PSORIASIS A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES
J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS
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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2003 by ICON Group International, Inc. Copyright 2003 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1
Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Psoriasis: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-83636-1 1. Psoriasis-Popular works. I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on psoriasis. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.
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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications. Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.
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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes & Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health
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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON PSORIASIS .................................................................................................. 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Psoriasis ...................................................................................... 11 E-Journals: PubMed Central ....................................................................................................... 79 The National Library of Medicine: PubMed ................................................................................ 80 CHAPTER 2. NUTRITION AND PSORIASIS ...................................................................................... 199 Overview.................................................................................................................................... 199 Finding Nutrition Studies on Psoriasis..................................................................................... 199 Federal Resources on Nutrition ................................................................................................. 206 Additional Web Resources ......................................................................................................... 207 CHAPTER 3. ALTERNATIVE MEDICINE AND PSORIASIS ................................................................ 211 Overview.................................................................................................................................... 211 National Center for Complementary and Alternative Medicine................................................ 211 Additional Web Resources ......................................................................................................... 237 General References ..................................................................................................................... 245 CHAPTER 4. DISSERTATIONS ON PSORIASIS .................................................................................. 247 Overview.................................................................................................................................... 247 Dissertations on Psoriasis.......................................................................................................... 247 Keeping Current ........................................................................................................................ 248 CHAPTER 5. CLINICAL TRIALS AND PSORIASIS ............................................................................ 249 Overview.................................................................................................................................... 249 Recent Trials on Psoriasis.......................................................................................................... 249 Keeping Current on Clinical Trials ........................................................................................... 257 CHAPTER 6. PATENTS ON PSORIASIS............................................................................................. 259 Overview.................................................................................................................................... 259 Patents on Psoriasis ................................................................................................................... 259 Patent Applications on Psoriasis ............................................................................................... 339 Keeping Current ........................................................................................................................ 355 CHAPTER 7. BOOKS ON PSORIASIS ................................................................................................ 357 Overview.................................................................................................................................... 357 Book Summaries: Federal Agencies............................................................................................ 357 Book Summaries: Online Booksellers......................................................................................... 358 The National Library of Medicine Book Index ........................................................................... 362 Chapters on Psoriasis................................................................................................................. 364 CHAPTER 8. MULTIMEDIA ON PSORIASIS ..................................................................................... 365 Overview.................................................................................................................................... 365 Video Recordings ....................................................................................................................... 365 Bibliography: Multimedia on Psoriasis...................................................................................... 366 CHAPTER 9. PERIODICALS AND NEWS ON PSORIASIS .................................................................. 369 Overview.................................................................................................................................... 369 News Services and Press Releases.............................................................................................. 369 Newsletter Articles .................................................................................................................... 375 Academic Periodicals covering Psoriasis ................................................................................... 380 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 383 Overview.................................................................................................................................... 383 NIH Guidelines.......................................................................................................................... 383 NIH Databases........................................................................................................................... 385 Other Commercial Databases..................................................................................................... 387 The Genome Project and Psoriasis ............................................................................................. 387
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APPENDIX B. PATIENT RESOURCES ............................................................................................... 393 Overview.................................................................................................................................... 393 Patient Guideline Sources.......................................................................................................... 393 Associations and Psoriasis ......................................................................................................... 407 Finding Associations.................................................................................................................. 410 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 413 Overview.................................................................................................................................... 413 Preparation................................................................................................................................. 413 Finding a Local Medical Library................................................................................................ 413 Medical Libraries in the U.S. and Canada ................................................................................. 413 ONLINE GLOSSARIES................................................................................................................ 419 Online Dictionary Directories ................................................................................................... 423 PSORIASIS DICTIONARY ......................................................................................................... 425 INDEX .............................................................................................................................................. 535
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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with psoriasis is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about psoriasis, using the most advanced research tools available and spending the least amount of time doing so. In addition to offering a structured and comprehensive bibliography, the pages that follow will tell you where and how to find reliable information covering virtually all topics related to psoriasis, from the essentials to the most advanced areas of research. Public, academic, government, and peer-reviewed research studies are emphasized. Various abstracts are reproduced to give you some of the latest official information available to date on psoriasis. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to psoriasis, these are noted in the text. E-book and electronic versions of this book are fully interactive with each of the Internet sites mentioned (clicking on a hyperlink automatically opens your browser to the site indicated). If you are using the hard copy version of this book, you can access a cited Web site by typing the provided Web address directly into your Internet browser. You may find it useful to refer to synonyms or related terms when accessing these Internet databases. NOTE: At the time of publication, the Web addresses were functional. However, some links may fail due to URL address changes, which is a common occurrence on the Internet. For readers unfamiliar with the Internet, detailed instructions are offered on how to access electronic resources. For readers unfamiliar with medical terminology, a comprehensive glossary is provided. For readers without access to Internet resources, a directory of medical libraries, that have or can locate references cited here, is given. We hope these resources will prove useful to the widest possible audience seeking information on psoriasis. The Editors
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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
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CHAPTER 1. STUDIES ON PSORIASIS Overview In this chapter, we will show you how to locate peer-reviewed references and studies on psoriasis.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and psoriasis, you will need to use the advanced search options. First, go to http://chid.nih.gov/index.html. From there, select the “Detailed Search” option (or go directly to that page with the following hyperlink: http://chid.nih.gov/detail/detail.html). The trick in extracting studies is found in the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Journal Article.” At the top of the search form, select the number of records you would like to see (we recommend 100) and check the box to display “whole records.” We recommend that you type “psoriasis” (or synonyms) into the “For these words:” box. Consider using the option “anywhere in record” to make your search as broad as possible. If you want to limit the search to only a particular field, such as the title of the journal, then select this option in the “Search in these fields” drop box. The following is what you can expect from this type of search: •
Bodily Suffering of Living With Severe Psoriasis: In-depth Interviews With 22 Hospitalized Patients With Psoriasis, The Source: Qualitative Health Research. 12(2): 250-61. February 2002. Summary: This journal article presents results from a qualitative study focusing on patients with severe psoriasis. Twenty-two hospitalized patients were interviewed in depth and shared their experiences of living with the disease. The interviews were consecutively analyzed according to grounded theory methodology. Bodily suffering emerged as a core variable in the data. Bodily suffering includes the following categories: the visible body, staying on an even keel, coping with an all-consuming disease, and social vulnerability. The results of this study indicate that the criterion for the management of psoriasis should be the patients' own perception of the consequences of the disease. 1 figure and 21 references. (AA).
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Treatment of Psoriasis: An Algorithm-Based Approach for Primary Care Physicians Source: American Family Physician. 61(3): 725-733. February 1, 2000. Contact: American Academy of Family Physicians. 11400 Tomahawk Creek Parkway, Leawood, KS 66211-2672. (800) 274-2237 or (913) 906-6000. E-mail:
[email protected]. Website: www.aafp.org. Summary: This journal article provides health professionals with information on the diagnosis and treatment of psoriasis. Although the primary cause of psoriasis remains unknown, abnormal epidermal cell kinetics and abnormal activation of immune mechanisms are thought to be the major contributors. Psoriasis is characterized by red, thickened plaques with a silvery scale. The lesions vary in size and degree of inflammation. Psoriasis is categorized as localized or generalized, based on the severity of the disease and its overall impact on the patient's quality of life and well being. The diagnosis of psoriasis can usually be made on the basis of the clinical presentation. If the diagnosis is uncertain, a biopsy can be performed or consultation with a dermatologist can be obtained. Once the diagnosis of psoriasis is made, patient education about the disease should begin. Points that should be emphasized about the disease initially include its noncontagious nature, the possibility of controlling but not curing it, and the factors that exacerbate the disease. In all cases, the therapeutic goal is to maximize treatment efficacy and the patient's quality of life while minimizing side effects. Topical therapy, including corticosteroids, calcipotriene, coal tar products, tazarotene, and anthralin, is the mainstay of treatment for localized disease. Psoriatic plaques that fail to respond to topical therapy may be improved by administration of intralesional corticosteroid injections. The patient who has refractory lesions may benefit from more advanced forms of treatment such as ultraviolet B alone or psoralens plus ultraviolet A; outpatient treatment at a clinic specializing in psoriasis; and systemic therapy with oral retinoids, methotrexate, or cyclosporine. Both physicians and patients need to understand that there is no definitive cure for psoriasis. 4 figures, 4 tables, and 17 references. (AA-M).
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Topical Psoriasis Therapy Source: American Family Physician. 59(4): 957-962. February 1999. Contact: American Academy of Family Physicians. 11400 Tomahawk Creek Parkway, Leawood, KS 66211-2672. (800) 274-2237 or (913) 906-6000. E-mail:
[email protected]. Website: www.aafp.org. Summary: This journal article provides health professionals with information on the efficacy and limitations of topical therapies used to treat psoriasis. Until recently, the mainstays of topical therapy have been corticosteroids, tars, anthralins, and keratolytics. Recently, however, vitamin D analogs, a new anthralin preparation, and topical retinoids have expanded the therapeutic armamentarium of physicians. Corticosteroids have anti-inflammatory, immunosuppressive, and antiproliferative properties. In general, mid-potency corticosteroids are used for lesions on the torso and extremities; low-potency corticosteroids are used for areas such as the face, genitals, or flexures; and high-potency corticosteroids are usually reserved for recalcitrant plaques or lesions on the palms of the hands and soles of the feet. Drawbacks of corticosteroid therapy include tachyphylaxis, skin atrophy, and adrenal suppression. Keratolytic agents help remove scales or hyperkeratosis. Salicylic acid is a commonly used keratolytic agent. Anthralin, which is available in ointment, cream, and paste forms, has been demonstrated to inhibit cell growth and restore cell differentiation. It is usually applied once daily at night and can be very irritating to normal skin. Coal tar appears to have
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antiproliferative and anti-inflammatory actions. However, it can cause contact allergy, and its use is limited by its inconvenience. Calcipotriene, a vitamin D analog, is generally well tolerated when applied twice daily. Like corticosteroids, calcipotriene can be considered a first-line agent and is available as an ointment, cream, or solution. Retinoids mediate cell differentiation and proliferation. Oral retinoids have many adverse systemic effects, so topical retinoids were developed to avoid many of them. Tazarotene, a topical retinoid, is rapidly metabolized in the skin and converted to tazarotenic acid. Local skin irritation and pruritis are frequent side effects. In addition, tazarotene may be teratogenic. 3 figures, 2 tables, and 26 references. (AA-M). •
Tazarotene, a Receptor-Selective Topical Retinoid, in the Treatment of Psoriasis Source: Today's Therapeutic Trends: Journal of New Developments in Clinical Medicine. 17(2): 133-145. 2nd Quarter 1999. Summary: This journal article provides health professionals with information on the use of tazarotene, a receptor-selective topical retinoid, in the treatment of psoriasis. Tazarotene is an acetylenic retinoid and prodrug of tazarotenic acid. A thin layer of tazarotene gel should be applied once daily in the evening to dry psoriatic plaques. Tazarotene normalizes keratinocyte differentiation, reverses keratinocyte hyperproliferation, and suppresses inflammation in treated plaques. Various studies have evaluated the effectiveness and safety of this agent, which has been shown to induce remission of psoriasis following the cessation of therapy. Although the drug is effective and well-tolerated as monotherapy, its efficacy can be further enhanced when it is used in combination with mid-or high-potency corticosteroids or ultraviolet B phototherapy. The combination of tazarotene and a mid-potency corticosteroid appears to be more efficacious than twice-daily dose of calcipotriene. Tazarotenic acid, the metabolite of tazarotene, has a short elimination half-life of 1 to 2 hours and does not accumulate in tissues. Very low plasma levels of tazarotene and its active metabolite have been detected, but treatment-related systemic adverse events have not been reported during clinical trials. Adverse effects, consisting primarily of dose-related local cutaneous itching, burning, erythema, and irritation, can be minimized with concurrent use of lubricants or medium-or high-potency corticosteroids. 1 table and 40 references. (Sum-M).
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Psoriasis: New Clues to Causation, New Ways To Treat Source: Patient Care. 33(9): 154-158,161-164. May 15, 1999. Summary: This journal article provides health professionals with information on the cause and treatment of psoriasis. This chronic, fluctuating, inflammatory skin condition ranges from mild to severe. The features of plaque psoriasis include circumscribed areas of thickening, redness, and overlying silvery scaling. Diagnosis is based on clinical examination. Patients who have mild, circumscribed psoriasis may be able to manage their symptoms with simple topical remedies. People who have more extensive skin involvement are likely to benefit from referral to a dermatologist or psoriasis specialty center. Medications available to treat psoriasis include traditional agents such as coal tar and anthralin preparations and topical corticosteroids, as well as newer agents such as the vitamin D derivative calcipotriene and the receptor-selective retinoid tazarotene. In addition, new topical options are in development or undergoing evaluation. Phototherapy with ultraviolet B (UVB) light remains the most widely used form of phototherapy. Trials of narrow-band UVB, which is expected to provide a significant advance, are under way. Photochemotherapy, which uses ultraviolet A light in combination with the photosensitizing agent and a psoralen compound, has been used
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successfully for more than 20 years. The main long-term concern of phototherapy is the development of squamous cell carcinoma and melanoma. Various systemic medications may be used to treat patients whose psoriasis does not respond to topical treatment or phototherapy. Systemic agents include methotrexate, oral retinoids, and cyclosporine. Many dermatologists try various different rotational programs to reduce the adverse effects and pharmacologic limitations associated with various agents and approaches. A long-term plan for disease management can also be helpful for patients. 8 figures and 13 references. •
New Topicals for Mild and Moderate Psoriasis Source: JAAPA: Official Journal of the American Academy of Physician Assistants. 12(4): 52-54,57-58,60. April 1999. Summary: This journal article provides health professionals with information on new topical agents for treating mild to moderate psoriasis. Although the cause of psoriasis is not clear, it is commonly accepted that a genetic predisposition combined with a triggering event such as skin trauma, psychologic stress, streptococcal infections, alcohol abuse, or ingestion of certain medications may initiate the process. Topical corticosteroids have been the mainstay of treatment because of their effectiveness, ease of use, and low cost. However, side effects limit their usefulness. Coal tar ointments and shampoos and anthralin also have unpleasant side effects. The limitations of these agents have led to the search for agents that can effectively relieve symptoms while avoiding the side effects and inconvenience of using them. The Food and Drug Administration approved the vitamin D analog calcipotriene and the vitamin A product tazarotene for topical treatment of psoriasis. Calcipotriene inhibits T lymphocyte proliferation. At 0.005 percent, calcipotriene is appropriate as a first or second line agent in moderate psoriasis. The drug has the efficacy of a medium potency topical corticosteroid. The ointment or cream is applied sparingly to the affected area twice a day for at least 2 to 6 weeks. Treatment may be continued for as long as 1 year. Side effects include hypercalciuria, hypercalcemia, and nephrolithiasis. The drug should not be used on the face or groin because of the risk of irritation. Tazarotene, a newly developed topical retinoid, targets retinoic acid receptors in the skin. The drug, which can be used for plaque psoriasis covering less than 20 percent of the body's surface area is applied in the evening. Several studies have demonstrated tazarotene's efficacy, which may be improved by combining it with a medium or high potency corticosteroid such as fluocinonide. The article provides guidelines on incorporating these new agents into patient care management. 1 table and 19 references.
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Koebner Phenomenon in Psoriasis Source: Postgraduate Medicine. 106(3): 39-40. September 1999. Summary: This journal article provides health professionals with information on the Koebner phenomenon in psoriasis. This phenomenon, which was first noted by Henrich Koebner in 1872, describes the appearance of new psoriatic lesions on otherwise normal skin in response to trauma. The phenomenon can be elicited by bites, burns, tattoos, lacerations, pressure, scratches, incisions, surgical scars, furuncles, vaccinations, sunburn, and radiation. Patients who have psoriasis should be cautioned to avoid preventable injury to the skin. The article presents the case of a 17 year old girl with a history of psoriasis since early childhood who experienced exacerbated disease on her elbows and knees and on her right lateral ankle at the site of a tattoo that had been applied a few months earlier. Following 1 month of treatment, her psoriasis improved 75 percent, but some disease activity remained on the extensor surfaces and the tattooed
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area. In this patient, the Koebner phenomenon that occurred in the recently tattooed area was identical in appearance to other lesions and was similarly resistant to certain treatments. 1 figure and 10 references. •
Corticosteroid-Induced Flare of Psoriasis: How to Control, Better Yet, Avoid Source: Postgraduate Medicine. 106(7): 31-32. December 1999. Summary: This journal article uses a case report to provide health professionals with information on corticosteroid induced flares of psoriasis. A 55 year old man who had a 25 year history of psoriasis experienced a generalized flare of the disease. Prior to the flare, the man had an exacerbation of asthma that was treated with systemic corticosteroids and prednisone. The prednisone dosage was started at 60 milligrams per day and tapered over 3 weeks. The man experienced a dramatic psoriasis flare during tapering. He was treated with the retinoid etretinate, emollients, and triamcinolone 0.1 percent cream. After 8 weeks, the psoriasis cleared completely, and clearance was maintained for a 6 month period using topical corticosteroids and low dose acitretin. Many genetic, environmental, and local factors can influence the pathogenesis of psoriasis. For example, as in this man's case, cessation of oral corticosteroids can trigger a severe flare or even cause progression to generalized pustular psoriasis. 2 figures and 8 references.
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Juvenile Psoriasis: Early Interventions Can Reduce Risks for Problems Later Source: Postgraduate Medicine. 103(4): 89-92, 95-96, 99-100. April 1998. Summary: This journal article for health professionals presents an overview of juvenile psoriasis. This skin disease is characterized by epidermal hyperplasia and greatly accelerated epidermal turnover. Lesions are usually discrete, erythematous papules and plaques covered with silvery scales. Lesions tend to be symmetric. Genetic, systemic, and environmental factors influence the course of psoriasis. Environmental factors, such as cutaneous trauma, drugs, low humidity, or stress, seem to be the most important in the course of juvenile psoriasis. It occurs in both sexes with nearly equal frequency. Estimates of total prevalence throughout the world range from 0.1 percent to 3 percent. Although the mean age at onset is 27.8 years, many patients were diagnosed before age 20. The guttate form of psoriasis is probably the most common in children. Many methods are available to treat psoriasis, including exposing the skin to sunlight and using topical preparations such as emollients and moisturizers, tar preparations, anthralin preparations, topical corticosteroid therapy, and vitamin D3 ointment. Systemic methods include cytotoxic antimetabolite drugs, photochemotherapy, and retinoids. However, these drugs are not safe for long-term use by infants and children. In addition, patient education is an important aspect of disease management. A totalcare approach is the optimal way of managing the disease. 6 figures, 3 tables, and 20 references.
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Psoriasis Drug Okay for Reproductive-age Women Source: Skin and Allergy News. 28(1):5; January 1997. Summary: This journal article for health professionals discusses the use of Soriatane for the treatment of severe psoriasis in women of childbearing age. This drug is a potential teratogen, so women must use reliable contraception while taking it and agree to avoid pregnancy for 3 years after therapy is completed. Other warnings and contraindications in the draft version of the drug's labeling deal with alcohol consumption and pregnancy
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testing prior to initiation of therapy. The manufacturer did not elaborate on plans for physician and patient education. •
Psoriasis: A Guide to Using Topical Therapy for Localized Disease Source: Consultant. 1171-1174,1177-1178,1180,1185; May 1997. Summary: This journal article for health professionals provides an overview of topical treatment options for localized psoriasis. Various topical agents help manage localized psoriasis, and they are also used as adjunctive therapy for widespread plaque psoriasis. Psoriasis localized to the trunk and extensors is usually treated with tar, salicylic acid, corticosteroids, anthralin, or calcipotriene. Topical corticosteroids or topical antifungals are the mainstay of therapy for facial skin psoriasis. These agents should be used in conjunction with moisturizing soaps, soap-free cleansers, and moisturizers. Topical corticosteroids, topical antifungals, and calcipotriene are useful for managing inverse psoriasis. Scalp psoriasis is generally treated with a combination of topical agents. Patients may benefit from using different kinds of shampoos, such as tars, selenium, zinc pyrithione, glycolic acid, salicylic acid, and ketoconazole. 1 reference, 9 figures, and 1 table. (AA-M).
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Nail Psoriasis Often Misdiagnosed as Onychomycosis Source: Skin and Allergy News. 28(10):32; October 1997. Summary: This journal article for health professionals reports on the misdiagnosis of nail psoriasis as onychomycosis. Nail psoriasis is difficult to diagnosis, and it may be caused by reactions to various irritants and allergens. A method of treating limited nail psoriasis is to inject triamcinolone acetonide into the proximal and lateral nail folds every four weeks until the nails are clear. In addition, other inflammatory nail conditions, such as alopecia universalis, can improve with intralesional injections. 1 photograph.
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New Treatment Options for Psoriasis Source: Dermatology Nursing. 9(5):295-306; October 1997. Summary: This journal article for health professionals is a continuing education offering on new treatment options for psoriasis. It discusses therapies for mild to moderate plaque psoriasis in terms of their side effects, efficacy, relapse rates, and cosmetic problems. Therapies include emollients, keratolytic agents, anthralin, calcipotriene, coal tar, and topical corticosteroids. A topical retinoid, tazarotene, is now available to treat mild to moderate plaque-type psoriasis. Its features, medical effectiveness, and side effects are presented. In addition, patient instructions for using tazarotene are provided. A multiple choice examination follows the article to test the reader's achievement of the article's educational objectives. 8 references, 12 figures, and 5 tables.
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Methotrexate Use in Psoriasis and Psoriatic Arthritis Source: Rheumatic Disease Clinics of North America. 23(4):797-809; November 1997. Summary: This journal article for health professionals discusses the use of methotrexate (MTX) in the treatment of psoriasis and psoriatic arthritis (PsA). It reviews studies on the efficacy of MTX therapy of psoriasis and PsA and on methotrexate-associated liver toxicity. Evidence shows that MTX is an extremely effective drug in treating these conditions, and it possesses a very high benefit-to-toxicity ratio compared with other therapies and immunosuppressive agents used in these disorders. Most adverse
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reactions related to MTX are mild, but serious and life-threatening reactions, particularly liver toxicity, may occur. Careful monitoring is needed to prevent most undesirable side effects. 75 references and 3 tables. (AA-M). •
Drugs for Psoriasis Therapy Target 'Killer' T Cells Source: Skin and Allergy News. 27(8):14-15. August 1996. Summary: This newsletter article for dermatologists treating patients with psoriasis discusses positive results of a new generation of immunosuppressive drugs that should be available before the end of the century. The author reports that some drugs target CD8 'killer' T cells which are found in large numbers in psoriatic epidermis while other drugs use synthetic T cell receptor peptides to destroy abnormal T cells or enhance T cell regulator activity. Clinical trials in 10 patients using CD8-acting drugs show clearing of disease in 4 patients and some clinical improvement in 4 others. Other approaches are using certain T cell receptor peptides as vaccines to prevent abnormal T cells from attacking the skin as well as to enhance T cell regulator activity, trying to restore the balance of activator and regulator cascades in psoriatic tissue. The article concludes with a discussion on psoriasis as multi-gene disease.
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Current Treatment Options in Psoriasis Source: Hospital Practice. 155-157,161-164,166; April 15, 1996. Summary: This journal article for health professionals presents an overview of psoriasis, a chronic scaly, inflammatory skin disease with relapsing and remitting course. The clinical features of various forms of psoriasis are described, focusing on plaque psoriasis, pustular psoriasis, guttate psoriasis, inverse psoriasis, and erythrodermic psoriasis. Other manifestations of psoriasis are highlighted. The pathophysiology of psoriasis is briefly explained. Topical and systemic treatments for psoriasis are discussed. The mainstays of topical treatment include emollients, corticosteroid ointments or creams, and calcipotriene ointment. Systemic therapies are used for patients with severe, extensive psoriasis who fail to respond to topical treatment. These therapies include ultraviolet B phototherapy, cyclosporine, and oral corticosteroids. New approaches to treating psoriasis are highlighted, including rotation therapy and the drug IL-2 fusion toxin. 3 figures and 4 tables.
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Treatment of Psoriasis With Polyethylene Sheet Bath PUVA Source: Journal of the American Academy of Dermatology. 35(2):208-210; Part one; August 1996. Summary: This journal article for health professionals describes a study that evaluated the safety and efficacy of sheet bath PUVA by restricting the volume of psoralen/bath water solution to 10 liters with the aid of a polyethylene sheet. Bath PUVA has been shown to be an effective alternative treatment for psoriasis with fewer systemic side effects than oral methoxsalen (8-MOP); however, the costs of 8- MOP and the need for a bath unit have prevented wider use of this treatment. Participants for the study were 58 patients with chronic plaque-type psoriasis who were treated with bath PUVA in a concentration of 0.5 milligrams of 8-MOP per liter of water. Results indicate that the group required a median of 17 baths for clearance. Patients with skin type II needed 14 baths, compared with 17 baths for patients with skin type III. Results demonstrate that even a low concentration of 8-MOP in bath water could be as effective as higher concentrations. Furthermore, with low concentrations, severe burns were absent and only mild erythema was observed in 6 of 19 patients with skin type II. Results also show
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that the total cost of the bath was reduced by 90 percent using the sheet bath method. 22 references and 1 table. (AA-M). •
Oral Lesions in Patients with Psoriasis: Clinical Presentation and Management Source: Journal of Periodontology. 71(12): 1896-1903. December 2000. Contact: Available from American Academy of Periodontology. Suite 800, 737 North Michigan Avenue, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: Psoriasis is a chronic inflammatory skin disease that rarely involves the oral cavity. In this article, the authors describe 2 cases, initially diagnosed with cutaneous psoriasis, that present with oral lesions on the attached gingiva (gums). The clinical appearance and differential diagnosis are presented and discussed. Case 1 describes the non surgical management of intraoral psoriasiform lesions and the use of a free gingival graft to restore an area of gingival recession resulting from an oral lesion. The second case outlines the use of topical corticosteroid therapy as an adjunct to non surgical periodontal therapy. Although patients with cutaneous psoriasis rarely present with oral involvement, the clinician should be aware that oral lesions may occur. Accurate diagnosis is dependent on a thorough clinical examination, a biopsy of the oral lesions, and a history of cutaneous psoriasis. 13 figures. 22 references.
•
Oral Mucositis with Features of Psoriasis: Report of a Case and Review of the Literature Source: Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics. 84(1): 61-67. July 1997. Summary: This article reports on an unusual case of oral mucositis with features of psoriasis and reviews the cases of oral psoriasis in the literature. The case reported involved a crusted lesion on the upper lip and erythematous lesions on the labial mucosa, buccal mucosa, and denture-bearing palatal mucosa. In addition, lesions resembling geographic tongue and ectopic geographic tongue were present. All lesions exhibited multiple small pustules. The review of the literature compares the distribution and clinical appearance of previously reported cases of oral psoriasis. 6 figures. 2 tables. 58 references. (AA-M).
•
Oral Psoriasis: Report of Six New Cases Source: Journal of Oral Pathology and Medicine. 24(1): 42-45. January 1995. Summary: This article presents six cases of oral psoriasis originally diagnosed by means of the histological changes found on biopsies of the oral lesions. Three of the patients presented with oral and skin psoriasis. Of the remaining three, two presented with oral manifestations alone, although their followup was short, while the third showed delayed dermatologic changes. Two of the cases were also complicated by psoriatic arthritis, one of them to the temporomandibular joint. 4 figures. 1 table. 23 references. (AA-M).
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Oral Psoriasis: Report of Case Source: Journal of Oral and Maxillofacial Surgery. 52(2): 185-187. February 1994. Summary: This article reports the case of a 39-year-old white man with oral psoriasis, a chronic, relapsing, inflammatory dermatologic disorder of the skin that occasionally involves mucous membranes. The authors describe the symptoms, diagnostic testing
Studies 11
done, and results. Additional discussion focuses on the histology of the man's condition; the three types of oral lesions seen in oral manifestations of psoriasis; the differential diagnosis; and the prognosis of psoriasis. The authors note that no specific form of therapy exists for oral psoriasis; treatment goals are generally directed toward palliation of symptomatic lesions. 3 figures. 11 references. •
Fissured Tongue in Generalized Pustular Psoriasis (editorial) Source: Archives of Dermatology. 129(10): 1346. October 1993. Summary: This letter describes 5 cases of fissured tongue in generalized pustular psoriasis. In pustular psoriasis, the tongue shows lesions that are clinically and histologically indistinguishable from geographic tongue. The author describes the series of five patients; four of five patients showed well-formed deep fissures that extended anteroposteriorly. Fissures extending laterally were also seen, but were superficial and less conspicuous. In one patient, fissues were more superficial and less marked than in the other four patients. All five patients had multiple smooth red patches of geographic tongue. The author concludes that fissured tongue is a fairly constant mucosal change in generalized pustular psoriasis. 1 figure. 4 references.
Federally Funded Research on Psoriasis The U.S. Government supports a variety of research studies relating to psoriasis. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to psoriasis. For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore psoriasis. The following is typical of the type of information found when searching the CRISP database for psoriasis: •
Project Title: INTERACTIONS
ANGIOSTATIN--MOLECULAR
MECHANISMS
AND
Principal Investigator & Institution: Sane, David C. Associate Professor; Internal Medicine; Wake Forest University Health Sciences Winston-Salem, NC 27157 Timing: Fiscal Year 2001; Project Start 30-SEP-1998; Project End 31-JUL-2003 Summary: (Adapted from Investigator's Abstract): Abnormalities in angiogenesis contribute to the pathogenesis of a variety of diseases including tumor growth and metastases, diabetic retinopathy, arthritis, psoriasis, and atherosclerosis. Angiostatin is a recently-discovered inhibitor of angiogenesis that has been shown to prevent the growth 2
Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
12 Psoriasis
and metastasis of experimental tumors. The goal of this proposal is to understand the molecular mechanisms by which angiostatin inhibits cellular growth and migration. Based on its striking homology with hepatocyte growth factor (HGF), a known inducer of angiogenesis, it is hypothesized that angiostatin may act as a competitive inhibitor of HGF, perhaps by binding, but not activating the c-met receptor. This hypothesis will be tested in cell proliferation and migration assays and with competitive cellular binding studies. Another potential mechanism of action of angiostatin involves its ability to displace plasminogen and thereby inhibit plasmin-mediated pericellular proteolytic activities, including the activation of procollagenases and the conversion of latent TGF-B to the active form. A final mechanism that to be examined is the potential ability of angiostatin to inhibit vitronectin-mediated haptotaxis, by disrupting urokinase receptor (UPAR) or integrin-mediated adherence of cells to this extracellular matrix protein. Recombinant vitronectin (wild and mutant forms) will be used to evaluate angiostatin's effect on VN-supported haptotaxis. Preliminary studies demonstrate that HGF (like angiostatin) binds to vitronectin. Domain deletion mutants of VN will be used to determine the VN binding site of HGF. The ability of angiostatin and HGF to compete for the same binding site on VN will also be examined using ELISA-based assays. By virtue of its ability to mediate haptotaxis and also approximate either pro or antiangiogenic factors close to the cell, VN may modulate angiogenesis. These studies will lead to a better understanding of the mechanisms of angiogenesis inhibition by angiostatin. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ASSEMBLY OF CORNIFIED CELL ENVELOPE IN TERMINALLY DIFFERENTIATED KERATINOCYTES Principal Investigator & Institution: Jarnik, Iichal; Brookhaven Science AssocBrookhaven Lab Brookhaven National Lab Upton, NY 11973 Timing: Fiscal Year 2001 Summary: Terminal differentiation of mammalian epidermal keratinocytes eventually creates a keratin filament matrix encased within a sheet of covalently cross-linked proteins called the cornified cell envelope (CE). Biogenesis of the CE is being studied in both normal and diseased states, e.g. psoriasis. - STEM measurements of mass/area on purified CEs allow one to evaluate their homogeneity and test for possible specialized areas within a given CE. CEs isolated from human epidermis (normal and psoriatic), mouse epidermis (normal and transgenic), other epithelia, and cultured keratinocytes are being studied. Several different methods of preparation have been examined since residual detergent between the CE's and the carbon substrate can affect mass measurements. The average thickness and mass/area of the mature envelopes are amazingly the same regardless of the tissue. Tliese results are helping to define the current model of CE assembly. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: ASSESSING FLUORESCENCE
PROTEIN
INTERACTIONS
IN
CELLS
BY
Principal Investigator & Institution: Clark, William A.; Pbl Biomedical Laboratories 131 Ethel Rd W, Ste 6 Piscataway, Nj 08854-5900, NJ 08854 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 30-JUN-2004 Summary: (provided by applicant): Interleukin-10 (IL-10) is a dominant molecule in anti-inflammatory and immunosuppressive pathways. The receptor for IL-10 consists of
Studies 13
two chains, IL-10R1 and IL-10R2. Despite a good deal of knowledge about the receptor components and signal transduction, no direct physical evidence has provided insight into the structure of the receptor on the cell surface in the presence and absence of ligand. By fusing blue and green fluorescent proteins (BFP, GFP and/or YFP/CFP) to the receptor chains and expressing them in cells, these fluorophores could be used to measure directly the interactions of the receptor chains on the cell surface in response to IL-10 by fluorescence resonance energy transfer (FRET). The specific aims are: 1) determine if the receptor chain pairs (specifically the R1 and R2 chains of the Interlerkin10 receptor) are pre-associated in the absence of ligand; 2) determine changes in receptor structure after engagement of ligand; 3) determine whether homotypic receptor chains are pre-assembled in the presence and absence of heterotypic chain and ligand, and 4) examine the potential for cross-talk between the IL-10 and IFN-gamma receptor complexes. The efficient accomplishment of these aims will not only provide a detailed understanding the Interleukin-10 receptor complex, but also will have ramifications for delineating the structure and dynamics of other receptors and for analyzing proteinprotein interactions, ligand-receptor interactions, signal transduction and many other cellular processes in live cells. Furthermore, questions relevant to protein interactions in cells that have been addressed indirectly should be able to be answered definitively with direct measurements by FRET and the time course of the events determined. In addition, applications to high throughput screening could be extensive not only for ligandreceptor interactions, but also for many cellular processes. This work has particularly strong potential to provide unique insights into the structural determinants that specifically underlie IL-10 receptor assembly, ligand binding, and signal transduction. IL-10 and the IL-10 receptor comprise a critical control point for a variety of antiinflammatory and immunosuppressive responses, the importance of which is underscored by the existence of IL-10 homologous sequences in certain viral genomes. The basic knowledge provided by this investigation coupled with the development of this FRET technology into a high-throughput screening approach for IL-10 receptor ligands may permit the discovery of novel peptide and non-peptide therapies for septic shock, graft survival, allergic inflammation, inflammatory bowel disease, psoriasis, and rheumatoid arthritis, among others. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: AUTOCRINE REGULATION OF KERATINOCYTES Principal Investigator & Institution: Piepkorn, Michael W. Professor; University of Washington Seattle, WA 98195 Timing: Fiscal Year 2001 Summary: The in vitro autocrine growth of human keratinocytes is principally attributable to the heparin-binding growth factors signaling through the epidermal growth factor receptor; amphiregulin and heparin-binding epidermal growth factor mediate most of this effect. Available evidence suggests that membrane heparan sulfate proteoglycans, such as splice variants of CD44V3, and cell density-dependent interactions with matrix beta1 integrin receptors regulate signaling. Moreover, heparan sulfate structure is modified during differentiation. Under the general hypothesis that the candidate regulatory mechanisms involving these molecules act to provide redundant control of autocrine cytokines, the specific hypotheses are: that endogenous CD44V3 isoforms, amphiregulin or heparin-binding epidermal growth factor, and epidermal growth factor receptor form a trimolecular signaling complex, wherein the CD44V3 heparan sulfate side chains act as multivalent templates to approximate the other reactants and to facilitate receptor oligomerization; that the complex is regulated
14 Psoriasis
by heterogeneity of heparan sulfate structure determined by the cell growth status; and that during the transition from migratory to stationary phenotype, relocalization of beta1 integrins correlates with alterations in cytolocalization and activity of the growth factors, which act to down regulate autocrine growth. The mechanisms by which heparan sulfates contribute to signaling will be investigated by determining binding constants of the cytokines to receptors, under conditions with and without blockade of heparan sulfate synthesis and in cell mutants defective in proteoglycan O-glycanation. Regulation of autocrine growth by heterogeneity of heparan sulfate structure will be tested by analyzing the structural motifs for the heparan sulfate side chains of recombinant and native isoforms of CD44V3 that correlate with growth arrest and with affinity for heparin-binding cytokines. Lastly, the effects of modulating alph-3-beta-1 integrin expression and localization on transcription, cellular distribution, processing, and juxtacrine activity of the membrane anchored cytokines will be characterized. The observation that amphiregulin is over- expressed in hyperproliferative disorders of the epidermis, including psoriasis, suggests that heparin-binding cytokines contribute pathophysiologically to up-regulated keratinocyte growth in neoplastic and nonneoplastic skin diseases. These considerations support the general objective to characterize the mechanisms of their signaling and the manner by which CD44V3 isoforms and beta-1 integrins regulate the process. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BIASED AUTOIMMUNITY
THYMIC
SELECTION
AND
CONSEQUENTIAL
Principal Investigator & Institution: Chervonsky, Alexander V. Staff Scientist; Jackson Laboratory 600 Main St Bar Harbor, ME 04609 Timing: Fiscal Year 2001; Project Start 20-APR-2001; Project End 31-MAR-2006 Summary: (Provided by the Applicant): The objective of this application is to study the connection between thymic-selection of a biased T-cell receptor (TCR) repertoire [due to expression of biased diversity of the complexes of peptides with Major Histocompatibility Complex (MHC) proteins] and organ-specific autoimmunity. Limitation of the MHC-peptide repertoire leads to diminished negative selection and gives a selective advantage to T-cells expressing receptors that have loose requirements for interactions with a specific peptide. Such receptors rely on other interactions (with MHC itself and especially with co-receptors) to achieve the level of signaling sufficient to allow T-cells to survive. If T-cells with such TCRs have autoreactive potential, they may be the cause of organ-specific autoimmunity after their egress from the thymus. We hypothesize that any strong bias of the repertoire of peptides bound to MHC molecules leads to imbalance in positive and negative selection allowing potentially autoreactive TCRs to slip through negative selection and trigger autoimmunity in the periphery. MM14.4 TCR transgenic animals have been made using TCR derived from a mouse with a restricted MHC-peptide repertoire. These mice develop severe autoimmunity in the forms of psoriasoform dermatitis (closely resembling human psoriasis) or lymphoid tissue-associated proliferative disease. The following specific aims will be pursued: I. Determine the mechanisms of selection of autoreactive T-cells produced in mice with a biased MHC-peptide repertoire. The role of MHC and co-receptors in selection of T-cells with autoreactive potential in mice with a constrained MHC-peptide repertoire will be studied. The frequency of selection of similar cells by biased peptide repertoire will be estimated. II. Elucidate the mechanisms of organ-specific autoimmune diseases caused by aberrant T-cell selection. General characterization of the autoimmunity in MM14.4 mice, the cellular components responsible for disease initiation and progression, and
Studies 15
target cells and antigens will be studied. The significance of the proposed research program is that it links together the expression of biased MEC-peptide repertoire, selection of altered T-cell repertoire, and resultant autoimmunity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BIOCHEMICAL PATHWAYS OF 12 HETE AND 12 KETE METABOLISM Principal Investigator & Institution: Rokach, Joshua; Professor & Director; None; Florida Institute of Technology Box 1150, 150 W University Blvd Melbourne, FL 32901 Timing: Fiscal Year 2001; Project Start 30-SEP-1992; Project End 30-NOV-2004 Summary: Psoriasis, asthma and inflammatory bowel disease (IBD) are characterized by a primary neutrophil and eosinophil infiltration at the inflammatory sites. 5-Oxo-ETE (5oxo-6E,8Z,11Z,14Z-eicosatetraenoic acid) is a potent activator of both neutrophils and eosinophils and among lipid mediators; it is the most active eosinophil chemoattractant so far tested. This raises the possibility that this compound is an important mediator of inflammation, especially in conditions associated with eosinophilia. The major focus of this application is the development of a variety of tools that will be used to investigate the biosynthesis, metabolism and physiological role of 5-oxo-ETE. A primary goal will be to synthesize affinity ligands and photoaffinity probes, based on 5-HETE, to permit the purification, labeling and ultimate cloning of 5-hydroxyeicosanoid dehydrogenase, the enzyme responsible for the formation of 5-oxo-ETE. Similar approaches will be used to develop affinity ligands related to 5-oxo-ETE. These will be used to characterize metabolic enzymes (5- oxo-eicosanoid-D6-reductase and 5-ketoreductase) as well as the 5-oxo-ETE receptor. We recently found that human platelets convert 5-oxo-ETE to a metabolite (5-oxo-12S-HETE) that antagonizes 5-oxo-ETE-induced calcium mobilization, and we propose to use this as a lead compound to develop more potent antagonists. Another major or goal is to investigate the metabolism of other oxo-eicosanoids, including 12-oxo-LTB4. We found that this compound is converted by keratinocytes in a highly stereospecific manner to a series of cysteinyl-containing metabolites c-LTB3, dLTB3 and e-LTB3, similar in structure to the potent cysteinyl-leukotrienes LTC4 and LTD4 and we propose to further investigate the mechanism for the formation of these compounds. In addition, we will investigate reductive pathways responsible for the conversion of 12-oxo-ETE to the potent proinflammatory agent 12-HETrE (12R-hydroxy5Z,8Z,14Z-eicosatrienoic acid). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: BIOLOGICAL FUNCTION OF BASONUCLIN Principal Investigator & Institution: Tseng, Hung; Dermatology; University of Pennsylvania 3451 Walnut Street Philadelphia, PA 19104 Timing: Fiscal Year 2001; Project Start 15-AUG-1996; Project End 31-MAR-2002 Summary: (Adapted from the applicant's abstract) - The long-term goal of the proposal is to understand the molecular regulatory mechanisms that maintain the cellular proliferative capacity and the signals that trigger the cells to cease proliferation. The principal investigator believes that understanding transcriptional regulation during the transition from proliferation to differentiation is an important step toward elucidation of these regulatory processes. The principal investigator has recently discovered a novel zinc finger protein, basonuclin. Basonuclin is present in the nuclei of keratinocytes in the proliferative compartment of epidermis and the germ cells in the seminiferous tubules of testis. The principal investigator hypothesizes that basonuclin is a transcription factor
16 Psoriasis
participating in the regulation of cellular proliferative potential (capability). Specific Aim 1 is to demonstrate that basonuclin is a DNA binding protein with sequence specificity. The approach is to select these targets from a pool of random sequences by electrophoresis mobility shift assay (EMSA) using zinc finger peptides. Specific Aim 2 will identify the genes whose promoters contain the basonuclin target sequence. The principal investigator aims to identify the genes that are controlled by basonuclin and thereby to understand the regulatory network in which basonuclin is a part. The principal investigator will search the DNA data base for promoters that contain the target sequence of basonuclin and to analyze the genomic fragments that are selected for their ability to bind to the bacterial produced full length basonuclin. Specific Aim 3 will map basonuclin's binding sites on mitotic chromosomes. The association of basonuclin with mitotic chromatin is highly unusual. The principal investigator aims to identify the mitotic chromosomes that contain basonuclin and to clone these binding sites, which may or may not be the same binding sites present on the bare DNA (lacking histones) that is studied in Aim 2. The virtue of molecules such as basonuclin in the study of biochemical and genetic regulation of cellular events is that it is a regulator that is also regulated. By studying it, the principal investigator expects to gain knowledge not only about basonuclin, but also about the regulatory hierarchy in which it is a part. The principal investigator believes that the proposed study of the biological function of basonuclin will enhance the knowledge about the molecular regulation of cellular proliferative potential. This knowledge is needed, he believes, to devise better medical treatment for proliferation-related abnormalities in the skin, such as cancer, psoriasis, and impaired wound healing. It is also essential for designing better culture conditions to produce large quantities of normal human cells for grafting and engineering purposes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BONE CELL REGULATION OF THE VITAMIN D RECEPTOR GENE Principal Investigator & Institution: Pike, J. Wesley. Professor; Biochemistry; University of Wisconsin Madison 750 University Ave Madison, WI 53706 Timing: Fiscal Year 2001; Project Start 01-JUL-1999; Project End 30-JUN-2003 Summary: Distinct signaling pathways exist for small lipophilic hormones such as the sex and adrenal steroids, thyroid hormone, and the vitamins A and D. These signaling pathways function to convey information from the cellular environment to the nucleus of the cell where they elicit unique transcriptional responses. Most cellular responses are initiated through interaction of a hormonal ligand with its unique receptor and culminate in receptor-mediated modifications in gene expression. Like other hormones, vitamin D is also capable of promoting both the differentiation of cells from precursors populations and regulating the expression of genes involved in differentiated cell function. The integration of these fundamental actions by vitamin D in target tissues likely accounts for its focal as well as global role as a calciotropic hormone. Since the ability of tissues to response to an external vitamin D stimulus revolves around the expression of the VDR gene, the goal of this project is to determine the molecular basis for its expression. We will focus on bone forming cells where the anabolic actions of vitamin D on both differentiation and differentiated-cell functions are well established. We will utilized primary human osteoblastic cells to establish the fundamentals of VDR regulation at the protein, mRNA, and transcriptional levels. We will focus upon basal expression of VDR as well as the gene's profile of inducibility by 1,25(OH)2D3 as well as bone relevant regulators such as PTH, retinoids, and glucocorticoids. While our efforts in these studies are directed towards bone cells, VDR expression studies will also be
Studies 17
carried out in intestinal-like HT-29 cells for comparison. Having established VDR expression and regulation in bone cells, the transcriptional component will be explored through an analysis of the activity and regulatory properties of the cloned human promoter for the VDR. We will use molecular approaches to identify determinants of both basal as well as inducible expression. We anticipate characterizing factors important to the expression and regulation of the VDR in bone cells such as PEBP2alphaA1/Cbfa1. Finally, we plan to prepare transgenic animals to assess the capacity of the cloned 4.0 kb hVDR promoter to direct faithful expression of firefly luciferase in bone cells and other tissues. Several additional mouse strains carrying mutant hVDR promoters will also be prepared to assess the role of specific cis elements. Our expectation is to more fully understand important determinants of human VDR regulation in bone cells as well as other cells at the transcriptional level. These determinants may be exploited together with novel vitamin D analogues in the treatment of bone diseases exemplified by osteoporosis and hypeproliferative diseases such as psoriasis and cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: C/EDB BETA AND CHOP IN EPIDERMAL DIFFERENTIATION Principal Investigator & Institution: Maytin, Edward V.; Cleveland Clinic Foundation 9500 Euclid Ave Cleveland, OH 44195 Timing: Fiscal Year 2001; Project Start 20-AUG-1998; Project End 30-JUN-2003 Summary: Mammalian skin is a vital organ that serves to maintain fluid and electrolyte balance, exclude toxins and pathogens, and participate in immune surveillance. These functions are largely attributable to the epithelial layer of the skin (the epidermis). Derangements in epidermal function in diseases such as psoriasis, or in environmental injuries such as exposure to ultraviolet light, result from abnormalities in the precise balance of keratinocyte proliferation and differentiation that constitute the normal epidermal differentiation program. This balance is regulated within cells at the level of gene transcription by a variety of transcription factors whose identities and mechanisms of action are only now being appreciated. This proposal will test the hypothesis that a relatively new family of nuclear transcription factors, the CCAAT-enhancer binding proteins (C/EBPs), plays an important regulatory role in epidermal differentiation. Based upon preliminary data that demonstrate the presence of C/EBPS in keratinocytes of the skin, both in vivo and in vitro, the proposed experiments will establish, in a causal manner, how two members of the C/EBP family (C/EBPbeta and CHOP) may be critical for the proper and orderly progression of the epidermal differentiation program. Stable keratinocyte cell lines, expressing doxycyline-inducible transgenes that encode both activators and inhibitors of C/EBPbeta and CHOP (including antisense RNA, and inhibitory protein isoforms of C/EBPs) will be studied in a calcium-dependent differentiation model in vitro. Alterations in parameters of growth and differentiation will be assayed after induction of the transgenes with doxycycline. As an in vivo correlate to these studies, stable keratinocyte lines will be grafted onto the backs of nude mice, to test for doxycycline-inducible changes in the epidermis formed at the graft site. Results of these studies may enhance our understanding of mechanisms that govern the switch from proliferation to differentiation, and in later events such as apoptosis, in the epidermis. These studies will build a foundation for later studies on the significance of observed changes in C/EBPbeta and CHOP expression in psoriasis and in skin exposed to UV light. Thus, changes in C/EBPbeta and CHOP-regulated gene expression are probably involved not only in the normal balance proliferation and differentiation in the
18 Psoriasis
epidermis, but also in epidermal disease and in responses of the skin to environmental injury. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CALCIUM, DIFFERENTIATION
S100
PROTEINS
AND
KERATINOCYTE
Principal Investigator & Institution: Eckert, Richard L. Professor; Physiology and Biophysics; Case Western Reserve University 10900 Euclid Ave Cleveland, OH 44106 Timing: Fiscal Year 2001; Project Start 03-MAY-2000; Project End 30-APR-2005 Summary: (Adapted from the applicant's abstract) - Calcium is the single most important regulator of keratinocyte differentiation. A major goal in keratinocyte biology is to understand how the calcium signal is transduced to drive keratinocyte differentiation. S100 proteins are an important class of protein that are required for calcium signal transduction. They are activated by a calcium binding-dependent conformation change, and then bind to and regulate the function of target proteins. The target proteins include regulators of cell proliferation and differentiation. Although keratinocytes express eight S100 proteins, little information is available regarding S100 protein function in keratinocytes. S100 proteins are thought to function as noncovalently associated homodimers. However, their recent study shows that the calcium-dependent enzyme, transglutaminase (TG), can modify S100 proteins by adding two interprotein covalent links, one linking each end of the antiparallel homodimer. They hypothesize that this regulates S100 function by altering the calcium-dependent conformation change. This hypothesis links transglutaminase, S 100 proteins, and calcium as components of a common regulatory unit. In this model, TG modification of S100 protein structure could provide a trigger to promote differentiation. The overall goals of this study are to characterize the S100 proteins expressed in keratinocytes with respect to (i) ability to act as a TG substrates and the effects of TG modification on function, (ii) subcellular and tissue distribution and the effects of physiological agents in this distribution, (iii) interaction with target proteins, and (iv) alteration in psoriasis. In preparation for these studies they have cloned cDNAs, expressed protein, and produced antibodies against S100A11, S100A10, and S100A7. They show that each of these proteins are TG substrates and in one case, S100A11; they identified the TG reactive sites by amino acid microsequencing. Their study is designed to provide new information on S100 protein function in keratinocytes. In Specific Aim 1, they clone, express, and generate antibodies to the remaining keratinocyte S100 proteins, S100A2, S100A4, S100A6, S100A8, and S100A9. These reagents are used (i) to determine whether these S100 proteins form TG-dependent covalent multimers in vivo and in cultured keratinocytes, (ii) to determine the structure of crosslinked products, (iii) to identify the amino acids involved in crosslink formation, and (iv) to study S100 protein function in psoriasis. The studies described in Specific Aim 2, are designed to determine whether TG-dependent modification of S100A11, their prototype S100 protein, alters its ability to interact with its target substrate, annexin I. This, they expect, will provide a direct test of their hypothesis that TG modification is a regulatory mechanism designed to alter S100 protein function. Localization can profoundly influence function. Their preliminary studies show that S100A11 is mobilized to the plasma membrane in response to calcium. In Specific Aim 3 they (i) use anti-S100 protein antibodies to localize the proteins in epidermis (normal and psoriatic), and in cultured cells, (ii) and examine the effects of physiological agents (calcium, etc.) on their subcellular distribution. S100 proteins transduce calcium signals by binding to target proteins; however, the targets are not known in keratinocytes. The goal of Specific Aim 4 is to identify these target proteins
Studies 19
using ligand blots, co-immunoprecipitation, affinity chromatography, and protein microsequencing. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CGMP DIFFERENTIATIONS
CHANNEL
ISOFORMS
AND
KERATINOCYTE
Principal Investigator & Institution: Mauro, Theodora M. Dermatology; University of California San Francisco 500 Parnassus Ave San Francisco, CA 94122 Timing: Fiscal Year 2001; Project Start 01-AUG-1997; Project End 30-JUN-2003 Summary: (Adapted from the applicant's abstract) - Calcium influx, required for keratinocyte differentiation, is enhanced by treatment with permeant cGMP. Moreover, the investigators have found a keratinocyte channel that is activated by cGMP. Finally, they have cloned complete and alternatively spliced isoforms of a cGMP channel that is similar to the calcium-permeable channel found in photoreceptor rod cells. The isoforms differ in their cGMP sensitivity, and their expression is unique in that it is developmentally regulated. The investigators hypothesize that this channel regulates keratinocyte differentiation through its role as cGMP-gated calcium influx pathway. The broad, long-term objective of these studies is to develop methods that modify keratinocyte differentiation by manipulating calcium influx into these cells. The healthrelatedness of the project stems from the fact that abnormal keratinocyte differentiation underlies common skin diseases, both benign; psoriasis, abnormal wound healing; and malignant: squamous cell carcinoma. Thus, new approaches to modifying cell differentiation would have wide clinical applications. The specific aims of the project are: 1) To correlate the exact proportion of each isoform with the degree of keratinocyte differentiation; 2) to compare channel characteristics in differentiating and undifferentiated keratinocytes; 3) to examine the channel's role in keratinocyte differentiation by overexpressing the native, alternatively spliced, or mutant isoforms in undifferentiated and differentiating keratinocytes. To accomplish these aims, the research design will first quantify the proportion of each isoform using the RNAse protection assay. Next, the functional difference conferred by the different isoforms will be examined by comparing 1) ion channel and whole cell current characteristics, using the patch clamp method; 2) calcium influx, using calcium-45 studies; and 3) intracellular calcium concentration, using Fluo-3 measurement. Finally, alteration of calcium influx and keratinocyte differentiation by overexpression of channel isoforms in keratinocytes will be tested. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CHARACTERIZATION OF THE MURINE WAVED 3 MUTATION Principal Investigator & Institution: Beier, David R. Associate Professor of Medicine; Brigham and Women's Hospital 75 Francis Street Boston, MA 02115 Timing: Fiscal Year 2001; Project Start 01-AUG-2000; Project End 31-JUL-2005 Summary: We have discovered a novel murine mutation which causes open eyes at birth and wavy hair. This phenotype is nearly identical to the waved 1 (wa1) and waved 2 (wa2) mutations. The gene affected in wa1 mice is transforming growth factor alpha (Tgfa), a widely expressed growth factor. Epidermal growth factor receptor (Egfr), the receptor for Tgfa, is mutated in wa2/wa2 mice. We mapped our waved mutation in an intercross and have localized it to proximal mouse Chr. 7. This shows that this mutation is not allelic with either wa1 or wa2, which map to Chr. 6 and 11 respectively, and we have designated it as waved 3 (wa3). The Tgfa/Egfr ligand/receptor pair has been
20 Psoriasis
investigated extensively; however, little is known about other genes that participate in the signaling process. Both of these genes are known to be over-expressed in many tumor cells, as well as in the skin disease psoriasis. While wa3 has not been proven to participate in the Tgfa signaling pathway, the phenotype is strikingly similar to wa1 and wa2. Furthermore, a number of studies of the biochemistry and genetics of Tgfa suggest that there are additional genes that function in the Tgfa signaling pathway. We suggest that the wa3 mutation is in such a gene, and propose experiments to test this hypothesis. Even in the case that wa3 is not in the Tgfa signaling pathway, its function is clearly important for normal development. We have been able to make considerable progress with respect to positional cloning of wa3. The wa3 non-recombinant interval has conserved homology with human chromosome 19q13.2, and the human genomic DNA corresponding to this interval has been nearly completely sequenced. Additionally, we have generated a complete mouse BAC contig across the wa3 interval. Analysis of the sequence in the region has already suggested several genes that can be characterized as candidates for the wa3 mutation. The combination of a positional cloning approach with a detailed characterization of the wa3 phenotype should provide insight into understanding genes that control normal skin development. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CHEMOKINE RECEPTOR STUDIES Principal Investigator & Institution: Richmond, Ann A. Professor; Cell and Developmental Biology; Vanderbilt University 3319 West End Ave. Nashville, TN 372036917 Timing: Fiscal Year 2001; Project Start 01-APR-1983; Project End 15-JUL-2002 Summary: (adapted from the investigator's abstract) Chemotactic cytokines, known as chemokines, modulate the inflammatory response, wound healing, tumorigenesis, angiogenesis, and pathogen entry into cells. Chemokine subfamilies are denoted based upon the structural presentation of the first two cysteine residues as CXC or CC. Chemokines exert their effects by binding to seven-transmembrane-G protein-coupled receptors and transducing intracellular signals which include activation of serine and tyrosine kinases and mobilization of calcium. Chemokine receptors (CXCR or CCR, depending upon the subfamily of chemokines the receptors bind) are present on leukocytes, endothelial cells, epithelial cells, melanocytes, macrophages, and dendritic cells. Disregulation of chemokine/ chemokine receptor expression is associated with a number of disorders: chronic inflammatory diseases such as rheumatoid arthritis, ARDS, and psoriasis, sepsis, angiogenesis associated with tumorigenesis, squamous cell carcinoma and melanoma. So that they might better understand the mechanism by which CXC chemokines regulate the immune response, wound healing and cell growth, they have partially characterized signal transduction through the CXCR2 receptor for CXC chemokines and the events involved in desensitization and sequestration of CXCR2. To further explore the hypothesis that CXC chemokines acting through CXCR2 regulate important events of cell migration, cell growth, and wound healing, they propose to more completely characterize the signal transduction pathway through CXCR2 and explore in vitro and in vivo models involving expression of gain and loss of function CXCR2 receptors in keratinocytes. There are three aims: 1) to develop in vitro and in vivo models to examine the biological consequence of gain or loss of function of CXCR2 receptors in the epidermis during wound healing; 2) to characterize the events which occur in response to ligand binding to CXCR2 which facilitate homologous/heterologous cross desensitization and CXCR2 sequestration; and 3) to characterize the role of tyrosine phosphorylation of pyk2, src, and p130CAS in the cell
Studies 21
motility responses mediated through CXCR2. Characterization of the events of signaling and receptor sequestration and desensitization will facilitate rationale drug design for disorders where sustained sensitivity to chemokines is essential for therapeutic efficacy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CHOROID PLEXUS SYNTHESIZED RETINOIC ACID REGULATION Principal Investigator & Institution: Mccaffrey, Peter; Eunice Kennedy Shriver Ctr Mtl Retardatn Waltham, MA 02254 Timing: Fiscal Year 2001; Project Start 01-SEP-1977; Project End 30-NOV-2005 Summary: (Adapted from applicant's Description) The transcriptional activator retinoic acid (RA) is essential for the normal development of the central nervous system. Defects in either the RA receptors or the enzymes that produce RA result in severe developmental abnormalities. The normal requirement for RA in development explain its teratogenicity and the use of RA for the treatment of acne, psoriasis, and leukemia renders this the most teratogenic compound in use. Disruptions in RA signaling have been suggested to be the basis of several congenital and toxin induced diseases, including Dandy-Walker and Arnold-Chiari malformations, as well as alcohol, dioxin, and PCB teratogenicity. Cerebellar malformations occur in all of these diseases and the investigators propose to study the cerebellar abnormalities in the mouse which result from the application of either an excess or insuffiency of RA. These conditions will be achieved by the use of RA receptor agonists and antagonists, chemical inhibitors of RA synthesis, and the use of viral vectors to misexpress RA synthesizing and catabolic enzymes. The investigators' preliminary data in migration as events that normally require RA. They plan to investigate the distribution of a transgenic reporter gene for RA signaling in the cerebellum; the influence of excess recep6tor ligand on cerebellar ligand on cerebellar development; and the influence of RA signal inhibition of cerebellar development. These results will assist in the identification of cerebellar events normally regulated by RA, as well as provide insights into the etiology of diseases that result from disruption of RA signaling. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: CLINICAL TRANSLATIONAL RESEARCH IN DERMATOLOGY Principal Investigator & Institution: Kang, Sewon; Associate Professor; Dermatology; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, MI 481091274 Timing: Fiscal Year 2001; Project Start 21-AUG-2000; Project End 31-JUL-2005 Summary: This application is in response to the Mid-career Investigator Award in Patient-Oriented Research (PA-98-053) which was created to support young, active and successful clinical investigators to overcome some of the major barriers to patientoriented research: time, resource and mentoring. Dr. Sewon Kang represents such a clinical researcher with years of specialty training and commitment to mentoring the next generation of clinical investigators. The objectives of this program are to further establish the candidate's independent patient-oriented clinical research program, especially in clinical translational research, and to provide him the time and resources necessary to mentor trainees pursuing clinical investigations in skin. The areas of activity of this project are Dr. Kang's research plan focused on therapeutic use of ultraviolet (UV)-A1 radiation in fibrosing skin diseases, effects of antioxidants in UVsignaling relevant to photoaging in human skin in vivo, and interleukin-10 in psoriasis, along with his plans for mentoring beginning clinical investigators. The three projects
22 Psoriasis
allow, in addition to the more traditional avenue of training in sound study design, execution, and analysis, opportunities for a novel avenue for training of clinical investigators to use tools required for reproducible observation and reliable documentation of molecular phenomenon relevant to human disease. The candidate has an established record of providing mentorship to pre- and post-doctoral trainees. Dr. Kang's research program will provide the context for him to continue to train beginning clinical investigators. His research and mentoring programs will be supported by the outstanding clinical research and training programs of the University of Michigan. These include the recently awarded institutional curriculum to teach the essentials of clinical research to young trainees and junior faculty (K-30), a well- funded General Clinical Research Center, the Center for Clinical Investigation and Therapeutics, educational program in Clinical Research Design and Statistical Analysis, and the School of Public Health. In summary, the candidate's expertise and accomplishments in patientoriented research, his ability and commitment to mentor beginning clinical investigators, and the research and training strengths of the University of Michigan combine to provide an ideal context to accomplish the specific aims of this proposal. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CO-FACILITATORS: NOVEL REGULATORS OF HORMONE METABOLISM Principal Investigator & Institution: Adams, John S. Professor; Cedars-Sinai Medical Center Box 48750, 8700 Beverly Blvd Los Angeles, CA 90048 Timing: Fiscal Year 2001; Project Start 01-SEP-2001; Project End 31-AUG-2005 Summary: The central hypothesis presented here holds that steroid hormone transit generally, and vitamin D metabolite transit specifically, into and within its metabolizing and/or target cell does not depend on the random movement of small, lipid-soluble, easily diffusible molecules. Rather, there exists a family of molecular chaperones that orchestrate the directional movement of vitamin D molecules to specific cellular destinations. It is proposed that this family of molecular shuttle proteins to be the hsp70-related intracellular vitamin D binding proteins (IDBPs) discovered in this laboratory. Confirmation of this central hypothesis requires that four corollary hypotheses be proved true: 1] IDBPs bind 25-hydroxylased vitamin D metabolites with sufficient capacity; 2] a favorable affinity gradient exists between and among intracellular binding proteins (i.e. megalin- bound serum vitamin D binding protein, other IDBPs, the vitamin- D-hydroxylases, vitamin D receptor) to facilitate the movement of ligand from one protein to the next; 3] a specific intermolecular interaction exists between the binding proteins that would narrow the diffusion distance for ligand exchange; and 4] altered expression of IDBPs must result in a definable effect on vitamin D metabolism or action. Specific Aim 1 will seek to prove that IDBPs are acceptor and delivery proteins for internalized vitamin D molecules by: 1] investigating the correlative traffic of fluorescently-labeled vitamin D metabolites and IDBPs within the cell; and 2] expanding our preliminary understanding of the specific intermolecular interaction of IDBPs with megalin and the vitamin-D-hydroxylases. Specific Aim 2 is designed to link the physical interactions described in Specific Aim 1 with a functional consequence by: 1] confirming that 1,25(OH)2D and 24,25(OH)2D production are dependent in part upon IDBP-directed delivery of substrate to the vitamin-Dhydroxylases; and 2] creating in vivo a transgenic mouse model of targeted overexpression of IDBP which recapitulates the functional observations made in vitro. It is anticipated that thus work will lay the foundation for an understanding of a previously unrecognized mode of control over the intracellular trafficking, metabolism
Studies 23
and action of sterol/steroid/retinoid/prostanoid hormones that is relevant to both human physiology and disease. Specifically, the current work will help to develop therapeutic strategies to counter common disease states that are worsened by vitamin D deficiency or resistance (i.e., osteoporosis) or that are improved or stabilized by enhancement of local vitamin D metabolite synthesis and action (i.e., leukemia, breast cancer, prostate cancer, psoriasis, etc.). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: COMPLEMENT INFLAMMATION
ANAPHYLATOXIN
RECEPTORS
IN
Principal Investigator & Institution: Wetsel, Rick A. Professor; None; University of Texas Hlth Sci Ctr Houston Box 20036 Houston, TX 77225 Timing: Fiscal Year 2001; Project Start 01-JUL-1987; Project End 28-FEB-2006 Summary: (provided by applicant): One of the major biological consequences of complement activation is the generation of three small cationic peptides C3a, C4a, and C5a, collectively referred to as complement anaphylatoxins. The complement anaphylatoxins are potent proinflammatory molecules that mediate numerous biological functions by binding to seven transmembrane G-protein coupled receptors expressed on specific target cells. The acute and chronic overproduction of complement anaphylatoxin peptides is considered to be a major contributor to the pathogenesis of numerous diseases, including rheumatoid arthritis, psoriasis, septic shock, myocardial ischemic injury, acute respiratory distress syndrome, and multiple system organ failure. The goal of this research program is to increase our understanding of the specific and overall roles that complement anaphylatoxin peptides and their receptors play in inflammation and immunity. During the next several years, the cellular expression and biological functions mediated by the C3a receptor will be examined in detail. In addition, the in vivo biological role of the C3a receptor will be studied and evaluated using a C3a receptor "knock-out" mouse in several well-characterized models of inflammation, infection, and autoimmunity. These studies will be accomplished by four major specific aims: 1) to determine the cells in peripheral blood and selected tissues that express the C3a anaphylatoxin receptor, and to delineate C3a mediated biological functions by cells expressing the C3a receptor, 2) to determine the effect of C3a receptor deficiency on pulmonary inflammation in established models of immune-complex injury, asthma, and bacterial infection and clearance, 3) to determine the effect of C3a receptor deficiency in the skin using established models of infectious dermatitis, immune-complex injury, and bullous pemphigoid, and 4) to determine the effect of C3a receptor deficiency in the peritoneum using established models of immune-complex peritonitis, acute septic peritonitis, and septic shock. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CONTROL OF MICROVASCULAR FUNCTION BY OXYGEN Principal Investigator & Institution: Jackson, William F. Professor; Biomedical Sciences; Western Michigan University 1903 W Michigan Ave Kalamazoo, MI 49008 Timing: Fiscal Year 2002; Project Start 31-OCT-1989; Project End 31-MAR-2007 Summary: (provided by the applicant): Blood flow to the body's organs and tissues is regulated to meet their metabolic demands. O2-dependent control of arteriolar tone has been implicated in this regulatory process for over a century. However, the cellular site where changes in PO2 are sensed, and how changes in PO2 are coupled to changes in arteriolar muscle tone remain unclear. Therefore, the overall aims of the research
24 Psoriasis
proposed are to 1.) identify the cellular location of the sensorthat mediates arteriolar O2 reactivity, and 2.) establish the mechanism of action of O2 on these microvessels. The focus of this proposal will be on arteriolar O2 reactivity, in the hamster cheek pouch, a common microcirculatory model. We are in a unique position to study arteriolar function in this tissue from the level of single ion channels in isolated arteriolar muscle cells in vitro, to responses of intact arterioles in the living microcirculation. The proposed studies will: acquire new information on the cellular location where changes in PO2 are sensed; establish the ionic basis of O2-induced changes in arteriolar tone; and improve our understanding of the mechanism of action of cysteinyl-leukotrienes (cysLTs) on arterioles in the microcirculation. These data will not only aid in understanding the basic physiology of blood flow regulation in the microcirculation, but may also provide new clues to the etiology or consequences of diseases that impact the microcirculation such as hypertension, diabetes, and atherosclerosis and well as diseases such as asthma, inflammatory bowel disease, psoriasis, renal disease, and eosinophilic inflammation in which cysLTs are implicated. The specific aimsof the research are to test five hypotheses concerning the site and mechanism of action of O2 on hamster cheek pouch arterioles. They are: 1. Cells that synthesize cysLTs (the signaling molecules that we propose mediated arteriolar O2 reactivity in the cheek pouch) are distributed, extravascularly along arterioles, 2. O2 and cysLTs depolarize, elevate [Ca2+], and contract arteriolar muscle cells by stimulating Ca2+ influx through L-type Ca2+ channels, which subsequently activate Ca2+-dependent Cl-efflux through Ca2+activated C1 about channels, 3. O2- and cysLT-induced depolarization and constriction are limited by activation of Ca2+activated K+ channels, 4. cysLTs initiate vasoconstriction that can be conducted along arterioles through an arteriolar muscle cell pathway and 5. 02-induced constriction is conducted along arterioles through an arteriolar muscle cell pathway. These hypotheses will be tested by integration of stateof-the-art methodologies including immunohistochemistry; laser scanning confocal microscopy; intravital videomicroscopy, ratiometric calcium measurements, enzymatic isolation of arteriolar muscle cells; single-channel and whole-cell patch clamp recording; and conventional microelectrode recording in cheek pouch arterioles from golden Syrian hamsters. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CYTOKINE NETWORKS IN PSORIASIS Principal Investigator & Institution: Lee, Edmund; Lab/Investigative Dermatology; Rockefeller University New York, NY 100216399 Timing: Fiscal Year 2003; Project Start 28-APR-2003; Project End 31-MAR-2008 Summary: (provided by applicant): Psoriasis is a common dermatosis affecting approximately 1-3% of the US population regardless of gender, age, ethnicity, or income group. Psoriasis is chronic, relapsing, and may be disabling. The presentation may be variable with some patients having only elbows and knees involved while others have 50% or more of their body surface area involved. Therapy depends on the severity of the disease. Treatment ranges from mild topical medications to potent parenteral drugs requiring hospitalization. Evidence implicates psoriasis as an immune disorder; mainly Th1. Activation of lymphocytes, as seen in psoriasis, results in interleukin-2 (IL-2) and interferon gamma (IFN-g) release. IFN-g interacts with many cell types and stimulates cytokine release. Ultraviolet light, in the 'B' spectrum, (UVB, 290-320nm) has been used for many years to treat psoriasis and is very effective, Evidence has demonstrated that UVB light is immunosuppressive and that a narrow portion of the UVB spectrum, 312nm or NB-UVB, is particularly effective. Data from our laboratory indicates that NB-
Studies 25
UVB light reduces the abnormally high levels of IFN-g expression in psoriatic skin as well as other genes regulated by IFN-g. For example, expression of IL-8 and IL-12 are reduced by NB-UVB. Our gene array data shows that the STAT1 gene, regulated by IFN-g, is modulated by NB-UVB. Our plan is to treat psoriasis patients with NB-UVB light, and then assess the cytokine and immune cell trafficking patterns in both skin and peripheral blood using RT-PCR, gene arrays, and immunohistochemistry. Current efforts towards new anti-psoriasis therapies focus on immunobiologics. For the near future, rotational-combination of new and old therapies will be the mainstay in treating psoriasis. Successful implementation of rotational-combination therapies depends on understanding molecular mechanisms of action. These studies will help us design rational rotational-combination therapies. In the future, individualized therapy, based on each patient's genetics, is the goal. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DERMAL ENDOTHELIAL INTERCELLULAR JUNCTIONS Principal Investigator & Institution: Kowalczyk, Andrew P. Assistant Professor; Dermatology; Emory University 1784 North Decatur Road Atlanta, GA 30322 Timing: Fiscal Year 2001; Project Start 15-AUG-1997; Project End 31-JUL-2002 Summary: This application for a Mentored Research Scientist Development Award is designed to provide the candidate with the opportunity to develop an independent area of research focusing on the molecular and cellular biology of dermal microvascular endothelial intercellular junctions. The research will be carried out at Northwestern University Medical School where the faculty have recognized expertise in the areas of intercellular junction assembly, endothelial cell biology, and dermatology. The formation of adhesive intercellular junctions by vascular endothelium is thought to be critical in the regulation of fluid balance between the plasma and tissue compartments. The loss of this barrier function of endothelial cells is a prevalent feature in numerous pathologies that involve inflammation and edema, and in the skin, this psoriasis and dermatitis. In addition, endothelial intercellular junctions may be regulated during angiogenesis and may provide control over endothelial cell migration into a wound area. Two types of approaches will be taken to investigate endothelial junction assembly. First, specific components of the junctions will be expressed in fibroblasts to reconstitute complexes that may form between proteins during junction assembly. This approach will allow for the identification of protein-protein interactions that can be further investigated using purified proteins in vitro. Secondly, mutants of the endothelial junction proteins will be expressed in endothelial cells to specifically inhibit the function of the endogenous protein and identify the role of each protein in junction assembly. By analyzing mutants that inhibit endothelial junction assembly, the impact of improper junction formation on endothelial cell function will be determined. Emphasis will be placed on understanding how endothelial junctions influence the ability of endothelial cells to function as a barrier to fluid and solutes and how endothelial junctions may regulate migration. It is anticipated that the results of this study will provide fundamental information regarding the altered behavior of endothelial cells in various cutaneous disorders that involve inflammation, edema, or angiogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DERMATOMYOSITIS SKIN DISEASE SEVERITY MEASURE VALIDATION Principal Investigator & Institution: Jorizzo, Jospeh L. Dermatology; Wake Forest University Health Sciences Winston-Salem, NC 27157
26 Psoriasis
Timing: Fiscal Year 2002; Project Start 05-SEP-2002; Project End 31-JUL-2004 Summary: (provided by applicant): Dermatomyositis is an inflammatory myopathy of unknown cause accompanied by a characteristic cutaneous eruption. Despite the frequently debilitating severity of the skin involvement, most studies have focused on the muscle disease and no controlled studies have been done to study systematically the skin disease in dermatomyositis or its treatment. This is in part due to the lack of standard methods for evaluating the skin involvement of dermatomyositis. Validated measures that can be used to judge the severity of skin involvement of patients with dermatomyositis and to evaluate and compare different therapies are not available yet. The purpose of this study is to validate a dermatomyositis skin disease severity measure (DSSI) developed based on the Psoriasis Area and Severity Index (PASI), to determine the clinical significance of changes in the DSSI, and to collect data on the expected effect size and variability of two common treatments. The hypothesis is that a modified version of the psoriasis severity measure can be used to accurately measure the severity of skin disease in patients with dermatomyositis. The successful completion of the study will permit future studies that assess the effectiveness of different treatments for dermatomyositis skin disease and provide data that could be used for power analysis calculations for designing future full-scale studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DEVELOPMENT INSTRUMENTATION
OF
BIOELECTRIC
FIELD
IMAGING
Principal Investigator & Institution: Nuccitelli, Richard L. Professor; Rpn Enterprises, Inc. 144 Carroll St New Britain, CT 06053 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JAN-2004 Summary: (provided by applicant): We have known for over a century, that human skin drives ionic current out of regions where the integrity of the epidermis has been breached (DuBois-Reymond, 1843,Ann.Phys.U.Chem.58:1) DuBois-Reymond used one of the earliest galvanometers to measure 1 uA leaving wounds in his skin. This has been confirmed using modern techniques and we now know that this current is driven out of the wound by the transepithelial potential generated across the epidermis by the apicalbasal transport of Na+. As this wound current traverses the epidermis it generates a local electric field that points towards the wound from all directions around it. While we know that wound currents exist, we do not know the local electric field strength that they generate as they move through the skin. It is this electric field that can influence wound healing by moving molecules by electrophoresis or attracting cells by galvanotaxis. Our goal is to measure this wound field in vivo. This field has been measured near guinea pig skin wounds but never in humans (Barker et al., 1982,Am.J.Physiol. 242:R358). Our company has been developing a new instrument called the Bioelectric Field Imager (BFI) that will be able to measure these lateral fields non-invasively. Just as the EKG can provide information about heart disease by measuring voltages between the limbs, the BFI technique provides information about skin disease. This will have many important applications to improving human health including the design of new electrical therapies for healing chronic wounds and possibly the early detection and diagnosis of skin diseases such as melanoma and psoriasis. Our Specific Aim is to adapt a prototype, BFI device to non-invasively measure the skin surface potential distribution in the region surrounding mammalian skin wounds. We will optimize vibration amplitude, distance between skin and probe, and signal averaging. We will introduce scanning capabilities that allow the two-dimensional mapping of the surface potential distribution around a skin wound. Finally we will
Studies 27
determine the reproducibility of the device by laboratory bench testing on well-defined mammalian wounds. This instrument will allow us to compare the endogenous fields near normally healing wounds with those near chronic wounds in order to determine if there are differences that might be reduced by electrotherapy. This technique also has the potential for early detection and diagnosis of various skin diseases including melanoma and psoriasis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DEVELOPMENT OF POTENT YET SAFER ANTI-INFLAMMATORY AGENTS: VIA MUTUAL PRODRUG APPR Principal Investigator & Institution: Mclean, Hugh M.; Hampton University E Queen & Tyler Sts Hampton, VA 23668 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2006 Summary: (provided by applicant): Chronic inflammatory diseases affect approximately 10% of the U.S. population. Although both anti-inflammatory steroids (glucocorticoids) and non-steroidal antiinflammatory drugs (NSAIDS) are routinely used to provide palliative therapy for many of these maladies, there is still a distinct paucity of "safe" and effective drugs, particularly for long term therapy of many inflammatory diseases such as asthma, psoriasis, ulcerative colitis and rheumatoid arthritis. Glucocorticoids are usually considered to be the drugs par excellence for relieving inflammatory symptoms, however their therapeutic use is restricted due to their propensity to elicit potentially serious adverse effects, particularly their suppressive effects on pituitary function and the immune system. The main thrust of the proposed study is the development of anti-inflammatory steroids with diminished penchant to elicit untoward systemic effects, via the mutual prodrug approach. To this end, the primary strategy is to incorporate a metabolically labile moiety, a carboxylic acid ester, into the steroid molecule (prednisolone), which would undergo facile systemic biotransformation to the less active and more readily excretable steroidal carboxylic acid. Such steroid acid esters have been dubbed antedrugs. To further enhance the topical potency and local/systemic activity ratios of these antedrugs, they will be conjugated via an ester linkage to selected NSAIDS (such as ibuprofen and indomethacin) at the 21-position of the glucocorticoids. Conjugates such as these have been dubbed mutual prodrugs, primarily because it is conceivable that upon administration, they would be biotransformed into the glucocorticoid and the NSAID, both of which could conceivably exhibit synergistic antiinflammatory activity. The results of these studies should establish axiomatically if the conjugation of glucocorticoids that are "antedrugs", and NSAIDS, is a fundamentally sound synthetic ploy in the development of potent yet safer anti-inflammatory steroids. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: INHIBITORS
DEVELOPMENT
OF
TOPICAL
NEUROINFLAMMATORY
Principal Investigator & Institution: Sachdeva, Mandip S. Professor; Pharmaceutical Sciences; Florida Agricultural and Mechanical Univ Tallahassee, FL 32307 Timing: Fiscal Year 2001; Project Start 01-SEP-2001; Project End 31-MAY-2006 Summary: (taken from the application?s abstract): There is increasing evidence that through the release of neuropeptides the cutaneous sensory neurological system plays an important role in the pathogenesis of inflammatory skin disorders. Certain skin diseases such as psoriasis, contact dermatitis and atopic dermatitis may have a significant neurogenic component. The hypothesis to be tested by the proposed research
28 Psoriasis
is that certain topically-delivered neuromodulators will prove to be effective therapeutic agents for the treatment of a wide range of inflammatory skin diseases. Thus, the longterm objective is to develop topical agents with novel anti-inflammatory activities. Specifically, agents such as calcitonin-gene-related peptide (CGRP), alpha-melanocyte stimulating hormone (alpha-MSH), substance P receptor (SPR) antagonists such as spantide II (peptide molecule) and SR 140333 (a non-peptide), which have antiinflammation properties or inhibit various aspects of neurogenic inflammation will be utilized as topical compounds to treat well-defined models of cutaneous inflammation. The specific aims of this research proposal are: Aim #1) The preparation of topical formulations (gels, creams and lotions) of neuromodulatory agents using prototype topical vehicles and screening these formulations for antiinflammatory effects in an animal model of cutaneous inflammation. Studies designed under this aim include formulation of topical agents (gels, creams and lotions) of neuromodulators and screening of these formulations for anti-inflammatory activity in a murine contact hypersensitivity model; Aim #2) The development, evaluation and optimization of various topical neuromodulatory formulations, which have shown promise in Specific Aim #1) Development of topical formulations includes compatibility and stability of neuromodulators in topical vehicles. The stable formulations will be optimized by ex vivo skin absorption and distribution studies in hairless mouse skin using Franz diffusion cells and; Aim #3) To determine the effectiveness of topically applied neuromodulatory agents to inhibit cutaneous inflammation. This will be accomplished by utilizing well-defined murine models of cutaneous inflammation such as allergic contact dermatitis, irritant contact dermatitis and acute photodermatitis. The effect of topical formulations on cutaneous inflammation will be compared with that of intravenous administration of these peptides. The results of these studies are intended to provide the basic information required for the development of novel skin disorders. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DEVELOPMENTAL PROGRAMS OF CELL CYCLE CONTROL Principal Investigator & Institution: O'farrell, Patrick H. Professor; Biochemistry and Biophysics; University of California San Francisco 500 Parnassus Ave San Francisco, CA 94122 Timing: Fiscal Year 2002; Project Start 01-JUL-1986; Project End 30-JUN-2006 Summary: (provided by applicant): The control of cell proliferation is important in normal growth and development, and its disruption has health consequences extending from psoriasis to cancer. Cell doubling involves a myriad of events, all accurately coordinated to avoid genetically destabilizing errors that can be oncogenic. The discovery of master cell cycle regulators, which was recognized in this year's Nobel Prize in Medicine, provided insight into mechanism and new avenues of drug design to target cancer cells. However, the links from the master regulators to cell biological events are largely unknown. In addition to triggering cell cycle transitions from one phase to the next, the master regulators appear to govern individual events in the cell cycle, defining when the events occur and enforcing the coordination required for accuracy. Our cell cycle studies in the model organism Drosophila have uncovered previously unrecognized regulatory roles of the cyclins. The mitotic cyclins are well known as activators of cyclin dependent kinase 1 (Cdk1) and as inducers of mitosis. Our results suggest that the accuracy of chromosome segregation at mitosis depends on an increase in the stability of kinetochore attachment to the spindle. This change, which occurs at the transition to anaphase, depends on the timely destruction of cyclin B. Similarly, cytokinesis follows destruction of cyclin B, which otherwise inhibits it. In
Studies 29
contrast, cytokinesis occurs in the presence of stable cyclin B3 despite persistence of a spindle and condensed chromosomes. Maintenance of the G2 phase of the cell cycle requires a catalytically repressed cyclin/Cdk1 complex, which, we propose, may specify this cell cycle state by acting as a protein ligand to influence other activities. Disruption of the controls that we are investigating results in segregation and replication defects resembling anomalies that are prominent in cancer cells. We will use genetic and cell biological tools to define the new regulatory pathways and will then pursue their biochemical dissection. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DIFFUSION OF DILUTE NANOFABRICATED CHANNELS
FLUORESCENT
MOLECULES
IN
Principal Investigator & Institution: Hess, Samuel T.; Cornell University Ithaca Office of Sponsored Programs Ithaca, NY 14853 Timing: Fiscal Year 2001 Summary: We propose to evaluate two-photon microscopy of BPD-MA to study subcellular localization under a variety of conditions. Benzoporphyrin Derivative is a second-generation photosensitizing compound currently undergoing phase II clinical trials for use in treating psoriasis, age-related macular degeneration as well as cutaneous oncology. Previous research has demonstrated that this drug is a potent sensitizer, with efficacy in cell killing demonstrated at concentrations below 200 ng/ml. Its primary subcellular target is believed to the mitochondria, where it has been demonstrated that BPD-MA can photodynamically uncouple oxidative phosphorylation in the isolated rat mitochondria. Our initial experiments have sought to optimize twophoton microscopy for observation of this drug. The two-photon cross section of BPDMA in a liposomal preparation has recently been measured from 820-980 nm. Having measured the cross section, we will be able to evaluate a detection threshold that will then be ve rified in adherent cell culture. Organelle localization studies have been outlined are expected to proceed in the near future. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ENDOTHELIAL LATERAL JUNCTIONS AND LEUKOCYTE EGRESS Principal Investigator & Institution: Goldberg, Peter L.; Brigham and Women's Hospital 75 Francis Street Boston, MA 02115 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2006 Summary: (provided by applicant): A critical event during an inflammatory response is the recruitment of blood leukocytes to the site of injury, immune response, or infection, resulting in transendothelial migration (TEM). Dysregulation of the inflammatory response is a factor in many diseases, such as inflammatory bowel disease (IBD), rheumatoid arthritis, atherosclerosis, asthma, and psoriasis. The TEM of leukocytes from the vasculature into the neighboring tissues has been studied extensively. However, there is limited information regarding the endothelium-dependant mechanisms that may contribute to leukocyte egress at endothelial cell (EC) lateral junctions. The focus of this application is to examine leukocyte egress at endothelial cellcell junctions, concentrating on the mechanisms that allow the rapid formation of interendothelial cell, claps by VE-cadherin during leukocyte TEM. Throughout this study we will make use of the a variety of in vitro molecular, biochemical, immunological, and biological techniques, including adenoviral constructs, fluorescence recovery after photobleaching and leukocyte TEM in flow chamber assays. Specifically, we will
30 Psoriasis
determine the 1) the lateral mobility of wild type VE-cadherin and a tailless mutant VEcadherin in vascular endothelium and 2) examine the lateral mobility of these proteins during leukocyte TEM. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EPIDERMAL COMMITMENT
STEM
CELL
MATURATION
AND
LINEAGE
Principal Investigator & Institution: Ambler, Carrie A.; Cancer Research - United Kingdom 44 Lincoln's Inn Fields London, Timing: Fiscal Year 2003; Project Start 15-MAR-2004 Summary: (provided by applicant): The epidermis is continually shed and replenished throughout life. Maintenance of the epidermis is dependent on a stem cell population found in the basal layer of the epidermis. These stem cells self-renew and contribute progenitors called transit amplifying cells. Stem cells and the subsequent transit amplifying cells contribute to multiple lineages of terminally differentiated cells including hair follicle cells, sebocytes, and interfollicular epidermal cells. Although it is clear that epidermal stem cells contribute to all three lineages, the role of transit amplifying cells in lineage commitment remains unknown and largely uninvestigated. The purpose of this proposal is to use in vitro and in vivo methods to investigate if transit amplifying cells contribute to one or multiple lineages. Specifically, the aims are to determine if human neonatal foreskin cultures can make sebocytes and hair follicle proteins, and to use this system to investigate the lineages that develop from a single transit amplifying cell. Additionally, the role of c-Myc and 13-catenin in lineage commitment of transit amplifying cells will be investigated, and using the BOLAP retroviral library, the fate of transit amplifying cells in vivo will be mapped. The process of stem cell maturation is essential to maintain the skin, and disruptions in the stem cell differentiation process have pathological implications in cancer, psoriasis, acne, and hair loss. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: FIVE DOSE TRIAL OF ABX IL8 IN TREATMENT OF SEVERE PLAQUE PSORIASIS Principal Investigator & Institution: Krueger, Gerald G.; University of Utah 200 S University St Salt Lake City, UT 84112 Timing: Fiscal Year 2001 Summary: ABX-IL-8 is a humanized monoclonal antibody generated in transgenic mice. The antibody has a high affinity for IL-8, and can neutralize IL-8, as demonstrated in several assay systems. The antibody inhibits binding to neutrophils, inhibits IL-8induced calcium flux, and inhibits MAC-1 expression, elastase release, and chemotaxis. Dr. Krueger did the developmental work for this protocol by demonstrating in an experimental system that unaffected skin from patients with psoriasis, grafted onto nude mice, generated psoriasis-like lesions when IL-8 was injected. This effect was totally blocked by administering ABX-IL-8. These animal data suggest that an antibody against IL-8 might be an effective method of treating plaque-phase psoriasis. From the study done on the GCRC, safety of the drug was determined, and then appropriate dosing ranges established. The drug proved remarkably effective in the treatment of plaque-phase psoriasis, and a manuscript describing the beneficial effects of this therapy is now in preparation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: FREQUENCY OF MIF GENE POLYMORPHISM AND CUTANEOUS EXPRESSION Principal Investigator & Institution: Kang, Insoo; Yale University 47 College Street, Suite 203 New Haven, CT 065208047 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2004 Summary: This is a new application for a YSDRCC pilot/feasibility grant from a clinically trained rheumatologist without NIH fundings who now seeks a financial support to initiate his research in determining Mif gene polymorphisms and cutaneous expression of MIF in patients with systemic lupus erythematosus (SLE). The mucocutaneous system is affected in 85% of patients with SLE. An important concept in the pathogenesis of SLE is that there is an intrinsically heightened state of T lymphocyte responsiveness that contributes to sustained T cell activation and autoantibody production. These events lead to recruitment and activation of inflammatory cells, such as macrophages, and subsequent tissue destruction in inflammatory sites. Several studies showed the requirement of macrophages in the development of murine lupus nephritis, suggesting an important role of macrophages as a pro-inflammatory migration inhibitory factor (MIF) is a pro-inflammatory cytokine secreted from monocytes, macrophages and T cells and has a pivotal, upstream role in activation of macrophages and T cells. Recently, a study identified promoter polymorphisms of the Mif gene that comprises the tetranuclotide repeat sequence (CATT)5-8. In rheumatoid arthritis (RA), a systemic autoimmune disease like SLE, a study showed that patients with RA had a decreased frequency of a single 5-CATT allele (lowest Mif expression), which was even lower in RA patients with mild disease. This suggests a potential role of Mif in the pathogenesis of T cell- and marcrophage-mediated autoimmune inflammatory diseases such as SLE and RA. Of interest, in psoriasis, an increased level of MIF was found in the skin and serum, suggesting a role of MIF in inflammatory skin diseases. Furthermore, a study showed induction of MIF in the skin by UVB, which is a well-known environmental factor for SLE. Based on these observations, a hypothesize that patients with SLE have increased expression of MIF, as a result of genetic predisposition, that promotes macrophasge-mediated inflammation and possibly T cell activation will be tested. To investigate this hypothesis, the following will be done. First, define the frequency of low- and high-expression Mif alleles in patients with SLE and correlate them with plasma MIF levels and disease activity. Second, determine the expression of MIF in skin lesions from patients with SLE and discoid lupus. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: FUCOSYLTRANSFERASE INHIBITORS WITH THERAPEUTIC POTENTIAL Principal Investigator & Institution: Magnani, John L.; Glycotech Corporation 14915 Broschart Rd, Ste 200 Rockville, MD 20850 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 31-MAR-2002 Summary: (applicant's abstract): Fucose-containing oligosaccharides are well documented to mediate important cell adhesion and cell communication events Including, trafficking of leukocytes, cancer metastasis, and host pathogen interactions. Blocking adhesion events involving fucosylated oligosaccharides represents a viable approach to the treatment of diverse indications such as chronic inflammatory disease and ulcers. One way to accomplish this is to prevent the synthesis of the carbohydrates themselves. A family of fucosyltransferases that are expressed in a tissue and cell type specific manner carries out attachment of fucose to carbohydrates. Thus, inhibition of a
32 Psoriasis
specific fucosyltransferase has the potential to be a highly selective method of disrupting cell adhesion events mediated by fucose containing carbohydrates. The proposed research is directed to characterizing the specificity and cell permeability of three new classes of fucosyltransferase inhibitors with in vitro IC50 values as low as 68 nM. Unlike previously reported inhibitors based on donor and acceptor substrates, they are uncharged, non-carbohydrate small molecule organic compounds. These inhibitors provide the basis for development of potent orally available fucosyltransferase inhibitors with potential for treatment of chronic inflammatory disease. PROPOSED COMMERCIAL APPLICATION: The fucosylated oligosaccharide sialyl-Lewis X is a key mediator of leukocyte trafficking in conditions of chronic inflammation. Thus, inhibitors of the fucosyltransferase FucT-VII are anticipated to be effective in treatment of chronic inflammatory conditions such as rheumatoid arthritis, multiple sclerosis and psoriasis. Each of these conditions comprises major unmet medical needs and has the potential for mufti-billion dollar markets. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: FUNCTIONAL ANALYSIS OF VEFZ1, A NOVEL ENDOTHELIAL MARKER Principal Investigator & Institution: Stuhlmann, Heidi; Associate Professor; Scripps Research Institute 10550 N Torrey Pines Rd San Diego, CA 920371000 Timing: Fiscal Year 2001; Project Start 04-FEB-2000; Project End 31-JAN-2004 Summary: The mammalian vascular system develops by two distinct processes, vasculogenesis and angiogenesis. Formation on the vascular system during embryogenesis from the lateral plate mesoderm and the extra embryonic mesoderm of the visceral folk sac is under complex genetic control, as suggested by the identification of a number of mutations in mice that affect its development. We have identified a novel gene, Zezf1, that we hypothesize is a key regulator of these processes. The gene, identified using retroviral entrapment vectors in murine ES cells, encodes a protein consisting of six zinc finger domains and is homologous to the human transcription factor, DB1. During embryogenesis, Vezf1 is expressed specifically in vascular endothelial cells, the cells that line the blood vessels, and in their precursors in the yolk sac blood islands. In adults, Vezf1 expression is primarily confined in the quiescent vascular endothelium, but is strongly up-regulated during angiogenesis and in response to vascular injury. The goal of this proposal is to understand the role of Vezf1 during blood vessel development. This will be accomplished using gain-of function and loss of function studies. Wild-type and dominant-negative mutants of Vezf1 will be generated and their effects in ES cells and on vasculogenesis and angiogenesis in transgenic mice will be investigated. In addition, the Vezf1 gene will be knocked-out in ES cells and in mice to study the consequences of its loss on these processes. Specifically, we will: 1. Investigate the function of VEZF1 as a transcription factor. 2. Determine the role of Vezf1 in vasculogenesis and angiogenesis using transgenic mice expressing gain-of function and dominant-negative mutations of Vezf1. 3. Determining the consequences of the loss of Vezf1 on mouse development using Vezf1 knock-out mice. These results will impact our understanding of the molecular mechanisms governing normal and abnormal processes of vasculogenesis and angiogenesis. These include congenital cardiovascular abnormalities and pathological conditions such as rheumatoid arthritis, retinopathies, hemangiomas, psoriasis, solid tumors and metastases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GANGLIOSIDE GENE MODULATION EFFECT ON CELL MOTILITY Principal Investigator & Institution: Paller, Amy S. Head; Children's Memorial Hospital (Chicago) Chicago, IL 606143394 Timing: Fiscal Year 2001; Project Start 01-MAY-1998; Project End 30-APR-2003 Summary: (Adapted from the applicant's abstract) - Human keratinocyte motility on fibronectin is critical in the reepithelialization of healing wounds and in the spread of cutaneous malignancy. The molecular events that influence this migration are poorly understood. Supplemental GT1b, a polysialyated ganglioside of keratinocytes, inhibits migration of keratinocytes on a fibronectin matrix at nM concentrations. Dr. Paller and colleagues propose that gangliosides modulate the alpha 5 beta 1/fibronectin interaction, probably by direct interaction with alpha 5 beta 1. The hypothesis is supported by the findings that: a)GT1b inhibition of keratinocyte migration occurs only on a fibronectin matrix; b)RGDS peptide competes with GT1b to inhibit cell adhesion to fibronectin; c)Preincubation of GT1b with the fibronectin matrix does not alter keratinocyte binding to the fibronectin; d)GT1b induces apoptosis of keratinocytes only when grown on a fibronectin matrix; e)FAK phosphorylation in response to fibronectin is decreased when keratinocytes are treated with GT1b; f)GT1b fails to inhibit the migration and proliferation of SCC13 and HaCaT cells, which have decreased expression of alpha 5 beta 1; and g)TGF-beta 1 increases HaCaT cell expression of alpha 5 beta 1, and induces cells to respond to the inhibitory effects of GT1b on adhesion to fibronectin. Dr. Paller and colleagues will explore the physiologic significance and mechanism(s) of the ganglioside action on epidermal cells by these specific aims: 1. Modulate the expression of ganglioside biosynthetic pathways by stable transfection of glycosyltransferase genes into a keratinocyte-derived line. In order to shift the endogenous production of gangliosides, including increasing expression GT1b, GalNAc transferase and sialyltransferase genes, driven by a progesterone antagonist-inducible system, will be transfected individually into SCC12 cells, a keratinocyte-derived GT1bresponsive cell line. 2. Examine the effects of changes in ganglioside expression on migration, adhesion, induction of apoptosis, and integrin signalling in cultured cells. The investigators will note changes in morphology, proliferative potential, apoptosis, and wound healing capability in an ex vivo transplantation model. They will also develop transgenic mice to study the effects of altered ganglioside content on proliferation, differentiation, and wound healing of normal keratinocytes in vivo. 3. Assess the mechanism of ganglioside inhibition of the alpha 5 beta 1/fibronectin interaction: The ganglioside/alpha 5 beta 1 interaction will be investigated in both a cellfree system using recombinant alpha 5 and beta 1 proteins, and with alpha 5 beta 1 immunoprecipitated from the transfected SCC12 cells. Dr. Paller will ask the following questions: a)Do gangliosides, including GT1b, bind directly to alpha 5 beta 1?; b)Do gangliosides interfere with alpha 5 beta 1 assembly?; c)Do gangliosides downregulate the expression of alpha 5 beta 1?; and d)Do alterations in ganglioside content affect membrane fluidity and thus the orientation of integrin receptors? Understanding the effect of gangliosides on the fibronectin-integrin interaction may lead to modulation of glycosyltransferase activity in normal or neoplastic keratinocytes as a novel therapeutic modality for treatment of chronic wounds, cutaneous neoplasia, and hyperproliferative epidermal disorders such as psoriasis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GENERAL CLINICAL RESEARCH CENTER Principal Investigator & Institution: Chobanian, Aram V. Director, Cardiovascular Institute; Medicine; Boston University Medical Campus 715 Albany St, 560 Boston, MA 02118 Timing: Fiscal Year 2001; Project Start 01-DEC-1978; Project End 30-NOV-2001 Summary: The General Clinical Research Center (GCRC) at Boston University School of Medicine is at the center of an effort to enhance clinical research at one of the best medical centers in the country in terms of clinical and basic research, clinical services and education programs targeted to the inner city. The Center is located in the new Boston Medical Center which is a full asset merger of Boston City Hospital and Boston University Medical Center Hospital. In addition, the Hospital and the Medical School have joined together with eight community health centers to form Boston HealthNet. The General Clinical Research Center supports inpatient and outpatient research services, specialized laboratories and a clinical research training program for physician scientists in Medicine, Surgery and Pediatrics. The facility provides investigators with: 1) the ability to conduct pharmacokinetic studies in a controlled environment in both adult and pediatric subjects; 2) the resources for timed collections of specimens and repetitive tests (e.g. echocardiograms, stress tests, bone density etc.); 3) the expertise to conduct esoteric laboratory testing and evaluation; 4) professionals to assist with statistical design and data analysis; 5) a private environment to explore patterns of behavior and 6) the location of education for future clinicians in patient oriented research. In conjunction with the new Office of Clinical Research at the Medical School, the Center plans to expand services to investigators including pharmacist support, state of the art PCR assays, and data management. Efforts are underway to afford inner city high school and college studies, as well as MD and MD-PhD students, an opportunity to see and learn about the exciting role clinical research plays in human health and disease. The Medical School will cost share in this expansion. The Center serves national recognized researchers focusing on the health of the inner city by studying AIDS in children and adults, hypertension in blacks, diabetes in Caribbean Latinos, hemoglobinopathies, substance abuse, angina in the elderly and maternal and child development. Bench to bedside research is being conducted in the Center on EBVassociated malignancies, nociception in newborns. Interleukin 16 in asthma, second generation active vitamin D analogues in psoriasis and immunotoxins for treating leukemia and lymphomas. In a changing health delivery system, the unique partnership of the Medical School, the Hospital and the Boston HealthNet provides a community driven urban health network that affords continued access to a patient population. The General Clinical Research Center is the place for NIH funded researchers to do bench to bedside research and physician scientists to address the full spectrum of health issues facing individuals living in the city. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GENETIC ANALYSIS OF PSORIASIS Principal Investigator & Institution: Bowcock, Anne M. Professor; Genetics; Washington University Lindell and Skinker Blvd St. Louis, MO 63130 Timing: Fiscal Year 2001; Project Start 01-JAN-1998; Project End 31-JAN-2002 Summary: (Adapted from the applicant's abstract) - Psoriasis is a complex disease that affects approximately 2% of the population. It results in abnormal proliferation of immature keratinocytes and recruitment of T cells to the dermis and epidermis. This results in three major features: induration, scaling, and erythema. A variety of novel
Studies 35
proteins have been identified in psoriatic skin that include pro-inflammatory cytokines, adhesion molecules, HLA-DR, keratins, and alteration in the cellular distribution of integrins. The mode of inheritance of psoriasis is complex, although a familial component is now accepted as a result of twin studies, sib pair studies, the identification of large numbers of multiply affected families, and more recently, by evidence for linkage to particular chromosomal regions in some families. The applicants previously provided strong evidence for linkage to the distal end of chromosome 17q. HOMOG estimates indicated that the disease is genetically heterogeneous. A second study recently showed evidence for linkage of psoriasis to chromosome 4 (near D4S1535) in five families from Ireland. In both of these studies, psoriasis susceptibility behaves as an autosomal dominant trait with high penetrance. There is also an autoimmune component to psoriasis, and Cw6 carriers are at 15-fold higher risk of disease. The applicants now propose to localize additional genes conferring susceptibility to psoriasis by performing a genome-wide linkage screen on 250 sib pairs and 27 multiply affected families. Markers will be selected at 3 cM intervals, and genotyping will be performed using an ABI 377. This will require the generation of 1,300,000 genotypes over 3 years (approximately 450,000 per year). Susceptibility loci will be identified by parametric and nonparametric means with GENEHUNTER. Regions where p<0.01 will be analyzed further by collaborators in an additional 250 sib pairs. The applicants will refine potential susceptibility regions with closely linked markers. The results of this study should be the localization of additional psoriasis susceptibility genes to defined regions of the genome. In the last year of funding any highly promising candidate genes in these regions will be screened for alterations in affected individuals from linked families and in sporadic cases. When alterations are found, they will be screened for in 100 unrelated controls to determine the possibility of their contributing to the development of psoriasis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENETICS OF LUPUS-RELATED AUTOIMMUNITY IN HUMANS Principal Investigator & Institution: Moser, Kathy L. Assistant Professor; Medicine; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, MN 554552070 Timing: Fiscal Year 2001; Project Start 20-SEP-1999; Project End 31-AUG-2003 Summary: The possibility that different autoimmune phenotypes might share particular genetic linkages has been bolstered by a meta-analysis of the available data (Becker, et al, PNAS 95:9979-9984, 1998). In addition, our collection of pedigrees multiplex for systemic lupus erythematosus (SLE), as a clinical disease, contain many members who do not have lupus, but who do have autoimmune findings. Examples include lupusrelated positive serology and other disorders thought to be autoimmune in origin such as myasthenia gravis, rheumatoid arthritis, scleroderma, Sjogren's syndrome, psoriasis, and diabetes. Recently, we published the results of a genome scan using clinical lupus as a phenotype (Moser, et al. PNAS 95:14869-14874, 1998). In 94 pedigrees studied, there are 223 confirmed SLE affecteds and 594 family members, 17 percent of who report the presence of another autoimmune disorder and over 30 percent with positive autoimmune serology. In classic work, Bias and coworkers (Am J Hum Genet 39:584602, 1986) have shown that pedigrees ascertained on lupus and evaluated using humoral autoimmunity as an intermediate phenotype segregate this trait in an autosomal dominant pattern. We propose to use our now larger collection of pedigrees multiplex for SLE as a basis from which to seek evidence for the predicted autosomal dominant linkage as well as for other genetic effects. We will use our currently available collection of 173 pedigrees containing 1300 individuals to: 1) evaluate for a Lupus-
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Related Autoimmune (LRA) phenotype, 2) seek linkage, and 3) perform fine mapping in regions providing evidence for linkage. Identification of genes that govern the propensity to develop autoimmunity has potential to provide important insight into mechanisms of etiology and pathogenesis that are common among multiple autoimmune diseases. Understanding these underlying pathological events will lead towards new opportunities for development of more effective mechanism-based therapeutic strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HOKT3 GAMMA 1 (ALA ALA) MONOCLONAL ANTIBODY FOR PSORIATIC ARTHRITIS Principal Investigator & Institution: Clark, Marcus R.; University of Chicago 5801 S Ellis Ave Chicago, IL 60637 Timing: Fiscal Year 2001 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: HOW AUTOIMMUNITY?
DOES
BLOCKADE
OF
CD40/CD40L
PREVENT
Principal Investigator & Institution: Von Herrath, Matthias G. Associate Professor with Tenure; La Jolla Institute for Allergy/Immunolgy Allergy and Immunology San Diego, CA 921211118 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 31-JUL-2006 Summary: (provided by applicant): All three projects of the consortium application are targeted at better understanding induction of long-term tolerance by costimulation blockade of CD40/CD40L interactions with aCD40L antibody. We believe that this immune-based intervention is one of the most promising and attractive approaches currently in clinical trials for several autoimmune disorders. Many of these ongoing interventions (psoriasis, transplantation etc.) show much promise and only one trial had to be stopped due to deleterious side effects (enhanced blood clotting), which was likely caused by the antibody preparation or too high dosages, since it did not occur in other clinical studies. Although it is known that CD40-CD40L interactions are required for dendritic cell maturation and activation, as well as generation of effector lymphocytes, many mechanistic issues remain unresolved. The most crucial of these will be tackled by the three projects united in the present U-19. Effects on lymphocyte differentiation and effector functions (Sarvetnick), T cell proliferation, differentiation and APC-trafficking (Miller) and induction of regulatory APCs or lymphocytes able to down-modulate aggressive autoimmune responses antigen specifically (von Herrath) will be studied by the single components. In addition to analyzing differential effector mechanisms, three distinct models for autoimmune diseases will be utilized (Sarvetnick, NOD; Miller, EAE; von Herrath, RIP-LCMV). This multi-focal approach will result in a more rapid and thorough understanding of a CD40L induced immune modulation and/or suppression. Furthermore, paradigms or discoveries applicable to a human situation should ideally be validated and tested in various animal models. Therefore, the direct comparison of three autoimmune models will enable us to define, which in vivo consequences of costimulation blockade occur more commonly and which are restricted to a given experimental situation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: HUMAN LYMPHOCYTE ACTIVATION--ROLE OF DENDRITIC CELLS Principal Investigator & Institution: Steinman, Ralph M.; Rockefeller University New York, NY 100216399 Timing: Fiscal Year 2001 Summary: Dendritic cells are a trace subpopulation of white blood cells. When antigens are presented on dendritic cells to the immune system, strong immune responses are induced. Methods have been developed to isolate dendritic cells from human blood, inflamed joints and skin. We use dendritic cells to study different aspects of the immune response in transplantation, arthritis, psoriasis, and resistance to tumors and infectious disease (influenza, AIDS). Our aims include: a) Develop monoclonal antibodies and DNA probes to cell surface and intracellular constituents of dendritic cells. b) Outline the range of inflammatory cytokines and cytokine receptors that are made by dendritic cells from blood and from diseased tissues. c) Clone T cells that may mediate autoreactivity in rheumatoid arthritis and psoriasis, and protective immunity in tumors, influenza, and AIDS. d) Study the transmission of a cytopathic infection with the AIDS virus from dendritic cells that have been exposed to the virus (HIV-1) to CD4+ T cells. Compare dendritic cells isolated from blood, skin, and inflammatory sites. Test the effect of different types of immune T cells and anti-HIV antibodies on this transmission. Generate HIV-specific immune T cells of both CD4 and CD8 subsets. Evaluate the effects of immune T cells on HIV-infected monocytes. e) Develop methods for generating large numbers of dendritic cells from immature progenitors, and use these to present antigens from tumors and infectious agents (influenza, HIV-1) to human T cells. f) Evaluate mechanisms whereby dendritic cells present superantigens to T cells, including attempts to identify superantigens that may be carried by dendritic cells in autoimmune disease. g) Evaluate in human allogeneic bone marrow chimeras the ontogeny and kinetics of dendritic cell engraftment, the role of dendritic cells in immune reconstitution, and the identification of dendritic cell progenitors and conditions supporting their growth. h) Use dendritic cells to generate antigen-specific cytolytic T lymphocytes (CTLs) to viral, tumor, and auto antigens. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ICM3 IN SUBJECTS WITH SEVERE PSORIASIS Principal Investigator & Institution: Ling, Mark; Emory University 1784 North Decatur Road Atlanta, GA 30322 Timing: Fiscal Year 2001 Summary: This is a placebo controlled dose escalation study to determine the safety, pharmacology, and immunogenicity of ICM3 when administered as an IV infusion compared to placebo in psoriatic disease and sensitization to a hapten antigen. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: IL-20 EXPRESSION AND FUNCTION IN SKIN Principal Investigator & Institution: Eynon, Elizabeth E.; Yale University 47 College Street, Suite 203 New Haven, CT 065208047 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2004 Summary: Interleukin-20 (IL-20) is a recently discovered cytokine which bears significant homology to IL-10, IL-19 and IL-24. IL-20 was first identified in keratinocytes but its functions are still largely unknown. Transgenic mice over-expressing IL-20
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exhibit a skin disorder very similar to psoriasis. In addition, the receptor for IL-20 is over expressed in human psoriasis, indicating that it is involved in the pathology of this common autoimmune disease. Phase II clinical trials are already underway using exogenous IL-10 to suppress autoimmunity in psoriasis patients. In contrast, IL-20 may enhance autoimmune responses in skin or directly influence keratinocyte growth in psoriatic lesions. In collaboration with Regeneron, we have developed an IL-20 knockout mouse* to test whether IL-20 is crucial for normal skin development and immune function. The initial aim of the pilot study will be to obtain data on the expression of IL-20 in mice using mRNA analysis, and the expression pattern of a LacZ gene knocked into the murine IL-20 sequence will be prepared and screened for use in western blot and FACS analysis. The data should validate our rationale for investigating the role of IL-20 in psoriasis and its potential as a novel target for therapy. *The IL-20 knock out mice to be used in these future experiments will be generated from IL-20 deficient embryonic stem cells provided by Regeneron Pharmaceuticals, Inc., subject to an in accordance with the terms of the Research Collaboration Agreement currently in effect between Dr. Richard Flavell, Yale University and Regeneron, on a nonexclusive basis as reasonably available for these studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: IMMUNOPATHOGENESIS OF PSORIASIS Principal Investigator & Institution: Nickoloff, Brian J. Professor; Pathology; Loyola University Medical Center Lewis Towers, 13Th Fl Chicago, IL 60611 Timing: Fiscal Year 2001; Project Start 20-JUN-1989; Project End 31-AUG-2003 Summary: (Adapted from the applicant's abstract) - Psoriasis is a common and enigmatic skin disease causing significant morbidity. No cure is available and current treatments provide only temporary relief associated with various side effects. Two major obstacles (one conceptual and one technological) have hindered progress in understanding and treating this complex cutaneous disorder. First, there has been great dispute as to whether psoriasis is fundamentally a disease of the immune system or keratinocyte. Undoubtedly, multiple factors contribute to the pathophysiology of psoriasis. However, there is now compelling evidence that the T lymphocyte is a key and central causal agent of psoriasis. Second, there has been no suitable animal model for studying the disease. This deficiency has now been overcome by an engraftment of human skin onto immunodeficient (SCID) mice. After transplantation, symptomless skin can be converted into full-fledged psoriatic plaques by injection of activated, autologous T cells derived from the blood of psoriatic patients. The hypothesis to be tested is that psoriasis is mediated by a specific subset of pathogenic T lymphocytes from the blood, which when activated and upon entrance into skin trigger proliferative responses by endothelial cells and keratinocytes. The long-term goal is to phenotype and genotype the pathogenic T cell responsible for causing psoriasis. The novel SCID mouse model engrafted with human skin will be used throughout the project In the first aim, requirements for T cell activation will be determined. In the second aim, causation of psoriasis by CD4+ or CD8+ T cells and a requirement for preferential expression of T cell receptor Vbeta repertoire will be examined. The third aim concerns establishment of pathogenic T cell lines and cell clones. The final aim will identify differentially expressed mRNA in pathogenic and regulatory T cells and psoriatic keratinocytes. The applicants expect that these studies will enhance our understanding of the causation of psoriasis and provide a basis for developing new and more effective treatments for this common and chronic disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: IMMUNOPATHOGENESIS OF PSORIASIS Principal Investigator & Institution: Kupper, Thomas S. Professor and Chair; Brigham and Women's Hospital 75 Francis Street Boston, MA 02115 Timing: Fiscal Year 2001 Summary: Psoriasis affects 2% of the world's population. Very recently, it was appreciated that psoriasis has many features of an autoimmune disease, and a pathogenic paradigm that implicates activated skin homing T cells responding to an as yet unknown epidermal antigen(s) has emerged. In support of this paradigm, it is clear that all effective treatments for psoriasis have T cells as their targets. Skin directed therapies, including UVB and PUVA, directly induce apoptosis of intraepidermal T cells, while systemic therapies such as low dose methotrexate and cyclosporin target activated T cells throughout the body. More recently, a number of clinical trials have been initiated that use novel immunomodulatory agents such as CTLAIg, DAB-IL-2, anti-CD40L, and LFA3-TIP. Because the prominent immunological component of psoriasis was only recently appreciated there are large gaps in our knowledge about the immunopathology of this disease. In this proposal, we hypothesize that psoriasis is mediated by a recirculating population of CD8+, CLA (cutaneous, lymphocyte antigen) + effector T cells that become activated in epidermis in response to autoantigen. In aim 1, we propose to compare the VbetaCDR3 spectratype profile of lesional psoriatic CD8+ (CD25+) T cells with the analogous profile found in the CLA+ CD8+ fraction of peripheral blood. It is predicted that substantial overlap will exist. In aim 2, using epidermal antigen as well as anti-CD3, we will isolate and expand clones of putative disease related (as well as unrelated) CD8+ T cells form both blood and epidermis. In our third aim, we will use an established SCID/Hu model, involving non-lesional psoriatic skin grafted onto SCID mice, to test whether putative disease related clones can induce a psoriatic phenotype in vivo. Using this model, we will also test the efficacy and mechanism of action of both anti CD40 ligand and LFA- 3TIP in treating psoriasis. Finally, in our fourth aim we will perform transcriptional profiling on T cells (including candidate disease related clones) and epidermal cells from psoriasis patients and from normal patients in an effort to carefully assess differences between these populations. The long term goal of this research is to better understand the nature of immune response underlying psoriasis. This will provide a means to understanding why certain therapeutic approaches are superior to others, as well as to developing novel approaches to therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: IMMUNOTHERAPY TRIAL IN NEW ONSET TYPE 1 DIABETES Principal Investigator & Institution: Gottlieb, Peter A. Assistant Professor; Pediatrics; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, CO 800450508 Timing: Fiscal Year 2001; Project Start 30-SEP-2000; Project End 31-AUG-2003 Summary: (adapted from the application) We propose a two arm randomized, partially blinded, placebo-controlled clinical trial to test the hypothesis that mycophenolate mofetil (MMF) alone or with daclizurnab (DZB) will prolong the period of C-peptide production in subjects with new onset type I diabetes. A second aim of this study will provide the clinical material for the validation of surrogate markers for immunity to islet Beta cells. The study will be conducted jointly by the Barbara Davis Center for Childhood Diabetes in Denver and the Virginia Mason Research Center in Seattle and takes advantage of the annual accrual of over 80 new onset type-l diabetes at these
40 Psoriasis
institutions. The metabolic end-points of this study will be fasting and stimulated Cpeptide, hemoglobin Alc, and total insulin dose. Levels of autoantibodies and T cell reactivity to islet autoantigens, both of which are surrogate immunological parameters specific for type I diabetes, will be followed. Measures of immune modulation will include serologic and T cell reactivity to recall antigens. The subject number allows for 80 percent power to detect differences significant at a 5 percent level. The study is innovative in that the agents to be tested have not previously been evaluated in type I diabetes, but are rational choices for interventions in an autoimmune disorder. The proposed surrogate markers use peptide tetramers to identify and enumerate antigenresponsive T cells. We believe the study is timely in that far less toxic immunosuppressive agents have been developed in the 10 year interval since Cyclosporine was found to preserve C-peptide production in new-onset patients. Our power projections are based on our extensive previous intervention studies and the choice of agents to be tested is supported by animal studies. MMF is an effective component of anti-rejection treatment of heart, kidney and liver recipients. It is effective for the treatment of psoriasis. The DZB anti-IL2 receptor antibody selected for use with MMF is effective in the treatment of acute renal rejection episodes. The safety of these agents in clinical use justifies a trial in type I diabetes, where 30 percent of new onset subjects run HbAlc levels that put them at high risk for vascular disease within 20 years. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INNATE MECHANISMS REGULATING CD8+T CELL IMMUNITY Principal Investigator & Institution: Fairchild, Robert L. Staff; Cleveland Clinic Foundation 9500 Euclid Ave Cleveland, OH 44195 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-AUG-2004 Summary: Many cutaneous immune responses, such as melanoma and psoriasis, are mediated by CD8+ T cells. The factors mediating recruitment of CD8+ T cells specific for antigens deposited in the skin remain unclear. Epicutaneous contact with haptens such as urushiol, the reactive agent in poison ivy, and subsequent challenge results in the development and elicitation of a CD8+ T cell-mediated inflammatory response termed contact hypersensitivity (CHS). Results from our laboratory have indicated that challenge of hapten-sensitized mice induces epidermal keratinocytes to produce the neutrophil chemoattractant Gro-alpha. This chemokine mediates neutrophil infiltration of the hapten challenge site and is required for the subsequent recruitment of the hapten-primed CD8+ effector T cells to the challenge site. On the basis of these results, we hypothesize that the antigen-specific T cell mediated immune response is elicited and regulated by cascades of chemokine production and cellular recruitment. This cascade is initiated by innate immune mechanisms which, in turn, mediate recruitment of the antigen- specific T cell component of the response. Following engagement of hapten, the CD8+ T cells produce IFN-gamma and this, in turn, stimulates stromal cells in the skin to produce potent chemoattractants (IP-10 and Mig) for antigen-primed T cells. These chemokines increase the inflammatory response by amlifying haptenprimed T cell infiltration into the challenge site. We further propose that hapten-specific T cells mediating down regulation of CHS inhibit chemokine production which recruits the innate and/or immune components to the hapten challenge site. Using histological, cellular immunology, an molecular approaches, this hypothesis will be tested by performing experiments proposed in three specific aims. In Specific Aim 1 we will test the role of Gro-alpha mediated neutrophil recruitment as the first step in the elicitation of CHS. In Specific Aim 2, we will test IP-10 and Mig as secondary chemokines required for the recruitment of CD4+ and CD8+ T cells during CHS. In Specific Aim 3 we will test
Studies 41
cytokine and molecular mechanisms which regulate chemokine production and leukocyte recruitment in CHS. The overall goal of these studies is to identify critical factors which regulate the recruitment of antigen-primed CD8+ T cells to defined antigens deposited in the skin. Definition of these factors will expose new strategies to limit the magnitude, duration and histopathology of T cell mediated inflammation in the skin. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INTERACTION BETWEEN PSORIATIC KERATINOCYTES AND T CELLS Principal Investigator & Institution: Cooper, Kevin D. Professor; Dermatology; Case Western Reserve University 10900 Euclid Ave Cleveland, OH 44106 Timing: Fiscal Year 2001; Project Start 15-AUG-1995; Project End 31-AUG-2003 Summary: Psoriasis is characterized by a marked T cell dependent hyperproliferation of the keratinocyte population within lesions of afflicted individuals. We have recently identified a clonogenic population of progenitor keratinocytes which, in normal skin, rarely undergo transition from the G0 stage of the cell cycle into the G1 cell cycle stage, however, in psoriatic lesions these progenitor cells are all actively cycling in G1 /S/G2/M. Relative to normals, clonogenic G0 keratinocytes hyper-respond to lymphokines from lesional T cell clones, in an ex vivo model of synchronized cell cycle induction from G0, particularly if stimulated with fibronectin (Fn). Changes in the clonogenic keratinocyte interactions with dermal/epidermal junction (DEJ) extracellular matrix may be a key link that confers psoriatic proliferation potential and T cell activation dependence in this disease. Both involved and uninvolved areas of psoriasis reveal increased Fn deposition at the DEJ. We show preliminary data that demonstrates that the Fn deposited is of an embryonic splice variant that splices in the EDA segment (EDA Fn). EDA which confers enhanced display of the RGD site, but is rarely stably expressed in adult human tissue. Further, keratinocytes from psoriatic individuals show increased alpha5beta1 integrin expression, a fibronectin receptor, enhanced integrin dependent spreading and focal adhesion kinase (FAK) activation, specifically on Fn. It is our hypothesis that increased Fn, Fn receptor, and Fn dependent functional activation in psoriasis are in response to the DEJ EDA Fn, and that an EDA-Fn rich versus poor ECM will regulate keratinocyte cell cycle progression and responsiveness to in combination with immune mediators. We propose to identify the cell type(s) in psoriasis responsible for production of EDA Fn, using assays for protein and mRNA with in situ localization. We will test whether or not EDA Fn regulates the FAK activation and proliferation of keratinocytes in a skin equivalent model in which keratinocytes engineered to overexpress EDA Fn production are used to form the epidermis. We will also test whether EDA Fn protein alone induces FAK phosphorylation, and its downstream kinase linked to cell cycle, MAPK, as well as cell cycle markers, in fresh ex-vivo normal and psoriatic keratinocytes. Blocking fragments of EDA Fn to the Fn matrix and specific integrin pair inhibitors will identify therapeutic intervention targets. This project will provide important and novel information that will translate rapidly to new treatments for psoriasis as well as to understand morphogenesis, with broad relevance to development, aging and cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
42 Psoriasis
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Project Title: SIGNALING
LANGERHANS
CELLS
AND
NERVES:
BIDIRECTIONAL
Principal Investigator & Institution: Granstein, Richard D. Professor; Dermatology; Weill Medical College of Cornell Univ New York, NY 10021 Timing: Fiscal Year 2001; Project Start 01-FEB-1992; Project End 31-AUG-2004 Summary: The overall goal of this application is to evaluate and define the bidirectional signaling between epidermal Langerhans cells (LC) and nerves This work is based on the following observations made in the initial funding period: (1) LC are anatomically-associated with calcitonin gene-related peptide (CGRP)-containing nerves, (2) CGRP regulates LC function, (3) LC express receptors for several other neuropeptides, as well as beta-adrenergic receptors, and some of these agonists regulate aspects of LC function including cytokine expression and antigen presenting function, and (4) LC are capable of producing neurotrophins. Thus, we hypothesize that bidirectional signaling occurs between nerves and LC with nerves influencing LC by production of neuron-derived signals while LC influence nerve cells by production of neurotrophins. This signaling allows regulation of immune function by neurons and may promote the formulation of the close association between nerves and LC that promotes this functional regulation. In Aim 1, we will test this hypothesis by examining LC for responses to neuropeptides and neuro-transmitters (effects on cytokine expression, co- stimulatory molecule expression and antigen presentation) and production of neurotrophins. Complementary in vivo experiments will test the physiological importance of neuropeptides and neurotransmitters in both induction and elicitation of immunity. Cytokine-deficient ("knock-out") mice will be used to test the involvement of certain cytokines in neural factor effects. In Aim 2, we will study the influence of primary neurons and neuropeptides on the migration of LC cells. Conversely, we will study the factors released by nerve cells that induce migration of LC towards nerve cells. The proposed studies will define an important locus of interaction between the nervous system and the immune system. The results obtained may provide a greater understanding of how the nervous system influences immunity within the skin, and how the association between the neural and immune systems in the skin is formed. These studies may lead to currently unforseen new therapeutic approaches to treat immunologic derangements, ranging form psoriasis to skin cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LINKAGE ANALYSIS OF FAMILIAL PSORIASIS Principal Investigator & Institution: Elder, James T. Professor; Dermatology; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, MI 481091274 Timing: Fiscal Year 2001; Project Start 10-MAR-1994; Project End 28-FEB-2003 Summary: (Adapted from the applicant's abstract)-Psoriasis is a common, HLAassociated disease of presumed immunopathogenesis. The hypothesis to be tested is that susceptibility to psoriasis is oligogenic, with at least one gene residing in the HLA region. Published results from a cohort of 224 affected sibling pairs have demonstrated three regions of suggestive linkage: HLA (Class I end, Zmax = 3.52), chromosome 16q (Zmax = 2.50), and chromosome 20p (Zmax = 2.62). Linkage to Class I and to 20p has been reported by others. The region in 16q overlaps with a recently identified locus for Crohn's disease. Since psoriasis occurs more commonly in patients with Crohn's disease than in controls (RR = 7. 1, p 1); (2) genotype candidate regions from Aim 1 at 5 cM intervals in all available pairs testing for linkage, increasing marker density to 0.5-1 cM in regions of suggestive or significant linkage (lod >2), and narrowing target intervals to
Studies 43
approximately cM by multipoint allele sharing and linkage disequilibrium techniques; and (3) identify genes residing in the intervals identified by Aim 2 and in the TNF-HLAC interval using the human transcript map. Allelic variation of the genes will be tested for segregation using TDT and MBSA, and by identifying alleles shared across haplotypes in regions of strong linkage disequilibrium. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MATRIX MEDIATORS OF WOUND HEALING Principal Investigator & Institution: Higgins, Paul J. Professor and Director; Micro/Immunol/Molec Genetics; Albany Medical College of Union Univ Union University Albany, NY 12208 Timing: Fiscal Year 2002; Project Start 01-MAY-1998; Project End 30-JUN-2006 Summary: (provided by applicant): Angiogensis is essential for wound healing. Deficient or exuberant angiogenesis, however, contributes to pathogenesis of cutaneous ulcers, ischemic injury, psoriasis, arthritis, vascular sclerosis, as well as the ocular and non-ocular complications of diabetes. Several proteolytic systems regulate the angiogenic process. Gene knockout and reconstitution studies have identified plasminogen activator inhibitor type-I (PAI-I), the major physiologic regulator of plasmin activation, as essential for neovascularization. PAI-I protects the stroma from excessive proteolysis, facilitates endothelial cell locomotion via regulation of cell-tomatrix adhesion and stabilizes nascent vessel structure. PAI-I transcription during endothelial cell activation and in vitro angiogenesis requires mitogen/ extracelIularregulated kinase (MEK) activity and involves binding of the helix-loop-helix transcription factor USF-1 to an E box motif (CACGTG). We propose to test the hypothesis that mitogen-activated protein (MAP) kinase-mediated USF-1 phosphorylation stimulates E box-dependent DNA binding and regulates PAI-I transcription as part of the switch to angiogenic phenotype. The following Aims will be addressed: 1. We will determine the requirements (i.e., USF-1 transcript expression, protein synthesis, nuclear translocation, phosphorylation) for USF-1 occupancy of the PAI-I box site and induced PAI-I transcription during endothelial growth activation and, migration. 2. We will clarify the MAP kinase type-specificity for USF-1 binding/ phosphorylation and identify the specific residues in USF-I that are phosphorylated by MAP kinases. 3. We will ascertain if the PAI-I E box is an expression "modulating" motif acting as a platform for replacement of the PAI-I transcriptional inhibitor USF-2a with a USF-1 containing complex during the switch from a quiescent to activated endothelial phenotype. 4. We will utilize genetic constructs that target PAI-I transcripts and modulate USF-1 function to assess effects of PAI-I expression perturbation on endothelial cell migration, proliferation and capillary structure. This work will provide information necessary to fashion targeted therapeutic strategies to treat pathologic angiogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISM BASED INHIBITORS OF SERINE PROTEINASES Principal Investigator & Institution: Groutas, William C. Distinguished Professor; Chemistry; Wichita State University Wichita, KS 67208 Timing: Fiscal Year 2001; Project Start 10-DEC-1997; Project End 30-NOV-2001 Summary: An array of inflammatory diseases such as pulmonary emphysema, chronic bronchitis, cystic fibrosis, psoriasis, rheumatoid arthritis and others, are characterized by an influx of neutrophils, and the presence of mediators of inflammation and
44 Psoriasis
cytokines that serve as neutrophil chemoattractants. The recruitment and degranulation of neutrophils in inflammatory states results in the production of reactive oxygen species and the extracellular release of the serine proteinases elastase, cathepsin G and proteinase 3. Poor regulation of the activity of these enzymes because of depressed levels of their physiological protein inhibitors leads to the degradation of the major components of the extracellular matrix and, ultimately the onset of disease. The use of innovative strategies that seek to counteract the damaging effects of the renegade enzymes be reestablishing a proteinase/antiproteinase inhibitor balance constitutes the long-term objective of the proposed research. The use of a potentially universal heterocyclic scaffold in the design of mechanism-based inhibitors that endows these inhibitors with unique mechanistic features and optimal biochemical properties is proposed. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MECHANISM OF ACTION OF PRO INFLAMMATORY CYTOKINES Principal Investigator & Institution: Davis, Roger J. Professor; Molecular Medicine; Univ of Massachusetts Med Sch Worcester Office of Research Funding Worcester, MA 01655 Timing: Fiscal Year 2001; Project Start 01-JUL-1995; Project End 30-APR-2005 Summary: (Adapted from applicant's abstract): The overall goal of this research program is to define the signal transduction mechanisms that mediate the response of cells to inflammatory cytokines and environmental stress. A focus of the study is the cJun NH2-terminal kinase (JNK) group of MAP kinases, which are activated in response to cytokines and stress. Many of the components of the JNK protein kinase signal transduction pathway have been identified by molecular cloning and have been characterized in biochemical studies. However, an understanding of the functional significance of the JNK signaling pathway in vivo has remained elusive. Recently, the PI has constructed mice with germ-line mutations in the three gene that encode the JNK protein kinases (Jnk1, Jnk2 and Jnk3) and in both of the genes that encode the protein kinases that phosphorylate and activate JNK (Mkk4 and Mkk7). Comparison of cells with wild-type and mutant genotypes can therefore provide important information concerning the physiological function of the JNK signaling pathway. A specific focus of this proposal is to define the functional significance of the JNK signal transduction pathway. Achievement of the goals of this proposal will increase understanding of the MAP kinase signal transduction in vivo. The information represents a basis for the design of novel therapeutic strategies for the treatment of [1] inflammation, and [2] proliferative diseases such as psoriasis and cancer. The specific aims of this proposal are to examine the effects of the JNK signaling pathway on : 1. Apoptosis and cell survival; 2. Oncogenic transformation and 3. Gene expression. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISM OF TRANSGLUTAMINASE TYPE I REGULATION BY HOXA7 Principal Investigator & Institution: La Celle, Peter T. Dermatology; University of Rochester Orpa - Rc Box 270140 Rochester, NY 14627 Timing: Fiscal Year 2001; Project Start 01-JUL-1999; Project End 30-JUN-2004 Summary: The inability to control proliferation and differentiation of epidermal keratinocytes is a major obstacle in wound healing following trauma or surgery, and in the treatment of diseases involving abnormal epidermal differentiation, from carcinomas to psoriasis. The long-range goal of this research is to identify the
Studies 45
mechanisms underlying the genetic regulatory pathways that specify the spectrum of proteins and the resulting cellular characteristics of particular stages of keratinocyte differentiation. To do this, we must identify the trans-acting factors and cis-acting elements that regulate differentiation-specific epidermal genes, such as transglutaminase type 1 (TGM1). The highly conserved homeobox (Hox) family of transcription factors can control cell identity and differentiation, and aberrant Hox regulation can lead to developmental abnormality or disease. Many Hox proteins recognize a common DNA sequence mainly via a small number of contacts in vitro, suggesting that additional mechanisms must underlie their diverse in vivo target specificity. Recent findings indicate that cooperative Hox interaction with cofactors can increase DNA specificity and affinity. We have identified the HOXA7 cDNA in a differentiating keratinocyte library through specific interaction with the KD-enhancer, that confers keratinocyte-specific activation to E6/E7 HPV-16 promoter. Sequence analysis indicates that KD-enhancer homology is present in the TGM1 5' promoter region (K3), which contains a Hox DNA recognition core element, as well as a binding site 90 percent identical to a known binding site for heterodimers of Hox and Pbx, the mammalian homolog of the Drosophila extradenticle. By transient transfection, HOXA7 suppresses transcriptional activity of K3 in neonatal keratinocytes, but strongly transactivates K3 in the epidermoid carcinoma cell line ME180. We propose that HOXA7 differentially regulates the keratinocyte differentiation marker gene TGM1 in neonatal keratinocytes and ME180, through interaction with co-factors, allowing cell-specific suppression or activation of the same gene. We will test this hypothesis by 1) determining the cis-acting elements in the TGM1 upstream regulatory region (K3) important in HOXA7 transactivation in neonatal keratinocytes and ME180 in vivo, and in HOXA7 binding in vitro, 2) identifying the functional domain of HOXA7 necessary for activation or repression of TGM1 in the two cell types in vivo, and for K3 binding in vitro, and 3) characterizing nuclear cofactors that form complexes with HOXA7 and K3 DNA. This study will begin to elucidate molecular mechanisms involved in HOX regulation of keratinocyte proliferation and differentiation, that in the long term may lead to new methods for controlling keratinocyte growth in re-epithelialization of wounds, and in treatment of cancers and other hyper-proliferative and disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MEDI-507 MONOCLONAL ANTIBODY IN PLAQUE PSORIASIS Principal Investigator & Institution: Langley, Richard Gb.; Massachusetts General Hospital 55 Fruit St Boston, MA 02114 Timing: Fiscal Year 2001 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MICROWAVE RADIOMETERS FOR HYPERTHERMIA ANTENNA ARRAYS Principal Investigator & Institution: Sterzer, Fred; Mmtc, Inc. 12 Roszel Rd, Ste A-203 Princeton, NJ 08540 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 30-SEP-2001 Summary: (Adapted from Applicant's Abstract): The long-term objective of this program is to improve the efficacy of hyperthermia treatments for patients with superficial skin diseases that cover large areas overlying contoured anatomies, such as chestwall recurrence of breast carcinoma or plaque psoriasis, To accomplish this
46 Psoriasis
objective, we propose to incorporate microwave radiometers that non-invasively measure subsurface tissue temperature into the Conformed Hypethermia Array Applicator System already in clinical use at the University of California, San Francisco (UCSF) to treat chestwall recurrence of breast carcinoma. The incorporation of temperature sensors into the UCSF system would make it possible to safely heat diseased tissues more uniformly and to higher therapeutic temperatures than is possible now. This would significantly increase the efficacy of the treatments and expand the number of patients with superficial disease that can be treated effectively with hyperthermia. The specific aim of the Phase I program is to develop a fast reading two frequency microwave radiometer and integrate it into the multiple elements of the Conformal Arrays. The goal of subsequent Phase II and III efforts will be to set up the capability for production of low cost custom shaped (patient and site specific) radiometrically controlled Conformal Arrays for heating large area surface disease. PROPOSED COMMERCIAL APPLICATION: The proposed integration of non-invasive temperature sensing, using microwave radiometers, with the hyperthermia antenna array should find wide use in clinics for treating superficial tissue diseases such as chestwall recurrence of breast carcinoma and mild to moderate plaque psoriasis. Celsion Corporation, a Silver Spring, MD manufacturer of hyperthermia equipment which has licensed several MMTP patents, has expressed interest in commercializing the radiometrically controlled Conformal Array applicator and multi-channel 915 MHz power equipment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOLECULAR PERMEABILITY
&
FUNCTIONAL
ASPECTS
OF
VASCULAR
Principal Investigator & Institution: Stan, Radu-Virgil; Cellular & Molecular Medicine; University of California San Diego 9500 Gilman Dr, Dept. 0934 La Jolla, CA 92093 Timing: Fiscal Year 2001; Project Start 20-AUG-2001; Project End 31-JUL-2005 Summary: The main function of vascular endothelium is the mediation and control of transendothelial exchanges of water and solutes (both small and large molecules) between blood plasma and the interstitial fluid. This function IS OBVIOUSLY "vital", judged on the dependency on it of all the cells from all tissues and organs. While the morphological structures involved in transendothelial exchanges have been identified (i.e. caveolae, transendothelial channels, fenestrae and intercellular junctions), there is very little to no biochemical evidence on the molecular composition of the structures involved, their biogenesis and regulation. The major goals of this research proposal are to elucidate the specific chemical composition and function of the endothelial differentiations such as fenestrae and caveolae and their stomatal diaphragms. The finding will also document a novel aspect of the transendothelial transport namely the possibility and ways of its modulation (in rate and components transported). Besides their impact on the understanding of the normal physiological process of the transendothelial transport, the data could be used further in the study of the pathophysiology of several human diseases (e.g. tumor angiogenesis, diabetes, retinopathy, psoriasis, pulmonary, fibrosis, thrombocytopenia, allergic encephalomyelitis, arterial hypertension) where such transport modulations have been shown to occur. These studies could also provide novel transport related endothelial specific molecular markers that could be used in designing strategies for drugs and gene targeting to selected microvascular beds. The techniques employed are cell fractionation, cell free-assays, in-vivo screening methods, two- dimensional electrophoresis, cell culture, transfections, light and electron microscopy.
Studies 47
Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOLECULAR MECHANISMS IN ACANTHOSIS NIGRICANS Principal Investigator & Institution: Bellus, Gary D. Dermatology; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, CO 800450508 Timing: Fiscal Year 2001; Project Start 01-MAY-1999; Project End 30-APR-2004 Summary: Acanthosis nigricans (AN) is a common skin disorder characterized by abnormal differentiation and hyperproliferation of keratinocytes in the epidermis and structural changes in the dermis. We hypothesize that the AN phenotype results from inappropriate stimulation of several different growth factors receptors expressed in keratinocytes and fibroblasts (eg IGFR, EGFR and FGFRs) which normally function to direct epidermal differentiation and regeneration. We propose to use AN as a model to better understand the regulation of keratinocyte proliferation and differentiation by growth factor receptor signaling. This will be accomplished by: 1.) using immunohistochemical and in situ hybridization techniques to characterize alterations in the expression of differentiation specific keratinocyte genes in skin biopsies of different types of AN; 2.) assessing alterations in growth parameters and gene expression in cultured keratinocytes, melanocytes and fibroblasts expressing endogenous or transfected FGFR mutations; and 3.) attempting to recapitulate the AN phenotype in a skin equivalent organ culture model using either keratinocytes and fibroblasts expressing FGFR mutations or by manipulation of growth factors in the culture media. These studies will provide a better understanding of how various growth factor receptor signaling pathways influence keratinocyte proliferation and differentiation pathways and should provide insights into wound healing and other disorders of abnormal keratinocyte proliferation and differentiation such as psoriasis, sebhorreic keratoses and skin cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MUTANTS FOR CELL ADHESION MOLECULES Principal Investigator & Institution: Beaudet, Arthur L. Professor and Chair; Molecular and Human Genetics; Baylor College of Medicine 1 Baylor Plaza Houston, TX 77030 Timing: Fiscal Year 2001; Project Start 01-JUL-1991; Project End 31-DEC-2001 Summary: (Adapted from the Investigator's Specific Aims): The overall goals of this project are to use genetic strategies to study the role of leukocyte and endothelial cell adhesion molecules in normal biology and in disease processes. Five Specific Aims are proposed: (1) Develop mutations in all three mouse selectin genes. (2) Perform phenotypic evaluation of knockout mice, including routine pathology, leukocyte counts, peritonitis, pneumonia, delayed type hypersensitivity reactions, and intravital microscopy. (3) Investigate the pathogenesis of psoriasis-like skin disease in CD18 deficient mice, specifically searching for a modifier gene or genes using a genomic-wide linkage strategy. (4) Develop cell-specific and inducible mutations using the loxP/Cre recombinase system, including an endothelial cell-specific mutation for VCAM-1 and an inducible mutations for ICAM-1. (5) Evaluate the role of adhesion molecules in the pathogenesis of atherosclerosis using apolipoprotein E-deficient mice. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NEW MRI SEQUENCES/RF COILS FOR HAND PSORIATIC ARTHRITIS Principal Investigator & Institution: Kwok, Wingchi E. Radiology; University of Rochester Orpa - Rc Box 270140 Rochester, NY 14627 Timing: Fiscal Year 2003; Project Start 15-JUL-2003; Project End 30-JUN-2006 Summary: (provided by applicant): The long-term objectives of our work are to establish an MR imaging technique to detect early changes of psoriaticarthritis (PsA) in the hand, and use that technique to improve our understanding of the disease mechanism and the effect of early treatment on the outcome of the disease. The recent work showed detection of lesions and cortical erosions with fat suppressed T2 weighted MRI have a significant role in the early stage of the disease, The purpose of this work is to advance the MR imaging technology to allow the detection of small lesions and early bone erosions in Spa in the hand. The specific aims of this work are: 1) to develop specifically designed phased arramy RF receiver coils for the hand and fingers to provide high signal sensitivity for high-resolution imaging of these specific anatomies; 2) to develop MR pulse sequences that improve fat suppression while acquiring both fat suppressed and non-fat suppressed images in a single scan time; 3) to evaluate the effect of chemical shift artifact elimination on the accurate measurements of anatomic structures and lesions in hand and fingers; 4) to conduct pilot evaluation of the usefulness of the new RF coil and pulse sequence technology in the detection of lesions in Spa patients. To accomplish our goal we will use our previous experience on phased array RF receiver coils to the design of special coils for the hand and for the fingers. Those coils will be tested on phantoms and normal subjects, and suitable ones will be used for further studies. The new pulse sequence development to acquire separate water and fat data in a single imaging time will be based on our preliminary experience in interleaved water and fat 3D gradient recall echo and 2D spin echo sequence development using spatial spectral excitation pulses. This will be further implemented on 2D spin echo, and 2D and 3Dfast spin echo sequences. We will develop post-processing algorithms to reconstruct water-only, fat-only and water plus-fat images from the acquired data. The new sequences will be tested on phantoms and normal subjects and their performance will be compared to that of the existing sequences. Fifteen patients with PsA as determined by plain film X-ray of the hand will be imaged using our new MRI technology to test its usefulness to detect PsA lesions. After completion of this study we will have the technology to detect early changes in PsA. This technology will allow us to start the clinical evaluation of the disease mechanism and the long-term effect of early treatment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NOVEL THERAPEUTIC APPROACH TO PSORIASIS Principal Investigator & Institution: Pershadsingh, Harrihar Pharmaceuticals, Inc. 1016 Lakeview Way Redwood City, CA 94062
A.;
Bethesda
Timing: Fiscal Year 2001; Project Start 30-SEP-1997; Project End 31-AUG-2003 Summary: (Applicant's abstract): Psoriasis is a common, inflammatory disease of the skin characterized by hyper-proliferation of keratinocytes. A variety of antipsoriatic therapies are available, however, due to problems with side effects and variability in clinical response, intense clinical and commercial interest remains in the development of new treatments. Thiazolidinediones, a novel class of compounds that activate the nuclear hormone receptor PPAR gamma, have recently been found to reversibly inhibit the proliferation of both normal and psoriatic human keratinocytes in vitro, and
Studies 49
ameliorate the histologic abnormalities of psoriatic skin in organ culture and in the scid mouse/human skin transplant model of psoriasis. In the current proposal, we will: 1) perform pilot studies of the antipsoriatic effects of orally administered thiazolidinediones in humans; 2) investigate the cellular mechanisms that mediate the antipsoriatic effects of thiazolidinediones, and 3) investigate the antipsoriatic potential of a recently developed series of novel thiazolidinediones that are expected to be more effective than existing compounds with respect to ameliorating the epidermal inflammation and hyperproliferation that characterizes psoriasis. By investigating clinical efficacy, by addressing therapeutic mechanisms, and by testing novel thiazolidinediones, the current Phase II studies will significantly advance the potential for Phase III commercial development of thiazolidinediones in the treatment of psoriasis. PROPOSED COMMERCIAL APPLICATION: NOT AVAILABLE Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: OSTEOCLASTIC BONE RESORPTION IN PSORIATIC ARTHRITIS Principal Investigator & Institution: Ritchlin, Christopher T. Medicine; University of Rochester Orpa - Rc Box 270140 Rochester, NY 14627 Timing: Fiscal Year 2001; Project Start 01-SEP-2001; Project End 31-AUG-2004 Summary: Psoriatic Arthritis is an inflammatory joint disease that can lead to chronic pain and disability. Joint destruction can be extensive and unique patterns of subchondral bone erosion have been noted but the mechanisms that underlie these changes are poorly understood. The overall goal of this project is for the Principal Investigator to develop the research skills necessary to become an independently funded investigator in patient-oriented research by studying osteoclast biology and bone resorption in the psoriatic joint under the mentorship of accomplished investigators in the field. In addition, protected time will allow the investigator to purse a Masters Degree in Public Health with a concentration in Clinical Investigation. These skills will be applied to defining the underlying mechanisms of bone resorption in psoriatic arthritis. Based on preliminary data from our laboratory, we hypothesize that: 1. Activated osteoclasts mediate focal bone resorption in the psoriatic joint. 2. Psoriatic synovial lining cells promote osteoclast differentiation and activation in adjacent bone through the expression of receptor activator of NFKB ligand (RANKL) which binds to its receptor RANK on the surface of osteoclasts and osteoclast precursors. 3. The circulating osteoclast precursor population is expanded in the peripheral blood of patients with PsA. 4. Treatment of PsA patients with the soluble TNF-p75 fusion protein (etanercept) will lessen joint inflammation and bone resorption through direct inhibition of TNF-a and down-regulation of TNF-mediated RANKL expression. To test these hypotheses we plan to perform studies with the following Specific Aims: 1. To demonstrate presence of osteoclasts at sites of bone resorption in PsA. 2. To define the expression pattern of TNF-a, RANK, RANKL and osteoprotegerin (OPG) in the psoriatic joint. 3. To determine if osteoclast precursors are expanded in the peripheral blood of patients with PsA. 4. To determine the effects of etanercept on inflammation, bone erosion, RANK and RANKL expression and circulating osteoclast precursor frequency as monitored by serial gadolinium enhanced MRI. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PATHOPHYSIOLOGICAL ROLE OF 12-R-LIPOXYGENASE Principal Investigator & Institution: Brash, Alan R. Professor; Pharmacology; Vanderbilt University 3319 West End Ave. Nashville, TN 372036917
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Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-AUG-2003 Summary: The products of metabolism of unsaturated fatty acids by oxygenases (prostaglandins, leukotrienes, and HETEs, Hydroxyeicosatetraenoic acids) are well established as important signaling molecules and mediators. Based on these precedents, the occurrence of a peculiar hydroxy fatty acid metabolite, 12R- HETE, in human epidermis, and particularly its prominence in proliferative skin diseases exemplified by psoriasis, is strongly suggestive of its significance to the pathophysiology of skin. Although 12R-HETE was usually considered a product of cytochrome P450, recently we established that a lipoxygenase is the enzyme type responsible for 12R-HETE synthesis in psoriasis. From human keratinocytes we have also cloned and expressed a 12Rlipoxygenase that can account for 12R-HETE overproduction in proliferative skin disease. In this project we will examine the role of this newly discovered enzyme by: 1. Characterization of the human 12R-lipoxygenase and its catalytic activities. 2. Establishing the tissue and cellular localization of the enzyme, including in psoriasis and other proliferative and inflammatory skin disease. 3. We will assess 12R-Lox expression in established mouse models of skin disease, and 4. Develop and characterize transgenic animals overexpressing the human 12R-lipoxygenase with targeted expression to epidermis. These studies will elucidate the sites and regulation of 12RHETE synthesis, assess its biosynthesis in normal and diseased tissues, elucidate the effects of 12R-HETE overexpression in animal models, and will prepare the way for a rational appraisal of lipoxygenase inhibitors as a potential therapy in proliferative skin disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PHOSPHOLIPASE D AND KERATINOCYTE DIFFERENTIATION Principal Investigator & Institution: Bollag, Wendy B. Associate Professor; Inst/Molecular Med & Genetics; Medical College of Georgia 1120 15Th St Augusta, GA 30912 Timing: Fiscal Year 2001; Project Start 25-APR-1998; Project End 31-MAR-2003 Summary: (Adapted from the applicant's abstract) - In epidermal keratinocytes the balance between proliferation and differentiation must be critically regulated in order to maintain the function of the skin as a protective barrier. Deregulation can lead to conditions such as skin cancer and psoriasis, a skin disorder characterized by hyperproliferation and abnormal differentiation. An understanding of the mechanisms involved in regulating normal growth and differentiation, as well as the alterations which lead to particular pathologic states, is important for developing better therapies for these conditions. 1,25-dihydroxyvitamin D3 is known to promote the differentiation of epidermal keratinocytes both in vitro and in vivo, and this compound and/or its analogs have been used successfully to treat psoriasis. However, the mechanism(s) through which 1,25-dihydroxyvitamin D3 exerts its effects are unclear. The investigators' recent data indicate that 1,25-dihydroxyvitamin D3 regulates the activity and expression of an isoform of PLD. PLD hydrolyzes membrane phospholipids to yield phosphatidic acid, which can, in turn, be dephosphorylated to generate diacylglycerol (DAG). Moreover, evidence from their laboratory and others suggests that this enzyme inhibits keratinocyte growth and promotes differentiation. Therefore, they hypothesize that PLD, via its production of phosphatidic acid and/or DAG, mediates the prodifferentiative effects of 1,25-dihydroxyvitamin D3. This proposal seeks to define the role of PLD and its lipid products in the 1,25-dihydroxyvitamin D3-mediated regulation of epidermal keratinocyte growth and differentiation. To accomplish this goal they will seek to answer several questions: 1) Does PLD activation and expression in response to
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1,25-dihydroxyvitamin D3 or its structural analogs correlate with their ability to induce differentiation? As a corollary to this question, the association between keratinocyte differentiation and PLD activation and expression will also be determined. 2) Do PLD and the products of its action mediate the prodifferentiative effects of 1,25dihydroxyvitamin D3? In these studies the roles of PLD, PLD-derived DAG and phosphatidic acid and PKC activity in 1,25-dihydroxyvitamin D3-induced differentiation will be defined. The data obtained from the proposed studies should provide critical information on the involvement of the PLD signaling system in regulating epidermal keratinocyte growth and differentiation and may suggest a new approach for the development of therapeutic agents for the treatment of psoriasis and basal and squamous carcinomas. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PHOSPHOLIPASE REGULATION OF MONOCYTE CHEMOTAXIS TO MCP-1 Principal Investigator & Institution: Cathcart, Martha K. Member; Molecular Medicine; Cleveland Clinic Lerner Col/Med-Cwru Cleveland, OH 44195 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 30-JUN-2007 Summary: (provided by applicant): Monocytes are major participants in inflammatory responses and are mediators of chronic inflammation. Monocyte chemotactic factor 1 (MCP-1) is a critical chemotactic factor involved in attracting monocytes from the blood into tissues. This chemotactic cytokine has been shown to be a particularly important for the extravasation of monocytes into vessel walls in atherogenesis. Atherosclerosis-prone mice, when rendered deficient in either MCP-1 or its receptor, CCR2, develop significantly less atherosclerosis than their normal counterparts. Furthermore, MCP-1 has also been associated with a series of other chronic human inflammatory diseases including rheumatoid arthritis, viral meningitis, psoriasis, and inflammatory bowel disease. To date, we have a very cursory understanding of the signal transduction pathways regulating the chemotactic response of monocytes to MCP-I. In this application we propose experiments to elucidate the pathways regulating this central inflammatory process. Recent studies from our laboratory have identified a novel role for phospholipases A2 in regulating monocyte chemotaxis. When primary monocytes are rendered deficient in the expression of either cPLA2 or iPLA2 they fail to respond to the chemotactic stimulus of MCP-I. These pathways appear to operate independently in regulating the chemotactic response. It is clear that lipid signaling pathways are integral regulators of this monocyte chemotactic response. In this proposal we present a research plan to investigate how these PEA2 pathways regulate chemotaxis. In Aim 1 we will determine how these phospholipases relate to the few other pathways that have been identified in regulating MCP-l-induced monocyte chemotaxis and in the process we will explore the best approaches for selectively intervening in this process. We will examine the contributions of phospholipase D and AA metabolites in regulating chemotaxis and will explore the role of phospholipases in influencing cytoskeletal rearrangement and other cell processes involved in monocytic responses to MCP-1. These studies will significantly advance our understanding of this key inflammatory event. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PILOT: DERMATOPROTEOME ARRAYS AS IMMUNODIAGNOSTIC TOOLS Principal Investigator & Institution: Mohan, Chandra; Associate Professor; University of Texas Sw Med Ctr/Dallas Dallas, TX 753909105
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Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2006 Summary: End-organ damage due to autoantibodies accounts for most of the morbidity seen in several dermatological diseases; including pemphigus vulgaris, pemphigus foliaceous, bullous pemphigoid and linear IgA disease. Given that autoantibodies are the pathogenic players in these diseases, it becomes important to understand what their antigenic (Ag) targets are. Although target antigens have been described for some of these, we do not still have a clear understanding of the full spectrum of relevant autoantigens in these diseases. In yet other dermatological diseases such as discoid lupus and psoriasis, our knowledge of target autoantigens is currently a black box. The current proposal seeks to address this knowledge gap by designing a proteome array that will enable parallel testing of patients' sera for reactivity to multiple skin Ags. The specific aims are: 1. To establish and optimize "dermatoproteome' arrays as immunoassay tools, 2. To ascertain the target antigen specificities of sera from patients with bullous diseases, and 3. To ascertain the target antigen specificities of sera from patients with discoid lupus. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PILOT: ELOX3 Principal Investigator & Institution: Schneider, Claus; Vanderbilt University 3319 West End Ave. Nashville, TN 372036917 Timing: Fiscal Year 2003; Project Start 01-MAY-2003; Project End 30-APR-2004 Summary: The main physiological function of lipoxygenases is the formation of mediators in inflammation and cellular differentiation. Most prominently, 5lipoxygenase and its leukotriene products are involved in bronchoconstriction and inflammation. A subgroup of epithelial lipoxygenases is suggested to play a role in the regulation or modulation of normal proliferation and differentiation of epithelial cells. For example, psoriasis and other proliferative skin diseases are associated with impaired function of epidermal lipoxygenases. Human eLOX3 is the most recent membr of the subfamily of epithelial lipoxygenases, and it is unique for two reasons: eLOX3 does not catalyze the normal lipoxygenase reaction, yet it does metabolize lipoxygenase products to skin-specific epoxy alcohols. Secondly, exon 1 of the human eLOX3 mRNA is unique among all lipoxygenases in that it has two functional translation initiation sites giving rise either to a cytosolic or to a nuclear form of the protein. The overall goal of this proposal is to provide initial insight into how the physiological role of eLOX3 is determined by its differential subcellular localization. I propose experiments that will establish the tissue distribution of the cytosolic and nuclear eLOX3, and provide insight into the regulation of eLOX3 expression and subcellular localization. To better understand the functional role of eLOX3 expression in the nucleus interacting proteins will be identified using a yeast two hybrid screening assay and coimmunoprecipitations. Finally, cultured keratinocytes will be used to investigate nuclear expression of eLOX3 during differentiation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PILOT: IL-24(MOB5) SIGNALING IN CUTANEOUS PATHOLOGY Principal Investigator & Institution: Liang, Peng; Associate Professor; Vanderbilt University 3319 West End Ave. Nashville, TN 372036917 Timing: Fiscal Year 2003; Project Start 01-MAY-2003; Project End 30-APR-2004 Summary: The overall objective of this research plan is to uncover the physiological functions of IL-24, a new cytokine that we recently discovered. IL-24 belongs to the IL-10
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family of cytokines that signal through highly related heterodimeric type II cytokine receptors. The relevance of IL-24 signaling to epidermal functions is based on the following evidence. First, epidermis (specifically keratinocytes) is one of the major target tissues of IL-24 based on the expression pattern of the two IL-24 receptors that we identified. Secondly, activated T lymphocytes, in particular the TH2 cells, are the major source of IL-24 production, and these cells are known to reside within epidermis (especially during wound healing) and psoriatic lesions. Accordingly, we hypothesize that IL-24 may be an important regulator for at least two epidermal functions. First, IL24 may function, in an analogous manner to IL-10 on hematopoietic cells, to inhibit the syntheses of proinflammatory cytokines such as IL-1 and TNF-alpha by epidermis. In this regard, IL-24, like IL-10, may function as a major anti-inflammatory cytokine that signals the attenuation or ultimate termination of inflammatory responses in the skin during the wound healing process. This is supported by the tissue specific nature of receptor expression for IL-10 in hematopoietic cells and for IL-24 in non-hematopoietic origins such as epidermis. Secondly, IL-24 may function as a signal for keratinocyte proliferation, migration and differentiation during tissue repair. We propose the following specific aims to test our hypothesis: Specific Aim 1: To determine the biological functions of IL-24 on keratinocytes - 1a: To determine if IL-24 can inhibit the production of proinflammatory cytokines by keratinocytes in response to bacterial lipopolysaccharide (LPS) - 1b: To determine if IL-24 can promote keratinocyte proliferation and migration - Specific Aim 2: To determine the expression pattern of IL24 and its receptors during tissue repair and psoriasis - 2a: Cellular localizations of IL-24 and IL-24 receptor expression in cutaneous excisional wounds - 2b: Comparison of the expression level of IL-24 and IL-24 receptors between normal and psoriatic skins Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PILOT--ACTIVIN IN SKIN WOUNDING AND PSORIASIS Principal Investigator & Institution: Hall, Alison K. Associate Professor; Case Western Reserve University 10900 Euclid Ave Cleveland, OH 44106 Timing: Fiscal Year 2003; Project Start 01-MAY-2003; Project End 30-APR-2006 Summary: There is no text on file for this abstract. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PILOT--FUNCTION AND REGULATION OF H2-CALPONIN IN KERATINOCYTES Principal Investigator & Institution: Jin, J-P P.; Case Western Reserve University 10900 Euclid Ave Cleveland, OH 44106 Timing: Fiscal Year 2003; Project Start 01-MAY-2003; Project End 30-APR-2006 Summary: In psoriasis, would healing, and other skin diseases normal keratinocyte differentiation process is altered and the cells display proliferation and increased motility. This change in cell behavior requires significant remodeling of the actin cytoskeleton. The goal of this study is to obtain new insights regarding the function of the actin cytoskeletal system, and proteins that regulate its function, in keratinocytes. The actin cytoskeleton is a dynamic filamentous network that must alter structure to permit cell proliferation, cell shape change, and cell movement. This network is regulated by calponins. Calponins comprise a family of actin filament-associated proteins that inhibit actin-activated myosin ATPase activity. This, in turn, leads to decreased cell motility and reduced remodeling of the actin cytoskeleton. Protein kinase C (PKC) catalyzed phosphorylation of calponin releases the calponin-dependent
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inhibition. Three homologous calponin genes have been identified. These encode h1, h2, and acidic calponin isoforms. H2-calponin is expressed in keratinocytes, but its function has not been investigated. We hypothesize that h2-calponin may function to regulate actin-associated filament formation in keratinocytes and modulate keratinocyte proliferation, motility, and differentiation in normal and diseased epidermis. Three specific aims are proposed in this Pilot and Feasibility study: Specific Aim 1: We will study the level of h2-calponin, and h2-calponin subcellular distribution as a function of keratinocyte proliferation rate. Specific Aim 2: We hypothesize that h2-calponin expression is elevated in proliferating keratinocytes to regulate actin-cytoskeleton remodeling during proliferation. We further hypothesize that overexpression of h2calponin will result in elevated levels of under-phosphorylated h2-calponin and that this will lead to suppression of cell proliferation. To test these hypotheses, we will use vector-mediated gene delivery to study the effect of over- and under-expression of h2calponin on keratinocyte profliferation. Specific Aim 3: We hypothesize that PKC modulates h2-calponin activity in proliferating karatinocytes. We will investigate the role of PKC-catalyzed phosphorylation of h2-calponin of keratinocyte proliferation and differentiation by over-expressing various PKC isoforms in the presence or absence over-expressed h2-calponin. Parallel experiments will manipulate PKC activity using pharmacologic agents. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PILOT--MONOCYTE DIRECTED GENE TRANSFER OF TGF BETA-1 Principal Investigator & Institution: Gilliam, Anita C. Associate Professor; Case Western Reserve University 10900 Euclid Ave Cleveland, OH 44106 Timing: Fiscal Year 2001; Project Start 30-SEP-1988; Project End 30-APR-2006 Summary: Monocyte/macrophages are critical immune cells in many skin diseases. They are bone marrow-derived leukocytes that leave the bloodstream, enter skin, and differentiate into tissue monocyte/macrophages. There they can present antigen and produce cytokines or differentiate toward phagocytes. They are prominent around cutaneous tumors (melanomas, sarcomas, and carcinomas), and appear in skin in large numbers after ultraviolet (UV) light exposure. We propose to develop a technique for site-specific immunotherapy using genetically altered monocytes that would naturally home to inflamed skin. TGFbeta1 plays a major role in cutaneous repair and fibrosis by promoting collagen synthesis We hypothesize that we can target transduced monocytes expressing murine TGFbeta1 to skin of mice using UV light to provide site-specific immune therapy, ultimately for wound healing. BALB/c bone marrow cells will be transduced by a replication deficient retrovirus carrying TGFbeta1 and then differentiated in vitro to monocyte/macrophages. These pilot studies will allow us to develop the in vitro methodology in preparation for in vivo studies in wound healing. Aim I: Can retrovirally transduced bone marrow cells be driven toward monocyte/macrophage differentiation in vitro and selectively targeted in vivo to the skin of normal mice with UV light? Aim II. What are the optimal conditions for in vitro and in vivo expression of TGFbeta1 in monocyte/macrophages transduced with a TGFbeta1-GFP-containing retroviral vector? Significance. The retroviral cassette can be potentially be loaded with any gene of interest (cytokine, chemokine, growth factor or other immunomodulatory protein), thereby targeting genetically altered monocyte/macrophages to specific cutaneous sites in a variety of severe refractory inflammatory skin diseases (psoriasis and scleroderma) and cutaneous tumors (melanoma, sarcomas, and carcinomas). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PROFILAGGRIN IN EPIDERMAL DIFFERENTIATION AND FUNCTION Principal Investigator & Institution: Presland, Richard B. Research Associate Professor; Oral Biology; University of Washington Seattle, WA 98195 Timing: Fiscal Year 2001; Project Start 01-MAY-1998; Project End 30-APR-2003 Summary: (Adapted from the applicant's abstract) - Profilaggrin is an abundant, highly phosphorylated, calcium-binding protein expressed in differentiating epidermal keratinocytes just prior to formation of cornified cells. Profilaggrin contains an Nterminal calcium-binding domain and multiple filaggrin units. Each region is proposed to have specific, distinct functions in vivo once profilaggrin is cleaved to yield the Nterminal and filaggrin peptides. The goal of this proposal is to understand the function(s) of these domains of profilaggrin by expression in keratinocytes of mutant proteins with a non-functional calcium-binding domain and by targeted disruption in embryonic stem cells to create profilaggrin-deficient mice. New evidence suggests that filaggrin, derived from profilaggrin by specific proteolysis, functions in cultured keratinocytes as a keratin-aggregating protein, leading to collapse of the keratin cytoskeleton, changes in cell shape, and cell cycle arrest. Filaggrin undergoes further proteolysis in vivo to free amino acids which bind water and are thought to maintain normal osmolarity of corneocytes. The hypotheses to be tested are (1) The calciumbinding domain of profilaggrin has a specific function(s) in regulating the calciumdependent events of epidermal cornification, including profilaggrin expression and proteolytic processing to filaggrin, and (2) filaggrin, through its roles as a keratinassociated protein and as the major source of hygroscopic amino acids, performs critical functions in regulating normal corneocyte maturation and function. To address these questions, the specific aims proposed are to (1) Determine the function of the N-terminal calcium-binding domain of profilaggrin by first abolishing its ability to bind calcium and then expressing it in stable keratinocyte cell lines and in transgenic mice and (2) determine the function(s) of profilaggrin in vivo by targeted disruption in mice. Profilaggrin-deficient mice will allow assessment of the functional significance of profilaggrin in vivo. This work should also provide a firm basis for understanding the biochemical significance of reduced or absent profilaggrin expression in skin diseases such as ichthyosis vulgaris and psoriasis and the failure of profilaggrin processing to filaggrin in the severe scaling disorder Harlequin ichthyosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RADIOMETRY CONTROLLED CONFORMAL ARRAY HEAT APPLICATOR Principal Investigator & Institution: Stauffer, Paul; Associate Professor; Radiation Oncology; University of California San Francisco 500 Parnassus Ave San Francisco, CA 94122 Timing: Fiscal Year 2003; Project Start 15-MAY-1996; Project End 28-FEB-2007 Summary: (provided by applicant): Adjuvant hyperthermia has been shown effective when sufficiently high thermal doses are delivered in close association with radiation or drug therapies. In previous work, we developed lightweight Conformal microwave Array (CMA) applicators from flexible printed circuit board (PCB) material and 6 mm thick water plus layers for heating large area superficial disease. These applicators were designed for treating chestwall recurrence of breast carcinoma and superficial melanomas <1.5 cm deep, but may eventually find use for treatment of other common skin diseases such as plaque psoriasis. While controllable heating of large contoured
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areas with CMA applicators has recently become an established IRB-approved procedure at UCSF with excellent heating effectiveness and patient acceptance, more widespread use awaits an improved patient interface that simplifies treatment setup and thermal monitoring/control of the large number of independent heat apertures. Thus, collaborative efforts have completed preliminary development of a microwave radiometer for non-invasive monitoring of subsurface tissue temperature. In this proposal, we plan to optimize the patient interface of current CMA applicators to allow integration of non-invasive temperature monitoring under each independent heat source. Such "Dual Mode" applicators will be characterized in terms of uniformity of power deposition and accuracy of temperature monitoring in chestwall tissue phantoms and comprehensive in vivo temperature distribution measurements in a small number of animals. Finally, applicator functionality in the clinic will be evaluated for improved operator convenience as well as for uniformity of heating, patient tolerance, and toxicity of higher minimum thermal dose treatments. The underlying goal of this development is to rekindle and significantly expand the use of hyperthermia therapy for superficial disease, a treatment that has been proven effective in randomized clinical trials but has stalled awaiting introduction of an easy to use applicator capable of effective heating of small areas with high resolution control, or large areas overlying contoured anatomy. Because of important new capabilities of integrated non-invasive volume-averaged tissue temperature monitoring and automatic self-balancing of applicator output, this applicator should facilitate new clinical protocols with exciting potential for improved therapy of diffuse superficial disease, such as longer duration low level heat in combination with systemic chemotherapy, heat enhanced drug delivery, and heat applied simultaneously with external beam radiation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: RATIONAL INFLAMMATORIES
DESIGN
OF
ADHESION
BLOCKING
ANTI-
Principal Investigator & Institution: Nagy, Jon O.; Ligocyte Pharmaceuticals, Inc. 920 Technology Blvd, Ste C Bozeman, MT 59715 Timing: Fiscal Year 2001; Project Start 01-AUG-1998; Project End 30-APR-2003 Summary: (Adapted from the Investigator's Abstract) The pathogenesis of many chronic and acute diseases of man has been demonstrated to have substantial involvement of cellular adhesion molecules known as selectins. The selectins mediate leukocyte recruitment into tissue sites to promote inflammatory injuries that underlies septic shock, ischemia-reperfusion injury, acute respiratory distress syndrome, and various chronic immune allergic disorders such as asthma and psoriasis. The goal of this project is to establish efficacy and safety data for potent selectin inhibitors to attract venture capital and/or a pharmaceutical partner to advance the PLN therapeutics through Phase I and II clinical trials. Through preliminary Phase I study the investigators have demonstrated that a defined group of multimerized selectin ligand analog expresses on UV-stabilized lyposomes termed PLN are very effective as selectin inhibitors in human cell shear assays systems and in mice. In this Phase II proposal the investigators seek to optimize the formulation and synthesis of PLN based therapeutics for comprehensive studies of animal models of human asthma and psoriasis in collaboration with the University of Michigan. These studies will serve as the basis for the toxicological and phramacokinetic studies that will serve to prepare PLN therapeutics for filing an IND/CTX. PROPOSED COMMERCIAL APPLICATION: NOT AVAILABLE Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: REGULATED PSORIATIC SKIN
GENES ISOLATED FROM WOUNDED AND
Principal Investigator & Institution: Rivas, Miriam V. Lab/Investigative Dermatology; Rockefeller University New York, NY 100216399 Timing: Fiscal Year 2001; Project Start 01-MAY-1999; Project End 31-OCT-2001 Summary: The candidate is a postdoctoral fellow at the Rockefeller University in the Laboratory for Investigative Dermatology. Her long-term career goal is to establish an independent laboratory, studying wound healing and skin diseases. The immediate career goal is to extend the work that she has begun on psoriasis and its relationship to wound healing, and further establish herself in the dermatology community in general and in the scientific community at large. Towards this end, research derived from the current proposal will be used to seek further advancement initially as a Research Associate progressing to Assistant Professor over the time frame of this award. The goal of this project is to advance our knowledge of the molecular events that convert a homeostatic epidermis to a physiological hyperproliferative epidermis in wound healing and to a pathological hyperproliferative epidermis in psoriasis. The specific plan is to functionally characterize four novel genes, that the candidate has recently cloned, which are differentially regulated in these skin conditions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATION AND FUNCTION OF KERATIN 6 GENES IN EPITHELIA Principal Investigator & Institution: Coulombe, Pierre A. Professor; Biological Chemistry; Johns Hopkins University 3400 N Charles St Baltimore, MD 21218 Timing: Fiscal Year 2001; Project Start 15-JUN-1995; Project End 30-JUN-2003 Summary: Keratins are the major structural proteins of epithelial cells in higher vertebrates, where they form 10 nm intermediate filaments (IFs) that significantly contribute to their trademark mechanical resilience. The greater than 40 keratin proteins are partitioned into two sequence types, I and II, both of which are required during filament polymerization in vivo and in vitro. In human, as in all mammalian species, type I and type II keratin genes are coordinately regulated in a pairwise, tissue- and differentiation-specific fashion, creating expression patterns that are tightly associated with the function of epithelia. Our studies are centered on K6, a type II keratin expressed in a variety of stratified epithelia under basal conditions but better known for its enhanced expression during wound repair and in chronic hyperproliferative diseases (psoriasis, carcinoma). We have shown the existence of multiple K6 isoforms in both human and mouse that are highly analogous in their primary sequence but differentially regulated at the transcriptional level. In doing so we have produced several tools including transgenic mouse strains that will enable us to examine three issues of broad and significant interest to skin biology. First, we will address the significance of having many K6 isoforms in the broader context of multiple type II keratin genes showing partially overlapping patterns of expression. We will inactivate the K6 alpha and K6 beta genes simultaneously by gene targeting and homologous recombination in 129 SvJ mice. The K6 null mice will be assessed in a variety of ways, including their ability to repair skin wounds and their susceptibility to two-step chemical carcinogenesis. We will attempt to complement the expected skin and oral mucosa phenotypes by reintroducing type II sequences in K6 null mice, such as K5 or K1, the two major type II keratins of skin. Second, we will pursue our characterization of the regulation of the K6 genes during wound repair in skin. We showed that the proximal 1.0 kilobase of
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5'upstream sequence from the human K6a gene is both necessary and sufficient to confer highly-specific wound-inducible expression to a reporter gene in transgenic mice. The transgene is induced as early as 2-3 hours following injury to mouse skin, coinciding with the endogenous K6 genes. We will carry out a molecular analysis of the cis-acting DNA regulatory sequences that underlie this expression pattern, with the goal of identifying the transcription factors and signalling pathways that are responsible for keratinocyte activation early after skin injury. Third, we will investigate the molecular pathogenesis of inherited skin blistering diseases involving mutations in keratin proteins. We created a transgenic mouse model in which the expression of a dominant negative K6 mutant protein, and hence the skin blistering phenotype, are inducible. We will examine the micromechanical properties of keratin filaments and of skin keratincytes isolated from transgenic mice expressing the mutant protein. Relating these data to the cytoarchitecture and mechanical resilience of epidermal tissue in transgenic mice in vivo should lead us to pinpoint the cellular basis for the heightened sensitivity to mechanical trauma. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATION OF ANGIOGENESIS BY TUMSTATIN Principal Investigator & Institution: Kalluri, Raghu; Associate Professor; Beth Israel Deaconess Medical Center St 1005 Boston, MA 02215 Timing: Fiscal Year 2003; Project Start 15-SEP-2003; Project End 30-JUN-2007 Summary: (provided by applicant): Angiogenesis is the formation of new capillaries from pre-existing capillaries. This process is most prevalent during development and growth of an organism, including humans. In adults, angiogenesis is mostly associated with wound healing, endometrial remodeling and the menstrual cycle. Pathogenic angiogenesis has been implicated in many different diseases, such as cancer, diabetic retinopathy, psoriasis, macular degeneration, rheumatoid arthritis, etc. Recent studies have reported identification of several endogenous inhibitors of angiogenesis, such as thrombopondin, angiostatin, endostatin and tumstatin. These endogenous inhibitors function in opposition to several pro-angiogenic factors such as VEGF, FGF, etc., and are thought to provide the regulatory balance for angiogenesis. In this grant proposal, we will investigate the mechanism behind the action of tumstatin, an endogenous inhibitor of angiogenesis. The focus of this grant is to better understand the need for the human body to generate endogenous inhibitors of angiogenesis. We hope to answer questions such as, what happens when endogenous inhibitors are genetically removed from the body? How do these inhibitors work? Why are they non-toxic and specific to dividing endothelial cells that are in the process of making new capillaries around tumor ceils? What is the molecular message sent by tumstatin to a dividing endothelial cell? Successful completion of the experiments proposed in this grant application will provide valuable insight into how these endogenous inhibitors function and their potential use as anti-tumor agents in the clinic. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RESEARCH NETWORK FOR DRUG-INDUCED LIVER DISEASE Principal Investigator & Institution: Bonkovsky, Herbert L. Professor of Medicine; Clinical Research Center; University of Connecticut Sch of Med/Dnt Bb20, Mc 2806 Farmington, CT 060302806 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2006
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Summary: (provided by applicant): Drugs and other chemicals have numerous salutary effects on humans, but they may also cause toxicity. Because of the central role played by the liver in metabolism, the liver is the most frequent and important site of drug- or chemical-induced tissue injury. As more drugs have been developed and used and more so-called complementary medicines (CAM) and herbal remedies are used, drug-induced liver disease (DILD) has become a problem of major and growing importance, and there is a growing need for better systems for early detection, characterization, and reporting of instances of DILD. Such systems should be applied both to drugs still under development and to drugs, CAM, and herbal remedies already on the market. The longterm aim of this research program is to develop a regional consortium and network in the Northeastern U.S.A. for the detection and clinico-pathological and molecular (genomic, proteomic) characterization of DILD. A key aspect of this work will be to develop a clinical, laboratory, and histopathological data base of "phenotypic" information on subjects with known or suspected DILD, and also to establish DNA, RNA, serum, and tissue banks on these same subjects. This will facilitate the development of "genotypic" (DNA), gene expression (RNA), and protein expression (proteomic) profiling of the same subjects, eventually permitting the detailed phenotypic-genotypic-proteomic correlations that will be possible as candidate genes and gene products involved in DILD are identified and characterized. Indeed, the regional and national data bases that will be established as a result of this program will aid us in discovering and identifying such genes and gene products, thereby bringing to fruition the enormous potential implicit in the successful sequencing of the human genome. The specific aims of this proposal are to: (1.) establish one of the national interactive Clinical Centers of the Hepatotoxicity Clinical Research Network, based at the University of Connecticut Health Center (UCHC). Our Center will serve as the coordinating center for a consortium of academic and practicing hepatologists and groups in the Northeastern U.S.A. We will take advantage of the strong research infrastructure of the UCHC Office of Clinical Research and the NIH-supported GCRC at UCHC; (2.) work with other members of the Network nationwide to develop consistent, standardized approaches and instruments to identify and fully characterize bona fide cases of drug-, CAM-, and toxin-induced liver injury, identified retrospectively. We will also obtain data from suitable control subjects thereby allowing for case-control studies, which will facilitate studies of the epidemiology and clinical spectrum of such hepatotoxicity; (3.) do prospective studies of selected, commonly used hepatotoxic drugs (HAART for HIV, INH for tuberculosis, methotrexate (MTX) for psoriasis); and (4.) obtain biological samples (blood, liver, plasma, serum) for study of the pathogenesis of DILD, using biochemical, serological, genetic, and proteomic techniques. The clinicopathological database and the tissue and DNA repositories will permit us to create and test numerous hypotheses relating to the pathogenesis and pharmacogenomics of DILD Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: RETINOIC ACID RECEPTORS: DYNAMICS, STABILITY AND FOLDING Principal Investigator & Institution: Schimerlik, Michael I. Professor; Biochemistry and Biophysics; Oregon State University Corvallis, OR 973391086 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2007 Summary: (provided by applicant): Retinoid X receptors (RXR) act as homodimers or heterodimers with retinoic acid receptors (RAR) or other nuclear hormone receptors to regulate gene expression. Among the genes regulated by retinoids are those that mediate apoptosis, cholesterol absorption and efflux, expression of xenobiotic
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metabolizing enzymes and the oncogene v-Erb A. Because of the important roles that RXR and RAR play in growth, development and cellular differentiation retinoids are of interest as chemopreventative and chemotherapeutic agents. They are also used in the treatment of acne, psoriasis and precancerous lesions. Although X-ray structures of several receptors for retinoids have been determined, information concerning the dynamics and stability of these proteins and the effects of ligands on these properties is lacking. This proposal will use mass spectrometry in conjunction with hydrogen/deuterium exchange to (1) examine the dynamics of the RARgamma and RXRalpha ligand binding domains and the effects of ligands and protein quaternary structure on solvent accessibility of structural elements, (2) probe the kinetic mechanism by which these proteins fold and (3) analyze conformational changes by differential protease sensitivity. Thermodynamic and kinetic studies are also proposed to examine the energetics and mechanisms of folding. These studies give information that complements the static, structural data, forms the foundation for future work to characterize the interactions of these proteins with other components of their signal transduction pathways and provides new data that may aid in the design of more effective drugs that act on receptors for retinoids. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF CONDITIONING IN THE PHARMACOTHERAPY OF PSORIASIS Principal Investigator & Institution: Ader, Robert; Professor and Director; Psychiatry; University of Rochester Orpa - Rc Box 270140 Rochester, NY 14627 Timing: Fiscal Year 2001; Project Start 14-AUG-2000; Project End 31-JUL-2005 Summary: (adapted from investigator's abstract): The lack of scientific attention devoted to the placebo effect as a phenomenon in its own right probably reflects the paucity of theoretical positions within which to organize the existing data and design new research. The proposed research is an attempt to advance from a descriptive to an experimental analysis of the placebo effect as a reflection of learning processes and examine the clinical implications of such an analysis in the case of an autoimmune disease. As such, this research addresses the clinical significance of behavior- immune system interactions. Conditioning is an inherent component of most pharmacotherapeutic regimens. The proposed research will capitalize on conditioned immunosuppressive responses to reduce the cumulative amount of corticosteroid medication used in the treatment of psoriasis. Patients would continue to be treated with steroid, but experimental patients would be shifted from their current schedule of continuous reinforcement (active drug whenever medication was applied) to a partial schedule of reinforcement (active drug a percentage of the time and placebo alone at other times). To equate amount of medication, other patients would be treated with a (reduced) dose of steroid in a standard (continuous schedule of reinforcement) treatment regimen. It is hypothesized that, holding cumulative dose constant, a partial schedule of reinforcement will enable patients to be maintained on lower cumulative amounts of corticosteriod than patients treated under a continuous schedule of active drug. Psoriasis is an especially appropriate model in which to evaluate the therapeutic affect of partial schedules of pharmacologic reinforcement which could decrease the amount of drug required to reduce psoriatic plaques and the deleterious "side" effects of long-term steroid treatment. Thus, it may be possible to increase the benefit: risk ratio of drug therapy and, at the same time, reduce the costs of medication. The proposed research is not an attempt to offer a behavioral alternative to drug treatment; it is an attempt to add a behavioral dimension to the design of drug treatment protocols. This is
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the first attempt to adopt conditioning principles and use schedules of reinforcement to design regimens of drug therapy. If proven effective, this new approach to pharmacotherapy and placebo effects is likely to stimulate new interdisciplinary research in neuropharmacology and behavioral pharmacology for the treatment of autoimmune and a variety of other chronic diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SCALP PSORIASIS TREATMENT WITH A FIBER OPTIC COMB Principal Investigator & Institution: Gourgouliatos, Zafirios F.; Bunsen Rush Laboratories, Inc. Woodbridge, CT 06525 Timing: Fiscal Year 2001; Project Start 28-AUG-2000; Project End 31-JUL-2002 Summary: Scalp psoriasis can be treated with a novel fiber optic delivery system that irradiates the psoriatic scalp of patients with UV-B light via an Optical Fiber Comb. The currently used methods for treatment of psoriasis with light are not applicable to the scalp because hair is usually blocking the light from reaching the affected skin. Our method overcomes this problem with the use of a "comb" that has optical fibers to deliver light directly to the skin. An UV-B Lightsource and a Fiber Optic Comb for use in clinics and doctor's offices have been developed during Phase I of this project. During Phase II this device will be evaluated in a clinical setting. The results of this trial will provide data about the effectiveness of the device. These results will be used to tailor the device before it is ready for volume production. In addition a lower cost device for home use will be developed, implementing the findings of the clinical trial and the experience gained during Phase I. If successful the UV-B Lightsource and Fiber Optic Comb will provide treatment to people affected with scalp psoriasis. At present, these people do not have any effective treatment available to them. PROPOSED COMMERCIAL APPLICATIONS: Psoriasis of the scalp affects more than two million people in the U.S. alone. Patients will require their own light combs, replaceable after 100- 200 uses. In a conservative scenario, assuming that only 1/3rd of affected patients were treated, in a physician's office, where one device might be used for 100 patients, 6,600 units would be needed in addition to several hundred thousand combs per year. Many patients would desire their own light source for convenience. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SIGNAL TRANSDUCTION MECHANISMS IN EPIDERMIS Principal Investigator & Institution: Blumenberg, Miroslav; Associate Professor; Dermatology; New York University School of Medicine 550 1St Ave New York, NY 10016 Timing: Fiscal Year 2001; Project Start 30-JUN-1994; Project End 31-JUL-2004 Summary: The long term objective of this work is to increase our understanding of the mechanisms that regulate gene expression in epidermis, and the changes in the mechanisms that occur in diseases. This increased understanding will lead to specific and effective treatments of such hyperproliferative and inflammatory processes as wound healing and psoriasis. The molecular signals in keratinocytes commonly activate multiple parallel intracellular pathways. Defining the pivotal signal transducing proteins, as well as the proteins that transduce the specific parallel effects will greatly increase our understanding of the regulatory processes in epidermis. The approach has four basic steps: to identify the molecular signals that operate in keratinocytes, to define the relevant signal transduction mechanisms, to characterize the patterns of transcription factor activation and to develop specific modifications of these processes
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using latest discoveries of molecular biology. Having already completed the first step, we focus in this proposal on the last three steps. Using DNA transfection and specific antibodies, the signal transduction mechanisms will be defined for two families of growth factors/cytokines, the EGF/TGFalpha and the TNFalpha/IL-1 family. Both are extremely important in cutaneous inflammatory processes. The patterns of transcription factor activation will be characterized for AP1, NFkappaB and C/EBPbeta proteins. These regulate gene expression in healthy and diseased epidermis. Finally, the proteins involved in signaling and regulation of gene expression will be inhibited using specific drugs, antisense oligonucleotides and target DNA binding sites in order to understand their roles in epidermal biology and pathology, and to develop specific therapeutic approaches. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SIMULATION OF PROTEIN AND HYDRIDE TRANSFER IN ENZYMES Principal Investigator & Institution: Hammes-Schiffer, Sharon; Professor; Chemistry; Pennsylvania State University-Univ Park 201 Old Main University Park, PA 16802 Timing: Fiscal Year 2003; Project Start 01-MAY-1998; Project End 30-APR-2007 Summary: (provided by applicant): The broad, long-term objectives of this research are to elucidate the fundamental principles and mechanisms of hydrogen transfer in enzyme catalysis and to address unresolved issues in biologically important systems. These objectives will be accomplished with a recently developed mixed quantumclassical molecular dynamics approach that includes electronic and nuclear quantum effects, as well as the motion of the entire solvated enzyme. The first specific aim is to determine the impact of enzyme structure and motion on catalysis. The second specific aim is to clarify the role of nuclear quantum effects such as zero point motion and hydrogen tunneling in enzyme catalysis. The remaining three specific aims address these issues for three enzyme reactions, which have been chosen on the basis of their biomedical importance and the availability of relevant experimental data. The third specific aim centers on the enzyme dihydrofolate reductase (DHFR), which is required for normal folate metabolism in prokaryotes and eukaryotes. This enzyme is essential for the maintenance of tetrahydrofolate levels required to support the biosynthesis of purines, pyrimidines, and amino acids. DHFR is medically relevant, in that inhibition of DHFR with potent antifolates has been used successfully in cancer chemotherapy. The fourth specific aim centers on the enzyme dihydroorotate dehydrogenase (DHOD). This enzyme catalyzes the only redox reaction in the biosynthesis of pyrimidines, which are required for the supply of precursors for RNA and DNA synthesis. DHOD is medically relevant, in that the immunosuppressive effects of inhibiting this enzyme have been used therapeutically. The fifth specific aim centers on lipoxygenase, which serves numerous vital roles in plants and mammals. In mammals, lipoxygenases are medically relevant, in that they mediate processes such as asthma, atherosclerosis, psoriasis, inflammatory diseases, and cancer growth. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SKIN DISEASES RESEARCH CORE CENTER Principal Investigator & Institution: Stricklin, George P. Professor and Chief; Medicine; Vanderbilt University 3319 West End Ave. Nashville, TN 372036917 Timing: Fiscal Year 2001; Project Start 01-MAY-1994; Project End 30-APR-2004
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Summary: This is the competitive renewal of the Skin Diseases Research Core Center at Vanderbilt University and the Department of Veterans Affairs Medical Center, Nashville. Skin relative research at this institutions has been characterized by a broadly based, interdisciplinary effort featuring collaborations with a number of Departments including Medicine (Dermatology), Biochemistry, Cell Biology, Pathology, Pharmacology and Surgery. The theme of this proposal, "Extracellular Matrix Cytokines and their Receptors in Skin Diseases," represents the interests and expertise in interacting, funded investigators performing skin related research in Dermatology Cell Biology, Pathology and Medicine. As the study of cytokines becomes related to skin disorders, it has become apparent that elucidating the role of cellular receptors is crucial, as gaining an understanding of cellular responses in the context of their surrounding connective tissue matrix. Research efforts are focused upon skin growth, development and repair through studies of cellular proliferation, migration, interactions with the connective tissue matrix and remodeling of that matrix. Cutaneous concerns relevant to these efforts include proliferative conditions such as psoriasis, benign and malignant neoplasms and wound healing. The objectives of this proposal are to encourage the growth and development of skin related research by enhancing the efficiency, interactions and productivity of its supporting funded investigators; attract, guide and support novel research and investigators new to skin related studies; and facilitate the involvement of our clinical trainees and faculty in skin research. To support this concept, COREs in Molecular Genetics, Morphology, and Animal & Cell Biology are proposed. A set of four Pilot & Feasibility projects present innovative proposals, several by investigators new to skin research, indicative of the resources available to dermatologic studies at this institution. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: STRESS VASODILATION
INDUCES
SKIN
MAST
CELL
ACTIVATION
&
Principal Investigator & Institution: Theoharides, Theoharis C. Professor; Pharmacol & Exper Therapeutics; Tufts University Boston Boston, MA 02111 Timing: Fiscal Year 2001; Project Start 13-APR-2001; Project End 31-JAN-2006 Summary: (applicant's abstract): Mast cells are located perivascularly close to nerve processes and can secrete many vasoactive and proinflammatory molecules. In addition to allergic triggers, mast cells can also be activated by direct nerve stimulation, by neuropeptides, and by acute immobilization stress through the local release of corticotropin releasing hormone (CRH) or urocortin (Ucn), which is more potent than CRH. Intradermal injections of CRH or Ucn induced rat skin mast cell activation and increased vascular permeability, both of which were inhibited by pretreatment with neutralizing antiserum to CRH or the CRH-receptor antagonist antalarmin. CRH or acute stress-induced skin vascular permeability measured with Evans blue extravasation was absent in W/W (v) mast cell deficient mice, but was present in their wt controls indicating it is mast cell dependent; this finding was supported by the fact that vascular permeability was also blocked by the "mast cell stabilizer" disodium cromoglycate (cromolyn). Similar results were obtained in rats and mice in response to acute immobilization stress. The in vivo, but not in situ, CRH action was absent in rodents treated with capsaicin to deplete sensory nerve fibers of their substance P (SP) content and was also inhibited by the neurotensin (NT) receptor antagonist SR48692. We are hypothesizing that acute stress releases CRH and/or Ucn in the skin leading, directly or through neuropeptides such as SP and NT, to mast cell activation and increased vascular permeability; leukocyte infiltration may then contribute to local
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inflammation and possibly to delayed-hypersensitivity (DTH) reactions. We propose to use normal and genetically deficient mice to investigate: (1) the effect of acute stress on (a) skin mast cell activation determined by image analysis, as well as residual skin histamine and mouse mast cell protease (MMCP)-6 content in CRH knock-out mice, and (b) vascular permeability quantitated by 99Technicium-gluceptate (99Tc) extravasation in CRH knock-out and W/W (v) mice and their +/+ controls; (2) any change in skin dorsal root ganglia (DRG) or spinal cord CRH, Ucn or CRH receptor expression after stress, using immunohistochemistry, Western and Northern analysis or RT-PCR; (3) the involvement of SP on stress-induced mast cell activation and vascular permeability in SP and NK-1 receptor knock-out mice, as well as the possible sequence of action of CRH or SP using combination of knock-out animals and CRH or SP-receptor antagonists; (4) the effect of CRH and Ucn on secretion of histamine, IL-6 and MMCP-6 or tryptase, respectively, from mouse purified skin and human umbilical cord-derived mast cells stimulated immunologically or by SP. These studies will help us understand how acute stress triggers skin mast cell activation, increased vascular permeability and possibly DTH. They will also help investigate the pathophysiology of skin syndromes exacerbated by stress, such as atopic dermatitis or psoriasis, especially since CRH and CRH receptors have been identified in human skin. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: STRUCTURAL BASIS OF CHEMOKINE RECEPTOR RECOGNITION Principal Investigator & Institution: Hodsdon, Michael E. Pharmacology; Yale University 47 College Street, Suite 203 New Haven, CT 065208047 Timing: Fiscal Year 2001; Project Start 01-JUL-2000; Project End 30-JUN-2004 Summary: The biological function of chemokines is critically dependent on their recognition and activation of specific G protein coupled receptors (GPCRs). The overall goal of the proposed project is to develop an understanding of the structural interactions between chemokines and their receptors. Unfortunately, these interactions cannot be directly observed by X-ray crystallography or nuclear magnetic resonance (NMR) spectroscopy due to the difficulty of working with full-length GPCRs. Mutagenesis studies have identified residues that are involved in functional protein-protein interactions, but the precise interactions that result in receptor recognition and activation remain uncharacterized. The approach adopted in the proposed research attempts to circumvent this problem by reconstructing the recognition interface using synthetic peptides derived from the extracellular domains of chemokine receptors. The conformation of these receptor-based peptides and their interactions with chemokines in solution will then be characterized using circular dichroism and NMR spectroscopy. The biological activity of the peptides will be determined using in vitro assays of neutrophil chemotaxis and receptor binding. The data will be analyzed in order to develop a structural model of chemokine receptor recognition which will be tested using sitedirected mutagenesis, followed by functional assays. Research into the structural basis of chemokine receptor recognition has wide-ranging relevance to human health and disease. Chemokines play a predominant role in a variety of allergic and rheumatic diseases including asthma, arthritis and psoriasis. Effects of chemokines on atherogenesis, angiogenesis and tumor growth have been reported. Some of the chemokine receptors function as HIV-1 coreceptors and have become attractive targets for identifying new anti-HIV compounds. A model of receptor recognition will guide experiments to delineate the biological roles of specific chemokine-receptor interactions. As well, therapeutic agents could be rationally designed to precisely inhibit single pairs of chemokines and their receptors which are specifically implicated in disease. The
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proposed project to be performed in the laboratory of Dr. Elias Lolis will allow me to continue my training in protein structural biology as well as introduce me to the science and techniques of immunobiology. My career development will be enhanced by this training and will prepare me for a future career in academic medical research. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: STRUCTURE/FUNCTION OF NUCLEAR RECEPTOR VITAMIN D HORMONE Principal Investigator & Institution: Collins, Elaine; San Jose State University Washington Square San Jose, CA 95192 Timing: Fiscal Year 2001 Summary: Most of the biological of the steroid hormone 1,25(OH)2 vitamin D3 are mediated through its interaction with the nuclear vitamin D receptor (VDR). VDR is a member of a superfamily of nuclear receptors which are ligand-dependent transcription factors. Other members of the family include receptors for steroid hormones, retinoids, thyroid hormone and several orphan receptors. Ligand binding induces conformational changes in the VDR that enable the receptor to form heterodimers with RXR, interact with other co-activators, and modulate gene transcription 1,25(oh)2D3, together with parathyroid hormone and calcitonin, is involved in the regulation of calcium homeostasis. Maintaining proper blood calcium levels is important for normal bone growth and maintenance. 1,25(OH)2D3 is also involved in the biological processes related to several diseases including osteoporosis, proliferative skin disorders like psoriasis, and some cancers including certain leukemias, breast and prostate cancers. The first steps in 1,25(OH)2D3 modulation of gene transcription involve binding of the 1,25(OH)2D3 ligand to VDR which results in conformational changes in the ligand binding domain (LBD) of VDR. We propose to investigate the molecular details of ligand binding and the relationship of binding to conformational changes in LBD. We propose the following specific aims to VDR that are important for binding 1,25(OH)2D3. 2) Determine if the VDR residues important for binding conformational changes in LBD of variant VDRs associated with binding 1,25(OH)2D3 or analogs of 1,25(oh)2D3. Together these experiments should help define the role of 1,25(OH_2D3 binding in the vitamin D signal transduction pathway and could lead to the development of more effective 1,25(oh)2D3 analogs for the treatment of particular diseases involving the vitamin D endocrine system. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: STUDIES ON VITAMIN D AND CALCIUM METABOLISM Principal Investigator & Institution: Norman, Anthony W. Distinguish Professor of Biochemistry An; Biochemistry; University of California Riverside 900 University Ave Riverside, CA 92521 Timing: Fiscal Year 2001; Project Start 01-JUN-1976; Project End 30-NOV-2005 Summary: The objective of this grant is to define at the cellular and molecular levels how the steroid hormone 1alpha,25 dihydroxyvitamin D3 [1a,25(OH)2D3] produces its biological responses. 1a,25(OH)2D3 is an unusually conformationally flexible molecule and consequently generates a wide array of molecular shapes that are available for binding to receptors. 1a,25(OH)2D3 generates biological responses via activation of at least two signal transduction pathways: (a) one shape of 1a,25(OH)2D3 interacts with a nuclear receptor [VDRnuc] to form a competent ligand-receptor partnership that, with other nuclear proteins, creates a transcription complex that regulates mRNA coding for
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selected proteins; and (b) a different shape of 1a,25(OH)2D3 interacts with a putative membrane [VDRmem] receptor to stimulate signal transduction events to activate raid responses [opening of Ca2+ and Cl- channels; activation of MAP-kinase; stimulation of intestinal Ca2+ transport or transcaltachia]. Functional analyses show that conformationally restricted analogs of 1 a,25(OH)2D3 VDRnuc and VDRmem bind distinctly different shapes of the hormone. Thus, the focus of the renewal of this 36-year grant is to define shapes of ligands and receptors for la,25(OH)D3 which will describe critical structure-function relationships between ligands (agonists and antagonists) and receptors. Aim 1: Using a 3D molecular model of the VDRnuc and site-directed mutagenesis in the ligand binding domain of VDRnuc, identify the specific amino acids that are critical for: (1.1) optimal ligand binding of the natural hormone 1a,25(OH)D3, and selected conformationally restricted agonist and potential antagonist analogs; and (1.2) formation of a complex between VDRnuc with the GRIP1 coactivator. Aim 2: Determine the shape of analogs of 1a,25(OH)2D3 which optimize their function as agonist or antagonist ligands for (2.1) the VDRnuc, and (2.2) the putative VDRmem. Aim 3; For the signal transduction pathway(s) associated with 1a,25(OH)D3-mediated rapid responses: (3.1) Describe upstream pathways of MAP-kinase activation and resultant downstream consequences in the nucleus in human leukemic NB4 cells; (3.2) Determine whether 1a,25(OH)2D3 activates MAP kinase and/or alters gene expression in VDRnucK0 mice; and (3.3) Clone the putative VDRmem/binding protein for 1a,25(OH)2D3 found in chick intestinal basal lateral membranes. The long-term clinical goal is to use rational drug design to chemically synthesize agonist and antagonist analogs of 1 a,25(OH)2D3 to selectively interact with VDRnuc and VDRmem. This may allow specific therapeutic intervention (e.g. type 1 diabetes, leukemia cancer control, psoriasis, immune disorders or osteoporosis) without hypercalcemia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: T CELLS BEARING INVARIANT GAMMA DELTA RECEPTORS Principal Investigator & Institution: Havran, Wendy L. Associate Professor; Scripps Research Institute 10550 N Torrey Pines Rd San Diego, CA 920371000 Timing: Fiscal Year 2001; Project Start 01-MAY-1992; Project End 30-APR-2003 Summary: Thy-1+ dendritic epidermal T cells (DETC) express an invariant gammadelta T cell receptor (TCR) and are only found in the skin. This population has been well characterized and represents the prototype invariant gammadelta T cell. DETC recognize and respond to self antigens expressed by neighboring keratinocytes after damage or disease. Once keratinocyte distress is detected, the DETC respond by the local secretion of KGF, an epithelial specific growth factor, and the production of chemokines which may direct other cell types to sites of damage in the epithelium. These results indicate a novel role for epithelial gammadelta T cells in recognition and repair of epithelial cells damaged by disease or insult. Identification of the antigen for the DETC is an important and necessary step in understanding the newly defined physiological role played by these cells. Identification of the antigen for the DETC is an important and necessary step in understanding the newly defined physiological role played by these cells. The goal of this project is to identify the antigen for the DETC and properties of antigen recognition in the following aims: (1) Identification of the DETC antigen. We have obtained highly-purified stimulatory material from keratinocytes and established that it is non-peptidic in nature. Ongoing analysis will provide complete identify. (2) Characterization of DETC antigen binding to TCR. Soluble Vgamma3Vdelta1 TCR molecules are being produced to examined antigen binding properties and structural features. (3) Dissection of the requirement for an antigen
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present molecule. We will isolate and characterize molecules that interact with antigen that may represent putative presenting molecules. Information gained in understanding antigens and properties of antigen recognition of the DETC may be applicable to populations of gammadelta T cells resident in other epithelial tissues. Once established, a paradigm for epithelial gammadelta T cell specificity will be useful for manipulation of the presence of these cells in epithelial diseases such as asthma, inflammatory bowel disease, psoriasis and wound healing. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TARGETING AUTOIMMUNITY
SIGNAL
TRANSDUCTION
PATHWAYS
IN
Principal Investigator & Institution: Rojas, Mauricio; Vanderbilt University 3319 West End Ave. Nashville, TN 372036917 Timing: Fiscal Year 2001; Project Start 01-MAY-1994; Project End 30-APR-2004 Summary: The ability to regulate and control the immune response has significant implications in areas like musculoskeletal and skin diseases, allergies, organ transplant and cancer. AA is an autoimmune disease of the hair follicle that causes loss of hair and is found in 2% of the population. The membrane- translocating sequence (MTS), which is a 12-aminoacid residue (AAVLLPVLLAAP) sequence with a function as a cellular import signal. In previous work we show that MTS sequence could efficiently deliver a large variety of proteins as fusion proteins, while also maintaining the function of the protein. In preliminary experiments to determine localization of the fusion protein we created a fusion protein, that contains a dominant negative form of the NF-kappaB inhibitor IkappaB-alpha(deltaN). It was possible to visualize the protein in the cytoplasm of cell. These finding suggested that the IkappaB-alpha(deltaN)-MTS fusion protein can be delivered efficiently into other cell types, such a T lymphocytes where it will be function as an inhibitor of Rel/NF-kappaB translocation and block the NFkappaB cascade. In this project we propose to test this the potential function of MTS protein in modification of an autoimmune disease hypothesis in the autoimmune skin disease, alopecia areata(AA) with the long-term prospect of intervening in other important skin disorders such psoriasis and graft vs host disease. To test this hypothesis, I propose the following specific aims: -Verify the function IkappaBalpha(deltaN)-MTS fusion protein in vitro using Jurkat T cells, to show that this protein blocks Rel/NF-kappaB nuclear translocation following T cell activation. - Determine if IkappaB(deltaN)-MTS alters the course of an autoimmune disease using the animal model of AA. To characterize the histologic changes in cellular composition of skin lesions induced by IkappaB- alpha(deltaN) MTS and to use mice that express a reporter for NF-kappaB activation as a transgene. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THE ROLE OF BACTERIAL TOXINS IN HUMAN SKIN DISEASE Principal Investigator & Institution: Leung, Donald Y. Head, Div of Pediatric Allergy & Immunol; National Jewish Medical & Res Ctr and Research Center Denver, CO 80206 Timing: Fiscal Year 2001; Project Start 17-JUL-1992; Project End 31-MAY-2005 Summary: Atopic dermatitis (AD) and psoriasis are the two most common chronic inflammatory skin diseases in the general population. Colonization and infection with S. aureus has been reported to exacerbate AD and psoriasis. The mechanisms by which bacteria participate in the pathogenesis of these skin diseases are unknown. Recent studies demonstrating that approximately 60% of Staphylococcus aureus from AD and
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psoriasis patients produce superantigens (SAgs) provide a plausible mechanism by which S. aureus could exacerbate skin inflammation. In particular, it has been shown that staphylococcal SAgs can engage HLA-DR on macrophages and activated keratinocytes to induce the release of cytokines and cause the selective stimulation of T cells expressing specific T cell receptor(TCR) Vbeta regions. Indeed in AD, SAg production has been associated with more severe skin disease. S aureus, which do not secrete SAgs, produce alpha toxin, a potent keratinocyte activator in vitro whose effects on the immune response in vivo is unknown. The specific aims of this competing renewal grant application will be: First, to determine whether AD and psoriasis skin lesions and their respective peripheral blood skin homing receptor positive T cells are associated with a selective expansion of T cells expressing TCR Vbeta regions that react with SAgs on lesional skin. Second, to investigate whether SAgs contribute to the severity of AD by inducing glucocorticoid insensitivity in skin homing T cells, and to assess the mechanisms by which this occurs. Third, to determine the histologic and immunologic effects of staphylococcal alpha toxin vs SAgs on the skin of normal controls vs patients with AD or psoriasis. Genetically-engineered mutant SAgs incapable of binding to either HLA-DR or the TCR will be used to decipher the molecular mechanisms of SAg-mediated skin inflammation in vivo. Fourth, to investigate the mechanisms leading to enhanced colonization of S aureus on the skin of patients with AD and psoriasis. Mutant S. aureus selectively deficient in various adhesin genes will be used to define the precise molecules involved in the attachment of S. aureus to inflamed skin surfaces. The role of bacterial toxins in the pathogenesis of skin diseases are poorly understood. The skin is an important model to study the pathogenesis of immunologic reactions in tissues. Thus, the elucidation of immune mechanisms by which SAgs exacerbate AD and psoriasis should have important consequences for the development of effective therapeutic modalities in the treatment of a variety of inflammatory diseases. With the increased prevalence of antibiotic resistant S. aureus and drug allergy, it is essential to develop new non-antibiotic strategies in combating bacterial toxin-mediated skin diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THE ROLE OF CCR4 IN SKIN LYMPHOCYTE HOMING AND IMMUNITY Principal Investigator & Institution: Campbell, James J.; Children's Hospital (Boston) Boston, MA 021155737 Timing: Fiscal Year 2001; Project Start 01-AUG-2001; Project End 30-JUN-2005 Summary: (provided by applicant): Chemoattractant cytokines (chemokines) are important mediators of lymphocyte trafficking from the circulation into sites of tissue damage and inflammation, and into secondary lymphoid organs. Certain chemokines rapidly trigger lymphocyte integrins, causing increased avidity with endothelial ligands, resulting in arrest of the lymphocyte on endothelial cells close to the chemokine source. Gradients of chemokine molecules can also attract arrested cells through the endothelium and into the surrounding tissue. A variety of chemokines are differentially expressed in various tissue types, suggesting a role in the differential homing of specific lymphocyte subsets to various types of tissue. We have found (in the human system) that the chemokines TARC and MDC efficiently attract circulating systemic memory T cells, especially skin-homing T cells expressing the cutaneous lymphocyte antigen, CLA. In contrast, intestinal (a4B7+) memory and naive T cells respond poorly. Immunohistochemistry reveals anti-TARC reactivity with venules involved in lymphocyte trafficking in chronically inflamed skin, but not in the gastrointestinal
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lamina propria, suggesting a potential role in circulating CLA+ lymphocyte recognition of skin vasculature. Consistent with this, TARC triggers integrin-dependent adhesion of CLA+ (but not a4B7hi intestinal) memory T cells to ICAM-1; and mediates rapid integrin-dependent arrest of lymphocytes rolling on the vascular CLA receptor, Eselectin, under physiologic flow conditions. The results suggest a fundamental role for TARC and its lymphocyte receptor CCR4 in lymphocyte-endothelial cell recognition and in differential trafficking of lymphocyte populations responsible for systemic vs. intestinal immunity. In order to define this role in detail, here we shall characterize CCR4 expression and responsiveness to TARC and MDC among specialized subsets of lymphocytes in man (Aim 1). We will determine if the preferential effects of TARC and MDC on systemic vs. mucosal lymphocytes are also observed in the mouse, and will ask if these responses are CCR4-dependent (Aim 2). The availability of a mutant CCR4deficient mouse line will allow us to explore the role of this receptor in targeted lymphocyte homing to inflamed skin (Aim 3) and its role in the inflammation process in models of DTH and autoimmune psoriasis (Aim 4). Monoclonal antibodies to mouse CCR4 and its ligands will facilitate these studies (Aim 5). These studies promise to define a critical component of lymphocyte recruitment to systemic sites inflammation, and may lead to novel therapeutic approaches in cutaneous (i.e. psoriasis) and other inflammatory diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THE ROLE OF INTEGRIN A5B1 IN ANGIOGENESIS & DISEASE Principal Investigator & Institution: Varner, Judith A. Assistant Professor; Cancer Center; University of California San Diego 9500 Gilman Dr, Dept. 0934 La Jolla, CA 92093 Timing: Fiscal Year 2001; Project Start 01-SEP-1999; Project End 30-JUN-2003 Summary: Angiogenesis promotes the growth and spread of cancers, exacerbates the joint-impairing disease arthritis, and contributes to the blindness associated with diabetes and aging as well as the severity of the skin disease known as psoriasis. New approaches to stop the development of these new blood vessels are sought as potential therapies for these diseases. Thus there is a need for continued research into new treatments that can stop new blood vessel growth. Potential new targets in angiogenesis therapy are the integrin alpha5beta1 and its ligand fibronectin. Both molecules are required for the development of the embryonic vasculature. Murine knockouts of both of these proteins are embryonic lethal with severe defects in blood vessel formation. Recent studies from our laboratory indicate that integrin alpha5beta1 and fibronectin are minimally expressed on blood vessels in normal tissues. In contrast, their expression is significantly Hupregulated on vasculature in solid tumor cancers and in response to particular angiogenic growth factors. Furthermore, our studies in animal models of angiogenesis indicate that growth factor and tumor induced angiogenesis, as well as tumor growth, can be significantly inhibited by three classes of antagonists of integrin alpha5beta1 (antibodies, cyclic peptides and small organic molecules) and by antibody antagonists of fibronectin, the major ligand for alpha5beta1. The overall objective of this proposal is to evaluate in depth the roles of integrin alpha5beta1 and fibronectin in angiogenesis. We will test the hypothesis that fibronectin and its receptor integrin alpha5beta1 play critical roles in pathological tumor and inflammatory angiogenesis. Thus we plan to characterize the expression of integrin alpha5beta1 and fibronectin on the vasculature in normal and pathological tissues. We will evaluate the roles of integrin alpha5beta1 and fibronectin in angiogenesis induced by different growth factors, using the chick chorioallantoic membrane, the nude mouse xenotransplant and the SCID
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mouse/human skin chimera models of angiogenesis. Finally, we will analyze the role of integrin alpha5beta1 and fibronectin in tumor angiogenesis and growth. We will evaluate the efficacy of the three classes of integrin alpha5beta1 antagonists in the treatment of angiogenesis associated with solid tumor cancer in the chick chorioallantoic membrane, nude mouse and SCID mouse/human chimera tumor xenotransplant models as well as in the Mtag, p53 (-/-) and p53 (-/+) murine spontaneous tumor models. These studies may lead to the development of new approaches for the therapeutic modulation of angiogenic disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THE ANGIOGENESIS
ROLE
OF
PLGF
IN
NORMAL
AND
NEOPLASTIC
Principal Investigator & Institution: Detmar, Michael J. Associate Professor; Beth Israel Deaconess Medical Center St 1005 Boston, MA 02215 Timing: Fiscal Year 2002; Project Start 13-JUN-2002; Project End 31-MAY-2007 Summary: (provided by applicant): Angiogenesis, the formation of new blood vessels from preexisting vessels, is a stepwise process involving vascular hyperpermeability, degradation of extracellular matrix, endothelial cell migration and proliferation, and formation and maturation of new capillary tubes. Whereas primary angiogenesis is a prominent feature of mammalian embryonic development, the normal adult body exhibits little vascular proliferation, with the exception of the female reproductive system and the cycling hair follicle. However, angiogenesis is a characteristic feature of inflammatory and neoplastic diseases and has been thought to represent a promising target for the development of novel anticancer therapies. While vascular endothelial growth factor (VEGF) has been suggested as the major skin and tumor angiogenesis factor, the biological function of placental growth factor (PlGF), an additional member of the vascular endothelial growth factor (VEGF) family of angiogenesis factors, has remained unknown. We recently found that two PlGF isoforms, PlGF-1 and PlGF-2, are upregulated in the chronic inflammatory skin disorder psoriasis and in squamous cell carcinomas of the skin, lesions that are characterized by richly angiogenic stroma. In vitro, epidermal PlGF expression is induced by transforming growth factor-alpha and by hypoxia, similar to VEGF. However, in contrast to VEGF, PlGF is also strongly expressed in dermal microvascular endothelial cells. PlGF-1 selectively activates the VEGF receptor-1 (VEGFR-1; Flt-1) on endothelial cells but not VEGFR-2 (KDR), in contrast to VEGF. PlGF-2 additionally binds to the neuropilin-1 receptor that is also shared by the neuronal guidance molecule semaphorin-D, acting as an antagonist. Recent findings in PlGF-deficient mice suggest that PlGF expression might be necessary for the biological activity of VEGF. To evaluate the importance of PlGF, alone or in concert with VEGF, in normal and pathological angiogenesis, we will investigate the following three aims: 1. Importance of PlGF in normal skin vascularization and in experimental skin inflammation, making use of PlGF-deficient mice, PlGF-2 transgenic mice, and of crosses with VEGF-transgenic mice. 2. Role of PlGF in the multistep process of skin carcinogenesis, elicited by a chemical carcinogen-promoter combination applied to normal, PlGF transgenic mice and PlGF-deficient mice. 3. Importance of transfected PlGF-1, PlGF-2, and semaphorin-D gene constructs for tumor growth, angiogenesis and metastasis of human squamous cell carcinoma and breast cancer xenotransplants. Understanding the molecular mechanisms that control skin and tumor angiogenesis will be the basis for the development of novel therapeutic approaches to treat inflammatory skin diseases and skin cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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•
Project Title: THERAPEUTIC INHIBITION OF LEUKOCYTE MIGRATION TO SKIN Principal Investigator & Institution: Dimitroff, Charles J.; Brigham and Women's Hospital 75 Francis Street Boston, MA 02115 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2004 Summary: Migration of leukocytes to skin is directed by adhesive interactions between vascular endothelial selectins and leukocyte selectin ligands. Leukocyte selectin ligands activity is conferred by specialized carbohydrate structures displayed on leukocyte cell surface proteins. These specialized carbohydrates, including the enzymes that biosynthesize them, are expressed on distinct subsets of leukocytes and impart the capacity of leukocytes to enter skin. Thus, controlling the migration of skin-homing leukocytes associated with skin disorders, such as allergic dermatitis and psoriasis, or preventing the progression of cutaneous leukemias with selecting ligand-modifying agents represents an attractive, yet novel, therapeutic strategy. Preliminary evidence has shown that fluorinated sugars analogs of naturally-occurring sugars, principally 4-FGlcNAc, modulate the structure and function of selectin ligands on human skin-homing leukocytes. Furthermore, 4-F-GlNAc treatment abrogates the capacity of murine skinhoming T helper 1 cells to bind to endothelial selectins, a process required for the elicitation of allergic-dependent cutaneous information. The objectives of studies outlined in this proposal are to evaluate the in vivo efficacy of 4-F- GlcNAc on cutaneous inflammation and the progression of cutaneous lymphoproliferative diseases. We aim to establish a dose of 4-F-GlcNAc that inhibits dermal leukocyte tropism, while neither affecting leukocyte proliferation nor leukocyte adhesion molecule function involved in other leukocyte migration patterns. Analysis of anti-inflammatory and antitumor effects of 4-F-GlcNAc will be performed utilizing mouse models of cutaneous inflammation and lymphoproliferative diseases. The overall goals of this preclinical evaluation 4-F-GlcNAc are to demonstrate its utility as a glycobiological tool for analyzing carbohydrate structure and function and to determine its therapeutic value against leukocyte- associated skin pathologies in treatment settings that require longterm administration with minimal side effects. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: THERAPY IN PSORIATIC ARTHRITIS--AN OPEN TRIAL OF 1,25 DIHYDROXYCHOLECALCIFEROL Principal Investigator & Institution: Felson, David; Boston University Medical Campus 715 Albany St, 560 Boston, MA 02118 Timing: Fiscal Year 2001 Summary: This study supplements an ongoing project, with (Principal Investigator Dr. Michael Holick) on the treatment of psoriasis with vitamin D. We will recruit patients with active psoriatic arthritis. The patients in this open trial will be part of a psoriasis study and will receive the same medication but will be assessed additionally for any improvement in their psoriatic arthritis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: TOLERABILITY OF BG9712 IN MODERATE TO SEVERE PLAQUE PSORIASIS Principal Investigator & Institution: Krueger, j; University of Utah 200 S University St Salt Lake City, UT 84112 Timing: Fiscal Year 2001
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Summary: In a preceding study, using an LFA-III molecule fused to an IgG1 protein, Dr. Krueger established that IV infusion was associated with minimal toxicity, was tolerated with no serious or unexpected adverse side effects, and some suggestions were generated that it had therapeutic effectiveness. The current study is a clinical trial to evaluate the effect of twelve weekly infusions of this agent given intravenously, subcutaneously, or intramuscularly with correlations to pharmacokinetics, safety, and toxicity. No preliminary data are yet available for analysis from this study. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TOPICAL CYCLOSPORIN A FOR DERMATITIS AND PSORIASIS Principal Investigator & Institution: Rothbard, Jonathon B. Chief Scientific Officer; Cellgate, Inc. 552 Del Rey Ave Sunnyvale, CA 94085 Timing: Fiscal Year 2001; Project Start 12-SEP-2001; Project End 31-AUG-2002 Summary: (Verbatim) The protective outer layer of the skin, the stratum corneum, serves to exclude therapeutic drugs like cyclosporin A (CsA). Preliminary experiments have unambiguously established that short polymers of arginine cross the stratum corneum of murine and human skin to enter the epidermal and dermal tissue. Similar penetration into all layers of the skin was observed when short polymers of arginine were conjugated to CsA, which in unconjugated form fails to penetrate skin. These conjugates reached infiltrating T cells in the dermis of inflamed skin. Related conjugates using a releasable linker provided therapeutically active CsA conjugates, thus providing a means of focally delivering systemically toxic drugs for the treatment of psoriasis and dermatitis while alleviating the problem of systemic toxicity. The goal of this proposal is to select a lead CsA -transporter conjugate for further development. This will entail the synthesis and evaluation of a series of GsA-transporter conjugates comprising a set of transporters with a range of tissue penetrating ability. A labeled subset will be assessed for tissue penetration and a corresponding releasable subset will be evaluated in vitro by assaying their ability to inhibit secretion of Il-2 by activated T cells and in vivo using an animal model of contact dermatitis. PROPOSED COMMERCIAL APPLICATION: Current topical therapies for dermatitis and psoriasis all have fundamental problems. When administered orally, immunosuppressants can be effective, and by, intralesional injection, CsA dramatically reduces or clears psoriatic lesions. CsA is not currently used to treat dermatitis and is used only in severe cases of psoriasis because of systemic toxicity. The proposed conjugates are expected to provide the first highly efficacious topical treatments for atopic/contact dermatitis and psoriasis, which together total >20 million US patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: TOPICAL PARATHYROID HORMONE ANALOG FOR TREATMENT OF PSORIASIS
RELATED
PEPTIDE
Principal Investigator & Institution: Malabanan, Alan Ona.; Boston University Medical Campus 715 Albany St, 560 Boston, MA 02118 Timing: Fiscal Year 2001 Summary: There is no text on file for this abstract. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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•
Project Title: TOPICALLY DIHYDROXYVITAMIN D2
ADMINISTERED
19
NOR
1ALPHA,
25
Principal Investigator & Institution: Holick, Dr M.; Boston University Medical Campus 715 Albany St, 560 Boston, MA 02118 Timing: Fiscal Year 2001 Summary: The goal of this pilot study is to determine the theraputic efficacy and safety of the vitamin D analog 19-nor-1 alfa, 25 dihydroxyvitamin D2 for the treatment of plaque type psoriasis in adults. This will be accompanied by evaluating the topical application of either placebo petrolatum or petrolatum that contain 1.5 microgram of 19 -nor-1, 25(OH)2 in 0.1 g petrolatum. Expected outcome: only 19-nor-1, 25(OH)2D2 will be effective for treating psoriasis. This study plans to recruit 20 adults patients who have lesions over at least 5% of their bodies. Study subjects will be male or female between ages 18 & 80. The patient will apply to a 50cm2 lesion 0.10 g of white petrolatum that comtains 1.5 mcg of 19-nor-1, 25(OH)2D2 once a day for 2 to 3 months. A comparable 50 cm2 psorasis lesion will recieve 15 mcg/g of white petrolatum daily. The study will be conducted in a double blind, right-left sided, self controlled fashion. Neither the physician nor study nurse who is making assessment will know which lesion is recieving which compound. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TOPS-ESTER: PHARMACOKINETICS AND IMAGING IN HUMAN SKIN Principal Investigator & Institution: Hsia, Carleton Jc.; Synzyme Technology, Inc. 1 Technology Dr, E-309 Irvine, CA 92618 Timing: Fiscal Year 2003; Project Start 15-SEP-2003; Project End 14-MAR-2004 Summary: (provided by applicant): TOPS-ester is a topical drug selected for development for it's unique ability to compartmentalize within skin cells and express antioxidant activity that limits oxidant mediated pathologies including psoriasis, sunburn, skin aging and skin cancer. The objective of this proposal is to use a noninvasive electron paramagnetic resonance (EPR) spectroscopy and imaging technique to monitor TOPS-ester (i.e. diethyl 2,2,6,6-tetramethyl-1-oxyl-4-piperidene succinate, or DETOPS) in human skin for the purpose of guiding the prophylactic and therapeutic treatment of skin disease. The DETOPS ester is a paramagnetic molecule and hence can be conveniently studied using EPR spectroscopy. Based on our preliminary data, we propose that after DETOPS penetrates cells of the epidermis and dermis, the succinateester moiety of the molecule is hydrolyzed by intracellular esterases to succinate anions; thereby facilitating intracellular retention of negatively charged carboxylate derivatives of DETOPS in the skin. The specific aims are to demonstrate the feasibility of distinguishing the difference between DETOPS and Tempol in their temporal distribution in human skin. The EPR measurements will be performed using the newly developed topical EPR imaging instrumentation for humans at the Johns Hopkins University. The skin penetration, compartmentalization and metabolism of the DETOPS in the forearm skin of human volunteers will be investigated using spatially resolved pharmacokinetic imaging data. It is expected that this preliminary study will lead to the evaluation of the therapeutic potential of the DETOPS formulation for the prevention and treatment of a variety of skin pathophysiological disorders. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TREATMENT OF AUTOIMMUNE DISEASE BY COSTIMULATORY SIGNAL* Principal Investigator & Institution: Khoury, Samia J. Associate Professor of Neurology; Brigham and Women's Hospital 75 Francis Street Boston, MA 02115 Timing: Fiscal Year 2003; Project Start 28-SEP-1999; Project End 31-MAR-2008 Summary: (provided by applicant): There have been tremendous advances in the field of autoimmunity in the last 20 years, and our understanding of the mechanisms underlying autoimmune disease has grown exponentially. True tolerance is likely to arise not from improved immunosuppression, but from improved understanding of the normal mechanisms that generate and maintain self-tolerance, and the ability to manipulate these mechanisms for the prevention and treatment of autoimmune diseases. The mechanisms of autoimmunity that underlie many diseases are similar, and an integrated multi-specialty approach for evaluating new and emerging therapies would provide the opportunity to integrate knowledge from the various specialties. We have chosen to study therapy of autoimmune disease by blocking co-stimulatory signals with CTLA4Ig and by blocking T cell activation with rapamycin. This strategy has two advantages. First, these are antigen non-specific steps in T cell activation and immune responses. This means that tolerance can be achieved without needing to know the identity of the antigen. Second, restricted delivery of signal two and alteration in cytokine production and profiles are probably involved in normal mechanisms of selftolerance. Third, by inhibiting T cell activation with rapamycin in addition to costimulatory signal blockade, we may be able to induce long term tolerance by allowing the occurrence of activation induced cell death. The human diseases that our program will focus on are multiple sclerosis (MS), autoimmune diabetes (IDDM), and psoriasis. All are organ specific diseases where T cells appear to be essential in initiating the immune response and lead to the particular disease pathology. Project #1 is the clinical trials project, in which we propose a clinical trial of CTLA4Ig in diabetes, a clinical trial of CTLA4Ig + rapamycin in early MS and describe the available patients and facilities for a potential psoriasis trial. The goals of project #2 are to investigate the role of NK T cells in human diabetes. Project #3 will take a direct approach by cloning T cells and NK T cells from the pancreas and pancreatic lymph nodes of patients with diabetes. The approach of treating autoimmune diseases by preventing T cell activation is timely and has a high likelihood of success. There is a body of evidence including clinical trials supporting the use of CTLA4Ig in autoimmune disease, and also evidence for the synergistic role of rapamycin. The data obtained from the clinical trials and the critical information from the basic science projects will be valuable in getting us closer to our goal of tolerance induction for autoimmune disease. PROJECT 1: Treatment of Autoimmune disease by costimulatory signal blockade (Khoury, Samia) PROJECT 1 (provided by applicant): The ultimate goal of immunotherapy in autoimmune diseases is to find immunologically specific, relatively non-toxic forms of therapy. Our understanding of the immunopathogenesis of T cell mediated autoimmune diseases implicates T cell activation as an important step in their pathogenesis. The CD28-B7 pathway of T cell costimulation plays a role in the pathogenesis of many T cell mediated autoimmune diseases as demonstrated by disease prevention after blocking this pathway in animal models. In experimental autoimmune encephalomyelitis (EAE) the animal model of MS, CTLA4Ig prevent disease and inhibits relapses. In a model of spontaneous diabetes (the NOD mouse) CTLA4Ig prevents the onset of diabetes. CTLA4Ig has shown effectiveness in a phase I clinical trial of psoriasis and more recently in clinical trials of rheumatoid arthritis. It is currently in clinical trials for multiple sclerosis (MS). It is likely that to achieve tolerance in autoimmune disease, one must target more than one pathway of immune activation. Data obtained from animal
Studies 75
models of transplantation suggest that a combination of costimulatory signal blockade and rapamycin can induce long term tolerance. Thus, our primary objective in this project is to study the safety and efficacy of CTLA4Ig treatment in patients with new onset type I diabetes, and the safety and efficacy of CTLA4Ig + rapamycin in patients with the earliest manifestations of multiple sclerosis. The outcome measures for the diabetes trial are safety, metabolic and immune effects of CTLA4Ig therapy. For the MS trial, we will compare the safety and efficacy of CTLA4Ig, rapamycin, and CTLA4Ig+rapamycin, to placebo in patients with clinically isolated syndrome of demyelination. The outcome measures are safety and the development of MS by McDonald criteria. Our group also has the interest and patient populations to participate in clinical trials of psoriasis. The Dermatology Clinical Investigations Unit (DCIU) of Massachusetts General Hospital is an established clinical trials unit with extensive experience. Current and past investigations include five trials of systemic medications in psoriasis similar to those we anticipate studying in trials associated with the ACE. In summary, this proposal encompasses three autoimmune diseases: MS, type I diabetes, and psoriasis. We are submitting clinical trial proposals for MS and diabetes with a particular focus on T cell activation pathways. We believe that the interactions among investigators from different clinical specialties will foster new ideas and crossfertilization leading to better treatment for autoimmune diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TRITIUM LABELLING OF RETINOIC ACID ANALOG: PSORIASIS & CANCER CHEMOTHERAPY Principal Investigator & Institution: Morimoto, Hiromi; University of Calif-Lawrenc Berkeley Lab Lawrence Berkeley National Laboratory Berkeley, CA 94720 Timing: Fiscal Year 2001 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: UNIVERSITY OF MICHIGAN RHEUMATIC DISEASES CORE CENTER Principal Investigator & Institution: Fox, David A. Professor; Internal Medicine; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, MI 481091274 Timing: Fiscal Year 2001; Project Start 28-SEP-2001; Project End 31-JUL-2006 Summary: The University of Michigan proposes to establish a Rheumatic Disease Core Center. This will be a broadly based effort involving approximately 80 faculty from clinical and basic science departments at the University of Michigan and neighboring institutions. The Center will apply a broad range of research skills, backgrounds, and approaches to investigation of fundamental issues in the etiology and pathogenesis of rheumatic diseases and in development of a scientific basis for novel therapeutics. The Center will focus its activities by grouping investigators in four Major Programs (Model Systems for Innovative Therapeutics, Autoimmunity, Cell and Cytokine Interactions in Organ Inflammation and Damage, and Genetics and Patterns of Gene Expression in the Rheumatic Diseases); and also in Disease Focused Working Groups (Osteoarthritis, Psoriasis/Psoriatic Arthritis, Rheumatoid Arthritis and Systemic Lupus Erythematosis). Activities of the Center will be supported by six Biomedical Core Facilities including Flow Cytometry, Hybridoma, Vector, Transgenic Animal, Protein Structure and DNA Sequencing Cores. UM-RDCC faculty will have access to core services for rheumatic
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disease-related research at substantially discounted recharge rates. Two Pilot and Feasibility Projected are proposed, each of which is led by new faculty recently recruited to the University of Michigan. The UM-RDCC and its administrative unit will be directed by David A. Fox, M.D., who is experienced in administration of a broadly based Center through more than ten years directing the University of Michigan Multipurpose Arthritis and Musculoskeletal Diseases Center. Rory Marks, M.D., Associate Professor of Rheumatology is proposed as the UM-RDCC Associate Director, with special responsibilities for supervision of the biomedical cores. The Center leadership will maintain close links between the basic research activities of the UMRDCC and expanding clinical investigation in the rheumatic diseases at the University of Michigan. The Center's administrative team will be assisted by an Executive Committee, an Internal Advisory Committee, and an External Scientific Advisor, Dr. Bennis Carson. We have constructed the UM- RDCC to maximally engage the talents and resources of the University of Michigan to focus on basic research in the rheumatic diseases in the rheumatic diseases, so as to achieve substantial progress in improving understanding of etiology, pathogenesis and treatment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: USE OF HUMANIZED CD25 (ANTI-TAC) IN THE TREATMENT OF PSORIASIS Principal Investigator & Institution: Krueger, James G. Professor; Rockefeller University New York, NY 100216399 Timing: Fiscal Year 2001 Summary: It is known that IL-2 receptor-bearing T-lymphocytes (CD3+, CD25+, CD122+) induce type I psoriasis. The hypothesis addressed in the current proposal is: (1) T-cell mediating psoriasis are MHC class I restricted and belong to the Tc1 subset of effector CD8+ lymphocytes. The following hypotheses regarding the mechanism will also be discussed: (2) CD4+ T cells (or other IL-2 receptor-bearing cells) are pathogenic. (3) Type I psoriasis is a primary disorder of keratinocytes with activation of T cells as a secondary event. (4) Activated Langerhans cells (or other dendritic antigen-presenting cell types) are directly pathogenic. IL-2 receptor-bearing T-lymphocytes (CD3+CD25+CD122+) induce type I psoriasis. T-cells mediating psoriasis are most likely MHC class I restricted and belong to the Tc1 subset of effector CD8+ lymphocytes. The major alternative hypothesis is that other IL-2 receptor-bearing cells, especially CD4+ T-cells, are pathogenic. Less likely alternative hypotheses are 1) that type I psoriasis is a primary disorder of keratinocytes with activation of T cells as a secondary event or 2) that activated Langerhans cells (or other dendritic antigen-presenting cell types) are directly pathogenic. This hypothesis is being tested by the in vivo administration of three novel immune-modulating drugs (which target activation and/or effector phases of immune responses) to patients with psoriasis vulgaris. Two of these agents directly target IL-2 receptors that are up-regulated on activated Tlymphocytes, and the other agent indirectly suppresses IL-2 receptor expression by Tlymphocytes. The agents being studied are DAB389IL2, a rationally engineered fusion toxin which binds selectively to activated T-lymphocytes; rh Interleukin-11, an antiinflammatory that modulates T-lymphocyte activation, and a humanized monoclonal antibody to CD25, the subunit of the IL-2 receptor that confers high-affinity interaction with IL-2. The major objectives of these studies are, first, to explore the safety and efficacy of novel immune-targeted therapeutic agents in the most common human immune-mediated disease (psoriasis vulgaris) and, secondly, to use these therapeutic agents as specific immune probes to dissect the contribution of different immune
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mechanisms to disease pathogenesis. Hence, our analysis plan is geared to investigate a broad range of immune pathways that might be affected by each agent. Proposed studies include analysis of (1) Molecules regulating early, mid, and late stages of T-cell activation, including expression of pathways such as CTLA4, Fas, and Fas ligand, believed to terminate immune responses; (2) Type I vs. type II cytokines synthesized by individual T-lymphocytes using new flow cytometry-based techniques (defines some subsets of effector lymphocytes); (3) Differentiation of memory vs. effector populations of CD8+ and CD4+ T-cell subsets using multiple molecular markers such as GMP-17 (TIA-1), CD27, CD28, CD57, CD45 isoforms, and CD29; (4) Trafficking of T-cells into psoriatic skin lesions, including expression of regulatory adhesion molecules such as CLA, CD11a, ICAM-1, CD29, and P/Eselectins; (5) Down-regulation of immune responses as measured by induction of T-cell apoptosis vs. induction of T-cell anergy. Furthermore, "mature" or activated Langerhans cells (as well as other types of dendritic antigen-presenting cells) may provide the stimulus for ongoing T-cell activation in psoriatic skin lesions. Hence, we will also study the effects of specific immune-blockade on the expression of co-stimulatory molecules (CD80, CD86, CD54, and CD40) that are up-regulated on dendritic cells in psoriatic skin lesions. Currently, the treatment of human autoimmune or immune-mediated diseases is hampered by 1) the lack of specific immune-directed therapeutics, especially agents without serious toxicity for non-immune cells and 2) a poor understanding of specific immune effector pathways and leukocyte or lymphocyte subsets that produce characteristic cellular pathology. As a whole, this group of diseases, which includes psoriasis, rheumatoid arthritis, inflammatory bowel disease, atopic dermatitis, type I diabetes, autoimmune thyroiditis, multiple sclerosis, and a variety of other disorders, constitutes a significant fraction of chronic human disease and overall health care costs. As the most common immunemediated human disease, psoriasis is the best model system with which to gain a comprehensive understanding of mechanisms involved in pathogenesis (it is accessible for study of leukocyte subsets in the diseased tissue; single-agent therapeutic trials can be conducted successfully in this disorder; and tissue-related pathology can be completely reversed by successful immune-directed therapy). Information about the safety, efficacy, and cellular/molecular mechanisms of new immune-directed therapeutics that are attained by the study of psoriasis can then be applied to other human immune-mediated diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: UV LIGHT AND THE CUTANEOUS NEUROSENSORY SYSTEM Principal Investigator & Institution: Glass, Jonathan D. Professor; Emory University 1784 North Decatur Road Atlanta, GA 30322 Timing: Fiscal Year 2002; Project Start 01-MAY-2002; Project End 30-APR-2004 Summary: Ultraviolet (UV) light affects the neurosensory system of the skin which likely plays an important pathophysiological role in various skin diseases. Mediators released from the cutaneous neurosensory system by UV irradiation participate in the sunburn reaction and UV-induced immunosupression, and in some skin diseases (e.g. psoriasis) the therapeutic effectiveness of UV treatment may be mediated by the cutaneous neurosensory system. This proposal will investigate the effect of UV light on the neurosensory system by measuring regulation of a number of soluble mediators released in response to UV irradiation. We will use cultured dorsal root ganglia (DRG) as a model of the peripheral nervous system (PNS) to investigate direct effects of UV light on sensory nerve fibers and their respective cell bodies. Responses measured in DRG will be compared to those in the intact neurocutaneous system in hairless mice. In
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Aim 1 we will analyze the effects of broadband and narrowband UVB irradiation on the sensory nerves from DRG. After single or repeated UVB exposure of DRG we will assess the UV effects on (i) the neuropeptides calcitonin gene-related peptide and substance P, (ii) the intracellular calcium levels of axons and ganglia cells, (iii) the expression of c-fos as a marker of neuronal activation, and (iv) the pattern and speed of axonal outgrowth. In Aim 2 we will compare the acute and chronic UV-induced effects observed in our "DRG-in vitro model" with the effects of acute and chronic UVB exposure on sensory nerves in the skin as well as on their respective cell bodies in the DRKs in hairless mice. The comparison of in vitro and in vivo data from our experiments should give us new insight in the effects of UV light on the cutaneous neurosensory system, and increase our understanding of direct and indirect interactions between UV irradiation and cutaneous nerves. In the future this knowledge could result in the improvement of present and the development of new treatments for skin diseases with neurosensory components. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: VITAMIN D3 FOR PSORIASIS Principal Investigator & Institution: Holick, Michael F.; Boston University Medical Campus 715 Albany St, 560 Boston, MA 02118 Timing: Fiscal Year 2001 Summary: This study is designed to evaluate the therapeutic efficacy of topically and orally administered 1.25-dihyroxyvitamin D3 in patients with psoriasis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: VITAMIN D--CHEMICAL AND RELATED STUDIES Principal Investigator & Institution: Okamura, William H. Professor; Chemistry; University of California Riverside 900 University Ave Riverside, CA 92521 Timing: Fiscal Year 2001; Project Start 01-APR-1977; Project End 31-MAR-2003 Summary: The goal of this investigation will continue to be the development of a detailed understanding at the molecular level of the mechanism of action of vitamin D. Through the design, chemical synthesis and biological evaluation of new analogs, appropriate structural evaluation of vitamin D metabolites and biological evaluation of new analogs, appropriate structural evaluation of vitamin D metabolites and analogs, both as the free ligand and bound to host proteins, and structure-function meta analyses of our own data together with literature data,a the long term goal is to define a more precise and practical protocol for treating disease states associated with vitamin Drelated endocrine disorders. From a biomedical standpoint, there are now many examples of pathological disruption of the normal state in which a drug form of vitamin D (an analog or metabolite) is proposed to be a potentially useful form of treatment, e.g. their use in treating various cancers (breast, colon and prostate cancers as well as leukemia), bone and kidney diseases (osteoporosis, renal osteodystrophy), skin diseases (psoriasis), neurological disorders (Alzheimer's disease), problems associated with the immune system (graft rejection and several autoimmune diseases) and also AIDS). The design of analogs to selectively interact with and then activate target tissues, presumably via a receptor mediated mechanism, is a continuing goal of medicinal chemistry. Structure determines function--it is this underlying thesis upon which this proposal is based. The specific aims of this proposal include; Aim 1, which concerns the chemical synthesis and nuclear magnetic resonance (NMR) spectroscopic investigations of protein bound, multiple C-13 labeled vitamin D metabolites [vitamin D3 (D3); 25-
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hydroxyvitamin D3 (25-D3); and 1alpha,25-dihydroxyvitamin D3 (1,25-D3)] as a means of assessing whether 6-s-cis or 6-s-trans conformations of ligand are involved in protein binding; Aim 2, which pertains tot he design and chemical synthesis and evaluation of 6-s-cis and related analogs of 1,25-D3 and other metabolites; Aim A-3, which addresses the problem of the design, chemical synthesis and biochemical evaluation of inhibitors of 25- hydroxyvitamin D3-1alpha-hydroxylase (25-D3-1-OHase), the key enzyme involved in the final step ina the metabolic activation of 25-D into its hormonally active form, 1,25-D3, and other aspects of vitamin D metabolism; Aim 4, which concerns studies of selected agonists and antagonists of vitamin D receptors; and Aim 5, which is expected to lead to the development of stereoselective chemical methods for synthesizing vitamin D and related polyenes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: XRAY STRUCTURE DETERMINATION OF RETINAL SPECIFIC DEHYDROGENASE Principal Investigator & Institution: Newcomer, Marcia E. Professor; Cornell University Ithaca Office of Sponsored Programs Ithaca, NY 14853 Timing: Fiscal Year 2001 Summary: The fibroblast growth factor (FGF) family is comprised of a group of at least nine cytokines which are characterized in part by binding to heparin, and which share 30-55% identity at the amino acid level. FGFs bind to a series of receptors among which is FGFR1 consisting of an intracellular split tyrosine portion, a transmembrane region, and an extracellular region comprised of two or three Ig domains, D(I), D (II), and D (III). In adult organisms, the FGFs are thought to play a role in would healing, in the pathology of tumor growth, rheumatoid arthritis, diabetic retinopathy, and psoriasis. New antagonists of FGF/FGFR1 interactions are expected to find applications for the control of angiogenesis and disease states that are neovascularization depdendent such as tumor growth and metastasis. To further understand the central role that the D(II) domain plays in the binding mechanism of the FGF system, we have undertaken a protein crystallization and x-ray diffraction study of this 118 residue fragment of FGFR1 expressed in E. coli. While we have obtained x-ray diffraction data to ~3 resolution from ~75 mm sized crystals using a storage phosphor detector and a Cu rotating anode source, we feel the combination of synchrotron radiation and cryocooling will give better quality and higher resolution data on these weakly diffracting crystals of the native protein. Phasing of the reflections will be done by MIR employing low resolution data collected using a rotating anode source. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and
3 4
Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.
With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age.
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unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “psoriasis” (or synonyms) into the search box. This search gives you access to fulltext articles. The following is a sample of items found for psoriasis in the PubMed Central database: •
Notch signalling is linked to epidermal cell differentiation level in basal cell carcinoma, psoriasis and wound healing. by Thelu J, Rossio P, Favier B. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=111189
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Proteasome inhibition reduces superantigen-mediated T cell activation and the severity of psoriasis in a SCID-hu model. by Zollner TM, Podda M, Pien C, Elliott PJ, Kaufmann R, Boehncke WH. 2002 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=150886
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Systematic review of comparative efficacy and tolerability of calcipotriol in treating chronic plaque psoriasis. by Ashcroft DM, Po AL, Williams HC, Griffiths CE. 2000 Apr 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27334
The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with psoriasis, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “psoriasis” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for psoriasis (hyperlinks lead to article summaries): •
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A case of childhood generalized pustular psoriasis treated with dapsone. Author(s): Yu HJ, Park JW, Park JM, Hwang DK, Park YW. Source: The Journal of Dermatology. 2001 June; 28(6): 316-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11476110&dopt=Abstract
The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print. 6 PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.
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A clinical evaluation of tazarotene 0.1% gel, with and without a high- or mid-highpotency corticosteroid, in patients with stable plaque psoriasis. Author(s): Green L, Sadoff W. Source: Journal of Cutaneous Medicine and Surgery. 2002 March-April; 6(2): 95-102. Epub 2002 February 13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11992180&dopt=Abstract
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A clinical study to determine the efficacy and safety of 1% methotrexate/Azone (MAZ) gel applied topically once daily in patients with psoriasis vulgaris. Author(s): Sutton L, Swinehart JM, Cato A, Kaplan AS. Source: International Journal of Dermatology. 2001 July; 40(7): 464-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11679005&dopt=Abstract
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A cognitive-behavioural symptom management programme as an adjunct in psoriasis therapy. Author(s): Fortune DG, Richards HL, Kirby B, Bowcock S, Main CJ, Griffiths CE. Source: The British Journal of Dermatology. 2002 March; 146(3): 458-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11952546&dopt=Abstract
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A comparative study of pediatric onset psoriasis with adult onset psoriasis. Author(s): Raychaudhuri SP, Gross J. Source: Pediatric Dermatology. 2000 May-June; 17(3): 174-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10886746&dopt=Abstract
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A comparative study of the expression of cytotoxic proteins in allergic contact dermatitis and psoriasis: spongiotic skin lesions in allergic contact dermatitis are highly infiltrated by T cells expressing perforin and granzyme B. Author(s): Yawalkar N, Hunger RE, Buri C, Schmid S, Egli F, Brand CU, Mueller C, Pichler WJ, Braathen LR. Source: American Journal of Pathology. 2001 March; 158(3): 803-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11238028&dopt=Abstract
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A comparison of psoralen plus ultraviolet A (PUVA) monotherapy, tacalcitol plus PUVA and tazarotene plus PUVA in patients with chronic plaque-type psoriasis. Author(s): Tzaneva S, Honigsmann H, Tanew A, Seeber A. Source: The British Journal of Dermatology. 2002 October; 147(4): 748-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12366423&dopt=Abstract
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A complementary note on the Morhenn's hypothesis on the pathomechanism of psoriasis. Author(s): Namazi MR. Source: Immunology Letters. 2003 February 3; 85(3): 223. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663134&dopt=Abstract
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A corticosteroid-induced flare of psoriasis. How to control or, better yet, avoid. Author(s): Brodell RT, Williams L. Source: Postgraduate Medicine. 1999 December; 106(7): 31-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10608962&dopt=Abstract
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A genome-wide search for genes predisposing to familial psoriasis by using a stratification approach. Author(s): Samuelsson L, Enlund F, Torinsson A, Yhr M, Inerot A, Enerback C, Wahlstrom J, Swanbeck G, Martinsson T. Source: Human Genetics. 1999 December; 105(6): 523-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10647885&dopt=Abstract
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A highly decreased binding of cyclic adenosine monophosphate to protein kinase A in erythrocyte membranes is specific for active psoriasis. Author(s): Schopf RE, Langendorf Y, Benz RE, Farber L, Benes P. Source: The Journal of Investigative Dermatology. 2002 July; 119(1): 160-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12164939&dopt=Abstract
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A host of novel agents for treating psoriasis, psoriatic arthritis stir interest. Author(s): Lamberg L. Source: Jama : the Journal of the American Medical Association. 2003 June 4; 289(21): 2779-80, 2783. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12783895&dopt=Abstract
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A multicenter dose-escalation trial with denileukin diftitox (ONTAK, DAB(389)IL-2) in patients with severe psoriasis. Author(s): Martin A, Gutierrez E, Muglia J, McDonald CJ, Guzzo C, Gottlieb A, Pappert A, Garland WT, Bagel J, Bacha P. Source: Journal of the American Academy of Dermatology. 2001 December; 45(6): 87181. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11712032&dopt=Abstract
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A new calcipotriol/betamethasone dipropionate formulation (Daivobet) is an effective once-daily treatment for psoriasis vulgaris. Author(s): Kaufmann R, Bibby AJ, Bissonnette R, Cambazard F, Chu AC, Decroix J, Douglas WS, Lowson D, Mascaro JM, Murphy GM, Stymne B. Source: Dermatology (Basel, Switzerland). 2002; 205(4): 389-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12444337&dopt=Abstract
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A new calcipotriol/betamethasone formulation with rapid onset of action was superior to monotherapy with betamethasone dipropionate or calcipotriol in psoriasis vulgaris. Author(s): Douglas WS, Poulin Y, Decroix J, Ortonne JP, Mrowietz U, Gulliver W, Krogstad AL, Larsen FG, Iglesias L, Buckley C, Bibby AJ. Source: Acta Dermato-Venereologica. 2002; 82(2): 131-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12125943&dopt=Abstract
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A new extended haplotype Cw*0602-B57-DRB1*0701-DQA1*0201-DQB1*0201 associated with psoriasis in the Croatian population. Author(s): Kastelan M, Gruber F, Cecuk-Jelicic E, Grubic Z, Kastelan A. Source: Clinical and Experimental Dermatology. 2003 March; 28(2): 200-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12653713&dopt=Abstract
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A novelliposomal formulation of dithranol for psoriasis: preliminary results. Author(s): Agarwal R, Saraswat A, Kaur I, Katare OP, Kumar B. Source: The Journal of Dermatology. 2002 August; 29(8): 529-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12227489&dopt=Abstract
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A practical guide to psoriasis. Author(s): Stollery NA. Source: Practitioner. 2002 November; 246(1640): 766-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12452120&dopt=Abstract
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A randomized, double-blind, multicenter trial comparing fluticasone propionate cream, 0.05%, and hydrocortisone-17-butyrate cream, 0.1%, applied twice daily for 4 weeks in the treatment of psoriasis. Author(s): James M. Source: Cutis; Cutaneous Medicine for the Practitioner. 2001 April; 67(4 Suppl): 2-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11338723&dopt=Abstract
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A randomized, double-blind, placebo-controlled phase III study evaluating efficacy and tolerability of 2 courses of alefacept in patients with chronic plaque psoriasis. Author(s): Krueger GG, Papp KA, Stough DB, Loven KH, Gulliver WP, Ellis CN; Alefacept Clinical Study Group. Source: Journal of the American Academy of Dermatology. 2002 December; 47(6): 82133. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12451365&dopt=Abstract
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A randomized, double-blind, placebo-controlled study of clobetasol propionate 0.05% foam in the treatment of nonscalp psoriasis. Author(s): Lebwohl M, Sherer D, Washenik K, Krueger GG, Menter A, Koo J, Feldman SR. Source: International Journal of Dermatology. 2002 May; 41(5): 269-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12100701&dopt=Abstract
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A randomized, observer-blinded trial of twice vs. three times weekly narrowband ultraviolet B phototherapy for chronic plaque psoriasis. Author(s): Cameron H, Dawe RS, Yule S, Murphy J, Ibbotson SH, Ferguson J. Source: The British Journal of Dermatology. 2002 November; 147(5): 973-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12410709&dopt=Abstract
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A review of the 308-nm excimer laser in the treatment of psoriasis. Author(s): Spann CT, Barbagallo J, Weinberg JM. Source: Cutis; Cutaneous Medicine for the Practitioner. 2001 November; 68(5): 351-2. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11766121&dopt=Abstract
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A role for mitogen-activated protein kinase activation by integrins in the pathogenesis of psoriasis. Author(s): Haase I, Hobbs RM, Romero MR, Broad S, Watt FM. Source: The Journal of Clinical Investigation. 2001 August; 108(4): 527-36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11518726&dopt=Abstract
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A simple technique for high-throughput screening of drugs that modulate normal and psoriasis-like differentiation in cultured human keratinocytes. Author(s): Pol A, Bergers M, van Ruissen F, Pfundt R, Schalkwijk J. Source: Skin Pharmacology and Applied Skin Physiology. 2002 July-August; 15(4): 25261. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12218287&dopt=Abstract
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A study of candidate genes for psoriasis near HLA-C in Chinese patients with psoriasis. Author(s): Chang YT, Tsai SF, Lee DD, Shiao YM, Huang CY, Liu HN, Wang WJ, Wong CK. Source: The British Journal of Dermatology. 2003 March; 148(3): 418-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12653732&dopt=Abstract
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A systematic review of adverse effects associated with topical treatments for psoriasis. Author(s): Bruner CR, Feldman SR, Ventrapragada M, Fleischer AB Jr. Source: Dermatology Online Journal [electronic Resource]. 2003 February; 9(1): 2. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12639460&dopt=Abstract
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A systematic review of antistreptococcal interventions for guttate and chronic plaque psoriasis. Author(s): Owen CM, Chalmers RJ, O'Sullivan T, Griffiths CE. Source: The British Journal of Dermatology. 2001 December; 145(6): 886-90. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11899140&dopt=Abstract
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Aberrant caveolin-1 expression in psoriasis: a signalling hypothesis. Author(s): Campbell L, Gumbleton M. Source: Iubmb Life. 2000 December; 50(6): 361-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11327308&dopt=Abstract
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Abnormalities of human genetic apparatus manifested in leukocyte proteins in psoriasis. Author(s): Paponov VD, Suntsova IG, Baidakova GV, Mordovtsev VN. Source: Bulletin of Experimental Biology and Medicine. 2001 March; 131(3): 260-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11427915&dopt=Abstract
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Activity of superoxide dismutase and catalase and the level of lipid peroxidation products reactive with TBA in patients with psoriasis. Author(s): Drewa G, Krzyzynska-Malinowska E, Wozniak A, Protas-Drozd F, MilaKierzenkowska C, Rozwodowska M, Kowaliszyn B, Czajkowski R. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2002 August; 8(8): Br338-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12165738&dopt=Abstract
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Acute pustular psoriasis complicated by leukocytoclastic vasculitis. Author(s): Welsch MJ. Source: J Drugs Dermatol. 2003 April; 2(2): 193-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12852373&dopt=Abstract
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Acute salicylate intoxication after percutaneous absorption in an HIV patient treated for psoriasis. Author(s): Peyriere H, Balmes N, Rouanet I, Mauboussin JM, Hillaire-Buys D, Arich C, Blayac JP, Vincent D. Source: Aids (London, England). 2002 September 6; 16(13): 1843-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12218404&dopt=Abstract
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Addition of low-dose methotrexate to infliximab in the treatment of a patient with severe, recalcitrant pustular psoriasis. Author(s): Barland C, Kerdel FA. Source: Archives of Dermatology. 2003 July; 139(7): 949-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12873907&dopt=Abstract
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Addition of pentoxifylline could reduce the side effects of fumaric acid esters in the treatment of psoriasis. Author(s): Friedrich M, Sterry W, Klein A, Ruckert R, Docke WD, Asadullah K. Source: Acta Dermato-Venereologica. 2001 November-December; 81(6): 429-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11859949&dopt=Abstract
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Advances in psoriasis therapy. Author(s): Lebwohl M. Source: Dermatologic Clinics. 2000 January; 18(1): 13-9, Vii. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10626107&dopt=Abstract
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Advances in psoriasis treatment. Author(s): Feldman S. Source: Dermatology Online Journal [electronic Resource]. 2000 September; 6(1): 4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11328614&dopt=Abstract
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Advances in systemic therapy for psoriasis. Author(s): Mrowietz U. Source: Clinical and Experimental Dermatology. 2001 June; 26(4): 362-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422190&dopt=Abstract
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Advances in the management of psoriasis: monoclonal antibody therapies. Author(s): Mehrabi D, DiCarlo JB, Soon SL, McCall CO. Source: International Journal of Dermatology. 2002 December; 41(12): 827-35. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492964&dopt=Abstract
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Advances in the search for psoriasis susceptibility genes. Author(s): Capon F, Dallapiccola B, Novelli G. Source: Molecular Genetics and Metabolism. 2000 September-October; 71(1-2): 250-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11001818&dopt=Abstract
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Adverse effects with long-term cyclosporin for severe psoriasis. Author(s): Markham T, Watson A, Rogers S. Source: Clinical and Experimental Dermatology. 2002 March; 27(2): 111-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11952700&dopt=Abstract
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Alcohol intake and psoriasis. Author(s): Wolf R, Wolf D, Ruocco V. Source: Clinics in Dermatology. 1999 July-August; 17(4): 423-30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10497727&dopt=Abstract
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Alefacept for chronic plaque psoriasis: a selective therapy with long-lasting disease remissions and an encouraging safety profile. Author(s): Leone G, Rolston K, Spaulding G. Source: Dermatology Nursing / Dermatology Nurses' Association. 2003 June; 15(3): 21620, 224-5; Quiz 226. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12875010&dopt=Abstract
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Alefacept therapy produces remission for patients with chronic plaque psoriasis. Author(s): Krueger GG, Ellis CN. Source: The British Journal of Dermatology. 2003 April; 148(4): 784-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12752139&dopt=Abstract
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Alefacept: potential new therapy for patients with moderate-to-severe psoriasis. Author(s): Shukla VK. Source: Issues Emerg Health Technol. 2003 April; (45): 1-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12680422&dopt=Abstract
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Alefacept-induced decreases in circulating blood lymphocyte counts correlate with clinical response in patients with chronic plaque psoriasis. Author(s): Ortonne JP, Lebwohl M, Em Griffiths C; Alefacept Clinical Study Group. Source: Eur J Dermatol. 2003 March-April; 13(2): 117-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12695125&dopt=Abstract
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Allelic distribution of complement components BF, C4A, C4B, and C3 in Psoriasis vulgaris. Author(s): Cislo M, Halasa J, Wasik F, Nockowski P, Prussak M, Manczak M, Kusnierczyk P. Source: Immunology Letters. 2002 March 1; 80(3): 145-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11803045&dopt=Abstract
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Allelic variants of drug metabolizing enzymes as risk factors in psoriasis. Author(s): Richter-Hintz D, Their R, Steinwachs S, Kronenberg S, Fritsche E, Sachs B, Wulferink M, Tonn T, Esser C. Source: The Journal of Investigative Dermatology. 2003 May; 120(5): 765-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12713578&dopt=Abstract
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Alopecia universalis associated with Zumbusch-type generalized pustular psoriasis. Author(s): Miyazaki Y, Yamamoto T, Watanabe K, Katayama I, Nishioka K. Source: Dermatology (Basel, Switzerland). 2002; 204(4): 308-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12077534&dopt=Abstract
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Alteration of the expression of Bcl-2, Bcl-x, Bax, Fas, and Fas ligand in the involved skin of psoriasis vulgaris following topical anthralin therapy. Author(s): Yamamoto T, Nishioka K. Source: Skin Pharmacology and Applied Skin Physiology. 2003 January-February; 16(1): 50-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12566829&dopt=Abstract
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Altered expression of angiopoietins and Tie2 endothelium receptor in psoriasis. Author(s): Kuroda K, Sapadin A, Shoji T, Fleischmajer R, Lebwohl M. Source: The Journal of Investigative Dermatology. 2001 May; 116(5): 713-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11348459&dopt=Abstract
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Altered expression of occludin and tight junction formation in psoriasis. Author(s): Yoshida Y, Morita K, Mizoguchi A, Ide C, Miyachi Y. Source: Archives of Dermatological Research. 2001 May; 293(5): 239-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11409568&dopt=Abstract
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An international, randomized, double-blind, placebo-controlled phase 3 trial of intramuscular alefacept in patients with chronic plaque psoriasis. Author(s): Lebwohl M, Christophers E, Langley R, Ortonne JP, Roberts J, Griffiths CE; Alefacept Clinical Study Group. Source: Archives of Dermatology. 2003 June; 139(6): 719-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810502&dopt=Abstract
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An open trial of oral macrolide treatment for psoriasis vulgaris. Author(s): Komine M, Tamaki K. Source: The Journal of Dermatology. 2000 August; 27(8): 508-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10989574&dopt=Abstract
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Analysis of phenotypic variation in psoriasis as a function of age at onset and family history. Author(s): Stuart P, Malick F, Nair RP, Henseler T, Lim HW, Jenisch S, Voorhees J, Christophers E, Elder JT. Source: Archives of Dermatological Research. 2002 July; 294(5): 207-13. Epub 2002 June 13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12115023&dopt=Abstract
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Angiogenesis in psoriasis. Author(s): Creamer D, Sullivan D, Bicknell R, Barker J. Source: Angiogenesis. 2002; 5(4): 231-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12906316&dopt=Abstract
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Annular pustular psoriasis--most common form of pustular psoriasis in children: report of three cases and review of the literature. Author(s): Liao PB, Rubinson R, Howard R, Sanchez G, Frieden IJ. Source: Pediatric Dermatology. 2002 January-February; 19(1): 19-25. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11860564&dopt=Abstract
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Annular verrucous psoriasis with exaggerated papillomatosis. Author(s): Erkek E, Bozdogan O. Source: The American Journal of Dermatopathology. 2001 April; 23(2): 133-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11285408&dopt=Abstract
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Antagonistic effects of the staphylococcal enterotoxin a mutant, SEA(F47A/D227A), on psoriasis in the SCID-hu xenogeneic transplantation model. Author(s): Boehncke WH, Hardt-Weinelt K, Nilsson H, Wolter M, Dohlsten M, Ochsendorf FR, Kaufmann R, Antonsson P. Source: The Journal of Investigative Dermatology. 2001 April; 116(4): 596-601. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11286628&dopt=Abstract
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Anti-CD4 monoclonal antibody treatment of moderate to severe psoriasis vulgaris: results of a pilot, multicenter, multiple-dose, placebo-controlled study. Author(s): Gottlieb AB, Lebwohl M, Shirin S, Sherr A, Gilleaudeau P, Singer G, Solodkina G, Grossman R, Gisoldi E, Phillips S, Neisler HM, Krueger JG. Source: Journal of the American Academy of Dermatology. 2000 October; 43(4): 595-604. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11004613&dopt=Abstract
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Anti-E-selectin is ineffective in the treatment of psoriasis: a randomized trial. Author(s): Bhushan M, Bleiker TO, Ballsdon AE, Allen MH, Sopwith M, Robinson MK, Clarke C, Weller RP, Graham-Brown RA, Keefe M, Barker JN, Griffiths CE. Source: The British Journal of Dermatology. 2002 May; 146(5): 824-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12000379&dopt=Abstract
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Antioxidant potential of propylthiouracil in patients with psoriasis. Author(s): Utas S, Kose K, Yazici C, Akdas A, Kelestimur F. Source: Clinical Biochemistry. 2002 May; 35(3): 241-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12074833&dopt=Abstract
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Anti-tumor necrosis factor alpha therapy in psoriatic arthritis and psoriasis. Author(s): Girolomoni G, Abeni D. Source: Archives of Dermatology. 2001 June; 137(6): 784-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11405771&dopt=Abstract
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Arginase 1 overexpression in psoriasis: limitation of inducible nitric oxide synthase activity as a molecular mechanism for keratinocyte hyperproliferation. Author(s): Bruch-Gerharz D, Schnorr O, Suschek C, Beck KF, Pfeilschifter J, Ruzicka T, Kolb-Bachofen V. Source: American Journal of Pathology. 2003 January; 162(1): 203-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12507903&dopt=Abstract
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Assessing the safety of immunologic modifiers for the treatment of chronic disease: the psoriasis paradigm. Author(s): Stern RS. Source: The Journal of Investigative Dermatology. 2003 February; 120(2): Xi-Xii. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12542547&dopt=Abstract
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Assessment of depression in subjects with psoriasis vulgaris and lichen planus. Author(s): Akay A, Pekcanlar A, Bozdag KE, Altintas L, Karaman A. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2002 July; 16(4): 347-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12224690&dopt=Abstract
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Association between psoriasis severity and transforming growth factor beta(1) and beta (2) in plasma and scales from psoriatic lesions. Author(s): Flisiak I, Chodynicka B, Porebski P, Flisiak R. Source: Cytokine. 2002 August 7; 19(3): 121-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12242078&dopt=Abstract
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Association of HIV infection, pyoderma gangrenosum and psoriasis. Author(s): Kreuter A, Gambichler T, Hoffmann K, Altmeyer P, Brockmeyer NH. Source: Acta Dermato-Venereologica. 2002; 82(2): 150-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12125953&dopt=Abstract
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Association of psoriasis vulgaris with HLA class I and class II antigens in the Turkish population, according to the age at onset. Author(s): Kundakci N, Oskay T, Olmez U, Tutkak H, Gurgey E. Source: International Journal of Dermatology. 2002 June; 41(6): 345-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12100689&dopt=Abstract
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Association of TAP and HLA-DM genes with psoriasis in Koreans. Author(s): Pyo CW, Hur SS, Kim YK, Kim TY, Kim TG. Source: The Journal of Investigative Dermatology. 2003 April; 120(4): 616-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12648225&dopt=Abstract
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Atypical pityriasis rosea or psoriasis guttata? Early examination is the key to a correct diagnosis. Author(s): Eslick GD. Source: International Journal of Dermatology. 2002 November; 41(11): 788-91. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12453007&dopt=Abstract
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Baseline relationships between psoriasis and psoriatic arthritis: analysis of 221 patients with active psoriatic arthritis. Department of Veterans Affairs Cooperative Study Group on Seronegative Spondyloarthropathies. Author(s): Cohen MR, Reda DJ, Clegg DO. Source: The Journal of Rheumatology. 1999 August; 26(8): 1752-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10451073&dopt=Abstract
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Basement membrane alterations in psoriasis are accompanied by epidermal overexpression of MMP-2 and its inhibitor TIMP-2. Author(s): Fleischmajer R, Kuroda K, Hazan R, Gordon RE, Lebwohl MG, Sapadin AN, Unda F, Iehara N, Yamada Y. Source: The Journal of Investigative Dermatology. 2000 November; 115(5): 771-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11069613&dopt=Abstract
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Basis of occlusive therapy in psoriasis: correcting defects in permeability barrier and calcium gradient. Author(s): Hwang SM, Ahn SK, Menon GK, Choi EH, Lee SH. Source: International Journal of Dermatology. 2001 March; 40(3): 223-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422532&dopt=Abstract
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B-cell lymphoma developing in a patient on cyclosporin for recalcitrant psoriasis. Author(s): Cliff S, Pettengell R, Gharge S, Marsden RA. Source: The British Journal of Dermatology. 1999 April; 140(4): 763-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10233345&dopt=Abstract
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Beneficial effects of fumarate therapy in psoriasis vulgaris patients coincide with downregulation of type 1 cytokines. Author(s): Litjens NH, Nibbering PH, Barrois AJ, Zomerdijk TP, Van Den Oudenrijn AC, Noz KC, Rademaker M, Van De Meide PH, Van Dissel JT, Thio B. Source: The British Journal of Dermatology. 2003 March; 148(3): 444-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12653735&dopt=Abstract
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Beta-blocker-induced psoriasis: a rare side effect--a case report. Author(s): Yilmaz MB, Turhan H, Akin Y, Kisacik HL, Korkmaz S. Source: Angiology. 2002 November-December; 53(6): 737-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12463630&dopt=Abstract
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Betamethasone valerate foam for treatment of nonscalp psoriasis. Author(s): Stein LF, Sherr A, Solodkina G, Gottlieb AB, Chaudhari U. Source: Journal of Cutaneous Medicine and Surgery. 2001 July-August; 5(4): 303-7. Epub 2001 July 18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11907840&dopt=Abstract
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Betamethasone valerate in foam vehicle is effective with both daily and twice a day dosing: a single-blind, open-label study in the treatment of scalp psoriasis. Author(s): Feldman SR, Ravis SM, Fleischer AB Jr, McMichael A, Jones E, Kaplan R, Shavin J, Weiss J, Bartruff JK, Levin DL, Del Rosso J, Kpea N. Source: Journal of Cutaneous Medicine and Surgery. 2001 September-October; 5(5): 3869. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11907847&dopt=Abstract
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Better patient compliance in psoriasis. Author(s): Chu T. Source: Practitioner. 2000 March; 244(1608): 238-42, 244. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10859810&dopt=Abstract
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Bilateral femoral avascular necrosis in a man with psoriasis: responsibility of topical corticosteroids and role of cyclosporine. Author(s): Reichert-Penetrat S, Trechot P, Barbaud A, Gillet P, Schmutz JL. Source: Dermatology (Basel, Switzerland). 2001; 203(4): 356-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11752834&dopt=Abstract
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Biologic effects of bacterial superantigens in a xenogeneic transplantation model for psoriasis. Author(s): Boehncke WH. Source: The Journal of Investigative Dermatology. Symposium Proceedings / the Society for Investigative Dermatology, Inc. [and] European Society for Dermatological Research. 2001 December; 6(3): 231-2. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11924833&dopt=Abstract
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Biologic therapy for psoriasis: a brief history, I. Author(s): Tutrone WD, Kagen MH, Barbagallo J, Weinberg JM. Source: Cutis; Cutaneous Medicine for the Practitioner. 2001 November; 68(5): 331-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11766118&dopt=Abstract
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Biologic therapy for psoriasis: a brief history, II. Author(s): Tutrone WD, Kagen MH, Barbagallo J, Weinberg JM. Source: Cutis; Cutaneous Medicine for the Practitioner. 2001 December; 68(6): 367-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11775769&dopt=Abstract
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Biologic therapy for psoriasis: the new therapeutic frontier. Author(s): Singri P, West DP, Gordon KB. Source: Archives of Dermatology. 2002 May; 138(5): 657-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12020229&dopt=Abstract
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Biologic therapy for psoriasis: the T-cell-targeted therapies efalizumab and alefacept. Author(s): Weinberg JM, Tutrone WD. Source: Cutis; Cutaneous Medicine for the Practitioner. 2003 January; 71(1): 41-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12553629&dopt=Abstract
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Biologic therapy for psoriasis: the tumor necrosis factor inhibitors infliximab and etanercept. Author(s): Weinberg JM, Saini R. Source: Cutis; Cutaneous Medicine for the Practitioner. 2003 January; 71(1): 25-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12553627&dopt=Abstract
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Biologic therapy for psoriasis--the first wave: infliximab, etanercept, efalizumab, and alefacept. Author(s): Weinberg JM, Saini R, Tutrone WD. Source: J Drugs Dermatol. 2002 December; 1(3): 303-10. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12851990&dopt=Abstract
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Biological activity of tyrosine kinase inhibitors: novel agents for psoriasis therapy. Author(s): Ben-Bassat H. Source: Curr Opin Investig Drugs. 2001 November; 2(11): 1539-45. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11763154&dopt=Abstract
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Blood thiols and malondialdehyde levels in psoriasis. Author(s): Relhan V, Gupta SK, Dayal S, Pandey R, Lal H. Source: The Journal of Dermatology. 2002 July; 29(7): 399-403. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12184635&dopt=Abstract
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Blood transfusions and psoriasis: is there a link? Author(s): O'Reilly MA, Decker S, Krueger GG. Source: Archives of Dermatology. 2000 February; 136(2): 270-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10677113&dopt=Abstract
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Body-weight-independent dosing of cyclosporine micro-emulsion and three times weekly maintenance regimen in severe psoriasis. A randomised study. Author(s): Thaci D, Brautigam M, Kaufmann R, Weidinger G, Paul C, Christophers E. Source: Dermatology (Basel, Switzerland). 2002; 205(4): 383-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12444336&dopt=Abstract
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Bone mineral density of patients with chronic plaque psoriasis. Author(s): Millard TP, Antoniades L, Evans AV, Smith HR, Spector TD, Barker JN. Source: Clinical and Experimental Dermatology. 2001 July; 26(5): 446-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11488836&dopt=Abstract
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Bullous and non-bullous ichthyosiform erythroderma associated with generalized pustular psoriasis of von Zumbusch type. Author(s): Ingen-Housz-Oro S, Vignon-Pennamen MD, Blanchet-Bardon C. Source: The British Journal of Dermatology. 2001 November; 145(5): 823-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11736910&dopt=Abstract
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Calcipotriol and betamethasone dipropionate (Dovobet, Daivobet): a new formulation for the treatment of psoriasis. Author(s): Poulin Y. Source: Skin Therapy Letter. 2002 June; 7(6): 1-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12223976&dopt=Abstract
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Calcipotriol ointment. A review of its use in the management of psoriasis. Author(s): Scott LJ, Dunn CJ, Goa KL. Source: American Journal of Clinical Dermatology. 2001; 2(2): 95-120. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11705309&dopt=Abstract
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Calcipotriol plus short-contact dithranol: a novel topical combination therapy for chronic plaque psoriasis. Author(s): Monastirli A, Georgiou S, Pasmatzi E, Sakkis T, Badavanis G, Drainas D, Sagriotis A, Tsambaos D. Source: Skin Pharmacology and Applied Skin Physiology. 2002 July-August; 15(4): 24651. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12218286&dopt=Abstract
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Calcipotriol solution for the treatment of scalp psoriasis: evaluation of efficacy, safety and acceptance in 3,396 patients. Author(s): Thaci D, Daiber W, Boehncke WH, Kaufmann R. Source: Dermatology (Basel, Switzerland). 2001; 203(2): 153-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11586015&dopt=Abstract
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Calcipotriol vs. tazarotene as combination therapy with narrowband ultraviolet B (311 nm): efficacy in patients with severe psoriasis. Author(s): Schiener R, Behrens-Williams SC, Pillekamp H, Kaskel P, Peter RU, Kerscher M. Source: The British Journal of Dermatology. 2000 December; 143(6): 1275-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11122033&dopt=Abstract
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Calcitriol 3 microg g-1 ointment in combination with ultraviolet B phototherapy for the treatment of plaque psoriasis: results of a comparative study. Author(s): Ring J, Kowalzick L, Christophers E, Schill WB, Schopf E, Stander M, Wolff HH, Altmeyer P. Source: The British Journal of Dermatology. 2001 March; 144(3): 495-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11260005&dopt=Abstract
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Calcitriol ointment and clobetasol propionate cream: a new regimen for the treatment of plaque psoriasis. Author(s): Lahfa M, Mrowietz U, Koenig M, Simon JC. Source: Eur J Dermatol. 2003 May-June; 13(3): 261-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12804986&dopt=Abstract
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Calcitriol shows greater persistence of treatment effect than betamethasone dipropionate in topical psoriasis therapy. Author(s): Camarasa JM, Ortonne JP, Dubertret L. Source: The Journal of Dermatological Treatment. 2003 January; 14(1): 8-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745849&dopt=Abstract
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Calcitriol vs. dithranol in combination with narrow-band ultraviolet B (311 nm) in psoriasis. Author(s): Hofmann UB, Eggert AA, Brocker EB, Goebeler M. Source: The British Journal of Dermatology. 2003 April; 148(4): 779-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12752138&dopt=Abstract
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Calcium channel blockers intake and psoriasis: a case-control study. Author(s): Cohen AD, Kagen M, Friger M, Halevy S. Source: Acta Dermato-Venereologica. 2001 October-November; 81(5): 347-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11800142&dopt=Abstract
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Calcium homeostasis remains unaffected after 12 weeks' therapy with calcitriol 3 microg/g ointment; no correlation with extent of psoriasis. Author(s): Barker JN, Berth-Jones J, Groves R, Omerod AD, Rizova E, Griffiths CE. Source: The Journal of Dermatological Treatment. 2003 January; 14(1): 14-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745850&dopt=Abstract
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Cancer risk in a population-based cohort of patients hospitalized for psoriasis in Sweden. Author(s): Boffetta P, Gridley G, Lindelof B. Source: The Journal of Investigative Dermatology. 2001 December; 117(6): 1531-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11886519&dopt=Abstract
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CD3+CD56+ NK T cells are significantly decreased in the peripheral blood of patients with psoriasis. Author(s): Koreck A, Suranyi A, Szony BJ, Farkas A, Bata-Csorgo Z, Kemeny L, Dobozy A. Source: Clinical and Experimental Immunology. 2002 January; 127(1): 176-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11882050&dopt=Abstract
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CD30+ T-cell lymphoma in a patient with psoriasis treated with ciclosporin and infliximab. Author(s): Mahe E, Descamps V, Grossin M, Fraitag S, Crickx B. Source: The British Journal of Dermatology. 2003 July; 149(1): 170-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890213&dopt=Abstract
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CD4+ T-cells from peripheral blood of a patient with psoriasis recognize keratin 14 peptide but not 'homologous' streptococcal M-protein epitope. Author(s): Kobayashi H, Takahashi M, Takahashi H, Ishida-Yamamoto A, Hashimoto Y, Sato K, Tateno M, Iizuka H. Source: Journal of Dermatological Science. 2002 December; 30(3): 240-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12443847&dopt=Abstract
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CD69, HLA-DR and the IL-2R identify persistently activated T cells in psoriasis vulgaris lesional skin: blood and skin comparisons by flow cytometry. Author(s): Ferenczi K, Burack L, Pope M, Krueger JG, Austin LM. Source: Journal of Autoimmunity. 2000 February; 14(1): 63-78. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10648117&dopt=Abstract
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CD8+ cell changes in psoriasis associated with roxithromycin-induced clinical improvement. Author(s): Ohshima A, Takigawa M, Tokura Y. Source: Eur J Dermatol. 2001 September-October; 11(5): 410-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11525946&dopt=Abstract
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Cell-kinetic evidence for increased recruitment of cycling epidermal cells in psoriasis: the ratio of histone and Ki-67 antigen expression is constant. Author(s): Castelijns FA, Gerritsen MJ, van Erp PE, van de Kerkhof PC. Source: Dermatology (Basel, Switzerland). 2000; 201(2): 105-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11053911&dopt=Abstract
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Cellular localization of fractalkine at sites of inflammation: antigen-presenting cells in psoriasis express high levels of fractalkine. Author(s): Raychaudhuri SP, Jiang WY, Farber EM. Source: The British Journal of Dermatology. 2001 June; 144(6): 1105-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422028&dopt=Abstract
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Changes in keratin 6 and keratin 10 (co-)expression in lesional and symptomless skin of spreading psoriasis. Author(s): Mommers JM, van Rossum MM, van Erp PE, van De Kerkhof PC. Source: Dermatology (Basel, Switzerland). 2000; 201(1): 15-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10971053&dopt=Abstract
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Changes of skin blood flow and color on lesional and control sites during PUVA therapy for psoriasis. Author(s): Suh DH, Kwon TE, Kim SD, Park SB, Kwon OS, Eun HC, Youn JI. Source: Journal of the American Academy of Dermatology. 2001 June; 44(6): 987-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11369911&dopt=Abstract
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Characterization of a T cell line bearing natural killer receptors and capable of creating psoriasis in a SCID mouse model system. Author(s): Nickoloff BJ, Bonish B, Huang BB, Porcelli SA. Source: Journal of Dermatological Science. 2000 December; 24(3): 212-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11084303&dopt=Abstract
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Childhood psoriasis. Author(s): Rogers M. Source: Current Opinion in Pediatrics. 2002 August; 14(4): 404-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12130902&dopt=Abstract
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Childhood psoriasis: a clinical review of 1262 cases. Author(s): Morris A, Rogers M, Fischer G, Williams K. Source: Pediatric Dermatology. 2001 May-June; 18(3): 188-98. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11437997&dopt=Abstract
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Chronic actinic dermatitis developed during phototherapy for psoriasis. Author(s): Fujii N, Uetsu N, Hamakawa M, Futamura S, Okamoto H, Horio T. Source: Photodermatology, Photoimmunology & Photomedicine. 2002 June; 18(3): 157-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12207682&dopt=Abstract
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Chronic plaque psoriasis. Author(s): Naldi L, Rzany B. Source: Clin Evid. 2002 June; (7): 1488-507. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12230765&dopt=Abstract
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Chronic tophaceous gout presenting as hyperpigmented nodules in the limbs of a patient with coexisting psoriasis. Author(s): Cho S, Koh GJ, Choi JH, Sung KJ, Moon KC, Koh JK. Source: The Journal of Dermatology. 2001 August; 28(8): 433-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11560160&dopt=Abstract
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Circulating natural killer cells in psoriasis. Author(s): Cameron AL, Kirby B, Griffiths CE. Source: The British Journal of Dermatology. 2003 July; 149(1): 160-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890211&dopt=Abstract
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Classical conditioning in the treatment of psoriasis. Author(s): Ader R. Source: Cutis; Cutaneous Medicine for the Practitioner. 2000 November; 66(5): 370-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11107523&dopt=Abstract
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Clearance can be a realistic expectation of psoriasis treatment. Author(s): Bowman PH, Koo JY. Source: Journal of the American Academy of Dermatology. 2001 September; 45(3): 476. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11511853&dopt=Abstract
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Clearance in psoriasis treatment. Author(s): Kumar B, Saraswat A. Source: Journal of the American Academy of Dermatology. 2001 July; 45(1): 153-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11423858&dopt=Abstract
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Clinical and histologic response to single-dose treatment of moderate to severe psoriasis with an anti-CD80 monoclonal antibody. Author(s): Gottlieb AB, Lebwohl M, Totoritis MC, Abdulghani AA, Shuey SR, Romano P, Chaudhari U, Allen RS, Lizambri RG. Source: Journal of the American Academy of Dermatology. 2002 November; 47(5): 692700. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12399760&dopt=Abstract
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Clinical and immunologic assessment of patients with psoriasis in a randomized, double-blind, placebo-controlled trial using recombinant human interleukin 10. Author(s): Kimball AB, Kawamura T, Tejura K, Boss C, Hancox AR, Vogel JC, Steinberg SM, Turner ML, Blauvelt A. Source: Archives of Dermatology. 2002 October; 138(10): 1341-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12374540&dopt=Abstract
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Clinical efficacy of narrow-band UVB (311 nm) combined with dithranol in psoriasis. An open pilot study. Author(s): Carrozza P, Hausermann P, Nestle FO, Burg G, Boni R. Source: Dermatology (Basel, Switzerland). 2000; 200(1): 35-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10681611&dopt=Abstract
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Clinical experience with topical calcitriol (1,25-dihydroxyvitamin D3) in psoriasis. Author(s): Kowalzick L. Source: The British Journal of Dermatology. 2001 April; 144 Suppl 58: 21-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11501509&dopt=Abstract
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Clinical management of psoriasis: principles and practice. Author(s): Lebwohl M, Feldman SR, Walther R, Shelk J, Morgan P, Gutkin SW. Source: Cutis; Cutaneous Medicine for the Practitioner. 2001 January; 67(1 Suppl): 1-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11210296&dopt=Abstract
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Clobetasol under hydrocolloid occlusion in psoriasis results in a complete block of proliferation and in a rebound of lesions following discontinuation. Author(s): Mommers JM, van Erp PE, van De Kerkhof PC. Source: Dermatology (Basel, Switzerland). 1999; 199(4): 323-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10640842&dopt=Abstract
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Coding haplotype analysis supports HCR as the putative susceptibility gene for psoriasis at the MHC PSORS1 locus. Author(s): Asumalahti K, Veal C, Laitinen T, Suomela S, Allen M, Elomaa O, Moser M, de Cid R, Ripatti S, Vorechovsky I, Marcusson JA, Nakagawa H, Lazaro C, Estivill X, Capon F, Novelli G, Saarialho-Kere U, Barker J, Trembath R, Kere J; Psoriasis Consortium. Source: Human Molecular Genetics. 2002 March 1; 11(5): 589-97. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11875053&dopt=Abstract
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Coexistence of epilepsy, myasthenia gravis and psoriasis vulgaris. Author(s): Kwan SY, Lin JH, Su MS. Source: Zhonghua Yi Xue Za Zhi (Taipei). 2000 February; 63(2): 153-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10677928&dopt=Abstract
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Coexistence of psoriasis vulgaris, bullous pemphigoid and vitiligo: a case report. Author(s): Pasic A, Ljubojevic S, Lipozencic J, Marinovic B, Loncaric D. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2002 July; 16(4): 426-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12224717&dopt=Abstract
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Combination of calcipotriene (Dovonex) ointment and tazarotene (Tazorac) gel versus clobetasol ointment in the treatment of plaque psoriasis: a pilot study. Author(s): Bowman PH, Maloney JE, Koo JY. Source: Journal of the American Academy of Dermatology. 2002 June; 46(6): 907-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12063489&dopt=Abstract
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Combination phototherapy of psoriasis with narrow-band UVB irradiation and topical tazarotene gel. Author(s): Behrens S, Grundmann-Kollmann M, Schiener R, Peter RU, Kerscher M. Source: Journal of the American Academy of Dermatology. 2000 March; 42(3): 493-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10688723&dopt=Abstract
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Combination regimens of topical calcipotriene in chronic plaque psoriasis: systematic review of efficacy and tolerability. Author(s): Ashcroft DM, Li Wan Po A, Williams HC, Griffiths CE. Source: Archives of Dermatology. 2000 December; 136(12): 1536-43. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11115167&dopt=Abstract
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Combination TL01 ultraviolet B phototherapy and topical calcipotriol for psoriasis: a prospective randomized placebo-controlled clinical trial. Author(s): Woo WK, McKenna KE. Source: The British Journal of Dermatology. 2003 July; 149(1): 146-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890208&dopt=Abstract
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Combination treatment seems rarely to be used in psoriasis. Author(s): Cullington D, Jhamatt A. Source: Bmj (Clinical Research Ed.). 2000 August 12; 321(7258): 452. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10991603&dopt=Abstract
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Combined mycophenolate mofetil and cyclosporin therapy for severe recalcitrant psoriasis. Author(s): Ameen M, Smith HR, Barker JN. Source: Clinical and Experimental Dermatology. 2001 September; 26(6): 480-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11678869&dopt=Abstract
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Combined segregation and linkage analysis of HLA markers in familial psoriasis. Author(s): Guo SW, Jenisch S, Stuart P, Lange EM, Kukuruga D, Nair R, Henseler T, Voorhees J, Christophers E, Elder JT. Source: European Journal of Human Genetics : Ejhg. 2002 May; 10(5): 327-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12082508&dopt=Abstract
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Combining lesional short-contact dithranol therapy of psoriasis with a potent topical corticosteroid. Author(s): Swinkels OQ, Prins M, Kucharekova M, de Boo T, Gerritsen MJ, van der Valk PG, van de Kerkhof PC. Source: The British Journal of Dermatology. 2002 April; 146(4): 621-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11966693&dopt=Abstract
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Comparative association analysis reveals that corneodesmosin is more closely associated with psoriasis than HLA-Cw*0602-B*5701 in German families. Author(s): Schmitt-Egenolf M, Windemuth C, Hennies HC, Albis-Camps M, von Engelhardt B, Wienker T, Reis A, Traupe H, Blasczyk R. Source: Tissue Antigens. 2001 May; 57(5): 440-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11556968&dopt=Abstract
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Comparative tolerability of systemic treatments for plaque-type psoriasis. Author(s): McClure SL, Valentine J, Gordon KB. Source: Drug Safety : an International Journal of Medical Toxicology and Drug Experience. 2002; 25(13): 913-27. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12381213&dopt=Abstract
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Comparison of calcipotriol and coal tar in conjunction with sun exposure in chronic plaque psoriasis: a pilot study. Author(s): Kaur I, Saraswat A, Kumar B. Source: The Journal of Dermatology. 2001 August; 28(8): 448-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11560163&dopt=Abstract
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Comparison of phototherapy two times and four times a week with low doses of narrow-band ultraviolet B in Asian patients with psoriasis. Author(s): Leenutaphong V, Nimkulrat P, Sudtim S. Source: Photodermatology, Photoimmunology & Photomedicine. 2000 October; 16(5): 202-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11068858&dopt=Abstract
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Comparison of the distribution and numbers of antigen-presenting cells among Tlymphocyte-mediated dermatoses: CD1a+, factor XIIIa+, and CD68+ cells in eczematous dermatitis, psoriasis, lichen planus and graft-versus-host disease. Author(s): Deguchi M, Aiba S, Ohtani H, Nagura H, Tagami H. Source: Archives of Dermatological Research. 2002 October; 294(7): 297-302. Epub 2002 July 27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12373334&dopt=Abstract
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Complete remission of chronic plaque psoriasis and gastric marginal zone B-cell lymphoma of MALT type after treatment with 2-chlorodeoxyadenosine. Author(s): Valencak J, Trautinger F, Fiebiger WC, Raderer M. Source: Annals of Hematology. 2002 November; 81(11): 662-5. Epub 2002 October 29. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12454707&dopt=Abstract
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Concurrent non-alcoholic steatohepatitis and psoriasis. Report of three cases from the POLI.ST.E.N.A. study. Author(s): Lonardo A, Loria P, Carulli N. Source: Dig Liver Dis. 2001 January-February; 33(1): 86-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11303985&dopt=Abstract
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Connections between psoriasis and Crohn's disease. Author(s): Najarian DJ, Gottlieb AB. Source: Journal of the American Academy of Dermatology. 2003 June; 48(6): 805-21; Quiz 822-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12789169&dopt=Abstract
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Consensus conference: acitretin in combination with UVB or PUVA in the treatment of psoriasis. Author(s): Lebwohl M, Drake L, Menter A, Koo J, Gottlieb AB, Zanolli M, Young M, McClelland P. Source: Journal of the American Academy of Dermatology. 2001 October; 45(4): 544-53. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11568745&dopt=Abstract
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Contrasting patterns of streptococcal superantigen-induced T-cell proliferation in guttate vs. chronic plaque psoriasis. Author(s): Davison SC, Allen MH, Mallon E, Barker JN. Source: The British Journal of Dermatology. 2001 August; 145(2): 245-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11531786&dopt=Abstract
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Corneodesmosin DNA polymorphisms in MHC haplotypes and Japanese patients with psoriasis. Author(s): Hui J, Oka A, Tamiya G, Tomizawa M, Kulski JK, Penhale WJ, Tay GK, Iizuka M, Ozawa A, Inoko H. Source: Tissue Antigens. 2002 July; 60(1): 77-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12366786&dopt=Abstract
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Corneodesmosin expression in psoriasis vulgaris differs from normal skin and other inflammatory skin disorders. Author(s): Allen M, Ishida-Yamamoto A, McGrath J, Davison S, Iizuka H, Simon M, Guerrin M, Hayday A, Vaughan R, Serre G, Trembath R, Barker J. Source: Laboratory Investigation; a Journal of Technical Methods and Pathology. 2001 July; 81(7): 969-76. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11454986&dopt=Abstract
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Cost of psoriasis: a study on the morbidity and financial effects of having psoriasis in Australia. Author(s): Jenner N, Campbell J, Plunkett A, Marks R. Source: The Australasian Journal of Dermatology. 2002 November; 43(4): 255-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12423431&dopt=Abstract
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Cost-effectiveness analysis of a psoriasis care instruction programme with dithranol compared with UVB phototherapy and inpatient dithranol treatment. Author(s): Hartman M, Prins M, Swinkels OQ, Severens JL, De Boo T, Van Der Wilt GJ, Van De Kerkhof PC, Van Der Valk PG. Source: The British Journal of Dermatology. 2002 September; 147(3): 538-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12207597&dopt=Abstract
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Cost-effectiveness comparison of therapy for psoriasis with a methotrexate-based regimen versus a rotation regimen of modified cyclosporine and methotrexate. Author(s): Ellis CN, Reiter KL, Bandekar RR, Fendrick AM. Source: Journal of the American Academy of Dermatology. 2002 February; 46(2): 242-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11807436&dopt=Abstract
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Crude coal tar treatment every day versus every other day for plaque psoriasis. Author(s): Danielsen AG, Heidenheim M, Wulf HC. Source: Acta Dermato-Venereologica. 2001 June-July; 81(3): 221-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11558890&dopt=Abstract
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Crusted scabies looking like psoriasis. Author(s): Gach JE, Heagerty A. Source: Lancet. 2000 August 19; 356(9230): 650. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10968439&dopt=Abstract
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Cryptococcal meningitis during cyclosporin treatment in a patient with psoriasis. Author(s): Cainelli F, Concia E, Vento S. Source: The British Journal of Dermatology. 2000 December; 143(6): 1327-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11122049&dopt=Abstract
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Current consensus and update on psoriasis therapy: a perspective from the U.S. Author(s): Koo JY. Source: The Journal of Dermatology. 1999 November; 26(11): 723-33. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10635614&dopt=Abstract
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Cushing's syndrome caused by topical steroid therapy for psoriasis. Author(s): Abma EM, Blanken R, De Heide LJ. Source: The Netherlands Journal of Medicine. 2002 April; 60(3): 148-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12164372&dopt=Abstract
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Cutaneous expression of cytochrome P450 CYP2S1: individuality in regulation by therapeutic agents for psoriasis and other skin diseases. Author(s): Smith G, Wolf CR, Deeni YY, Dawe RS, Evans AT, Comrie MM, Ferguson J, Ibbotson SH. Source: Lancet. 2003 April 19; 361(9366): 1336-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12711469&dopt=Abstract
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Cyclosporin in childhood psoriasis. Author(s): Perrett CM, Ilchyshyn A, Berth-Jones J. Source: The Journal of Dermatological Treatment. 2003 June; 14(2): 113-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775319&dopt=Abstract
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Cyclosporin trough levels: is monitoring necessary during short-term treatment in psoriasis? A systematic review and clinical data on trough levels. Author(s): Heydendael VM, Spuls PI, Ten Berge IJ, Opmeer BC, Bos JD, de Rie MA. Source: The British Journal of Dermatology. 2002 July; 147(1): 122-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12100194&dopt=Abstract
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Cyclosporine in childhood psoriasis. Author(s): Mahe E, Bodemer C, Pruszkowski A, Teillac-Hamel D, de Prost Y. Source: Archives of Dermatology. 2001 November; 137(11): 1532-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11708969&dopt=Abstract
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Cyclosporine in severe psoriasis. Results of a meta-analysis in 579 patients. Author(s): Faerber L, Braeutigam M, Weidinger G, Mrowietz U, Christophers E, Schulze HJ, Mahrle G, Meffert H, Drechsler S. Source: American Journal of Clinical Dermatology. 2001; 2(1): 41-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11702620&dopt=Abstract
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Cyclosporine in the treatment of psoriasis. Author(s): Gulliver WP. Source: Cutis; Cutaneous Medicine for the Practitioner. 2000 November; 66(5): 365-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11107522&dopt=Abstract
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Cytokine gene polymorphisms in psoriasis. Author(s): Craven NM, Jackson CW, Kirby B, Perrey C, Pravica V, Hutchinson IV, Griffiths CE. Source: The British Journal of Dermatology. 2001 April; 144(4): 849-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11298547&dopt=Abstract
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Cytokines may favor a role for human papillomaviruses in the pathogenesis of psoriasis. Author(s): Majewski S, Jablonska S, Favre M, Orth G. Source: Archives of Dermatology. 2001 October; 137(10): 1373. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11594869&dopt=Abstract
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Decreased expression levels of L-selectin on subsets of leucocytes and increased serum L-selectin in severe psoriasis. Author(s): Inaoki M, Sato S, Shimada Y, Kawara S, Steeber DA, Tedder TF, Takehara K. Source: Clinical and Experimental Immunology. 2000 December; 122(3): 484-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11122259&dopt=Abstract
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Depression modulates pruritus perception. A study of pruritus in psoriasis, atopic dermatitis and chronic idiopathic urticaria. Author(s): Gupta MA, Gupta AK. Source: Annals of the New York Academy of Sciences. 1999 October 20; 885: 394-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10816673&dopt=Abstract
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Dermatomyositis-like eruption and leg ulceration caused by hydroxyurea in a patient with psoriasis. Author(s): Kirby B, Gibson LE, Rogers S, Pittelkow M. Source: Clinical and Experimental Dermatology. 2000 May; 25(3): 256-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10844510&dopt=Abstract
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Dermatomyositis-like eruption and leg ulceration caused by hydroxyurea in a patient with psoriasis. Author(s): Varma S, Lanigan SW. Source: Clinical and Experimental Dermatology. 1999 May; 24(3): 164-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10354169&dopt=Abstract
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Detection of telomerase activity in psoriasis lesional skin and correlation with Ki-67 expression and suppression by retinoic acid. Author(s): Jang HS, Oh CK, Jo JH, Kim YS, Kwon KS. Source: Journal of Korean Medical Science. 2001 October; 16(5): 623-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11641534&dopt=Abstract
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Development of the PSORIQoL, a psoriasis-specific measure of quality of life designed for use in clinical practice and trials. Author(s): McKenna SP, Cook SA, Whalley D, Doward LC, Richards HL, Griffiths CE, Van Assche D. Source: The British Journal of Dermatology. 2003 August; 149(2): 323-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932239&dopt=Abstract
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Developments in the treatment of nail psoriasis, melanonychia striata, and onychomycosis. A review of the literature. Author(s): Van Laborde S, Scher RK. Source: Dermatologic Clinics. 2000 January; 18(1): 37-46. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10626110&dopt=Abstract
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Diabetes but not psoriasis. Author(s): Uwaifo GI, Muzzammil A, Shoukri K, Whitaker-Worth DL. Source: Lancet. 1999 August 7; 354(9177): 480. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10465174&dopt=Abstract
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Diagnosis: psoriasis or not? What are the clues? Author(s): Altman EM, Kamino H. Source: Semin Cutan Med Surg. 1999 March; 18(1): 25-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10188839&dopt=Abstract
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Different transcriptional activity and in vitro TNF-alpha production in psoriasis patients carrying the TNF-alpha 238A promoter polymorphism. Author(s): Kaluza W, Reuss E, Grossmann S, Hug R, Schopf RE, Galle PR, MaerkerHermann E, Hoehler T. Source: The Journal of Investigative Dermatology. 2000 June; 114(6): 1180-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10844563&dopt=Abstract
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Differential association of polymorphisms in the TNFalpha region with psoriatic arthritis but not psoriasis. Author(s): Hohler T, Grossmann S, Stradmann-Bellinghausen B, Kaluza W, Reuss E, de Vlam K, Veys E, Marker-Hermann E. Source: Annals of the Rheumatic Diseases. 2002 March; 61(3): 213-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11830425&dopt=Abstract
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Differential expression of interferon gamma by mitogen-stimulated peripheral blood mononuclear cells among Kuwaiti psoriasis patients. Author(s): Mahmoud F, Abul H, al-Seleh Q, Morgan G, Haines D, al-Ramly M, Burleson J, Kreutzer D. Source: The Journal of Dermatology. 1999 January; 26(1): 23-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10063208&dopt=Abstract
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Disease mechanisms in psoriasis and psoriatic arthritis. Author(s): Costello P, FitzGerald O. Source: Curr Rheumatol Rep. 2001 October; 3(5): 419-27. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11564374&dopt=Abstract
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Dislipidemia and oxidative stress in mild and in severe psoriasis as a risk for cardiovascular disease. Author(s): Rocha-Pereira P, Santos-Silva A, Rebelo I, Figueiredo A, Quintanilha A, Teixeira F. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 2001 January; 303(1-2): 33-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11163020&dopt=Abstract
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Dithranol and dimethylfumarate suppress the interferon-gamma-induced upregulation of cytokeratin 17 as a putative psoriasis autoantigen in vitro. Author(s): Bonnekoh B, Bockelmann R, Ambach A, Gollnick H. Source: Skin Pharmacology and Applied Skin Physiology. 2001 July-August; 14(4): 21725. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11464104&dopt=Abstract
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Dithranol treatment of psoriasis in dithranol-sensitive patients. Author(s): Prins M, Swinkels OQ, Mommers JM, Gerritsen MJ, van der Valk PG. Source: Contact Dermatitis. 1999 August; 41(2): 116-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10445706&dopt=Abstract
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Do specific human papillomavirus types cause psoriasis? Author(s): de Villiers EM, Ruhland A. Source: Archives of Dermatology. 2001 March; 137(3): 384. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11255361&dopt=Abstract
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Domain structure of erythrocyte membranes in psoriasis: an EPR study. Author(s): Gornicki A. Source: Journal of Dermatological Science. 2002 September; 29(3): 214-221. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12234712&dopt=Abstract
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Dominant lesional T cell receptor rearrangements persist in relapsing psoriasis but are absent from nonlesional skin: evidence for a stable antigen-specific pathogenic T cell response in psoriasis vulgaris. Author(s): Vollmer S, Menssen A, Prinz JC. Source: The Journal of Investigative Dermatology. 2001 November; 117(5): 1296-301. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11710947&dopt=Abstract
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Double-blind clinical study reveals synergistic action between alpha-hydroxy acid and betamethasone lotions towards topical treatment of scalp psoriasis. Author(s): Kostarelos K, Teknetzis A, Lefaki I, Ioannides D, Minas A. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2000 January; 14(1): 5-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10877245&dopt=Abstract
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Double-blind, placebo-controlled, randomized, right-left study comparing calcipotriol monotherapy with a combined treatment of calcipotriol and diflucortolone valerate in chronic plaque psoriasis. Author(s): Salmhofer W, Maier H, Soyer HP, Honigsmann H, Hodl S. Source: Acta Derm Venereol Suppl (Stockh). 2000; (211): 5-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11234559&dopt=Abstract
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Downregulation and altered spatial pattern of caveolin-1 in chronic plaque psoriasis. Author(s): Campbell L, Laidler P, Watson RE, Kirby B, Griffiths CE, Gumbleton M. Source: The British Journal of Dermatology. 2002 October; 147(4): 701-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12366416&dopt=Abstract
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Drug interactions in psoriasis: the pros and cons of combining topical psoriasis therapies. Author(s): Endzweig-Gribetz CH, Brady C, Lynde C, Sibbald D, Lebwohl M. Source: Journal of Cutaneous Medicine and Surgery. 2002 May-June; 6(3 Suppl): 12-6. Epub 2002 April 30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11976987&dopt=Abstract
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Drug-induced psoriasis. Recognition and management. Author(s): Tsankov N, Angelova I, Kazandjieva J. Source: American Journal of Clinical Dermatology. 2000 May-June; 1(3): 159-65. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11702297&dopt=Abstract
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Drug-induced suppression of phosphorylase kinase activity correlates with resolution of psoriasis as assessed by clinical, histological and immunohistochemical parameters. Author(s): Heng MC, Song MK, Harker J, Heng MK. Source: The British Journal of Dermatology. 2000 November; 143(5): 937-49. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11069500&dopt=Abstract
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Duration of improvement in psoriasis after treatment with tazarotene 0.1% gel plus clobetasol propionate 0.05% ointment: comparison of maintenance treatments. Author(s): Lebwohl M, Lombardi K, Tan MH. Source: International Journal of Dermatology. 2001 January; 40(1): 64-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11277960&dopt=Abstract
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Duration of remission of psoriasis therapies. Author(s): Koo J, Lebwohl M. Source: Journal of the American Academy of Dermatology. 1999 July; 41(1): 51-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10411411&dopt=Abstract
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Early onset of action and efficacy of a combination of calcipotriene and betamethasone dipropionate in the treatment of psoriasis. Author(s): Papp KA, Guenther L, Boyden B, Larsen FG, Harvima RJ, Guilhou JJ, Kaufmann R, Rogers S, van de Kerkhof PC, Hanssen LI, Tegner E, Burg G, Talbot D, Chu A. Source: Journal of the American Academy of Dermatology. 2003 January; 48(1): 48-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12522370&dopt=Abstract
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Effect of propylthiouracil on adenosine deaminase activity and thyroid function in patients with psoriasis. Author(s): Kose K, Utas S, Yazici C, Akdas A, Kelestimur F. Source: The British Journal of Dermatology. 2001 June; 144(6): 1121-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422030&dopt=Abstract
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Effect of topical PPARbeta/delta and PPARgamma agonists on plaque psoriasis. A pilot study. Author(s): Kuenzli S, Saurat JH. Source: Dermatology (Basel, Switzerland). 2003; 206(3): 252-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673084&dopt=Abstract
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Effect of vitamin D3 on the increased expression of Bcl-xL in psoriasis. Author(s): Fukuya Y, Higaki M, Higaki Y, Kawashima M. Source: Archives of Dermatological Research. 2002 February; 293(12): 620-5. Epub 2001 December 19. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11875645&dopt=Abstract
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Effects of administration of a single dose of a humanized monoclonal antibody to CD11a on the immunobiology and clinical activity of psoriasis. Author(s): Gottlieb A, Krueger JG, Bright R, Ling M, Lebwohl M, Kang S, Feldman S, Spellman M, Wittkowski K, Ochs HD, Jardieu P, Bauer R, White M, Dedrick R, Garovoy M. Source: Journal of the American Academy of Dermatology. 2000 March; 42(3): 428-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10688712&dopt=Abstract
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Effects of alefacept on health-related quality of life in patients with psoriasis: results from a randomized, placebo-controlled phase II trial. Author(s): Ellis CN, Mordin MM, Adler EY; Randomized, placebo-controlled phase II trial. Source: American Journal of Clinical Dermatology. 2003; 4(2): 131-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12553852&dopt=Abstract
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Effects of cyclosporin A on immune activation markers in patients with active psoriasis. Author(s): Economidou J, Barkis J, Demetriou Z, Avgerinou G, Psarra K, Degiannis D, Vareltzidis A, Katsambas A. Source: Dermatology (Basel, Switzerland). 1999; 199(2): 144-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10559581&dopt=Abstract
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Efficacy and safety of a new combination of calcipotriol and betamethasone dipropionate (once or twice daily) compared to calcipotriol (twice daily) in the treatment of psoriasis vulgaris: a randomized, double-blind, vehicle-controlled clinical trial. Author(s): Guenther L, Van de Kerkhof PC, Snellman E, Kragballe K, Chu AC, Tegner E, Garcia-Diez A, Springborg J. Source: The British Journal of Dermatology. 2002 August; 147(2): 316-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12174105&dopt=Abstract
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Efficacy and safety of infliximab monotherapy for plaque-type psoriasis: a randomised trial. Author(s): Chaudhari U, Romano P, Mulcahy LD, Dooley LT, Baker DG, Gottlieb AB. Source: Lancet. 2001 June 9; 357(9271): 1842-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11410193&dopt=Abstract
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Efficacy and tolerance of topical calcitriol 3 microg g(-1) in psoriasis treatment: a review of our experience in Poland. Author(s): Langner A, Stapor W, Ambroziak M. Source: The British Journal of Dermatology. 2001 April; 144 Suppl 58: 11-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11501507&dopt=Abstract
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Efficacy of acitretin and commercial tanning bed therapy for psoriasis. Author(s): Carlin CS, Callis KP, Krueger GG. Source: Archives of Dermatology. 2003 April; 139(4): 436-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707089&dopt=Abstract
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Efficacy of acitretin in severe psoriasis. Author(s): Geiger JM. Source: Skin Therapy Letter. 2003 April-May; 8(4): 1-3, 7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12858231&dopt=Abstract
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Efficacy of betamethasone valerate mousse in comparison with standard therapies on scalp psoriasis: an open, multicentre, randomized, controlled, cross-over study on 241 patients. Author(s): Andreassi L, Giannetti A, Milani M; Scale Investigators Group. Source: The British Journal of Dermatology. 2003 January; 148(1): 134-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534607&dopt=Abstract
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Efficacy of calcipotriol ointment applied under hydrocolloid occlusion in psoriasis. Author(s): Castelijns FA, Gerritsen MJ, van Erp PE, van de Kerkhof PC. Source: Dermatology (Basel, Switzerland). 2000; 200(1): 25-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10681609&dopt=Abstract
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Efficacy of fumaric acid ester monotherapy in psoriasis pustulosa palmoplantaris. Author(s): Stander H, Stadelmann A, Luger T, Traupe H. Source: The British Journal of Dermatology. 2003 July; 149(1): 220-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890235&dopt=Abstract
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Efficacy of sirolimus (rapamycin) administered concomitantly with a subtherapeutic dose of cyclosporin in the treatment of severe psoriasis: a randomized controlled trial. Author(s): Reitamo S, Spuls P, Sassolas B, Lahfa M, Claudy A, Griffiths CE; Sirolimus European Psoriasis Study Group. Source: The British Journal of Dermatology. 2001 September; 145(3): 438-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11531834&dopt=Abstract
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Efficacy of the 308-nm excimer laser for treatment of psoriasis: results of a multicenter study. Author(s): Feldman SR, Mellen BG, Housman TS, Fitzpatrick RE, Geronemus RG, Friedman PM, Vasily DB, Morison WL. Source: Journal of the American Academy of Dermatology. 2002 June; 46(6): 900-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12063488&dopt=Abstract
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Elevated B-lymphocyte levels in lesional tissue of non-arthritic psoriasis. Author(s): Mahmoud F, Abul H, al Saleh Q, Hassab-el Naby H, Kajeji M, Haines D, Burleson J, Morgan G. Source: The Journal of Dermatology. 1999 July; 26(7): 428-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10458082&dopt=Abstract
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Elevated plasma levels of vascular endothelial growth factor and plasminogen activator inhibitor-1 decrease during improvement of psoriasis. Author(s): Nielsen HJ, Christensen IJ, Svendsen MN, Hansen U, Werther K, Brunner N, Petersen LJ, Kristensen JK. Source: Inflammation Research : Official Journal of the European Histamine Research Society. [et Al.]. 2002 November; 51(11): 563-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12540021&dopt=Abstract
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Epidermal CD8+ T cells in chronic plaque psoriasis are Tc1 cells producing heterogeneous levels of interferon-gamma. Author(s): Ovigne JM, Baker BS, Brown DW, Powles AV, Fry L. Source: Experimental Dermatology. 2001 June; 10(3): 168-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11380612&dopt=Abstract
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Epidermal CD8+ T cells reactive with group A streptococcal antigens in chronic plaque psoriasis. Author(s): Ovigne JM, Baker BS, Davison SC, Powles AV, Fry L. Source: Experimental Dermatology. 2002 August; 11(4): 357-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12190945&dopt=Abstract
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Epidermal HLA-DR and the enhancement of cutaneous reactivity to superantigenic toxins in psoriasis. Author(s): Travers JB, Hamid QA, Norris DA, Kuhn C, Giorno RC, Schlievert PM, Farmer ER, Leung DY. Source: The Journal of Clinical Investigation. 1999 November; 104(9): 1181-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10545517&dopt=Abstract
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Epidermal remodelling in psoriasis (III): a hexagonally-arranged cylindrical papilla model reveals the nature of psoriatic architecture. Author(s): Iizuka H, Honda H, Ishida-Yamamoto A. Source: Journal of Dermatological Science. 1999 September; 21(2): 105-12. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10511479&dopt=Abstract
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Erythema gyratum repens in a case of resolving psoriasis. Author(s): Bryan ME, Lienhart K, Smoller BR, Johnson SM. Source: J Drugs Dermatol. 2003 June; 2(3): 315-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12848115&dopt=Abstract
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Erythema gyratum repens-like psoriasis. Author(s): Jablonska S, Blaszczyk M, Kozlowska A. Source: International Journal of Dermatology. 2000 September; 39(9): 695-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11044195&dopt=Abstract
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Erythrocyte membrane fluidity changes in psoriasis: an EPR study. Author(s): Gornicki A, Gutsze A. Source: Journal of Dermatological Science. 2001 September; 27(1): 27-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11457641&dopt=Abstract
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Erythrodermic psoriasis precipitated by radiologic contrast media. Author(s): Evans AV, Parker JC, Russell-Jones R. Source: Journal of the American Academy of Dermatology. 2002 June; 46(6): 960-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12063501&dopt=Abstract
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Establishing a practical and effective psoriasis treatment center. Author(s): Bagel J. Source: Dermatologic Clinics. 2000 April; 18(2): 349-57, Xi. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10791162&dopt=Abstract
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Etanercept for severe psoriasis and psoriatic arthritis: observations on combination therapy. Author(s): Iyer S, Yamauchi P, Lowe NJ. Source: The British Journal of Dermatology. 2002 January; 146(1): 118-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11841377&dopt=Abstract
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Etanercept for severe psoriasis and psoriatic arthritis: observations on combination therapy. Author(s): Davison SC, Bunker CB, Basarab T. Source: The British Journal of Dermatology. 2002 October; 147(4): 831-2; Author Reply 832. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12366452&dopt=Abstract
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Etanercept in the treatment of psoriatic arthritis and psoriasis: a randomised trial. Author(s): Mease PJ, Goffe BS, Metz J, VanderStoep A, Finck B, Burge DJ. Source: Lancet. 2000 July 29; 356(9227): 385-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10972371&dopt=Abstract
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Etanercept, a TNF antagonist for treatment for psoriatic arthritis and psoriasis. Author(s): Mease PJ. Source: Skin Therapy Letter. 2003 January; 8(1): 1-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12728284&dopt=Abstract
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Evaluating the potential clinical benefits of switching patients with plaque psoriasis from calcipotriene to tazarotene treatment. Author(s): Coynik D. Source: Cutis; Cutaneous Medicine for the Practitioner. 2000 December; 66(6 Suppl): 1924. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11147087&dopt=Abstract
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Evaluation of skin surface hydration in Korean psoriasis patients: a possible factor influencing psoriasis. Author(s): Kim SD, Huh CH, Seo KI, Suh DH, Youn JI. Source: Clinical and Experimental Dermatology. 2002 March; 27(2): 147-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11952709&dopt=Abstract
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Evaluation of the atherogenic tendency of lipids and lipoprotein content and their relationships with oxidant-antioxidant system in patients with psoriasis. Author(s): Vanizor Kural B, Orem A, Cimsit G, Yandi YE, Calapoglu M. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 2003 February; 328(1-2): 71-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12559600&dopt=Abstract
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Evidence for a major psoriasis susceptibility locus at 6p21(PSORS1) and a novel candidate region at 4q31 by genome-wide scan in Chinese hans. Author(s): Zhang XJ, He PP, Wang ZX, Zhang J, Li YB, Wang HY, Wei SC, Chen SY, Xu SJ, Jin L, Yang S, Huang W. Source: The Journal of Investigative Dermatology. 2002 December; 119(6): 1361-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12485440&dopt=Abstract
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Evidence for interaction between psoriasis-susceptibility loci on chromosomes 6p21 and 1q21. Author(s): Capon F, Semprini S, Dallapiccola B, Novelli G. Source: American Journal of Human Genetics. 1999 December; 65(6): 1798-800. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10577939&dopt=Abstract
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Evidence for the involvement of bacterial superantigens in psoriasis, atopic dermatitis, and Kawasaki syndrome. Author(s): Yarwood JM, Leung DY, Schlievert PM. Source: Fems Microbiology Letters. 2000 November 1; 192(1): 1-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11040420&dopt=Abstract
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Exacerbation of chronic large plaque psoriasis associated with Olanzepine therapy. Author(s): Ascari-Raccagni A, Baldari U, Rossi E, Alessandrini F. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2000 July; 14(4): 315-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11204528&dopt=Abstract
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Exacerbation of psoriasis by interferon-alpha therapy for hepatitis C. Author(s): Downs AM, Dunnill MG. Source: Clinical and Experimental Dermatology. 2000 June; 25(4): 351-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10971502&dopt=Abstract
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Exacerbation of psoriasis by thalidomide in Behcet's syndrome. Author(s): Dobson CM, Parslew RA. Source: The British Journal of Dermatology. 2003 August; 149(2): 432-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932265&dopt=Abstract
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Examining day-case and inpatient psoriasis care. Author(s): Haynes M. Source: Prof Nurse. 2000 November; 16(2): 893-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12029866&dopt=Abstract
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Excess mortality related to alcohol and smoking among hospital-treated patients with psoriasis. Author(s): Poikolainen K, Karvonen J, Pukkala E. Source: Archives of Dermatology. 1999 December; 135(12): 1490-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10606054&dopt=Abstract
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Exclusion of CARD15/NOD2 as a candidate susceptibility gene to psoriasis in the Italian population. Author(s): Borgiani P, Vallo L, D'Apice MR, Giardina E, Pucci S, Capon F, Nistico S, Chimenti S, Pallone F, Novelli G. Source: Eur J Dermatol. 2002 November-December; 12(6): 540-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12459523&dopt=Abstract
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Exfoliative dermatitis after long-term methotrexate treatment of severe psoriasis. Author(s): Peters T, Theile-Ochel S, Chemnitz J, Sohngen D, Hunzelmann N, Scharffetter-Kochanek K. Source: Acta Dermato-Venereologica. 1999 September; 79(5): 391-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10494723&dopt=Abstract
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Exorex for psoriasis: the importance of randomized controlled trials in testing “new” products. Author(s): Williams HC. Source: Archives of Dermatology. 2001 December; 137(12): 1637-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11735715&dopt=Abstract
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Experience in treating recalcitrant scalp psoriasis with automated shampooing and debridement. Author(s): King L Jr, Webb B, Zanolli M. Source: Journal of the American Academy of Dermatology. 1999 October; 41(4): 638-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10495388&dopt=Abstract
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Experiences of stigmatization play a role in mediating the impact of disease severity on quality of life in psoriasis patients. Author(s): Vardy D, Besser A, Amir M, Gesthalter B, Biton A, Buskila D. Source: The British Journal of Dermatology. 2002 October; 147(4): 736-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12366421&dopt=Abstract
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Experimental therapies for psoriasis. Author(s): Asadullah K, Volk HD, Friedrich M, Sterry W. Source: Arch Immunol Ther Exp (Warsz). 2002; 50(6): 411-20. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12546067&dopt=Abstract
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Explosive diaper pustular psoriasis. Author(s): Watanabe M, Tabata N, Tagami H. Source: Pediatric Dermatology. 2002 November-December; 19(6): 564-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12437567&dopt=Abstract
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Expression and function of beta 2 integrin CD11B/CD18 on leukocytes from patients with psoriasis. Author(s): Sjogren F, Ljunghusen O, Baas A, Coble BI, Stendahl O. Source: Acta Dermato-Venereologica. 1999 March; 79(2): 105-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10228626&dopt=Abstract
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Expression of a retinoid-inducible tumor suppressor, Tazarotene-inducible gene-3, is decreased in psoriasis and skin cancer. Author(s): Duvic M, Helekar B, Schulz C, Cho M, DiSepio D, Hager C, DiMao D, Hazarika P, Jackson B, Breuer-McHam J, Young J, Clayman G, Lippman SM, Chandraratna RA, Robinson NA, Deucher A, Eckert RL, Nagpal S. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2000 August; 6(8): 3249-59. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10955811&dopt=Abstract
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Expression of dipeptidyl-peptidase IV (CD26) on CD8+ T cells is significantly decreased in patients with psoriasis vulgaris and atopic dermatitis. Author(s): Bock O, Kreiselmeyer I, Mrowietz U. Source: Experimental Dermatology. 2001 December; 10(6): 414-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11737260&dopt=Abstract
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Expression of IL-18 in psoriasis. Author(s): Ohta Y, Hamada Y, Katsuoka K. Source: Archives of Dermatological Research. 2001 July; 293(7): 334-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11550806&dopt=Abstract
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Expression of p53 protein before and after PUVA treatment in psoriasis. Author(s): Hannuksela-Svahn A, Paakko P, Autio P, Reunala T, Karvonen J, Vahakangas K. Source: Acta Dermato-Venereologica. 1999 May; 79(3): 195-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10384915&dopt=Abstract
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Expression of the psoriasis-associated antigen, Pso p27, is inhibited by cyclosporin A. Author(s): Dalaker M, Jacobsen T, Lysvand H, Iversen OJ. Source: Acta Dermato-Venereologica. 1999 July; 79(4): 281-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10429984&dopt=Abstract
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Expression pattern of the bcl-2 homologous protein bad in normal skin, psoriasis vulgaris and keratinocytic tumors. Author(s): Tomkova H, Fujimoto W, Arata J. Source: Journal of Dermatological Science. 2000 February; 22(2): 132-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10674827&dopt=Abstract
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Extensive psoriasis induced by interferon alfa treatment for chronic hepatitis C. Author(s): Taylor C, Burns DA, Wiselka MJ. Source: Postgraduate Medical Journal. 2000 June; 76(896): 365-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10824054&dopt=Abstract
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Extensive striae distensae as a result of topical corticosteroid therapy in psoriasis vulgaris. Author(s): Rogalski C, Haustein UF, Glander HJ, Paasch U. Source: Acta Dermato-Venereologica. 2003; 83(1): 54-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12636026&dopt=Abstract
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Factors associated with increased aqueous flare in psoriasis. Author(s): Okamoto F, Umebayasi Y, Ohtsuka F, Hommura S. Source: Japanese Journal of Ophthalmology. 2001 March-April; 45(2): 172-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11313050&dopt=Abstract
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Failure to demonstrate therapeutic tachyphylaxis to topically applied steroids in patients with psoriasis. Author(s): Miller JJ, Roling D, Margolis D, Guzzo C. Source: Journal of the American Academy of Dermatology. 1999 October; 41(4): 546-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10495373&dopt=Abstract
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Familial association of pseudohypoparathyroidism and psoriasis: case report. Author(s): Montenegro RM Jr, Albuquerque de Paula FJ, Foss NT, Foss MC. Source: Sao Paulo Medical Journal = Revista Paulista De Medicina. 2002 January 3; 120(1): 23-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11836550&dopt=Abstract
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Familial scarring alopecia associated with scalp psoriasis. Author(s): Cockayne SE, Messenger AG. Source: The British Journal of Dermatology. 2001 February; 144(2): 425-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11251592&dopt=Abstract
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Family history of psoriasis, stressful life events, and recent infectious disease are risk factors for a first episode of acute guttate psoriasis: results of a case-control study. Author(s): Naldi L, Peli L, Parazzini F, Carrel CF; Psoriasis Study Group of the Italian Group for Epidemiological Research in Dermatology. Source: Journal of the American Academy of Dermatology. 2001 March; 44(3): 433-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11209111&dopt=Abstract
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Family-based analysis using a dense single-nucleotide polymorphism-based map defines genetic variation at PSORS1, the major psoriasis-susceptibility locus. Author(s): Veal CD, Capon F, Allen MH, Heath EK, Evans JC, Jones A, Patel S, Burden D, Tillman D, Barker JN, Trembath RC. Source: American Journal of Human Genetics. 2002 September; 71(3): 554-64. Epub 2002 July 29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12148091&dopt=Abstract
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Fatal group A streptococcal necrotizing fasciitis and toxic shock syndrome in a patient with psoriasis and chronic renal impairment. Author(s): Chong AH, Burrows NP. Source: The Australasian Journal of Dermatology. 2002 August; 43(3): 194-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12121397&dopt=Abstract
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Fine mapping of the PSORS4 psoriasis susceptibility region on chromosome 1q21. Author(s): Capon F, Semprini S, Chimenti S, Fabrizi G, Zambruno G, Murgia S, Carcassi C, Fazio M, Mingarelli R, Dallapiccola B, Novelli G. Source: The Journal of Investigative Dermatology. 2001 May; 116(5): 728-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11348461&dopt=Abstract
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First biotech drug to treat psoriasis. Author(s): Mitchell P. Source: Nature Biotechnology. 2002 July; 20(7): 640-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12089534&dopt=Abstract
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Flow cytometric assessment of clearance and relapse characteristics in psoriasis vulgaris after treatment with weekly clobetasol lotion under hydrocolloid occlusion versus twice-daily clobetasol ointment. Author(s): Glade CP, van der Vleuten CJ, van Erp PE, van de Kerkhof PC. Source: Skin Pharmacology and Applied Skin Physiology. 2002 March-April; 15(2): 92-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11867965&dopt=Abstract
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Flow cytometric characterization of lesional T cells in psoriasis: intracellular cytokine and surface antigen expression indicates an activated, memory/effector type 1 immunophenotype. Author(s): Friedrich M, Krammig S, Henze M, Docke WD, Sterry W, Asadullah K. Source: Archives of Dermatological Research. 2000 October; 292(10): 519-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11142774&dopt=Abstract
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Follow-up survey of 308-nm laser treatment of psoriasis. Author(s): Rodewald EJ, Housman TS, Mellen BG, Feldman SR. Source: Lasers in Surgery and Medicine. 2002; 31(3): 202-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12224094&dopt=Abstract
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Frequency of patch-test positivity in patients with psoriasis: a prospective controlled study. Author(s): Malhotra V, Kaur I, Saraswat A, Kumar B. Source: Acta Dermato-Venereologica. 2002; 82(6): 432-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12575849&dopt=Abstract
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Frequent use of tobacco and alcohol in Chinese psoriasis patients. Author(s): Zhang X, Wang H, Te-Shao H, Yang S, Wang F. Source: International Journal of Dermatology. 2002 October; 41(10): 659-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390188&dopt=Abstract
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Fumaric acid esters: an alternative systemic treatment for psoriasis. Author(s): Ameen M, Russell-Jones R. Source: Clinical and Experimental Dermatology. 1999 September; 24(5): 361-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10564321&dopt=Abstract
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Gene polymorphisms (G82S, 1704G/T, 2184A/G and 2245G/A) of the receptor of advanced glycation end products (RAGE) in plaque psoriasis. Author(s): Vasku V, Kankova K, Vasku A, Muzik J, Izakovicova Holla L, Semradova V, Vacha J. Source: Archives of Dermatological Research. 2002 May; 294(3): 127-30. Epub 2002 April 09. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12029499&dopt=Abstract
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Generalised pustular psoriasis induced by cyclosporin a withdrawal responding to the tumour necrosis factor alpha inhibitor etanercept. Author(s): Kamarashev J, Lor P, Forster A, Heinzerling L, Burg G, Nestle FO. Source: Dermatology (Basel, Switzerland). 2002; 205(2): 213-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12218252&dopt=Abstract
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Generalized pustular and erythrodermic psoriasis associated with bupropion treatment. Author(s): Cox NH, Gordon PM, Dodd H. Source: The British Journal of Dermatology. 2002 June; 146(6): 1061-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12072078&dopt=Abstract
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Generalized pustular psoriasis developing during withdrawal of short-term cyclosporin therapy. Author(s): Georgala S, Koumantaki E, Rallis E, Papadavid E. Source: The British Journal of Dermatology. 2000 May; 142(5): 1057-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10809879&dopt=Abstract
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Generalized pustular psoriasis following withdrawal of oral cyclosporin treatment for palmo-plantar pustulosis. Author(s): De Silva BD, Benton EC, Tidman MJ. Source: Clinical and Experimental Dermatology. 1999 January; 24(1): 10-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10233640&dopt=Abstract
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Generalized pustular psoriasis of pregnancy (impetigo herpetiformis). Author(s): Breier-Maly J, Ortel B, Breier F, Schmidt JB, Honigsmann H. Source: Dermatology (Basel, Switzerland). 1999; 198(1): 61-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10026404&dopt=Abstract
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Generalized pustular psoriasis or drug-induced toxic pustuloderma? The use of patch testing. Author(s): Whittam LR, Wakelin SH, Barker JN. Source: Clinical and Experimental Dermatology. 2000 March; 25(2): 122-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10733635&dopt=Abstract
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Generalized pustular psoriasis with hypoparathyroidism. Author(s): Kawamura A, Kinoshita MT, Suzuki H. Source: Eur J Dermatol. 1999 October-November; 9(7): 574-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10523741&dopt=Abstract
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Genetic analysis of PSORS1 distinguishes guttate psoriasis and palmoplantar pustulosis. Author(s): Asumalahti K, Ameen M, Suomela S, Hagforsen E, Michaelsson G, Evans J, Munro M, Veal C, Allen M, Leman J, David Burden A, Kirby B, Connolly M, Griffiths CE, Trembath RC, Kere J, Saarialho-Kere U, Barker JN. Source: The Journal of Investigative Dermatology. 2003 April; 120(4): 627-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12648227&dopt=Abstract
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Genetic aspects of psoriasis. Author(s): Barker JN. Source: Clinical and Experimental Dermatology. 2001 June; 26(4): 321-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422183&dopt=Abstract
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Genetic basis of psoriasis vulgaris and its pharmacogenetic potential. Author(s): Ameen M. Source: Pharmacogenomics. 2003 May; 4(3): 297-308. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12718720&dopt=Abstract
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Genetic linkage of childhood atopic dermatitis to psoriasis susceptibility loci. Author(s): Cookson WO, Ubhi B, Lawrence R, Abecasis GR, Walley AJ, Cox HE, Coleman R, Leaves NI, Trembath RC, Moffatt MF, Harper JI. Source: Nature Genetics. 2001 April; 27(4): 372-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11279517&dopt=Abstract
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Genetic polymorphisms in the cell growth regulated gene, SC1 telomeric of the HLAC gene and lack of association of psoriasis vulgaris. Author(s): Teraoka Y, Naruse TK, Oka A, Matsuzawa Y, Shiina T, Iizuka M, Iwashita K, Ozawa A, Inoko H. Source: Tissue Antigens. 2000 March; 55(3): 206-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10777095&dopt=Abstract
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Genomewide scan in german families reveals evidence for a novel psoriasissusceptibility locus on chromosome 19p13. Author(s): Lee YA, Ruschendorf F, Windemuth C, Schmitt-Egenolf M, Stadelmann A, Nurnberg G, Stander M, Wienker TF, Reis A, Traupe H. Source: American Journal of Human Genetics. 2000 October; 67(4): 1020-4. Epub 2000 September 13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10986047&dopt=Abstract
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Genomic structure, promoter characterisation and mutational analysis of the S100A7 gene: exclusion of a candidate for familial psoriasis susceptibility. Author(s): Semprini S, Capon F, Bovolenta S, Bruscia E, Pizzuti A, Fabrizi G, Schietroma C, Zambruno G, Dallapiccola B, Novelli G. Source: Human Genetics. 1999 February; 104(2): 130-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10190323&dopt=Abstract
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Genotype association of C(-735)T polymorphism in matrix metalloproteinase 2 gene with G(8002)A endothelin 1 gene with plaque psoriasis. Author(s): Vasku V, Vasku A, Tschoplova S, Izakovicova Holla L, Semradova V, Vacha J. Source: Dermatology (Basel, Switzerland). 2002; 204(4): 262-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12077518&dopt=Abstract
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Genotyping psoriasis. Author(s): Christophers E. Source: The Journal of Investigative Dermatology. 2003 April; 120(4): Xvii. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12648245&dopt=Abstract
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Geographic tongue (migrant glossitis) and psoriasis. Author(s): Femiano F. Source: Minerva Stomatol. 2001 June; 50(6): 213-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11535977&dopt=Abstract
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Gingival hyperplasia in psoriasis patients treated with cyclosporin. Author(s): Kirby B, Rogers S. Source: Clinical and Experimental Dermatology. 2000 January; 25(1): 97-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10819606&dopt=Abstract
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Glomerulopathies associated with psoriasis: a report of three cases. Author(s): Sirolli V, Bonomini M. Source: Nephron. 2000 September; 86(1): 89-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10971159&dopt=Abstract
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Glucagonoma syndrome presenting as psoriasis. Author(s): Beattie PE, Fleming CJ, Evans AT, Sheppard DG, Leese GP, Dow E, Tait IS. Source: Qjm : Monthly Journal of the Association of Physicians. 2002 December; 95(12): 834-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12454329&dopt=Abstract
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Gluten and psoriasis. Author(s): Chalmers RJ, Kirby B. Source: The British Journal of Dermatology. 2000 January; 142(1): 5-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10651687&dopt=Abstract
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Graft vs autoimmunity following allogeneic non-myeloablative blood stem cell transplantation in a patient with chronic myelogenous leukemia and severe systemic psoriasis and psoriatic polyarthritis. Author(s): Slavin S, Nagler A, Varadi G, Or R. Source: Experimental Hematology. 2000 July; 28(7): 853-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10907647&dopt=Abstract
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Guess what! Psoriasis of the lips. Author(s): Tosti A, Misciali C, Cameli N, Vincenzi C. Source: Eur J Dermatol. 2001 November-December; 11(6): 589-90. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11701417&dopt=Abstract
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Guttate psoriasis following Kawasaki disease. Author(s): Garty B, Mosseri R, Finkelstein Y. Source: Pediatric Dermatology. 2001 November-December; 18(6): 507-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11841639&dopt=Abstract
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Guttate psoriasis triggered by perianal streptococcal dermatitis in a four-year-old boy. Author(s): Herbst RA, Hoch O, Kapp A, Weiss J. Source: Journal of the American Academy of Dermatology. 2000 May; 42(5 Pt 2): 885-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10767696&dopt=Abstract
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Haem oxygenase-1: a novel player in cutaneous wound repair and psoriasis? Author(s): Hanselmann C, Mauch C, Werner S. Source: The Biochemical Journal. 2001 February 1; 353(Pt 3): 459-66. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11171041&dopt=Abstract
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Haemorrhage into chronic plaque psoriasis as a consequence of disseminated intravascular coagulation. Author(s): Short KA, Groves RW, Novelli MR. Source: Clinical and Experimental Dermatology. 2002 September; 27(6): 471-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12372088&dopt=Abstract
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Hairy psoriasis. Author(s): Scarisbrick JJ, Wall K, Groves RW. Source: Clinical and Experimental Dermatology. 2001 November; 26(8): 727-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11722466&dopt=Abstract
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Half-side comparison of erythemogenic versus suberythemogenic UVA doses in oral photochemotherapy of psoriasis. Author(s): Tanew A, Ortel B, Honigsmann H. Source: Journal of the American Academy of Dermatology. 1999 September; 41(3 Pt 1): 408-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10459114&dopt=Abstract
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Haplotype analysis of distantly related populations implicates corneodesmosin in psoriasis susceptibility. Author(s): Capon F, Toal IK, Evans JC, Allen MH, Patel S, Tillman D, Burden D, Barker JN, Trembath RC. Source: Journal of Medical Genetics. 2003 June; 40(6): 447-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12807967&dopt=Abstract
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Haplotype associations of the major histocompatibility complex with psoriasis in Northeastern Thais. Author(s): Choonhakarn C, Romphruk A, Puapairoj C, Jirarattanapochai K, Romphruk A, Leelayuwat C. Source: International Journal of Dermatology. 2002 June; 41(6): 330-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12100686&dopt=Abstract
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HAX-1, identified by differential display reverse transcription polymerase chain reaction, is overexpressed in lesional psoriasis. Author(s): Mirmohammadsadegh A, Tartler U, Michel G, Baer A, Walz M, Wolf R, Ruzicka T, Hengge UR. Source: The Journal of Investigative Dermatology. 2003 June; 120(6): 1045-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12787133&dopt=Abstract
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Health-related quality of life in patients with psoriasis and atopic dermatitis measured with SF-36, DLQI and a subjective measure of disease activity. Author(s): Lundberg L, Johannesson M, Silverdahl M, Hermansson C, Lindberg M. Source: Acta Dermato-Venereologica. 2000 November-December; 80(6): 430-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11243637&dopt=Abstract
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Help young people tackle the problem of psoriasis. Author(s): Decker S, Silverberg NB. Source: Cutis; Cutaneous Medicine for the Practitioner. 2001 September; 68(3): 178. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11579779&dopt=Abstract
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Hepatitis C virus infection: prevalence in psoriasis and psoriatic arthritis. Author(s): Taglione E, Vatteroni ML, Martini P, Galluzzo E, Lombardini F, Delle Sedie A, Bendinelli M, Pasero G, Bencivelli W, Riente L. Source: The Journal of Rheumatology. 1999 February; 26(2): 370-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9972971&dopt=Abstract
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High frequency of ultraviolet mutations at the INK4a-ARF locus in squamous cell carcinomas from psoralen-plus-ultraviolet-A-treated psoriasis patients. Author(s): Kreimer-Erlacher H, Seidl H, Back B, Cerroni L, Kerl H, Wolf P. Source: The Journal of Investigative Dermatology. 2003 April; 120(4): 676-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12648234&dopt=Abstract
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High macrophage migration inhibitory factor (MIF) serum levels associated with extended psoriasis. Author(s): Shimizu T, Nishihira J, Mizue Y, Nakamura H, Abe R, Watanabe H, Ohkawara A, Shimizu H. Source: The Journal of Investigative Dermatology. 2001 June; 116(6): 989-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11407993&dopt=Abstract
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High prevalence of an IgG response against murine leukemia virus (MLV) in patients with psoriasis. Author(s): Moles JP, Hadi JC, Guilhou JJ. Source: Virus Research. 2003 August; 94(2): 97-101. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902038&dopt=Abstract
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High-concentration (20 mug/g) tacalcitol ointment therapy on refractory psoriasis vulgaris with low response to topical corticosteroids. Author(s): Katayama I, Ohkawara A, Ohkido M, Harada S, Tamaki K, Nakagawa H, Hori Y, Nishiyama S. Source: Eur J Dermatol. 2002 November-December; 12(6): 553-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12459526&dopt=Abstract
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High-dose 308-nm excimer laser for the treatment of psoriasis. Author(s): Trehan M, Taylor CR. Source: Journal of the American Academy of Dermatology. 2002 May; 46(5): 732-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12004316&dopt=Abstract
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Higher levels of antibodies against the psoriasis-associated antigen pso p27 in cerebrospinal fluid from patients with low back pain and sciatica. Author(s): Zwart JA, Iversen OJ, Sand T, Dale LG, Unsgard G. Source: Spine. 1999 February 15; 24(4): 373-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10065522&dopt=Abstract
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Histochemical analysis of macrophage migration inhibitory factor in psoriasis vulgaris. Author(s): Shimizu T, Nishihira J, Mizue Y, Nakamura H, Abe R, Watanabe H, Ishibashi T, Shimizu H. Source: Histochemistry and Cell Biology. 2002 September; 118(3): 251-7. Epub 2002 July 04. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12271361&dopt=Abstract
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Histological changes in naevi with superimposed psoriasis. Author(s): Fabrizi G, Massi G. Source: The British Journal of Dermatology. 2000 September; 143(3): 688-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10971378&dopt=Abstract
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Histopathology of psoriasis treated with zinc pyrithione. Author(s): Aliaga A. Source: The American Journal of Dermatopathology. 2001 April; 23(2): 161-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11285418&dopt=Abstract
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Histopathology of psoriasis treated with zinc pyrithione. Author(s): Rowlands CG, Danby FW. Source: The American Journal of Dermatopathology. 2000 June; 22(3): 272-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10871074&dopt=Abstract
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HIV-associated psoriasis. Author(s): Mallon E, Bunker CB. Source: Aids Patient Care and Stds. 2000 May; 14(5): 239-46. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10833810&dopt=Abstract
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HLA antigens may influence the age of onset of psoriasis and psoriatic arthritis. Author(s): Queiro R, Torre JC, Gonzalez S, Lopez-Larrea C, Tinture T, Lopez-Lagunas I. Source: The Journal of Rheumatology. 2003 March; 30(3): 505-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610809&dopt=Abstract
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HLA class II haplotypic association and DQCAR microsatellite polymorphisms in Croatian patients with psoriasis. Author(s): Grubic Z, Zunec R, Kastelan M, Cecuk-Jelicic E, Gruber F, Kastelan A. Source: Coll Antropol. 2002 June; 26(1): 61-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12137324&dopt=Abstract
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HLA-B27-positive familial case of a daughter with juvenile pustular psoriasis and her father with ankylosing spondylitis. Author(s): Isogai Z, Tsuji T, Kurita K, Iwata H. Source: Pediatric Dermatology. 1999 November-December; 16(6): 491-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10651571&dopt=Abstract
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HLA-C and guttate psoriasis. Author(s): Mallon E, Bunce M, Savoie H, Rowe A, Newson R, Gotch F, Bunker CB. Source: The British Journal of Dermatology. 2000 December; 143(6): 1177-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11122018&dopt=Abstract
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HLA-Cw6 and the genetic predisposition to psoriasis: a meta-analysis of published serologic studies. Author(s): Mallon E, Newson R, Bunker CB. Source: The Journal of Investigative Dermatology. 1999 October; 113(4): 693-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10504461&dopt=Abstract
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HLA-Cw6-positive and HLA-Cw6-negative patients with Psoriasis vulgaris have distinct clinical features. Author(s): Gudjonsson JE, Karason A, Antonsdottir AA, Runarsdottir EH, Gulcher JR, Stefansson K, Valdimarsson H. Source: The Journal of Investigative Dermatology. 2002 February; 118(2): 362-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11841557&dopt=Abstract
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Human papillomavirus in cutaneous squamous cell carcinoma and cervix of a patient with psoriasis and extensive ultraviolet radiation exposure. Author(s): Rust A, McGovern RM, Gostout BS, Persing DH, Pittelkow MR. Source: Journal of the American Academy of Dermatology. 2001 April; 44(4): 681-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11260548&dopt=Abstract
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Hydroxyurea in psoriasis. Author(s): Reynolds N. Source: Clinical and Experimental Dermatology. 1999 November; 24(6): 496. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10681171&dopt=Abstract
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Hypercalcaemia and hypercalciuria after topical treatment of psoriasis with excessive amounts of calcipotriol. Author(s): Georgiou S, Tsambaos D. Source: Acta Dermato-Venereologica. 1999 January; 79(1): 86. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10086871&dopt=Abstract
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Hyporesponsiveness of peripheral blood lymphocytes to streptococcal superantigens in patients with guttate psoriasis: evidence for systemic stimulation of T cells with superantigens released from focally infecting Streptococcus pyogenes. Author(s): Tokura Y, Seo N, Ohshima A, Wakita H, Yokote R, Furukawa F, Takigawa M. Source: Archives of Dermatological Research. 1999 July-August; 291(7-8): 382-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10482006&dopt=Abstract
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Ichthyosis and psoriasis in a patient with Down syndrome. Author(s): Nomura K. Source: The Journal of Dermatology. 1999 August; 26(8): 538-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10487012&dopt=Abstract
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Identification of a commonly used CDR3 region of infiltrating T cells expressing Vbeta13 and Vbeta15 derived from psoriasis patients. Author(s): Hwang HY, Bahk YY, Kim TG, Kim TY. Source: The Journal of Investigative Dermatology. 2003 March; 120(3): 359-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12603847&dopt=Abstract
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Identification of a novel psoriasis susceptibility locus at 1p and evidence of epistasis between PSORS1 and candidate loci. Author(s): Veal CD, Clough RL, Barber RC, Mason S, Tillman D, Ferry B, Jones AB, Ameen M, Balendran N, Powis SH, Burden AD, Barker JN, Trembath RC. Source: Journal of Medical Genetics. 2001 January; 38(1): 7-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11134234&dopt=Abstract
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Identification of a psoriasis susceptibility candidate gene by linkage disequilibrium mapping with a localized single nucleotide polymorphism map. Author(s): Hewett D, Samuelsson L, Polding J, Enlund F, Smart D, Cantone K, See CG, Chadha S, Inerot A, Enerback C, Montgomery D, Christodolou C, Robinson P, Matthews P, Plumpton M, Wahlstrom J, Swanbeck G, Martinsson T, Roses A, Riley J, Purvis I. Source: Genomics. 2002 March; 79(3): 305-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11863360&dopt=Abstract
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Identification of Malassezia species isolated from scalp skin of patients with psoriasis and healthy subjects. Author(s): Prohic A. Source: Acta Dermatovenerol Croat. 2003; 11(1): 10-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12718790&dopt=Abstract
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Identification of pituitary adenylate cyclase activating polypeptide (PACAP) and PACAP type 1 receptor in human skin: expression of PACAP-38 is increased in patients with psoriasis. Author(s): Steinhoff M, McGregor GP, Radleff-Schlimme A, Steinhoff A, Jarry H, Schmidt WE. Source: Regulatory Peptides. 1999 March 17; 80(1-2): 49-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10235634&dopt=Abstract
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Identifying a gene for psoriasis on chromosome 6 (Psors1) Author(s): Burden AD. Source: The British Journal of Dermatology. 2000 August; 143(2): 238-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10951128&dopt=Abstract
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IL-1 beta and IFN-gamma induce the regenerative epidermal phenotype of psoriasis in the transwell skin organ culture system. IFN-gamma up-regulates the expression of keratin 17 and keratinocyte transglutaminase via endogenous IL-1 production. Author(s): Wei L, Debets R, Hegmans JJ, Benner R, Prens EP. Source: The Journal of Pathology. 1999 February; 187(3): 358-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10398092&dopt=Abstract
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Images in nephrology. Recurrence of psoriasis in an arteriovenous fistula. Author(s): Levy JB, Clutterbuck EJ. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1999 November; 14(11): 2738-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10534524&dopt=Abstract
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Immunobiologic agents for the treatment of psoriasis: clinical research delivers new hope for patients with psoriasis. Author(s): Gottlieb A. Source: Archives of Dermatology. 2003 June; 139(6): 791-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810512&dopt=Abstract
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Immunogenetic profile of patients with psoriatic arthritis varies according to the age at onset of psoriasis. Author(s): Rahman P, Schentag CT, Gladman DD. Source: Arthritis and Rheumatism. 1999 April; 42(4): 822-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10211902&dopt=Abstract
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Immunohistochemical localization of transforming growth factor-alpha and epithelial growth factor receptor in human fetal developing skin, psoriasis and restrictive dermopathy. Author(s): Sergi C, Kahl P, Otto HF. Source: Pathology Oncology Research : Por. 2000; 6(4): 250-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11173656&dopt=Abstract
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Immunomodulation by interleukin-10 therapy decreases the incidence of relapse and prolongs the relapse-free interval in Psoriasis. Author(s): Friedrich M, Docke WD, Klein A, Philipp S, Volk HD, Sterry W, Asadullah K. Source: The Journal of Investigative Dermatology. 2002 April; 118(4): 672-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11918715&dopt=Abstract
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Immunotherapy for psoriasis: from serendipity to selectivity. Author(s): Griffiths CE. Source: Lancet. 2002 January 26; 359(9303): 279-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11830192&dopt=Abstract
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Implications of psoriasis as a new disease. Author(s): Altschuler EL. Source: Dermatology (Basel, Switzerland). 1999; 199(1): 1-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10449948&dopt=Abstract
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Improved quality of life among patients with psoriasis after supervised climate therapy at the Canary Islands. Author(s): Mork C, Wahl A. Source: Journal of the American Academy of Dermatology. 2002 August; 47(2): 314-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12140483&dopt=Abstract
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Improved response of plaque psoriasis after multiple treatments with topical 5aminolaevulinic acid photodynamic therapy. Author(s): Robinson DJ, Collins P, Stringer MR, Vernon DI, Stables GI, Brown SB, Sheehan-Dare RA. Source: Acta Dermato-Venereologica. 1999 November; 79(6): 451-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10598759&dopt=Abstract
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Improvement in psoriasis after intradermal administration of delipidated, deglycolipidated Mycobacterium vaccae (PVAC): results of an open-label trial. Author(s): Balagon MV, Tan PL, Prestidge R, Cellona RV, Abalos RM, Tan EV, Walsh GP, Watson JD, Walsh DS. Source: Clinical and Experimental Dermatology. 2001 May; 26(3): 233-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422164&dopt=Abstract
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Improvement in psoriasis after intradermal administration of heat-killed Mycobacterium vaccae. Author(s): Balagon MV, Walsh DS, Tan PL, Cellona RV, Abalos RM, Tan EV, Fajardo TT, Watson JD, Walsh GP. Source: International Journal of Dermatology. 2000 January; 39(1): 51-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10651968&dopt=Abstract
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Improvement of psoriasis during imatinib therapy in a patient with a metastatic gastrointestinal stromal tumour. Author(s): Miyagawa S, Fujimoto H, Ko S, Hirota S, Kitamura Y. Source: The British Journal of Dermatology. 2002 August; 147(2): 406-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12174137&dopt=Abstract
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Improvement of Pyoderma gangrenosum and psoriasis associated with Crohn disease with anti-tumor necrosis factor alpha monoclonal antibody. Author(s): Tan MH, Gordon M, Lebwohl O, George J, Lebwohl MG. Source: Archives of Dermatology. 2001 July; 137(7): 930-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11453813&dopt=Abstract
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Improving psoriasis care through a nurse-led service. Author(s): Penzer R. Source: Community Nurse. 2000 March; 6(2): 19. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11144204&dopt=Abstract
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In vivo study of skin mechanical properties in psoriasis vulgaris. Author(s): Dobrev H. Source: Acta Dermato-Venereologica. 2000 July-August; 80(4): 263-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11028858&dopt=Abstract
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Incidence and risk factors associated with a second squamous cell carcinoma or basal cell carcinoma in psoralen + ultraviolet a light-treated psoriasis patients. Author(s): Katz KA, Marcil I, Stern RS. Source: The Journal of Investigative Dermatology. 2002 June; 118(6): 1038-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12060400&dopt=Abstract
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Incidence of Candida in psoriasis--a study on the fungal flora of psoriatic patients. Author(s): Waldman A, Gilhar A, Duek L, Berdicevsky I. Source: Mycoses. 2001 May; 44(3-4): 77-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11413927&dopt=Abstract
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Increased oxidative damage to fibroblasts in skin with and without lesions in psoriasis. Author(s): Dimon-Gadal S, Gerbaud P, Therond P, Guibourdenche J, Anderson WB, Evain-Brion D, Raynaud F. Source: The Journal of Investigative Dermatology. 2000 May; 114(5): 984-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10771481&dopt=Abstract
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Increased serum cutaneous T cell-attracting chemokine (CCL27) levels in patients with atopic dermatitis and psoriasis vulgaris. Author(s): Kakinuma T, Saeki H, Tsunemi Y, Fujita H, Asano N, Mitsui H, Tada Y, Wakugawa M, Watanabe T, Torii H, Komine M, Asahina A, Nakamura K, Tamaki K. Source: The Journal of Allergy and Clinical Immunology. 2003 March; 111(3): 592-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12642842&dopt=Abstract
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Increased T-cell receptor vbeta2 chain expression in skin homing lymphocytes in psoriasis. Author(s): Davison S, Allen M, Harmer A, Vaughan R, Barker JN. Source: The British Journal of Dermatology. 1999 May; 140(5): 845-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10354020&dopt=Abstract
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Infantile psoriasis: successful treatment with topical calcipotriol. Author(s): Choi YJ, Hann SK, Chang SN, Park WH. Source: Pediatric Dermatology. 2000 May-June; 17(3): 242-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10886765&dopt=Abstract
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Infantile pustular psoriasis--may mimic seborrhic dermatitis. Author(s): Nayek K, Dasgupta MK. Source: Indian Pediatrics. 2001 September; 38(9): 1059. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11568388&dopt=Abstract
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Inflammatory joint manifestations are prevalent in psoriasis: prevalence study of joint and axial involvement in psoriatic patients, and evaluation of a psoriatic and arthritic questionnaire. Author(s): Alenius GM, Stenberg B, Stenlund H, Lundblad M, Dahlqvist SR. Source: The Journal of Rheumatology. 2002 December; 29(12): 2577-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12465155&dopt=Abstract
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Inflammatory linear verrucous epidermal nevus (ILVEN) and psoriasis in a child? Author(s): Menni S, Restano L, Gianotti R, Boccardi D. Source: International Journal of Dermatology. 2000 January; 39(1): 30-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10651962&dopt=Abstract
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Infliximab for psoriasis and psoriatic arthritis. Author(s): Antoni C, Manger B. Source: Clin Exp Rheumatol. 2002 November-December; 20(6 Suppl 28): S122-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12463461&dopt=Abstract
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Infliximab for the treatment of severe pustular psoriasis. Author(s): Elewski BE. Source: Journal of the American Academy of Dermatology. 2002 November; 47(5): 796-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12399781&dopt=Abstract
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Infliximab monotherapy provides rapid and sustained benefit for plaque-type psoriasis. Author(s): Gottlieb AB, Chaudhari U, Mulcahy LD, Li S, Dooley LT, Baker DG. Source: Journal of the American Academy of Dermatology. 2003 June; 48(6): 829-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12789171&dopt=Abstract
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Information resources for psoriasis patients. Author(s): Monk B. Source: Journal of the Royal Society of Medicine. 1999 September; 92(9): 492-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10645309&dopt=Abstract
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Inhibition of keratinocyte apoptosis by IL-15: a new parameter in the pathogenesis of psoriasis? Author(s): Ruckert R, Asadullah K, Seifert M, Budagian VM, Arnold R, Trombotto C, Paus R, Bulfone-Paus S. Source: Journal of Immunology (Baltimore, Md. : 1950). 2000 August 15; 165(4): 2240-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10925312&dopt=Abstract
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Inhibitors of the enzyme purine nucleoside phosphorylase as potential therapy for psoriasis. Author(s): Morris PE Jr, Omura GA. Source: Current Pharmaceutical Design. 2000 June; 6(9): 943-59. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10828318&dopt=Abstract
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Inhibitors of tyrosine kinases in the treatment of psoriasis. Author(s): Ben-Bassat H, Klein BY. Source: Current Pharmaceutical Design. 2000 June; 6(9): 933-42. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10828317&dopt=Abstract
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Inhibitors of tyrosine kinases in the treatment of psoriasis. Author(s): Ben-Bassat H, Levitzki A. Source: Isr Med Assoc J. 2000 July; 2 Suppl: 69-73. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10909421&dopt=Abstract
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Injection of pre-psoriatic skin with CD4+ T cells induces psoriasis. Author(s): Nickoloff BJ, Wrone-Smith T. Source: American Journal of Pathology. 1999 July; 155(1): 145-58. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10393847&dopt=Abstract
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Inpatient hospital care for psoriasis: a vanishing practice in the United States. Author(s): Stern RS; PUVA Follow-up Study. Source: Journal of the American Academy of Dermatology. 2003 September; 49(3): 44550. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12963908&dopt=Abstract
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Insights into psoriasis and other inflammatory diseases from large-scale gene expression studies. Author(s): Bowcock AM, Shannon W, Du F, Duncan J, Cao K, Aftergut K, Catier J, Fernandez-Vina MA, Menter A. Source: Human Molecular Genetics. 2001 August 15; 10(17): 1793-805. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11532989&dopt=Abstract
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Insulin-like growth factor II induces interleukin-6 expression via NFkappaB activation in psoriasis. Author(s): Kwon YW, Jang ER, Lee YM, Kim YS, Kwon KS, Jang HS, Oh CK, Kim KW. Source: Biochemical and Biophysical Research Communications. 2000 November 19; 278(2): 312-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11097836&dopt=Abstract
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Interferon gamma in keratinocytes in psoriasis. Author(s): McKenzie RC, Sabin E, Szepietowski JC, Gracie JA, Forsey RJ, Howie S. Source: Eur J Dermatol. 2003 May-June; 13(3): 315-6. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12822559&dopt=Abstract
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Interleukin 10 treatment of psoriasis: clinical results of a phase 2 trial. Author(s): Asadullah K, Docke WD, Ebeling M, Friedrich M, Belbe G, Audring H, Volk HD, Sterry W. Source: Archives of Dermatology. 1999 February; 135(2): 187-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10052405&dopt=Abstract
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Interleukin 12 and psoriasis. Author(s): de Rie MA. Source: Dermatology (Basel, Switzerland). 1999; 199(2): 101. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10636696&dopt=Abstract
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Interleukin-10 promoter polymorphism IL10.G and familial early onset psoriasis. Author(s): Hensen P, Asadullah K, Windemuth C, Ruschendorf F, Huffmeier U, Stander M, Schmitt-Egenolf M, Wienker TF, Reis A, Traupe H. Source: The British Journal of Dermatology. 2003 August; 149(2): 381-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932247&dopt=Abstract
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Interleukin-10 promoter polymorphism in psoriasis. Author(s): Asadullah K, Eskdale J, Wiese A, Gallagher G, Friedrich M, Sterry W. Source: The Journal of Investigative Dermatology. 2001 June; 116(6): 975-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11407990&dopt=Abstract
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Interleukin-11 therapy selectively downregulates type I cytokine proinflammatory pathways in psoriasis lesions. Author(s): Trepicchio WL, Ozawa M, Walters IB, Kikuchi T, Gilleaudeau P, Bliss JL, Schwertschlag U, Dorner AJ, Krueger JG. Source: The Journal of Clinical Investigation. 1999 December; 104(11): 1527-37. Erratum In: J Clin Invest 2000 February; 105(3): 396. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10587516&dopt=Abstract
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Interleukin-12 p40 gene (IL12B) 3'-untranslated region polymorphism is associated with susceptibility to atopic dermatitis and psoriasis vulgaris. Author(s): Tsunemi Y, Saeki H, Nakamura K, Sekiya T, Hirai K, Fujita H, Asano N, Kishimoto M, Tanida Y, Kakinuma T, Mitsui H, Tada Y, Wakugawa M, Torii H, Komine M, Asahina A, Tamaki K. Source: Journal of Dermatological Science. 2002 November; 30(2): 161-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12413772&dopt=Abstract
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Interleukin-4 therapy of psoriasis induces Th2 responses and improves human autoimmune disease. Author(s): Ghoreschi K, Thomas P, Breit S, Dugas M, Mailhammer R, van Eden W, van der Zee R, Biedermann T, Prinz J, Mack M, Mrowietz U, Christophers E, Schlondorff D, Plewig G, Sander CA, Rocken M. Source: Nature Medicine. 2003 January; 9(1): 40-6. Epub 2002 December 02. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12461524&dopt=Abstract
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Interleukin-8 plays its role at local level in psoriasis vulgaris. Author(s): Sticherling M, Sautier W, Schroder JM, Christophers E. Source: Acta Dermato-Venereologica. 1999 January; 79(1): 4-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10086849&dopt=Abstract
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Interleukin-8-positive neutrophils in psoriasis. Author(s): Duan H, Koga T, Kohda F, Hara H, Urabe K, Furue M. Source: Journal of Dermatological Science. 2001 June; 26(2): 119-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11378328&dopt=Abstract
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Intermittent short courses of cyclosporin (Neoral(R)) for psoriasis unresponsive to topical therapy: a 1-year multicentre, randomized study. The PISCES Study Group. Author(s): Ho VC, Griffiths CE, Albrecht G, Vanaclocha F, Leon-Dorantes G, Atakan N, Reitamo S, Ohannesson A, Mork NJ, Clarke P, Pfister P, Paul C. Source: The British Journal of Dermatology. 1999 August; 141(2): 283-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10468801&dopt=Abstract
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Intermittent short courses of cyclosporine microemulsion for the long-term management of psoriasis: a 2-year cohort study. Author(s): Ho VC, Griffiths CE, Berth-Jones J, Papp KA, Vanaclocha F, Dauden E, Beard A, Puvanarajan L, Paul C. Source: Journal of the American Academy of Dermatology. 2001 April; 44(4): 643-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11260540&dopt=Abstract
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Interventions for guttate psoriasis. Author(s): Chalmers RJ, O'Sullivan T, Owen CM, Griffiths CE. Source: Cochrane Database Syst Rev. 2000; (2): Cd001213. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10796758&dopt=Abstract
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Intra-individual comparison of the cutaneous safety and efficacy of calcitriol 3 microg g(-1) ointment and calcipotriol 50 microg g(-1) ointment on chronic plaque psoriasis localized in facial, hairline, retroauricular or flexural areas. Author(s): Ortonne JP, Humbert P, Nicolas JF, Tsankov N, Tonev SD, Janin A, Czernielewski J, Lahfa M, Dubertret L. Source: The British Journal of Dermatology. 2003 February; 148(2): 326-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12588387&dopt=Abstract
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Intraosseous epidermoid cyst mimicking psoriasis. Author(s): Bhagwandas K, Nicolaou N, Roberts DL. Source: The British Journal of Dermatology. 2001 August; 145(2): 366-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11531821&dopt=Abstract
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Inverse psoriasis induced by terbinafine. Author(s): Pauluzzi P, Boccucci N. Source: Acta Dermato-Venereologica. 1999 September; 79(5): 389. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10494721&dopt=Abstract
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Investigation of cytomegalovirus and human herpes viruses 6 and 7 as possible causative antigens in psoriasis. Author(s): Kirby B, Al-Jiffri O, Cooper RJ, Corbitt G, Klapper PE, Griffiths CE. Source: Acta Dermato-Venereologica. 2000 November-December; 80(6): 404-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11243630&dopt=Abstract
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Investigator-masked comparison of tazarotene gel q.d. plus mometasone furoate cream q.d. vs. mometasone furoate cream b.i.d. in the treatment of plaque psoriasis. Author(s): Koo JY, Martin D. Source: International Journal of Dermatology. 2001 March; 40(3): 210-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422529&dopt=Abstract
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Involvement of insulin-like growth factor-I in psoriasis as a paracrine growth factor: dermal fibroblasts play a regulatory role in developing psoriatic lesions. Author(s): Miura H, Sano S, Higashiyama M, Yoshikawa K, Itami S. Source: Archives of Dermatological Research. 2000 December; 292(12): 590-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11214819&dopt=Abstract
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Is an epitope on keratin 17 a major target for autoreactive T lymphocytes in psoriasis? Author(s): Gudmundsdottir AS, Sigmundsdottir H, Sigurgeirsson B, Good MF, Valdimarsson H, Jonsdottir I. Source: Clinical and Experimental Immunology. 1999 September; 117(3): 580-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10469066&dopt=Abstract
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Is psoriasis a neuroimmunologic disease? Author(s): Farber EM, Raychaudhuri SP. Source: International Journal of Dermatology. 1999 January; 38(1): 12-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10065603&dopt=Abstract
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Is psoriasis a T-cell disease? Author(s): Nickoloff BJ, Schroder JM, von den Driesch P, Raychaudhuri SP, Farber EM, Boehncke WH, Morhenn VB, Rosenberg EW, Schon MP, Holick MF. Source: Experimental Dermatology. 2000 October; 9(5): 359-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11016857&dopt=Abstract
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Is renal function altered in patients with psoriasis vulgaris?--A short review. Author(s): Szepietowski JC, Szepietowski T. Source: The Journal of Dermatology. 2000 September; 27(9): 569-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11052231&dopt=Abstract
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Is the search for serum antibodies to gliadin, endomysium and tissue transglutaminase meaningful in psoriatic patients? Relationship between the pathogenesis of psoriasis and coeliac disease. Author(s): Cardinali C, Degl'innocenti D, Caproni M, Fabbri P. Source: The British Journal of Dermatology. 2002 July; 147(1): 187-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12154772&dopt=Abstract
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Isolated tenosynovitis associated with psoriasis triggered by physical injury. Author(s): Padula A, Belsito F, Barozzi L, Cantini F, Salvarani C, Pavlica P, Olivieri I. Source: Clin Exp Rheumatol. 1999 January-February; 17(1): 103-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10084042&dopt=Abstract
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Itching in patients suffering from psoriasis. Author(s): Szepietowski JC, Reich A, Wisnicka B. Source: Acta Dermatovenerol Croat. 2002 December; 10(4): 221-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12588672&dopt=Abstract
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John Updike on psoriasis: At war with my skin, from the journal of a leper. Author(s): Jackson R. Source: Journal of Cutaneous Medicine and Surgery. 2000 April; 4(2): 113-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11179937&dopt=Abstract
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Juvenile generalized circinate pustular psoriasis treated with oral cyclosporin A. Author(s): Wollina U, Funfstuck V. Source: Eur J Dermatol. 2001 March-April; 11(2): 117-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11275806&dopt=Abstract
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Juvenile psoriatic arthritis with nail psoriasis in the absence of cutaneous lesions. Author(s): Duran-McKinster C, Ortiz-Solis D, Granados J, Tamayo L, OrozcoCovarrubias L, Ruiz-Maldonado R. Source: International Journal of Dermatology. 2000 January; 39(1): 32-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10651963&dopt=Abstract
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Keeping psoriasis under wraps. Author(s): Griffiths CE. Source: The Journal of Dermatological Treatment. 2001 September; 12(3): 133. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12243702&dopt=Abstract
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Keratinocyte CDw60 expression is modulated by both a Th-1 type cytokine IFNgamma and Th-2 cytokines IL-4 and IL-13: relevance to psoriasis. Author(s): Huang BB, Bonish BK, Chaturvedi V, Qin JZ, Nickoloff BJ. Source: The Journal of Investigative Dermatology. 2001 February; 116(2): 305-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11180008&dopt=Abstract
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Keratinocytes from patients with atopic dermatitis and psoriasis show a distinct chemokine production profile in response to T cell-derived cytokines. Author(s): Giustizieri ML, Mascia F, Frezzolini A, De Pita O, Chinni LM, Giannetti A, Girolomoni G, Pastore S. Source: The Journal of Allergy and Clinical Immunology. 2001 May; 107(5): 871-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11344355&dopt=Abstract
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Koebner phenomenon in psoriasis. A common response to skin trauma. Author(s): Mohla G, Brodell RT. Source: Postgraduate Medicine. 1999 September; 106(3): 39-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10494263&dopt=Abstract
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Lack of association between NOD2 3020InsC frameshift mutation and psoriasis. Author(s): Nair RP, Stuart P, Ogura Y, Inohara N, Chia NV, Young L, Henseler T, Jenisch S, Christophers E, Voorhees JJ, Nunez G, Elder JT. Source: The Journal of Investigative Dermatology. 2001 December; 117(6): 1671-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11886540&dopt=Abstract
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Lack of association of TNF-238A and -308A in Japanese patients with psoriasis vulgaris, psoriatic arthritis and generalized pustular psoriasis. Author(s): Nishibu A, Oyama N, Nakamura K, Kaneko F. Source: Journal of Dermatological Science. 2002 September; 29(3): 181-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12234707&dopt=Abstract
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Lack of efficacy of topical mycophenolic acid in psoriasis vulgaris. Author(s): Geilen CC, Mrowietz U. Source: Journal of the American Academy of Dermatology. 2000 May; 42(5 Pt 1): 837-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10775867&dopt=Abstract
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Lack of evidence of relationship between Helicobacter pylori infection and psoriasis in childhood. Author(s): Fabrizi G, Carbone A, Lippi ME, Anti M, Gasbarrini G. Source: Archives of Dermatology. 2001 November; 137(11): 1529. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11708968&dopt=Abstract
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Langerhans cells, nitric oxide, keratinocytes and psoriasis. Author(s): Kolb-Bachofen V, Bruch-Gerharz D. Source: Immunology Today. 1999 June; 20(6): 289. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10354555&dopt=Abstract
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Large increments in psoralen-ultraviolet A (PUVA) therapy are unsuitable for fairskinned individuals with psoriasis. Author(s): Kirby B, Buckley DA, Rogers S. Source: The British Journal of Dermatology. 1999 April; 140(4): 661-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10233317&dopt=Abstract
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Leukotriene inhibitor may be effective in treatment of psoriasis. Author(s): Zemtsov A, Ali-Moncada S. Source: Acta Dermato-Venereologica. 2000 September-October; 80(5): 389. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11200848&dopt=Abstract
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Levels of endothelial cell stimulating angiogenesis factor and vascular endothelial growth factor are elevated in psoriasis. Author(s): Bhushan M, McLaughlin B, Weiss JB, Griffiths CE. Source: The British Journal of Dermatology. 1999 December; 141(6): 1054-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10606852&dopt=Abstract
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Levels of proelafin peptides in the sera of the patients with generalized pustular psoriasis and pustulosis palmoplantaris. Author(s): Tanaka N, Fujioka A, Tajima S, Ishibashi A, Hirose S. Source: Acta Dermato-Venereologica. 2000 March-April; 80(2): 102-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10877128&dopt=Abstract
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Limited application of fluticasone propionate ointment, 0.005% in patients with psoriasis of the face and intertriginous areas. Author(s): Lebwohl MG, Tan MH, Meador SL, Singer G. Source: Journal of the American Academy of Dermatology. 2001 January; 44(1): 77-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11148481&dopt=Abstract
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Linkage disequilibrium analysis of familial psoriasis: identification of multiple disease-associated MHC haplotypes. Author(s): Jenisch S, Westphal E, Nair RP, Stuart P, Voorhees JJ, Christophers E, Kronke M, Elder JT, Henseler T. Source: Tissue Antigens. 1999 February; 53(2): 135-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10090613&dopt=Abstract
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Lipid profile, insulin secretion, and insulin sensitivity in psoriasis. Author(s): Reynoso-von Drateln C, Martinez-Abundis E, Balcazar-Munoz BR, BustosSaldana R, Gonzalez-Ortiz M. Source: Journal of the American Academy of Dermatology. 2003 June; 48(6): 882-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12789179&dopt=Abstract
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Localization of calcineurin/NFAT in human skin and psoriasis and inhibition of calcineurin/NFAT activation in human keratinocytes by cyclosporin A. Author(s): Al-Daraji WI, Grant KR, Ryan K, Saxton A, Reynolds NJ. Source: The Journal of Investigative Dermatology. 2002 May; 118(5): 779-88. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11982754&dopt=Abstract
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Localization of psoriasis-susceptibility locus PSORS1 to a 60-kb interval telomeric to HLA-C. Author(s): Nair RP, Stuart P, Henseler T, Jenisch S, Chia NV, Westphal E, Schork NJ, Kim J, Lim HW, Christophers E, Voorhees JJ, Elder JT. Source: American Journal of Human Genetics. 2000 June; 66(6): 1833-44. Epub 2000 May 05. Erratum In: Am J Hum Genet 2002 April; 70(4): 1074. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10801386&dopt=Abstract
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Localized pustular psoriasis with onycholysis representing a Kobner phenomenon. Author(s): Gniadecki R, Petersen CS, Rossen K. Source: Acta Dermato-Venereologica. 2000 May; 80(3): 208. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10954214&dopt=Abstract
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Long-term continuous versus intermittent cyclosporin: therapy for psoriasis. Author(s): Ohtsuki M, Nakagawa H, Sugai J, Ozawa A, Ohkido M, Nakayama J, Hanada J, Morimoto Y, Jimbow K, Horikoshi T, Kitahara H, Tamaki K, Urabe K, Hori Y. Source: The Journal of Dermatology. 2003 April; 30(4): 290-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707465&dopt=Abstract
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Long-term efficacy and safety of tacalcitol ointment in patients with chronic plaque psoriasis. Author(s): van de Kerkhof PC, Berth-Jones J, Griffiths CE, Harrison PV, Honigsmann H, Marks R, Roelandts R, Schopf E, Trompke C. Source: The British Journal of Dermatology. 2002 March; 146(3): 414-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11952541&dopt=Abstract
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Long-term safety and efficacy of high-concentration (20 microg/g) tacalcitol ointment in psoriasis vulgaris. Author(s): Miyachi Y, Ohkawara A, Ohkido M, Harada S, Tamaki K, Nakagawa H, Hori Y, Nishiyama S. Source: Eur J Dermatol. 2002 September-October; 12(5): 463-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12370136&dopt=Abstract
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Long-term safety aspects of systemic therapy with fumaric acid esters in severe psoriasis. Author(s): Hoefnagel JJ, Thio HB, Willemze R, Bouwes Bavinck JN. Source: The British Journal of Dermatology. 2003 August; 149(2): 363-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932244&dopt=Abstract
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Longterm treatment of psoriasis using fumaric acid preparations can be associated with severe proximal tubular damage. Author(s): Raschka C, Koch HJ. Source: Human & Experimental Toxicology. 1999 December; 18(12): 738-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10627662&dopt=Abstract
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Long-term treatment of psoriasis with calcipotriol scalp solution and cream. Author(s): Barnes L, Altmeyer P, Forstrom L, Stenstrom MH. Source: Eur J Dermatol. 2000 April-May; 10(3): 199-204. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10725818&dopt=Abstract
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Loss of heterozygosity and PCR artifacts in a microsatellite analysis of psoriasis and colorectal cancer. Author(s): Hyun JS, Jo BK, Park CJ, Yi JY, Lee JY, Rhyu MG. Source: Journal of Korean Medical Science. 2002 October; 17(5): 641-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12378016&dopt=Abstract
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Low DNA repair is a risk factor in skin carcinogenesis: a study of basal cell carcinoma in psoriasis patients. Author(s): Dybdahl M, Frentz G, Vogel U, Wallin H, Nexo BA. Source: Mutation Research. 1999 January 26; 433(1): 15-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10047775&dopt=Abstract
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Low dose cyclosporin A and methotrexate in the treatment of psoriasis. Author(s): Wong KC, Georgouras K. Source: Acta Dermato-Venereologica. 1999 January; 79(1): 87. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10086872&dopt=Abstract
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Low dose cyclosporin A treatment in generalized pustular psoriasis. Author(s): Kilic SS, Hacimustafaoglu M, Celebi S, Karadeniz A, Ildirim I. Source: Pediatric Dermatology. 2001 May-June; 18(3): 246-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11438009&dopt=Abstract
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Magnetic resonance imaging of acquired Brown syndrome in a patient with psoriasis. Author(s): Thorne JE, Volpe NJ, Liu GT. Source: American Journal of Ophthalmology. 1999 February; 127(2): 233-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10030581&dopt=Abstract
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Malignant melanoma in patients treated for psoriasis with PUVA. Author(s): Stern RS. Source: Photodermatology, Photoimmunology & Photomedicine. 1999 February; 15(1): 37-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9990669&dopt=Abstract
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Malignant tumours and psoriasis: a follow-up study. Author(s): Frentz G, Olsen JH. Source: The British Journal of Dermatology. 1999 February; 140(2): 237-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10233215&dopt=Abstract
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Management of guttate and generalized psoriasis vulgaris: prospective randomized study. Author(s): Caca-Biljanovska NG, V'lckova-Laskoska MT. Source: Croatian Medical Journal. 2002 December; 43(6): 707-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12476481&dopt=Abstract
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Management of moderate to severe plaque psoriasis with biologic therapy. Author(s): Pariser DM. Source: Manag Care. 2003 April; 12(4): 36-44. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747028&dopt=Abstract
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Management of nail psoriasis. Author(s): de Berker D. Source: Clinical and Experimental Dermatology. 2000 July; 25(5): 357-62. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11012585&dopt=Abstract
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Management of psoriasis in childhood. Author(s): Burden AD. Source: Clinical and Experimental Dermatology. 1999 September; 24(5): 341-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10564317&dopt=Abstract
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Management of psoriasis vulgaris with methotrexate 0.25% in a hydrophilic gel: a placebo-controlled, double-blind study. Author(s): Syed TA, Hadi SM, Qureshi ZA, Nordstrom CG, Ali SM. Source: Journal of Cutaneous Medicine and Surgery. 2001 July-August; 5(4): 299-302. Epub 2001 July 18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11907839&dopt=Abstract
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Management of psoriasis. Author(s): Cowen P. Source: Aust Fam Physician. 2001 November; 30(11): 1033-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11759451&dopt=Abstract
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Management of scalp psoriasis: guidelines for corticosteroid use in combination treatment. Author(s): van der Vleuten CJ, van de Kerkhof PC. Source: Drugs. 2001; 61(11): 1593-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11577796&dopt=Abstract
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Managing the patient with psoriasis. Author(s): Wong C, Kirby B. Source: Practitioner. 2001 November; 245(1628): 913-8, 920, 922. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11727344&dopt=Abstract
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Marginal acrokeratoderma and psoriasis: Is there an association? Author(s): Rai R, Saraswat A, Kaur I, Kumar B. Source: International Journal of Dermatology. 2000 December; 39(12): 936-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11168667&dopt=Abstract
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Mathematical modelling of nitric oxide regulation of rete peg formation in psoriasis. Author(s): Savill NJ, Weller R, Sherratt JA. Source: Journal of Theoretical Biology. 2002 January 7; 214(1): 1-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11786028&dopt=Abstract
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Matrix metalloproteinase-19 is expressed by keratinocytes in psoriasis. Author(s): Suomela S, Kariniemi AL, Impola U, Karvonen SL, Snellman E, Uurasmaa T, Peltonen J, Saarialho-Kere U. Source: Acta Dermato-Venereologica. 2003; 83(2): 108-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12735638&dopt=Abstract
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Measuring health-related quality of life in patients with mild to moderate eczema and psoriasis: clinical validity, reliability and sensitivity to change of the DLQI. The Cavide Research Group. Author(s): Badia X, Mascaro JM, Lozano R. Source: The British Journal of Dermatology. 1999 October; 141(4): 698-702. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10583119&dopt=Abstract
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Mediation of systemic vascular hyperpermeability in severe psoriasis by circulating vascular endothelial growth factor. Author(s): Creamer D, Allen M, Jaggar R, Stevens R, Bicknell R, Barker J. Source: Archives of Dermatology. 2002 June; 138(6): 791-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12056961&dopt=Abstract
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Medical backgrounder: psoriasis. Author(s): Travis L, Weinberg JM. Source: Drugs Today (Barc). 2002 December; 38(12): 847-65. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12582473&dopt=Abstract
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Medium-dose 308-nm excimer laser for the treatment of psoriasis. Author(s): Trehan M, Taylor CR. Source: Journal of the American Academy of Dermatology. 2002 November; 47(5): 701-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12399761&dopt=Abstract
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Methotrexate in psoriasis: 26 years' experience with low-dose long-term treatment. Author(s): Haustein UF, Rytter M. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2000 September; 14(5): 382-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11305380&dopt=Abstract
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Methotrexate in the treatment of psoriasis. Author(s): Bright RD. Source: Cutis; Cutaneous Medicine for the Practitioner. 1999 November; 64(5): 332-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10582158&dopt=Abstract
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Methotrexate versus cyclosporine in moderate-to-severe chronic plaque psoriasis. Author(s): Heydendael VM, Spuls PI, Opmeer BC, de Borgie CA, Reitsma JB, Goldschmidt WF, Bossuyt PM, Bos JD, de Rie MA. Source: The New England Journal of Medicine. 2003 August 14; 349(7): 658-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917302&dopt=Abstract
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MICA 5.1 allele is a susceptibility marker for psoriasis in the Korean population. Author(s): Choi HB, Han H, Youn JI, Kim TY, Kim TG. Source: Tissue Antigens. 2000 December; 56(6): 548-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11169245&dopt=Abstract
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Microalbuminuria as a subclinical marker of renal impairment in subjects with psoriasis vulgaris. Author(s): Szepietowski JC, Bielicka E, Wasik F, Kopec W, Szepietowski T. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2000 November; 14(6): 513-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11444279&dopt=Abstract
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Microbiology of infected pustular psoriasis lesions. Author(s): Brook I, Frazier EH, Yeager JK. Source: International Journal of Dermatology. 1999 August; 38(8): 579-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10487445&dopt=Abstract
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Microorganisms in intertriginous psoriasis: no evidence of Candida. Author(s): Flytstrom I, Bergbrant IM, Brared J, Brandberg LL. Source: Acta Dermato-Venereologica. 2003; 83(2): 121-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12735640&dopt=Abstract
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Microscopic inflammatory changes in colon of patients with both active psoriasis and psoriatic arthritis without bowel symptoms. Author(s): Scarpa R, Manguso F, D'Arienzo A, D'Armiento FP, Astarita C, Mazzacca G, Ayala F. Source: The Journal of Rheumatology. 2000 May; 27(5): 1241-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10813294&dopt=Abstract
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Molecular classification of psoriasis disease-associated genes through pharmacogenomic expression profiling. Author(s): Oestreicher JL, Walters IB, Kikuchi T, Gilleaudeau P, Surette J, Schwertschlag U, Dorner AJ, Krueger JG, Trepicchio WL. Source: The Pharmacogenomics Journal. 2001; 1(4): 272-87. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11911124&dopt=Abstract
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Mucocutaneous adverse effects of hydroxyurea: a prospective study of 30 psoriasis patients. Author(s): Kumar B, Saraswat A, Kaur I. Source: Clinical and Experimental Dermatology. 2002 January; 27(1): 8-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11952660&dopt=Abstract
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Nail changes in psoriasis: a study of 167 patients. Author(s): Kaur I, Saraswat A, Kumar B. Source: International Journal of Dermatology. 2001 September; 40(9): 601-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11737461&dopt=Abstract
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Nail psoriasis: a combined treatment using calcipotriol cream and clobetasol propionate cream. Author(s): Rigopoulos D, Ioannides D, Prastitis N, Katsambas A. Source: Acta Dermato-Venereologica. 2002; 82(2): 140. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12125946&dopt=Abstract
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Nailfold video capillaroscopy in psoriasis. Author(s): Bhushan M, Moore T, Herrick AL, Griffiths CE. Source: The British Journal of Dermatology. 2000 June; 142(6): 1171-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10848742&dopt=Abstract
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Narrowband UV-B (TL-01) phototherapy vs oral 8-methoxypsoralen psoralen-UV-A for the treatment of chronic plaque psoriasis. Author(s): Markham T, Rogers S, Collins P. Source: Archives of Dermatology. 2003 March; 139(3): 325-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12622624&dopt=Abstract
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Narrowband UV-B phototherapy clears psoriasis through a combination of local and systemic effects. Author(s): Gibbs NK. Source: Archives of Dermatology. 2003 May; 139(5): 665; Author Reply 665-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756108&dopt=Abstract
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Narrowband UVB phototherapy for psoriasis: results with fixed increments by skin type (as opposed to percentage increments). Author(s): Halasz CL. Source: Photodermatology, Photoimmunology & Photomedicine. 1999 April; 15(2): 81-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10321520&dopt=Abstract
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Narrowband UVB phototherapy for the treatment of psoriasis: a review and update. Author(s): Barbagallo J, Spann CT, Tutrone WD, Weinberg JM. Source: Cutis; Cutaneous Medicine for the Practitioner. 2001 November; 68(5): 345-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11766120&dopt=Abstract
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Narrowband UV-B phototherapy vs photochemotherapy in the treatment of chronic plaque-type psoriasis: a paired comparison study. Author(s): Tanew A, Radakovic-Fijan S, Schemper M, Honigsmann H. Source: Archives of Dermatology. 1999 May; 135(5): 519-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10328190&dopt=Abstract
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Natural killer and natural killer-T cells in psoriasis. Author(s): Cameron AL, Kirby B, Fei W, Griffiths CE. Source: Archives of Dermatological Research. 2002 November; 294(8): 363-9. Epub 2002 October 08. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12420105&dopt=Abstract
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Natural killer cell activity, serum immunoglobulins, complement proteins, and zinc levels in patients with psoriasis vulgaris. Author(s): Ozturk G, Erbas D, Gelir E, Gulekon A, Imir T. Source: Immunological Investigations. 2001 August; 30(3): 181-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11570639&dopt=Abstract
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Nerve growth factor and its receptor system in psoriasis. Author(s): Raychaudhuri SP, Jiang WY, Smoller BR, Farber EM. Source: The British Journal of Dermatology. 2000 July; 143(1): 198-200. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10886162&dopt=Abstract
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Nerve growth factor and keratinocytes: a role in psoriasis. Author(s): Pincelli C. Source: Eur J Dermatol. 2000 March; 10(2): 85-90. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10694304&dopt=Abstract
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New dermatological agents for the treatment of psoriasis. Author(s): Thacher SM, Vasudevan J, Tsang KY, Nagpal S, Chandraratna RA. Source: Journal of Medicinal Chemistry. 2001 February 1; 44(3): 281-97. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11462969&dopt=Abstract
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New developments in the treatment of psoriasis. Author(s): Lebwohl M. Source: Archives of Dermatology. 2002 May; 138(5): 686-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12020234&dopt=Abstract
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New developments in the treatment of psoriasis. Author(s): van De Kerkhof PC. Source: Skin Pharmacology and Applied Skin Physiology. 2001 May-June; 14(3): 129-35. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11408843&dopt=Abstract
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New drugs in the treatment of psoriasis. Author(s): DiSepio D, Chandraratna RA. Source: Expert Opinion on Investigational Drugs. 2000 January; 9(1): 79-93. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11060662&dopt=Abstract
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New topical treatments change the pattern of treatment of psoriasis: dermatologists remain the primary providers of this care. Author(s): Feldman SR, Fleischer AB Jr, Cooper JZ. Source: International Journal of Dermatology. 2000 January; 39(1): 41-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10651966&dopt=Abstract
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New topicals for mild and moderate psoriasis. Author(s): Cooper CW. Source: Jaapa. 1999 April; 12(4): 52-4, 57-60. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10728082&dopt=Abstract
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New treatments for psoriasis. Author(s): Granstein RD. Source: The New England Journal of Medicine. 2001 July 26; 345(4): 284-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11474669&dopt=Abstract
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Newly available treatments for psoriatic arthritis and their impact on skin psoriasis. Author(s): Galadari H, Fuchs B, Lebwohl M. Source: International Journal of Dermatology. 2003 March; 42(3): 231-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12653923&dopt=Abstract
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No additional effect of calcipotriol ointment on low-dose narrow-band UVB phototherapy in psoriasis. Author(s): Brands S, Brakman M, Bos JD, de Rie MA. Source: Journal of the American Academy of Dermatology. 1999 December; 41(6): 991-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10570386&dopt=Abstract
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Noninvasive characterization of human stratum corneum of undiseased skin of patients with atopic dermatitis and psoriasis as studied by Fourier transform Raman spectroscopy. Author(s): Wohlrab J, Vollmann A, Wartewig S, Marsch WC, Neubert R. Source: Biopolymers. 2001; 62(3): 141-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11343282&dopt=Abstract
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Non-M protein(s) on the cell wall and membrane of group A streptococci induce(s) IFN-gamma production by dermal CD4+ T cells in psoriasis. Author(s): Brown DW, Baker BS, Ovigne JM, Fischetti VA, Hardman C, Powles AV, Fry L. Source: Archives of Dermatological Research. 2001 April; 293(4): 165-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11380148&dopt=Abstract
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Normal keratinocytes express Toll-like receptors (TLRs) 1, 2 and 5: modulation of TLR expression in chronic plaque psoriasis. Author(s): Baker BS, Ovigne JM, Powles AV, Corcoran S, Fry L. Source: The British Journal of Dermatology. 2003 April; 148(4): 670-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12752123&dopt=Abstract
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Normal proliferative responses of peripheral blood mononuclear cells to streptococcal preparation OK-432 in patients with pustulosis palmaris et plantaris constitute a distinct feature from the reduced responses observed in those with psoriasis vulgaris, pustular psoriasis, and acrodermatitis continua of Hallopeau. Author(s): Takahashi K, Aiba S, Uddin Z, Kasai H, Tagami H. Source: Journal of Dermatological Science. 2001 January; 25(1): 87-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11154870&dopt=Abstract
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Novel biological immunotherapies for psoriasis. Author(s): Kanitakis J, Butnaru AC, Claudy A. Source: Expert Opinion on Investigational Drugs. 2003 July; 12(7): 1111-21. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12831347&dopt=Abstract
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Novel genetic association between the corneodesmosin (MHC S) gene and susceptibility to psoriasis. Author(s): Tazi Ahnini R, Camp NJ, Cork MJ, Mee JB, Keohane SG, Duff GW, di Giovine FS. Source: Human Molecular Genetics. 1999 June; 8(6): 1135-40. Erratum In: Hum Mol Genet 2000 March 1; 9(4): 659. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10332047&dopt=Abstract
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Novel immune-based therapies for psoriasis. Author(s): Kirby B, Griffiths CE. Source: The British Journal of Dermatology. 2002 April; 146(4): 546-51. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11966683&dopt=Abstract
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Novel immunoglobulin superfamily gene cluster, mapping to a region of human chromosome 17q25, linked to psoriasis susceptibility. Author(s): Speckman RA, Wright Daw JA, Helms C, Duan S, Cao L, Taillon-Miller P, Kwok PY, Menter A, Bowcock AM. Source: Human Genetics. 2003 January; 112(1): 34-41. Epub 2002 October 24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12483297&dopt=Abstract
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Novel immunotherapies for psoriasis. Author(s): Asadullah K, Volk HD, Sterry W. Source: Trends in Immunology. 2002 January; 23(1): 47-53. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11801454&dopt=Abstract
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Novel mechanisms of T-cell and dendritic cell activation revealed by profiling of psoriasis on the 63,100-element oligonucleotide array. Author(s): Zhou X, Krueger JG, Kao MC, Lee E, Du F, Menter A, Wong WH, Bowcock AM. Source: Physiological Genomics. 2003 March 18; 13(1): 69-78. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12644634&dopt=Abstract
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Novel therapies for psoriasis. Author(s): Cather J, Menter A. Source: American Journal of Clinical Dermatology. 2002; 3(3): 159-73. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11978137&dopt=Abstract
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Objective assessment of photoageing effects using high-frequency ultrasound in PUVA-treated psoriasis patients. Author(s): Sator PG, Schmidt JB, Honigsmann H. Source: The British Journal of Dermatology. 2002 August; 147(2): 291-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12174102&dopt=Abstract
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Observer-blind, randomized, intrapatient comparison of a novel 1% coal tar preparation (Exorex) and calcipotriol cream in the treatment of plaque type psoriasis. Author(s): Tzaneva S, Honigsmann H, Tanew A. Source: The British Journal of Dermatology. 2003 August; 149(2): 350-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932242&dopt=Abstract
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Occlusive versus nonocclusive calcipotriol ointment treatment for palmoplantar psoriasis. Author(s): Duweb GA, Abuzariba O, Rahim M, al-Taweel M, al-Alem S, Abdulla SA. Source: Int J Tissue React. 2001; 23(2): 59-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11447774&dopt=Abstract
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Occupational post-traumatic psoriasis. Author(s): Kanerva L, Estlander T. Source: Contact Dermatitis. 2001 May; 44(5): 317-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11382217&dopt=Abstract
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Oligoclonal expansion of intraepidermal T cells in psoriasis skin lesions. Author(s): Lin WJ, Norris DA, Achziger M, Kotzin BL, Tomkinson B. Source: The Journal of Investigative Dermatology. 2001 December; 117(6): 1546-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11886521&dopt=Abstract
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On the immunopathogenesis of psoriasis. Author(s): Jablonska S, Majewski S. Source: Archives of Dermatology. 2001 February; 137(2): 229-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11176704&dopt=Abstract
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Once-daily vs twice-daily triamcinolone acetonide cream for psoriasis. Author(s): Kanzler MH, Chui C, Gorsulowsky DC. Source: Archives of Dermatology. 2001 November; 137(11): 1529-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11708967&dopt=Abstract
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Optimized UVB treatment of psoriasis: a controlled, left-right comparison trial. Author(s): Selvaag E, Caspersen L, Bech-Thomsen N, de Fine Olivarius F, Wulf HC. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2000 January; 14(1): 19-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10877248&dopt=Abstract
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Oral lesions in patients with psoriasis: clinical presentation and management. Author(s): Brice DM, Danesh-Meyer MJ. Source: J Periodontol. 2000 December; 71(12): 1896-903. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11156048&dopt=Abstract
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Oral liarozole in the treatment of palmoplantar pustular psoriasis: a randomized, double-blind, placebo-controlled study. Author(s): Bhushan M, Burden AD, McElhone K, James R, Vanhoutte FP, Griffiths CE. Source: The British Journal of Dermatology. 2001 October; 145(4): 546-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11703279&dopt=Abstract
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Oral propylthiouracil for the treatment of resistant plaque psoriasis. Author(s): Chowdhury MM, Marks R. Source: The Journal of Dermatological Treatment. 2001 June; 12(2): 81-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12243663&dopt=Abstract
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Oral psoriasis in a patient with hepatitis C virus infection. Author(s): Yamamoto T, Nishioka K. Source: Eur J Dermatol. 2002 January-February; 12(1): 75-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11809602&dopt=Abstract
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Oral psoriasis. Author(s): Bruce AJ, Rogers RS 3rd. Source: Dermatologic Clinics. 2003 January; 21(1): 99-104. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12622272&dopt=Abstract
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Overexpression of CD1d by keratinocytes in psoriasis and CD1d-dependent IFNgamma production by NK-T cells. Author(s): Bonish B, Jullien D, Dutronc Y, Huang BB, Modlin R, Spada FM, Porcelli SA, Nickoloff BJ. Source: Journal of Immunology (Baltimore, Md. : 1950). 2000 October 1; 165(7): 4076-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11034419&dopt=Abstract
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Overexpression of monocyte-derived cytokines in active psoriasis: a relation to coexistent arthropathy. Author(s): Nishibu A, Han GW, Iwatsuki K, Matsui T, Inoue M, Akiba H, Kaneko R, Kaneko F. Source: Journal of Dermatological Science. 1999 September; 21(1): 63-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10468194&dopt=Abstract
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Oxidative stress in keratinocytes as an etiopathogenetic factor of psoriasis. Author(s): Shilov VN, Sergienko VI. Source: Bulletin of Experimental Biology and Medicine. 2000 April; 129(4): 309-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10977902&dopt=Abstract
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Palmoplantar lesions in psoriasis: a study of 3065 patients. Author(s): Kumar B, Saraswat A, Kaur I. Source: Acta Dermato-Venereologica. 2002; 82(3): 192-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12353710&dopt=Abstract
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Paroxetine-associated psoriasis. Author(s): Osborne SF, Stafford L, Orr KG. Source: The American Journal of Psychiatry. 2002 December; 159(12): 2113. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12450972&dopt=Abstract
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Pathophysiology of psoriasis: science behind therapy. Author(s): Guenther LC, Ortonne JP. Source: Journal of Cutaneous Medicine and Surgery. 2002 May-June; 6(3 Suppl): 2-7. Epub 2002 April 30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11976985&dopt=Abstract
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Patient notes: psoriasis. Author(s): Landow K. Source: Postgraduate Medicine. 2002 July; 112(1): 91-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12146096&dopt=Abstract
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Patients' strategies for coping with psoriasis. Author(s): Fortune DG, Richards HL, Main CJ, Griffiths CE. Source: Clinical and Experimental Dermatology. 2002 May; 27(3): 177-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12072002&dopt=Abstract
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Patients with psoriasis prefer solution and foam vehicles: a quantitative assessment of vehicle preference. Author(s): Housman TS, Mellen BG, Rapp SR, Fleischer AB Jr, Feldman SR. Source: Cutis; Cutaneous Medicine for the Practitioner. 2002 December; 70(6): 327-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12502121&dopt=Abstract
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Patterns of adaptation in asthma and psoriasis. Author(s): Rubino IA, Tozzi F, Pischedda S, Ciani N. Source: Percept Mot Skills. 2001 April; 92(2): 569-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11361323&dopt=Abstract
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Pediatric psoriasis revisited. Author(s): Marcoux D, Prost Y. Source: Journal of Cutaneous Medicine and Surgery. 2002 May-June; 6(3 Suppl): 22-8. Epub 2002 April 30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11976986&dopt=Abstract
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Perforin and granzyme B may contribute to skin inflammation in atopic dermatitis and psoriasis. Author(s): Yawalkar N, Schmid S, Braathen LR, Pichler WJ. Source: The British Journal of Dermatology. 2001 June; 144(6): 1133-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422032&dopt=Abstract
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Performance of the self-administered psoriasis area and severity index in evaluating clinical and sociodemographic subgroups of patients with psoriasis. Author(s): Sampogna F, Sera F, Mazzotti E, Pasquini P, Picardi A, Abeni D; IDI Multipurpose Psoriasis Research on Vital Experiences (IMPROVE) Study Group. Source: Archives of Dermatology. 2003 March; 139(3): 353-8; Discussion 357. Erratum In: Arch Dermatol. 2003 July; 139(7): 950. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12622629&dopt=Abstract
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Pharmacodynamic and pharmacokinetic response to anti-tumor necrosis factor-alpha monoclonal antibody (infliximab) treatment of moderate to severe psoriasis vulgaris. Author(s): Gottlieb AB, Masud S, Ramamurthi R, Abdulghani A, Romano P, Chaudhari U, Dooley LT, Fasanmade AA, Wagner CL. Source: Journal of the American Academy of Dermatology. 2003 January; 48(1): 68-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12522373&dopt=Abstract
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Pharmacoeconomic evaluation of calcipotriol (Daivonex/Dovonex) and UVB phototherapy in the treatment of psoriasis: a Markov model for The Netherlands. Author(s): de Rie MA, de Hoop D, Jonsson L, Bakkers EJ, Sorensen M. Source: Dermatology (Basel, Switzerland). 2001; 202(1): 38-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11244227&dopt=Abstract
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Pharmacokinetics and pharmacodynamics of low-dose methotrexate in the treatment of psoriasis. Author(s): Chladek J, Grim J, Martinkova J, Simkova M, Vaniekova J, Koudelkova V, Noiekova M. Source: British Journal of Clinical Pharmacology. 2002 August; 54(2): 147-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12207634&dopt=Abstract
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Phototherapy for psoriasis. Author(s): Honigsmann H. Source: Clinical and Experimental Dermatology. 2001 June; 26(4): 343-50. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422187&dopt=Abstract
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Phototherapy of psoriasis: update with practical pearls. Author(s): Lui H. Source: Journal of Cutaneous Medicine and Surgery. 2002 May-June; 6(3 Suppl): 17-21. Epub 2002 April 30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11976982&dopt=Abstract
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Phototherapy utilization for psoriasis is declining in the United States. Author(s): Housman TS, Rohrback JM, Fleischer AB Jr, Feldman SR. Source: Journal of the American Academy of Dermatology. 2002 April; 46(4): 557-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11907508&dopt=Abstract
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Physicians' response to a letter to confirm diagnosis in a genetic study of psoriasis. Author(s): Mahe E, Lahfa M, Mansouri S, Mosharraf-Olmolk H, Rebours JL, Prud'Homme JF, Fischer J. Source: Eur J Dermatol. 2002 January-February; 12(1): 66-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11809599&dopt=Abstract
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Pimecrolimus identifies a common genomic anti-inflammatory profile, is clinically highly effective in psoriasis and is well tolerated. Author(s): Rappersberger K, Komar M, Ebelin ME, Scott G, Burtin P, Greig G, Kehren J, Chibout SD, Cordier A, Holter W, Richter L, Oberbauer R, Stuetz A, Wolff K. Source: The Journal of Investigative Dermatology. 2002 October; 119(4): 876-87. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12406334&dopt=Abstract
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Pneumonitis complicating methotrexate therapy for pustular psoriasis. Author(s): Ameen M, Taylor DA, Williams IP, Wells AU, Barkert JN. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2001 May; 15(3): 247-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11683290&dopt=Abstract
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Polymorphism of the vitamin D(3) receptor in patients with psoriasis. Author(s): Okita H, Ohtsuka T, Yamakage A, Yamazaki S. Source: Archives of Dermatological Research. 2002 July; 294(4): 159-62. Epub 2002 May 28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12111344&dopt=Abstract
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Polymorphisms of vitamin D receptor gene in Japanese patients with psoriasis vulgaris. Author(s): Saeki H, Asano N, Tsunemi Y, Takekoshi T, Kishimoto M, Mitsui H, Tada Y, Torii H, Komine M, Asahina A, Tamaki K. Source: Journal of Dermatological Science. 2002 November; 30(2): 167-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12413773&dopt=Abstract
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Positive family history of psoriasis does not affect the clinical expression and course of juvenile idiopathic arthritis patients with oligoarthritis. Author(s): Tsitsami E, Bozzola E, Magni-Manzoni S, Viola S, Pistorio A, Ruperto N, Martini A, Ravelli A. Source: Arthritis and Rheumatism. 2003 August 15; 49(4): 488-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12910554&dopt=Abstract
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Potential role of the chemokine receptors CXCR3, CCR4, and the integrin alphaEbeta7 in the pathogenesis of psoriasis vulgaris. Author(s): Rottman JB, Smith TL, Ganley KG, Kikuchi T, Krueger JG. Source: Laboratory Investigation; a Journal of Technical Methods and Pathology. 2001 March; 81(3): 335-47. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11310827&dopt=Abstract
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Potential use of leukotriene inhibitors in treatment of psoriasis. Author(s): Zemtsov A, Bucchino S, McDowell MR. Source: Dermatology (Basel, Switzerland). 2003; 206(2): 179-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592092&dopt=Abstract
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Practical management of psoriasis in the elderly: epidemiology, clinical aspects, quality of life, patient education and treatment options. Author(s): Yosipovitch G, Tang MB. Source: Drugs & Aging. 2002; 19(11): 847-63. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12428994&dopt=Abstract
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Pretreatment of psoriasis with the vitamin D3 derivative tacalcitol increases the responsiveness to 311-nm ultraviolet B: results of a controlled, right/left study. Author(s): Messer G, Degitz K, Plewig G, Rocken M. Source: The British Journal of Dermatology. 2001 March; 144(3): 628-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11260031&dopt=Abstract
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Prevalence of psoriasis in Spain (Epiderma Project: phase I). Author(s): Ferrandiz C, Bordas X, Garcia-Patos V, Puig S, Pujol R, Smandia A. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2001 January; 15(1): 20-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11451315&dopt=Abstract
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Profiles of activated T lymphocytes in peripheral blood of Kuwaiti psoriasis vulgaris patients. Author(s): Abul H, Mahmoud F, Al-Saleh Q, Khajeji M, Haines D. Source: The Journal of Dermatology. 2002 April; 29(4): 202-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12027084&dopt=Abstract
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Promoter polymorphisms of the genes encoding tumor necrosis factor-alpha and interleukin-1beta are associated with different subtypes of psoriasis characterized by early and late disease onset. Author(s): Reich K, Mossner R, Konig IR, Westphal G, Ziegler A, Neumann C. Source: The Journal of Investigative Dermatology. 2002 January; 118(1): 155-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11851889&dopt=Abstract
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Promoter region polymorphism of the CD14 gene (C-159T) is not associated with psoriasis vulgaris. Author(s): Karhukorpi J, Ikaheimo I, Karvonen J, Karttunen R. Source: European Journal of Immunogenetics : Official Journal of the British Society for Histocompatibility and Immunogenetics. 2002 February; 29(1): 57-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11841490&dopt=Abstract
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Proteasome inhibition reduces superantigen-mediated T cell activation and the severity of psoriasis in a SCID-hu model. Author(s): Zollner TM, Podda M, Pien C, Elliott PJ, Kaufmann R, Boehncke WH. Source: The Journal of Clinical Investigation. 2002 March; 109(5): 671-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11877475&dopt=Abstract
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Psoriasiform acral dermatitis: a peculiar clinical presentation of psoriasis in children. Author(s): Patrizi A, Bardazzi F, Neri I, Fanti PA. Source: Pediatric Dermatology. 1999 November-December; 16(6): 439-43. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10632940&dopt=Abstract
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Psoriasis and parapsoriasis: since 200 and 100 years, respectively. Author(s): Holubar K. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2003 March; 17(2): 126-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12705739&dopt=Abstract
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Psoriasis and pregnancy. Author(s): Tauscher AE, Fleischer AB Jr, Phelps KC, Feldman SR. Source: Journal of Cutaneous Medicine and Surgery. 2002 November-December; 6(6): 561-70. Epub 2002 October 09. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12362257&dopt=Abstract
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Psoriasis and psoriatic arthritis, axial type. Author(s): White KL. Source: Dermatology Online Journal [electronic Resource]. 2001 December; 7(2): 12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12165228&dopt=Abstract
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Psoriasis and radiotherapy. Author(s): Tomlinson MJ. Source: Clin Oncol (R Coll Radiol). 2001; 13(2): 145. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11565503&dopt=Abstract
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Psoriasis and side-effects of mesotherapy. Author(s): Rosina P, Chieregato C, Miccolis D, D'Onghia FS. Source: International Journal of Dermatology. 2001 September; 40(9): 581-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11737454&dopt=Abstract
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Psoriasis arthropathy and lymphedema. Author(s): Yamamoto T, Nishioka K. Source: The Journal of Dermatology. 2002 December; 29(12): 812-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12532050&dopt=Abstract
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Psoriasis as a model for T-cell-mediated disease: immunobiologic and clinical effects of treatment with multiple doses of efalizumab, an anti-CD11a antibody. Author(s): Gottlieb AB, Krueger JG, Wittkowski K, Dedrick R, Walicke PA, Garovoy M. Source: Archives of Dermatology. 2002 May; 138(5): 591-600. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12020219&dopt=Abstract
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Psoriasis bullosa acquisita. Author(s): Morris SD, Mallipeddi R, Oyama N, Gratian MJ, Harman KE, Bhogal BS, Black MM, Eady RA, Hashimoto T, McGrath JA. Source: Clinical and Experimental Dermatology. 2002 November; 27(8): 665-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12472542&dopt=Abstract
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Psoriasis concomitant with chronic opisthorchiasis: ultrastructural changes in cell populations of gastroduodenal mucosa. Author(s): Khardikova SA, Aidagulova SV, Lapii GA, Nepomnyashchikh DL. Source: Bulletin of Experimental Biology and Medicine. 2002 December; 134(6): 588-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12660845&dopt=Abstract
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Psoriasis from the patient's point of view. Author(s): Finlay AY. Source: Archives of Dermatology. 2001 March; 137(3): 352-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11255339&dopt=Abstract
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Psoriasis guttata in association with hepatocellular carcinoma. Author(s): Tsunemi Y, Ihn H, Idezuki T, Okochi H, Tamaki K. Source: Acta Dermato-Venereologica. 2003; 83(1): 70-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12636036&dopt=Abstract
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Psoriasis in a 5-month-old girl with HIV infection. Author(s): Carnero L, Betlloch I, Ramon R, Albares MP, Guijarro J, Botella R. Source: Pediatric Dermatology. 2001 January-February; 18(1): 87-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11207987&dopt=Abstract
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Psoriasis in children: a guide to its diagnosis and management. Author(s): Leman J, Burden D. Source: Paediatric Drugs. 2001; 3(9): 673-80. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11688598&dopt=Abstract
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Psoriasis in infancy: therapy with calcipotriene ointment. Author(s): Travis LB, Silverberg NB. Source: Cutis; Cutaneous Medicine for the Practitioner. 2001 November; 68(5): 341-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11766119&dopt=Abstract
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Psoriasis in the eastern Saudi Arabia. Author(s): Fatani MI, Abdulghani MH, Al-Afif KA. Source: Saudi Med J. 2002 February; 23(2): 213-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11938399&dopt=Abstract
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Psoriasis is associated with a SNP haplotype of the corneodesmosin gene (CDSN). Author(s): Orru S, Giuressi E, Casula M, Loizedda A, Murru R, Mulargia M, Masala MV, Cerimele D, Zucca M, Aste N, Biggio P, Carcassi C, Contu L. Source: Tissue Antigens. 2002 October; 60(4): 292-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12472658&dopt=Abstract
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Psoriasis of early and late onset: a clinical and epidemiologic study from Spain. Author(s): Ferrandiz C, Pujol RM, Garcia-Patos V, Bordas X, Smandia JA. Source: Journal of the American Academy of Dermatology. 2002 June; 46(6): 867-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12063483&dopt=Abstract
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Psoriasis of the scalp. Diagnosis and management. Author(s): van de Kerkhof PC, Franssen ME. Source: American Journal of Clinical Dermatology. 2001; 2(3): 159-65. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11705093&dopt=Abstract
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Psoriasis patients who are homozygous for the HLA-Cw*0602 allele have a 2.5-fold increased risk of developing psoriasis compared with Cw6 heterozygotes. Author(s): Gudjonsson JE, Karason A, Antonsdottir A, Runarsdottir EH, Hauksson VB, Upmanyu R, Gulcher J, Stefansson K, Valdimarsson H. Source: The British Journal of Dermatology. 2003 February; 148(2): 233-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12588373&dopt=Abstract
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Psoriasis predicts a poor short-term outcome in patients with spondylarthropathy. Author(s): Stafford L, Kane D, Murphy E, Duffy T, Lassere M, Youssef PP, Bresnihan B, Fitzgerald O. Source: Arthritis and Rheumatism. 2001 December; 45(6): 485-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11762682&dopt=Abstract
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Psoriasis scales contain C5a as the predominant chemotaxin for monocyte-derived dendritic cells. Author(s): Mrowietz U, Koch WA, Zhu K, Wiedow O, Bartels J, Christophers E, Schroder JM. Source: Experimental Dermatology. 2001 August; 10(4): 238-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11493312&dopt=Abstract
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Psoriasis update. Author(s): Franz R. Source: Dermatology Nursing / Dermatology Nurses' Association. 2001 June; 13(3): 2312. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11917460&dopt=Abstract
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Psoriasis vulgaris and acute guttate psoriasis in a family. Author(s): Banno T, Fujisawa H, Satomi H, Imakado S, Otsuka F. Source: International Journal of Dermatology. 2001 April; 40(4): 285-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11454089&dopt=Abstract
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Psoriasis vulgaris and arthritis psoriatica gravis mutilans. Author(s): Vrzogic P, Pasic A, Podobnik-Takac T. Source: Acta Dermatovenerol Croat. 2003; 11(1): 22-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12718792&dopt=Abstract
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Psoriasis vulgaris and Poland's syndrome in the same patient. Author(s): Sasmaz S, Coban YK, Boran C, Gumusalan Y. Source: The Journal of Dermatology. 2002 December; 29(12): 773-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12532042&dopt=Abstract
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Psoriasis vulgaris associated with Vogt-Koyanagi-Harada syndrome. Author(s): Yokota K, Shimizu H. Source: Clinical and Experimental Dermatology. 2001 May; 26(3): 308-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11426444&dopt=Abstract
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Psoriasis vulgaris in a male with partial deletion 18p. Author(s): Mikelsaar RV, Muru K, Kulla A, Suvari A. Source: American Journal of Medical Genetics. 2002 March 15; 108(3): 252-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11891697&dopt=Abstract
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Psoriasis vulgaris--a sterile antibacterial skin reaction mediated by cross-reactive T cells? An immunological view of the pathophysiology of psoriasis. Author(s): Prinz JC. Source: Clinical and Experimental Dermatology. 2001 June; 26(4): 326-32. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422184&dopt=Abstract
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Psoriasis, its treatment, and cancer in a cohort of Finnish patients. Author(s): Hannuksela-Svahn A, Pukkala E, Laara E, Poikolainen K, Karvonen J. Source: The Journal of Investigative Dermatology. 2000 March; 114(3): 587-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10692122&dopt=Abstract
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Psoriasis, psoriatic arthropathy and relapsing orbital myositis. Author(s): Ajitsaria R, Dale R, Ferguson V, Mayou S, Cavanagh N. Source: Clinical and Experimental Dermatology. 2001 May; 26(3): 274-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422174&dopt=Abstract
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Psoriasis. Author(s): Lebwohl M. Source: Lancet. 2003 April 5; 361(9364): 1197-204. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12686053&dopt=Abstract
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Psoriasis: current perspectives with an emphasis on treatment. Author(s): Linden KG, Weinstein GD. Source: The American Journal of Medicine. 1999 December; 107(6): 595-605. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10625029&dopt=Abstract
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Psoriasis: new drugs on the horizon? Author(s): Bonney RC. Source: Am Clin Lab. 2001 September; 20(8): 30-1. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11586939&dopt=Abstract
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Psoriasis: response to high-dose intravenous immunoglobulin in three patients. Author(s): Gurmin V, Mediwake R, Fernando M, Whittaker S, Rustin MH, Beynon HL. Source: The British Journal of Dermatology. 2002 September; 147(3): 554-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12207600&dopt=Abstract
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Psoriasis: the future. Author(s): Kirby B, Griffiths CE. Source: The British Journal of Dermatology. 2001 April; 144 Suppl 58: 37-43. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11501513&dopt=Abstract
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Psoriasis: the plot thickens. Author(s): Schon MP, Ruzicka T. Source: Nature Immunology. 2001 February; 2(2): 91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11175798&dopt=Abstract
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Psoriasis: the role of the genetic research nurse. Author(s): Ronda L. Source: Nurs Times. 2001 May 3-9; 97(18): 37-8. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11957886&dopt=Abstract
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Psoriasis: to cut or not to cut, what say you? Author(s): Saini R, Shupack JL. Source: Dermatologic Surgery : Official Publication for American Society for Dermatologic Surgery [et Al.]. 2003 July; 29(7): 735-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828697&dopt=Abstract
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Psoriasis--epidemiology and clinical spectrum. Author(s): Christophers E. Source: Clinical and Experimental Dermatology. 2001 June; 26(4): 314-20. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422182&dopt=Abstract
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Psychiatric morbidity in psoriasis and vitiligo: a comparative study. Author(s): Sharma N, Koranne RV, Singh RK. Source: The Journal of Dermatology. 2001 August; 28(8): 419-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11560158&dopt=Abstract
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Psychiatric morbidity in vitiligo and psoriasis: a comparative study from India. Author(s): Mattoo SK, Handa S, Kaur I, Gupta N, Malhotra R. Source: The Journal of Dermatology. 2001 August; 28(8): 424-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11560159&dopt=Abstract
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Psychological distress impairs clearance of psoriasis in patients treated with photochemotherapy. Author(s): Fortune DG, Richards HL, Kirby B, McElhone K, Markham T, Rogers S, Main CJ, Griffiths CE. Source: Archives of Dermatology. 2003 June; 139(6): 752-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810506&dopt=Abstract
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Psychological influences in psoriasis. Author(s): Griffiths CE, Richards HL. Source: Clinical and Experimental Dermatology. 2001 June; 26(4): 338-42. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422186&dopt=Abstract
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Psychological stress, distress and disability in patients with psoriasis: consensus and variation in the contribution of illness perceptions, coping and alexithymia. Author(s): Fortune DG, Richards HL, Griffiths CE, Main CJ. Source: The British Journal of Clinical Psychology / the British Psychological Society. 2002 June; 41(Pt 2): 157-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12034003&dopt=Abstract
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Pustular psoriasis of the nails: treatment and long-term follow-up of 46 patients. Author(s): Piraccini BM, Tosti A, Iorizzo M, Misciali C. Source: The British Journal of Dermatology. 2001 May; 144(5): 1000-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11359388&dopt=Abstract
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Quality of life and clinical outcome in psoriasis patients using intermittent cyclosporin. Author(s): Touw CR, Hakkaart-Van Roijen L, Verboom P, Paul C, Rutten FF, Finlay AY. Source: The British Journal of Dermatology. 2001 May; 144(5): 967-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11359382&dopt=Abstract
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Quality of life and prevalence of arthritis reported by 5,795 members of the Nordic Psoriasis Associations. Data from the Nordic Quality of Life Study. Author(s): Zachariae H, Zachariae R, Blomqvist K, Davidsson S, Molin L, Mork C, Sigurgeirsson B. Source: Acta Dermato-Venereologica. 2002; 82(2): 108-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12125937&dopt=Abstract
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Quality of life considerations in psoriasis treatment. Author(s): Weiss SC, Bergstrom KG, Weiss SA, Kimball AB. Source: Dermatology Nursing / Dermatology Nurses' Association. 2003 April; 15(2): 120, 123-7; Quiz 128. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12751346&dopt=Abstract
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Quality of life in 6497 Nordic patients with psoriasis. Author(s): Zachariae R, Zachariae H, Blomqvist K, Davidsson S, Molin L, Mork C, Sigurgeirsson B. Source: The British Journal of Dermatology. 2002 June; 146(6): 1006-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12072069&dopt=Abstract
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Quality of life of psoriasis patients. Author(s): Gupta MA, Gupta AK. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2000 July; 14(4): 241-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11204506&dopt=Abstract
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Quality of life, health-state utilities and willingness to pay in patients with psoriasis and atopic eczema. Author(s): Lundberg L, Johannesson M, Silverdahl M, Hermansson C, Lindberg M. Source: The British Journal of Dermatology. 1999 December; 141(6): 1067-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10606854&dopt=Abstract
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Quantifying the harmful effect of psoriasis on health-related quality of life. Author(s): Weiss SC, Kimball AB, Liewehr DJ, Blauvelt A, Turner ML, Emanuel EJ. Source: Journal of the American Academy of Dermatology. 2002 October; 47(4): 512-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12271293&dopt=Abstract
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Quantitative assessments of physiological and biological parameters in psoriatic lesions and its correlations to the clinical severity of psoriasis. Author(s): Chen GS, Wu TM, Yang SA, Yu HS. Source: Kaohsiung J Med Sci. 2001 August; 17(8): 408-18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11715840&dopt=Abstract
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Quantitative real-time reverse transcription-polymerase chain reaction analysis of drug metabolizing and cytoprotective genes in psoriasis and regulation by ultraviolet radiation. Author(s): Smith G, Dawe RS, Clark C, Evans AT, Comrie MM, Wolf CR, Ferguson J, Ibbotson SH. Source: The Journal of Investigative Dermatology. 2003 August; 121(2): 390-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12880432&dopt=Abstract
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Randomized clinical trials for psoriasis 1977-2000: the EDEN survey. Author(s): Naldi L, Svensson A, Diepgen T, Elsner P, Grob JJ, Coenraads PJ, Bavinck JN, Williams H; European Dermato-Epidemiology Network. Source: The Journal of Investigative Dermatology. 2003 May; 120(5): 738-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12713574&dopt=Abstract
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Rapid improvement of psoriasis vulgaris during drug-induced agranulocytosis. Author(s): Toichi E, Tachibana T, Furukawa F. Source: Journal of the American Academy of Dermatology. 2000 August; 43(2 Pt 2): 3915. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10901732&dopt=Abstract
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Rapid response to infliximab in severe pustular psoriasis, von Zumbusch type. Author(s): Newland MR, Weinstein A, Kerdel F. Source: International Journal of Dermatology. 2002 July; 41(7): 449-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12121565&dopt=Abstract
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Rationale for use and clinical responsiveness of hexafluoro-1,25-dihydroxyvitamin D3 for the treatment of plaque psoriasis: a pilot study. Author(s): Durakovic C, Malabanan A, Holick MF. Source: The British Journal of Dermatology. 2001 March; 144(3): 500-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11260006&dopt=Abstract
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Reactivation of herpes simplex keratitis during TL01 phototherapy for psoriasis. Author(s): Wong GA, Kaye SB, Parslew R. Source: Clinical and Experimental Dermatology. 2003 July; 28(4): 453-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12823318&dopt=Abstract
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Recent developments in the understanding of the pathogenesis of psoriasis. Author(s): Ortonne JP. Source: The British Journal of Dermatology. 1999 April; 140 Suppl 54: 1-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10731127&dopt=Abstract
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Reciprocal altered expression of T-cadherin and P-cadherin in psoriasis vulgaris. Author(s): Zhou S, Matsuyoshi N, Takeuchi T, Ohtsuki Y, Miyachi Y. Source: The British Journal of Dermatology. 2003 August; 149(2): 268-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932231&dopt=Abstract
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Recombinantly engineered human proteins: transforming the treatment of psoriasis. Author(s): Gottlieb AB, Bos JD. Source: Clinical Immunology (Orlando, Fla.). 2002 November; 105(2): 105-16. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12482385&dopt=Abstract
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Recurrent cholestatic jaundice associated with generalized pustular psoriasis: evidence for a neutrophilic cholangitis. Author(s): Allez M, Roux ME, Bertheau P, Erlinger S, Degott C, Morel P, Modigliani R, Rybojad M. Source: Journal of Hepatology. 2000 July; 33(1): 160-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10905601&dopt=Abstract
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Recurrent erythrodermic psoriasis in a thiuram-allergic patient due to contact with nurses' rubber gloves. Author(s): Pagliaro JA, Jones SK. Source: The British Journal of Dermatology. 1999 March; 140(3): 567-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10233815&dopt=Abstract
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Rediscovering hydroxyurea: its role in recalcitrant psoriasis. Author(s): Kumar B, Saraswat A, Kaur I. Source: International Journal of Dermatology. 2001 August; 40(8): 530-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11703528&dopt=Abstract
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Relationship between lymphocyte cyclosporin sensitivity and clinical progress of psoriasis. Author(s): Umezawa Y, Oh-i T, Koga M. Source: Journal of Dermatological Science. 2001 June; 26(2): 94-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11378324&dopt=Abstract
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Remission and relapse of chronic plaque psoriasis treated once a week with clobetasol propionate occluded with a hydrocolloid dressing versus twice daily treatment with clobetasol propionate alone. Author(s): Volden G, Kragballe K, Van De Kerkhof PC, Aberg K, White RJ. Source: The Journal of Dermatological Treatment. 2001 September; 12(3): 141-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12243704&dopt=Abstract
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Remission of psoriasis after treatment with interferon-alfa and 2chlordeoxyadenosine for hairy cell leukemia. Author(s): Ilyas W, Myers D, Mann R, Seraly MP. Source: Journal of the American Academy of Dermatology. 1999 August; 41(2 Pt 2): 3168. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10426918&dopt=Abstract
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Remissions of psoriasis with excimer laser treatment. Author(s): Feldman SR. Source: J Drugs Dermatol. 2002 July; 1(1): 13-4. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847749&dopt=Abstract
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Remissions of psoriasis with excimer laser treatment. Author(s): Feldman SR. Source: Dermatology Online Journal [electronic Resource]. 2002 October; 8(2): 23. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12546777&dopt=Abstract
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Renal failure and cholestatic jaundice as unusual complications of childhood pustular psoriasis. Author(s): Li SP, Tang WY, Lam WY, Wong SN. Source: The British Journal of Dermatology. 2000 December; 143(6): 1292-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11122037&dopt=Abstract
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Repeat courses of intravenous alefacept in patients with chronic plaque psoriasis provide consistent safety and efficacy. Author(s): Lowe NJ, Gonzalez J, Bagel J, Caro I, Ellis CN, Menter A. Source: International Journal of Dermatology. 2003 March; 42(3): 224-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12653922&dopt=Abstract
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Repeated exposure to blue light does not improve psoriasis. Author(s): Maari C, Viau G, Bissonnette R. Source: Journal of the American Academy of Dermatology. 2003 July; 49(1): 55-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12833008&dopt=Abstract
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Resetting the research agenda for psoriasis. Author(s): Chalmers RJ, Griffiths CE. Source: The Journal of Investigative Dermatology. 2003 May; 120(5): Ix-X. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12713600&dopt=Abstract
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Resolution of psoriasis after allogeneic bone marrow transplantation for chronic myelogenous leukemia: late complications of therapy. Author(s): Adkins DR, Abidi MH, Brown RA, Khoury H, Goodnough LT, Vij R, Westervelt P, DiPersio JF. Source: Bone Marrow Transplantation. 2000 December; 26(11): 1239-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11149740&dopt=Abstract
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Resolution of psoriasis following allogeneic bone marrow transplantation for chronic myelogenous leukemia: case report and review of the literature. Author(s): Kanamori H, Tanaka M, Kawaguchi H, Yamaji S, Fujimaki K, Tomita N, Fujisawa S, Ishigatsubo Y. Source: American Journal of Hematology. 2002 September; 71(1): 41-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12221673&dopt=Abstract
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Response of psoriasis to interleukin-10 is associated with suppression of cutaneous type 1 inflammation, downregulation of the epidermal interleukin-8/CXCR2 pathway and normalization of keratinocyte maturation. Author(s): Reich K, Garbe C, Blaschke V, Maurer C, Middel P, Westphal G, Lippert U, Neumann C. Source: The Journal of Investigative Dermatology. 2001 February; 116(2): 319-29. Erratum In: J Invest Dermatol 2001 May; 116(5): 829. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11180010&dopt=Abstract
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Response of psoriasis to sunbed treatment: comparison of conventional ultraviolet A lamps with new higher ultraviolet B-emitting lamps. Author(s): Das S, Lloyd JJ, Walshaw D, Diffey BL, Farr PM. Source: The British Journal of Dermatology. 2002 November; 147(5): 966-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12410708&dopt=Abstract
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Response of severe psoriasis to infliximab. Author(s): Mang R, Stege H, Ruzicka T, Krutmann J. Source: Dermatology (Basel, Switzerland). 2002; 204(2): 156-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11937748&dopt=Abstract
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Retinoids and psoriasis: novel issues in retinoid pharmacology and implications for psoriasis treatment. Author(s): Saurat JH. Source: Journal of the American Academy of Dermatology. 1999 September; 41(3 Pt 2): S2-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10459139&dopt=Abstract
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Retinoids for the treatment of psoriasis: outlook for the future. Author(s): Kuenzli S, Saurat JH. Source: Curr Opin Investig Drugs. 2001 May; 2(5): 625-30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11569936&dopt=Abstract
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Reversal of epidermal hyperproliferation in psoriasis by insulin-like growth factor I receptor antisense oligonucleotides. Author(s): Wraight CJ, White PJ, McKean SC, Fogarty RD, Venables DJ, Liepe IJ, Edmondson SR, Werther GA. Source: Nature Biotechnology. 2000 May; 18(5): 521-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10802619&dopt=Abstract
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Risk of malignancies in psoriasis patients treated with cyclosporine: a 5 y cohort study. Author(s): Paul CF, Ho VC, McGeown C, Christophers E, Schmidtmann B, Guillaume JC, Lamarque V, Dubertret L. Source: The Journal of Investigative Dermatology. 2003 February; 120(2): 211-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12542524&dopt=Abstract
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Risk of malignancy associated with cyclosporin use in psoriasis. Author(s): Paul C, Hornig F. Source: Dermatology (Basel, Switzerland). 1999; 198(3): 320-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10419287&dopt=Abstract
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Risk of melanoma with psoralen/ultraviolet A therapy for psoriasis. Do the known risks now outweigh the benefits? Author(s): Lindelof B. Source: Drug Safety : an International Journal of Medical Toxicology and Drug Experience. 1999 April; 20(4): 289-97. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10230579&dopt=Abstract
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Risk-benefit assessment of methotrexate in the treatment of severe psoriasis. Author(s): Kuijpers AL, van de Kerkhof PC. Source: American Journal of Clinical Dermatology. 2000 January-February; 1(1): 27-39. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11702302&dopt=Abstract
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Role of neutrophils in induction of acute inflammation in T-cell-mediated immune dermatosis, psoriasis: a neutrophil-associated inflammation-boosting loop. Author(s): Terui T, Ozawa M, Tagami H. Source: Experimental Dermatology. 2000 February; 9(1): 1-10. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10688368&dopt=Abstract
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Role of Pityrosporum ovale in guttate psoriasis. Author(s): Sandhu K, Jain R, Kaur I, Kumar B. Source: The Journal of Dermatology. 2003 March; 30(3): 252-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12692367&dopt=Abstract
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Rupioid psoriasis with arthropathy. Author(s): Murakami T, Ohtsuki M, Nakagawa H. Source: Clinical and Experimental Dermatology. 2000 July; 25(5): 409-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11012598&dopt=Abstract
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S gene (Corneodesmosin) diversity and its relationship to psoriasis; high content of cSNP in the HLA-linked S gene. Author(s): Enerback C, Enlund F, Inerot A, Samuelsson L, Wahlstrom J, Swanbeck G, Martinsson T. Source: The Journal of Investigative Dermatology. 2000 June; 114(6): 1158-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10844560&dopt=Abstract
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S100 protein subcellular localization during epidermal differentiation and psoriasis. Author(s): Broome AM, Ryan D, Eckert RL. Source: The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society. 2003 May; 51(5): 675-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12704215&dopt=Abstract
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S100A2 coding sequence polymorphism: characterization and lack of association with psoriasis. Author(s): Stoll SW, Chia NV, Nair RP, Woods TL, Stuart P, Henseler T, Jenisch S, Christophers E, Voorhees JJ, Elder JT. Source: Clinical and Experimental Dermatology. 2001 January; 26(1): 79-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11260185&dopt=Abstract
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Sacroiliitis, hyperostosis sternoclavicularis, and psoriasis palmoplantaris in monozygotic twins. Author(s): Hoffmann A, Dinser R, Linder R, Neufang KF, Krone W. Source: Arthritis and Rheumatism. 1999 March; 42(3): 574-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10088783&dopt=Abstract
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Salient features and HLA markers of childhood psoriasis in Kuwait. Author(s): Nanda A, Al-Fouzan AS, El-Kashlan M, Al-Sweih N, Al-Muzairai I. Source: Clinical and Experimental Dermatology. 2000 March; 25(2): 147-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10733642&dopt=Abstract
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Sarcoidosis associated with psoriasis vulgaris. Author(s): Usuki K, Hamada H, Terasaki Y, Hiwatashi S, Hisadome H, Setoyama M, Kanzaki T, Mera S. Source: The Journal of Dermatology. 2001 February; 28(2): 86-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11320712&dopt=Abstract
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Sartans, angiotensin II receptor antagonists, can induce psoriasis. Author(s): Marquart-Elbaz C, Grosshans E, Lipsker D, Lipsker D. Source: The British Journal of Dermatology. 2002 September; 147(3): 617-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12207619&dopt=Abstract
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Scalp psoriasis: topical calcipotriol 50 micrograms/g/ml solution vs. betamethasone valerate 1% lotion. Author(s): Duweb GA, Abuzariba O, Rahim M, al-Taweel M, Abdulla SA. Source: Int J Clin Pharmacol Res. 2000; 20(3-4): 65-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11314240&dopt=Abstract
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Scalp psoriasis: topical therapies. Author(s): Watts J. Source: Community Nurse. 1999 September; 5(8): 33-4, 37. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10732560&dopt=Abstract
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Scanning electron microscopy study of hair shaft disorders in psoriasis. Author(s): Plozzer C, Coletti C, Kokelj F, Trevisan G. Source: Acta Derm Venereol Suppl (Stockh). 2000; (211): 9-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11234560&dopt=Abstract
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Schizophrenia associated with psoriasis vulgaris: three case reports. Author(s): Miyaoka T, Seno H, Inagaki T, Ishino H, Ueda D, Ohno T, Dekio S. Source: Schizophrenia Research. 2000 January 21; 41(2): 383-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10708349&dopt=Abstract
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Search for the psoriasis susceptibility gene: the Newfoundland Study. Author(s): Nall L, Gulliver W, Charmley P, Farber EM. Source: Cutis; Cutaneous Medicine for the Practitioner. 1999 November; 64(5): 323-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10582157&dopt=Abstract
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Searching for psoriasis susceptibility genes in Italy: genome scan and evidence for a new locus on chromosome 1. Author(s): Capon F, Novelli G, Semprini S, Clementi M, Nudo M, Vultaggio P, Mazzanti C, Gobello T, Botta A, Fabrizi G, Dallapiccola B. Source: The Journal of Investigative Dermatology. 1999 January; 112(1): 32-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9886260&dopt=Abstract
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Searching for the major histocompatibility complex psoriasis susceptibility gene. Author(s): Capon F, Munro M, Barker J, Trembath R. Source: The Journal of Investigative Dermatology. 2002 May; 118(5): 745-51. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11982750&dopt=Abstract
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Selection of conserved TCR VDJ rearrangements in chronic psoriatic plaques indicates a common antigen in psoriasis vulgaris. Author(s): Prinz JC, Vollmer S, Boehncke WH, Menssen A, Laisney I, Trommler P. Source: European Journal of Immunology. 1999 October; 29(10): 3360-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10540348&dopt=Abstract
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Selective response of dermal Th-1 cells to 20-50 kDa streptococcal cell-wall proteins in chronic plaque psoriasis. Author(s): Baker BS, Ovigne JM, Fischetti VA, Powles A, Fry L. Source: Scandinavian Journal of Immunology. 2003 September; 58(3): 335-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12950680&dopt=Abstract
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Selective targeting of T cell subsets: focus on alefacept - a remittive therapy for psoriasis. Author(s): Krueger GG. Source: Expert Opinion on Biological Therapy. 2002 April; 2(4): 431-41. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11955280&dopt=Abstract
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Sensitivity of the Dermatology Life Quality Index to clinical change in patients with psoriasis. Author(s): Mazzotti E, Picardi A, Sampogna F, Sera F, Pasquini P, Abeni D; IDI Multipurpose Psoriasis Research on Vital Experiences study group. Source: The British Journal of Dermatology. 2003 August; 149(2): 318-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932238&dopt=Abstract
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Sequence, organization, chromosomal localization, and alternative splicing of the human serine protease inhibitor gene hurpin (PI13) which is upregulated in psoriasis. Author(s): Abts HF, Welss T, Scheuring S, Scott FL, Irving JA, Michel G, Bird PI, Ruzicka T. Source: Dna and Cell Biology. 2001 March; 20(3): 123-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11313015&dopt=Abstract
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Serum adenosine deaminase levels in patients with psoriasis: a prospective casecontrol study. Author(s): Bukulmez G, Akan T, Ciliv G. Source: Eur J Dermatol. 2000 June; 10(4): 274-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10846253&dopt=Abstract
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Serum cytokine levels in psoriasis vulgaris. Author(s): el Barnawi NY, Giasuddin AS, Ziu MM, Singh M. Source: British Journal of Biomedical Science. 2001; 58(1): 40-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11284224&dopt=Abstract
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Serum levels of interleukin-18 and s-ICAM-1 in patients affected by psoriasis: preliminary considerations. Author(s): Gangemi S, Merendino RA, Guarneri F, Minciullo PL, DiLorenzo G, Pacor M, Cannavo SP. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2003 January; 17(1): 42-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12602967&dopt=Abstract
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Serum lipid levels in psoriasis. Author(s): Piskin S, Gurkok F, Ekuklu G, Senol M. Source: Yonsei Medical Journal. 2003 February; 44(1): 24-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12619171&dopt=Abstract
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Serum lipids and apolipoproteins in patients with psoriasis. Author(s): Uyanik BS, Ari Z, Onur E, Gunduz K, Tanulku S, Durkan K. Source: Clinical Chemistry and Laboratory Medicine : Cclm / Fescc. 2002 January; 40(1): 65-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11916273&dopt=Abstract
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Severe combined immunodeficiency mouse-human skin chimeras: a unique animal model for the study of psoriasis and cutaneous inflammation. Author(s): Raychaudhuri SP, Dutt S, Raychaudhuri SK, Sanyal M, Farber EM. Source: The British Journal of Dermatology. 2001 May; 144(5): 931-9. Review. Erratum In: Br J Dermatol 2001 October; 145(4): 689. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11359377&dopt=Abstract
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Sex-specific differences in the treatment of severe psoriasis. Author(s): Hotard RS, Feldman SR, Fleischer AB Jr. Source: Journal of the American Academy of Dermatology. 2000 April; 42(4): 620-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10727307&dopt=Abstract
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Short-term cyclosporin monotherapy for chronic severe plaque-type psoriasis. Author(s): Jan V, Vaillant L, Bressieux JM, Barthelemy H, Legoux A, Steiner HG, Reigneau O. Source: Eur J Dermatol. 1999 December; 9(8): 615-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10586127&dopt=Abstract
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Short-term resolution of psoriasis after total thyroidectomy for euthyroid multinodular goitre. Author(s): Kuchel J, Barakate M, Delbridge L, Agarwal G, Beattie J, Barnetson R. Source: The Australasian Journal of Dermatology. 2002 August; 43(3): 214-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12121402&dopt=Abstract
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Simple horizontal averaging programme enables shade correction for image analysis in psoriasis. Author(s): Tanaka M, Gaskell S, Edwards C, Marks R. Source: Clinical and Experimental Dermatology. 2000 June; 25(4): 323-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10971496&dopt=Abstract
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Simultaneous onset of psoriasis vulgaris in monozygotic twins. Author(s): Glaser R, Mrowietz U, Jenisch S, Simeoni E, Christophers E. Source: American Journal of Clinical Dermatology. 2001; 2(3): 183-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11705095&dopt=Abstract
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Skin CD4+ T cells produce interferon-gamma in vitro in response to streptococcal antigens in chronic plaque psoriasis. Author(s): Brown DW, Baker BS, Ovigne JM, Hardman C, Powles AV, Fry L. Source: The Journal of Investigative Dermatology. 2000 March; 114(3): 576-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10692120&dopt=Abstract
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Skin innate immune system in psoriasis: friend or foe? Author(s): Nickoloff BJ. Source: The Journal of Clinical Investigation. 1999 November; 104(9): 1161-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10545511&dopt=Abstract
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Skin T cell proliferative response to M protein and other cell wall and membrane proteins of group A streptococci in chronic plaque psoriasis. Author(s): Baker BS, Brown DW, Fischetti VA, Ovigne JM, Porter W, Powles A, Fry L. Source: Clinical and Experimental Immunology. 2001 June; 124(3): 516-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11472417&dopt=Abstract
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SLURP-2, a novel member of the human Ly-6 superfamily that is up-regulated in psoriasis vulgaris. Author(s): Tsuji H, Okamoto K, Matsuzaka Y, Iizuka H, Tamiya G, Inoko H. Source: Genomics. 2003 January; 81(1): 26-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12573258&dopt=Abstract
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Social coping strategies associated with quality of life decrements among psoriasis patients. Author(s): Rapp SR, Cottrell CA, Leary MR. Source: The British Journal of Dermatology. 2001 October; 145(4): 610-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11703288&dopt=Abstract
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Somatostatin- and factor XIIIa-immunoreactive cells in psoriasis during clobetasol propionate and calciprotriol treatment. Author(s): Talme T, Schultzberg M, Sundqvist KG, Marcusson JA. Source: Acta Dermato-Venereologica. 1999 January; 79(1): 44-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10086858&dopt=Abstract
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Somatostatin immunoreactive cells and Merkel cells in psoriasis. Author(s): Talme T, Schultzberg M. Source: Acta Dermato-Venereologica. 1999 September; 79(5): 388-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10494720&dopt=Abstract
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Specific human papillomaviruses could participate in epidermal hyperproliferation and autoimmune phenomena in psoriasis. Author(s): Majewski S, Favre M, Orth G, Jablonska S. Source: Acta Dermato-Venereologica. 2001 August-September; 81(4): 312. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11720190&dopt=Abstract
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Spinal hyperostosis--a rare skeletal manifestation of psoriasis vulgaris. Author(s): Rahman P, Alderdice C, Curtis B, Battcock S, Pike E. Source: The Journal of Rheumatology. 2000 October; 27(10): 2513-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11036854&dopt=Abstract
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Spontaneous clearance of psoriasis during the course of Kikuchi-Fujimoto disease. Author(s): Kato A, Kono T, Ishii M, Wakasa K, Taniguchi S. Source: Journal of the American Academy of Dermatology. 2002 November; 47(5 Suppl): S287-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12399754&dopt=Abstract
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Spontaneous rupture of the tibialis anterior tendon in a patient with psoriasis. Author(s): Aydingoz U, Aydingoz O. Source: Clinical Imaging. 2002 May-June; 26(3): 209-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11983476&dopt=Abstract
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Squamous cell carcinoma-related antigen (SCCr-Ag), sICAM-1 and beta 2microglobulin are useful markers of disease activity in psoriasis. Author(s): De Pita O, Frezzolini A, Cianetti A, De Sanctis G, Fontana L, Bottari V. Source: Acta Dermato-Venereologica. 1999 March; 79(2): 132-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10228632&dopt=Abstract
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Staphylococcal scalded skin syndrome complicating acute generalized pustular psoriasis. Author(s): Sharkey MP, Muir JB. Source: The Australasian Journal of Dermatology. 2002 August; 43(3): 199-201. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12121398&dopt=Abstract
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Stigmatization and psoriasis. Author(s): Richards HL, Fortune DG, Main CJ, Griffiths CE. Source: The British Journal of Dermatology. 2003 July; 149(1): 209-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890228&dopt=Abstract
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Strategies to optimize efficacy, duration of remission, and safety in the treatment of plaque psoriasis by using tazarotene in combination with a corticosteroid. Author(s): Lebwohl M. Source: Journal of the American Academy of Dermatology. 2000 August; 43(2 Pt 3): S436. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10898829&dopt=Abstract
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Stratum corneum chymotryptic enzyme in psoriasis. Author(s): Ekholm E, Egelrud T. Source: Archives of Dermatological Research. 1999 April; 291(4): 195-200. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10335915&dopt=Abstract
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Streptococcal infection distinguishes different types of psoriasis. Author(s): Weisenseel P, Laumbacher B, Besgen P, Ludolph-Hauser D, Herzinger T, Roecken M, Wank R, Prinz JC. Source: Journal of Medical Genetics. 2002 October; 39(10): 767-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12362037&dopt=Abstract
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Stronger association with HLA-Cw6 than with corneodesmosin (S-gene) polymorphisms in Swedish psoriasis patients. Author(s): Enerback C, Nilsson S, Enlund F, Inerot A, Samuelsson L, Wahlstrom J, Swanbeck G, Martinsson T. Source: Archives of Dermatological Research. 2000 November; 292(11): 525-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11194889&dopt=Abstract
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Stronger proliferative response to membrane versus cell-wall Streptococcal proteins by peripheral blood T cells in chronic plaque psoriasis. Author(s): Baker BS, Brown D, Fischetti VA, Ovigne JM, Porter W, Powles A, Fry L. Source: Scandinavian Journal of Immunology. 2001 December; 54(6): 619-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11902338&dopt=Abstract
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Subclinical microbial infection in patients with chronic plaque psoriasis. Author(s): Bartenjev I, Rogl Butina M, Potocnik M. Source: Acta Derm Venereol Suppl (Stockh). 2000; (211): 17-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11234557&dopt=Abstract
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Suberythemogenic narrow-band UVB is markedly more effective than conventional UVB in treatment of psoriasis vulgaris. Author(s): Walters IB, Burack LH, Coven TR, Gilleaudeau P, Krueger JG. Source: Journal of the American Academy of Dermatology. 1999 June; 40(6 Pt 1): 893900. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10365919&dopt=Abstract
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Successful in vivo blockade of CD25 (high-affinity interleukin 2 receptor) on T cells by administration of humanized anti-Tac antibody to patients with psoriasis. Author(s): Krueger JG, Walters IB, Miyazawa M, Gilleaudeau P, Hakimi J, Light S, Sherr A, Gottlieb AB. Source: Journal of the American Academy of Dermatology. 2000 September; 43(3): 44858. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10954656&dopt=Abstract
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Successful treatment of severe generalized pustular psoriasis with basiliximab (interleukin-2 receptor blocker) Author(s): Salim A, Emerson RM, Dalziel KL. Source: The British Journal of Dermatology. 2000 November; 143(5): 1121-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11069550&dopt=Abstract
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Successful treatment of severe psoriasis with basiliximab, an interleukin-2 receptor monoclonal antibody. Author(s): Owen CM, Harrison PV. Source: Clinical and Experimental Dermatology. 2000 May; 25(3): 195-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10844492&dopt=Abstract
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Successful treatment of severe recalcitrant psoriasis with combination infliximab and methotrexate. Author(s): Kirby B, Marsland AM, Carmichael AJ, Griffiths CE. Source: Clinical and Experimental Dermatology. 2001 January; 26(1): 27-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11260172&dopt=Abstract
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Suprabasal overexpression of the hsRPB7 gene in psoriatic epidermis as identified by a reverse transcriptase-polymerase chain reaction differential display model comparing psoriasis plaque tissue with peritonsillar mucosa. Author(s): Bockelmann R, Neugebauer P, Paseban ND, Huttemann M, Gollnick H, Bonnekoh B. Source: American Journal of Pathology. 2001 February; 158(2): 367-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11159173&dopt=Abstract
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Sustained improvement of the quality of life of patients with psoriasis after hospitalization. Author(s): Vensel E, Hilley T, Trent J, Taylor JR, Kirsner RS, Kerdel FA, Taylor JR, Schwartzberg JB. Source: Journal of the American Academy of Dermatology. 2000 November; 43(5 Pt 1): 858-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11050595&dopt=Abstract
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Sympathetic skin response in psoriasis and vitiligo. Author(s): Bir LS, Aktan S. Source: Journal of the Autonomic Nervous System. 1999 July 7; 77(1): 68-71. Erratum In: J Auton Nerv Syst 2000 April 12; 80(1-2): 114. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10494752&dopt=Abstract
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Systematic review of comparative efficacy and tolerability of calcipotriol in treating chronic plaque psoriasis. Author(s): Ashcroft DM, Po AL, Williams HC, Griffiths CE. Source: Bmj (Clinical Research Ed.). 2000 April 8; 320(7240): 963-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10753146&dopt=Abstract
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Systemic photodynamic therapy is a safe and effective treatment for psoriasis. Author(s): Boehncke WH, Elshorst-Schmidt T, Kaufmann R. Source: Archives of Dermatology. 2000 February; 136(2): 271-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10677114&dopt=Abstract
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Systemic sclerosis could mask the presentation of psoriasis in a patient with symptomatic and bilateral sacroiliitis. Author(s): di Girolamo C, Rengo C, Ferrucci MG, Miniero E, Cuomo G, Crisci C, Valentini G. Source: Scandinavian Journal of Rheumatology. 2003; 32(3): 186-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892259&dopt=Abstract
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Systemic sequential therapy of psoriasis: a new paradigm for improved therapeutic results. Author(s): Koo J. Source: Journal of the American Academy of Dermatology. 1999 September; 41(3 Pt 2): S25-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10459144&dopt=Abstract
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Systemic therapy of psoriasis using methotrexate. Author(s): Smith KC. Source: Skin Therapy Letter. 2000; 6(3): 1-2; 5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11176041&dopt=Abstract
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Systemic toxicity following administration of sirolimus (formerly rapamycin) for psoriasis: association of capillary leak syndrome with apoptosis of lesional lymphocytes. Author(s): Kaplan MJ, Ellis CN, Bata-Csorgo Z, Kaplan RS, Endres JL, Fox DA. Source: Archives of Dermatology. 1999 May; 135(5): 553-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10328196&dopt=Abstract
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Tacalcitol ointment for long-term control of chronic plaque psoriasis in dermatological practice. Author(s): Lambert J, Trompke C. Source: Dermatology (Basel, Switzerland). 2002; 204(4): 321-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12077538&dopt=Abstract
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Tacrolimus ointment for the treatment of psoriasis on the face and intertriginous areas. Author(s): Freeman AK, Linowski GJ, Brady C, Lind L, Vanveldhuisen P, Singer G, Lebwohl M. Source: Journal of the American Academy of Dermatology. 2003 April; 48(4): 564-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664020&dopt=Abstract
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Tamoxifen-induced remission of psoriasis. Author(s): Boyd AS, King LE Jr. Source: Journal of the American Academy of Dermatology. 1999 November; 41(5 Pt 2): 887-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10534679&dopt=Abstract
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Targeting interleukin-2 as a treatment for psoriasis. Author(s): Salim A, Emerson R. Source: Curr Opin Investig Drugs. 2001 November; 2(11): 1546-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11763155&dopt=Abstract
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Tazarotene 0.1% gel for psoriasis of the fingernails and toenails: an open, prospective study. Author(s): Bianchi L, Soda R, Diluvio L, Chimenti S. Source: The British Journal of Dermatology. 2003 July; 149(1): 207-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890227&dopt=Abstract
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Tazarotene 0.1% gel in the treatment of fingernail psoriasis: a double-blind, randomized, vehicle-controlled study. Author(s): Scher RK, Stiller M, Zhu YI. Source: Cutis; Cutaneous Medicine for the Practitioner. 2001 November; 68(5): 355-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11766122&dopt=Abstract
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Tazarotene cream in the treatment of psoriasis: Two multicenter, double-blind, randomized, vehicle-controlled studies of the safety and efficacy of tazarotene creams 0.05% and 0.1% applied once daily for 12 weeks. Author(s): Weinstein GD, Koo JY, Krueger GG, Lebwohl MG, Lowe NJ, Menter MA, Lew-Kaya DA, Sefton J, Gibson JR, Walker PS; Tazarotene Cream Clinical Study Group. Source: Journal of the American Academy of Dermatology. 2003 May; 48(5): 760-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12734506&dopt=Abstract
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Terbinafine exacerbates psoriasis: case report with a literature review. Author(s): Szepietowski JC. Source: Acta Dermatovenerol Croat. 2003; 11(1): 17-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12718791&dopt=Abstract
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The bodily suffering of living with severe psoriasis: in-depth interviews with 22 hospitalized patients with psoriasis. Author(s): Wahl AK, Gjengedal E, Hanestad BR. Source: Qualitative Health Research. 2002 February; 12(2): 250-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11837374&dopt=Abstract
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The chemokine receptor CCR6 identifies interferon-gamma expressing T cells and is decreased in atopic dermatitis as compared with psoriasis. Author(s): Ong PY, Leung DY. Source: The Journal of Investigative Dermatology. 2002 December; 119(6): 1463-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12485455&dopt=Abstract
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The coexistence of photosensitive psoriasis with chronic actinic dermatitis. Author(s): Sahoo B, Kumar B. Source: Dermatology (Basel, Switzerland). 2002; 204(1): 77-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11834857&dopt=Abstract
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The combination of calcipotriol and methotrexate compared with methotrexate and vehicle in psoriasis: results of a multicentre placebo-controlled randomized trial. Author(s): de Jong EM, Mork NJ, Seijger MM, De La Brassine M, Lauharanta J, Jansen CT, Guilhou JJ, Guillot B, Ostrojic A, Souteyrand P, Vaillant L, Barnes L, Rogers S, Klaber MR, Van De Kerkhof PC. Source: The British Journal of Dermatology. 2003 February; 148(2): 318-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12588386&dopt=Abstract
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The contribution of perceptions of stigmatisation to disability in patients with psoriasis. Author(s): Richards HL, Fortune DG, Griffiths CE, Main CJ. Source: Journal of Psychosomatic Research. 2001 January; 50(1): 11-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11259795&dopt=Abstract
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The correlation between activity and a circulating lymphocyte pattern in plasma of patients with psoriasis preceded by an infection. Author(s): Lecewicz-Torun B, Pietrzak A, Rolinski J. Source: Ann Univ Mariae Curie Sklodowska [med]. 1999; 54: 269-76. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11205775&dopt=Abstract
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The cost effectiveness of tapered versus abrupt discontinuation of oral cyclosporin microemulsion for the treatment of psoriasis. Author(s): Hakkaart-van Roijen L, Verboom P, Redekop WK, Touw KR, Rutten FF. Source: Pharmacoeconomics. 2001; 19(5 Pt 2): 599-608. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11465304&dopt=Abstract
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The direct cost of care for psoriasis and psoriatic arthritis in the United States. Author(s): Javitz HS, Ward MM, Farber E, Nail L, Vallow SG. Source: Journal of the American Academy of Dermatology. 2002 June; 46(6): 850-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12063481&dopt=Abstract
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The effect of PUVA treatment on sister chromatid exchange (SCE) values in psoriasis vulgaris patients. Author(s): Baysal V, Sahin F, Erel A, Oruk S, Menevse S. Source: The Journal of Dermatological Treatment. 2003 January; 14(1): 22-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745851&dopt=Abstract
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The effectiveness of tumor necrosis factor alpha antibody (infliximab) in treating recalcitrant psoriasis: a report of 2 cases. Author(s): O'Quinn RP, Miller JL. Source: Archives of Dermatology. 2002 May; 138(5): 644-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12020227&dopt=Abstract
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The effects of topical corticosteroids and a coal tar preparation on dithranol-induced irritation in patients with psoriasis. Author(s): Swinkels OQ, Kucharekova M, Prins M, Gerritsen MJ, van der Valk PG, van de Kerkhof PC. Source: Skin Pharmacology and Applied Skin Physiology. 2003 January-February; 16(1): 12-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12566824&dopt=Abstract
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The effects of ultraviolet B treatment on the expression of adhesion molecules by circulating T lymphocytes in psoriasis. Author(s): Sigmundsdottir H, Gudjonsson JE, Valdimarsson H. Source: The British Journal of Dermatology. 2003 May; 148(5): 996-1000. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12786832&dopt=Abstract
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The evaluation of the sociodemographic and clinical features of Turkish psoriasis patients. Author(s): Kundakci N, Tursen U, Babiker MO, Gurgey E. Source: International Journal of Dermatology. 2002 April; 41(4): 220-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12031031&dopt=Abstract
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The FDA guidelines for the treatment of psoriasis using cyclosporine A: are they adequate? Author(s): Zackheim HS. Source: Cutis; Cutaneous Medicine for the Practitioner. 2002 November; 70(5): 288-90. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12469783&dopt=Abstract
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The genetic epidemiology of psoriasis vulgaris in Chinese Han. Author(s): Zhang X, Wang H, Te-Shao H, Yang S, Chen S. Source: International Journal of Dermatology. 2002 October; 41(10): 663-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390189&dopt=Abstract
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The HCR gene on 6p21 is unlikely to be a psoriasis susceptibility gene. Author(s): O'Brien KP, Holm SJ, Nilsson S, Carlen L, Rosenmuller T, Enerback C, Inerot A, Stahle-Backdahl M. Source: The Journal of Investigative Dermatology. 2001 May; 116(5): 750-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11348465&dopt=Abstract
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The 'heartbreak of psoriasis' has met its match! Author(s): Morrow T. Source: Manag Care. 2003 June; 12(6): 13, 17-8. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854254&dopt=Abstract
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The immunologic basis for the treatment of psoriasis with new biologic agents. Author(s): Krueger JG. Source: Journal of the American Academy of Dermatology. 2002 January; 46(1): 1-23; Quiz 23-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11756941&dopt=Abstract
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The impact of psoriasis on quality of life. Author(s): de Arruda LH, De Moraes AP. Source: The British Journal of Dermatology. 2001 April; 144 Suppl 58: 33-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11501512&dopt=Abstract
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The impact of psoriasis on quality of life: results of a 1998 National Psoriasis Foundation patient-membership survey. Author(s): Krueger G, Koo J, Lebwohl M, Menter A, Stern RS, Rolstad T. Source: Archives of Dermatology. 2001 March; 137(3): 280-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11255325&dopt=Abstract
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The influence of heredity for psoriasis on the ILAR classification of juvenile idiopathic arthritis. Author(s): Berntson L, Fasth A, Andersson-Gare B, Herlin T, Kristinsson J, Lahdenne P, Marhaug G, Nielsen S, Pelkonen P, Rygg M. Source: The Journal of Rheumatology. 2002 November; 29(11): 2454-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12415608&dopt=Abstract
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The International Psoriasis Genetics Study: assessing linkage to 14 candidate susceptibility loci in a cohort of 942 affected sib pairs. Author(s): International Psoriasis Genetics Consortium. Source: American Journal of Human Genetics. 2003 August; 73(2): 430-7. Epub 2003 July 07. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12851855&dopt=Abstract
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The level of prosaposin is decreased in the skin of patients with psoriasis vulgaris. Author(s): Alessandrini F, Stachowitz S, Ring J, Behrendt H. Source: The Journal of Investigative Dermatology. 2001 March; 116(3): 394-400. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11231313&dopt=Abstract
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The National Psoriasis Foundation Psoriasis Score (NPF-PS) system versus the Psoriasis Area Severity Index (PASI) and Physician's Global Assessment (PGA): a comparison. Author(s): Gottlieb AB, Chaudhari U, Baker DG, Perate M, Dooley LT. Source: J Drugs Dermatol. 2003 June; 2(3): 260-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12848110&dopt=Abstract
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The persistent risk of genital tumors among men treated with psoralen plus ultraviolet A (PUVA) for psoriasis. Author(s): Stern RS, Bagheri S, Nichols K; PUVA Follow Up Study. Source: Journal of the American Academy of Dermatology. 2002 July; 47(1): 33-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12077578&dopt=Abstract
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The potential role of hypocortisolism in the pathophysiology of PTSD and psoriasis. Author(s): Thaller V, Vrkljan M, Hotujac L, Thakore J. Source: Coll Antropol. 1999 December; 23(2): 611-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10646236&dopt=Abstract
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The prevalence of psoriasis in the world. Author(s): Raychaudhuri SP, Farber EM. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2001 January; 15(1): 16-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11451313&dopt=Abstract
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The relationship between infection with group A beta hemolytic streptococci and the development of psoriasis. Author(s): Rasmussen JE. Source: The Pediatric Infectious Disease Journal. 2000 February; 19(2): 153-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10694004&dopt=Abstract
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The response of uninvolved skin of patients with psoriasis to single and repeated applications of dithranol cream: an immunohistochemical assessment. Author(s): Swinkels OQ, Prins M, van Vlijmen-Willems IM, Gerritsen MJ, van der Valk PG, van de Kerkhof PC. Source: Skin Pharmacology and Applied Skin Physiology. 2002 November-December; 15(6): 385-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12476012&dopt=Abstract
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The risk of malignancy associated with psoriasis. Author(s): Margolis D, Bilker W, Hennessy S, Vittorio C, Santanna J, Strom BL. Source: Archives of Dermatology. 2001 June; 137(6): 778-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11405770&dopt=Abstract
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The role of oxidants and antioxidants in psoriasis. Author(s): Yildirim M, Inaloz HS, Baysal V, Delibas N. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2003 January; 17(1): 34-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12602965&dopt=Abstract
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The role of T cells in psoriasis. Author(s): Prinz JC. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2003 May; 17(3): 257-70. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12702062&dopt=Abstract
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The role of the Duffy antigen-related chemokine receptor in psoriasis vulgaris. Author(s): Sticherling M, Baisch C, Bornscheuer E, Schroder JM, Christophers E. Source: Cytokine. 2002 June 21; 18(6): 329-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12160521&dopt=Abstract
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The role of the low energy diet in psoriasis vulgaris treatment. Author(s): Rucevic I, Perl A, Barisic-Drusko V, Adam-Perl M. Source: Coll Antropol. 2003; 27 Suppl 1: 41-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12955890&dopt=Abstract
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The skin fungus-induced Th1- and Th2-related cytokine, chemokine and prostaglandin E2 production in peripheral blood mononuclear cells from patients with atopic dermatitis and psoriasis vulgaris. Author(s): Kanda N, Tani K, Enomoto U, Nakai K, Watanabe S. Source: Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology. 2002 August; 32(8): 1243-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12190666&dopt=Abstract
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The suitability of quality-of-life questionnaires for psoriasis research: a systematic literature review. Author(s): De Korte J, Mombers FM, Sprangers MA, Bos JD. Source: Archives of Dermatology. 2002 September; 138(9): 1221-7; Discussion 1227. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12224984&dopt=Abstract
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The therapeutic potential of calcipotriol in diseases other than psoriasis. Author(s): Holm EA, Jemec GB. Source: International Journal of Dermatology. 2002 January; 41(1): 38-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11895512&dopt=Abstract
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The use of 0.25% zinc pyrithione spray does not enhance the efficacy of clobetasol propionate 0.05% foam in the treatment of psoriasis. Author(s): Housman TS, Keil KA, Mellen BG, McCarty MA, Fleischer AB Jr, Feldman SR. Source: Journal of the American Academy of Dermatology. 2003 July; 49(1): 79-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12833013&dopt=Abstract
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The Woronoff ring in psoriasis. Author(s): Varma S, Finlay AY. Source: The British Journal of Dermatology. 2003 January; 148(1): 170. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534616&dopt=Abstract
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Thioguanine for refractory psoriasis: a 4-year experience. Author(s): Mason C, Krueger GG. Source: Journal of the American Academy of Dermatology. 2001 January; 44(1): 67-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11148479&dopt=Abstract
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TNF-alpha and apoptosis: implications for the pathogenesis and treatment of psoriasis. Author(s): Victor FC, Gottlieb AB. Source: J Drugs Dermatol. 2002 December; 1(3): 264-75. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12851985&dopt=Abstract
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Topical agents for the treatment of psoriasis, past, present and future. Author(s): Tremblay JF, Bissonnette R. Source: Journal of Cutaneous Medicine and Surgery. 2002 May-June; 6(3 Suppl): 8-11. Epub 2002 April 30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11976984&dopt=Abstract
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Topical application of mycophenolate mofetil in plaque-type psoriasis. Author(s): Wohlrab J, Jahn K, Plaetzer M, Neubert R, Marsch WC. Source: The British Journal of Dermatology. 2001 June; 144(6): 1263-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422055&dopt=Abstract
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Topical calcipotriol plus oral fumaric acid is more effective and faster acting than oral fumaric acid monotherapy in the treatment of severe chronic plaque psoriasis vulgaris. Author(s): Gollnick H, Altmeyer P, Kaufmann R, Ring J, Christophers E, Pavel S, Ziegler J. Source: Dermatology (Basel, Switzerland). 2002; 205(1): 46-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12145434&dopt=Abstract
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Topical preparations for the treatment of psoriasis: a systematic review. Author(s): Mason J, Mason AR, Cork MJ. Source: The British Journal of Dermatology. 2002 March; 146(3): 351-64. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11952534&dopt=Abstract
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Topical PTH (1-34) is a novel, safe and effective treatment for psoriasis: a randomized self-controlled trial and an open trial. Author(s): Holick MF, Chimeh FN, Ray S. Source: The British Journal of Dermatology. 2003 August; 149(2): 370-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932245&dopt=Abstract
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Topical tacrolimus for facial psoriasis. Author(s): Clayton TH, Harrison PV, Nicholls R, Delap M. Source: The British Journal of Dermatology. 2003 August; 149(2): 419-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932257&dopt=Abstract
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Topical tazarotene therapy for psoriasis, acne vulgaris, and photoaging. Author(s): Guenther LC. Source: Skin Therapy Letter. 2002 March; 7(3): 1-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12007011&dopt=Abstract
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Topical treatment of psoriasis in children. Author(s): Coffey J, Landells I. Source: Skin Therapy Letter. 2002 April; 7(4): 4-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12097995&dopt=Abstract
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Topiramate in the treatment of psoriasis: a pilot study. Author(s): Ryback R. Source: The British Journal of Dermatology. 2002 July; 147(1): 130-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12100195&dopt=Abstract
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Toxicity of methotrexate treatment in psoriasis and psoriatic arthritis--short- and long-term toxicity in 104 patients. Author(s): Wollina U, Stander K, Barta U. Source: Clinical Rheumatology. 2001; 20(6): 406-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11771523&dopt=Abstract
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Transgenic delivery of VEGF to mouse skin leads to an inflammatory condition resembling human psoriasis. Author(s): Xia YP, Li B, Hylton D, Detmar M, Yancopoulos GD, Rudge JS. Source: Blood. 2003 July 1; 102(1): 161-8. Epub 2003 March 20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649136&dopt=Abstract
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Treating severe psoriasis: how to navigate safely between scylla and charybdis? Author(s): Paul CF. Source: The Journal of Investigative Dermatology. 2003 August; 121(2): Ix-X. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12880444&dopt=Abstract
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Treatment of atopic dermatitis and psoriasis vulgaris with bupropion-SR: a pilot study. Author(s): Modell JG, Boyce S, Taylor E, Katholi C. Source: Psychosomatic Medicine. 2002 September-October; 64(5): 835-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12271115&dopt=Abstract
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Treatment of chronic plaque psoriasis by selective targeting of memory effector T lymphocytes. Author(s): Ellis CN, Krueger GG; Alefacept Clinical Study Group. Source: The New England Journal of Medicine. 2001 July 26; 345(4): 248-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11474662&dopt=Abstract
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Treatment of inverse psoriasis with the 308 nm excimer laser. Author(s): Mafong EA, Friedman PM, Kauvar AN, Bernstein LJ, Alexiades-Armenakas M, Geronemus RG. Source: Dermatologic Surgery : Official Publication for American Society for Dermatologic Surgery [et Al.]. 2002 June; 28(6): 530-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12081686&dopt=Abstract
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Treatment of plaque psoriasis. Author(s): Hanauer L. Source: The New England Journal of Medicine. 2001 December 20; 345(25): 1854; Author Reply 1854-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11803920&dopt=Abstract
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Treatment of plaque psoriasis. Author(s): Haserick JR. Source: The New England Journal of Medicine. 2001 December 20; 345(25): 1854; Author Reply 1854-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11803919&dopt=Abstract
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Treatment of psoriasis in children: is there a role for antibiotic therapy and tonsillectomy? Author(s): Wilson JK, Al-Suwaidan SN, Krowchuk D, Feldman SR. Source: Pediatric Dermatology. 2003 January-February; 20(1): 11-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12558839&dopt=Abstract
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Treatment of psoriasis with 6-thioguanine and hepatic venoocclusive disease. Author(s): Romagosa R, Kerdel F, Shah N. Source: Journal of the American Academy of Dermatology. 2002 December; 47(6): 970-2; Author Reply 972. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12451396&dopt=Abstract
Studies 191
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Treatment of psoriasis with the chimeric monoclonal antibody against tumor necrosis factor alpha, infliximab. Author(s): Schopf RE, Aust H, Knop J. Source: Journal of the American Academy of Dermatology. 2002 June; 46(6): 886-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12063486&dopt=Abstract
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Treatment of psoriasis: an algorithm-based approach for primary care physicians. Author(s): Pardasani AG, Feldman SR, Clark AR. Source: American Family Physician. 2000 February 1; 61(3): 725-33, 736. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10695585&dopt=Abstract
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Treatment of psoriatic arthritis and psoriasis vulgaris with the tumor necrosis factor inhibitor infliximab. Author(s): Cauza E, Spak M, Cauza K, Hanusch-Enserer U, Dunky A, Wagner E. Source: Rheumatology International. 2002 November; 22(6): 227-32. Epub 2002 September 04. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12426660&dopt=Abstract
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Treatment of psoriatic arthritis with antitumour necrosis factor-alpha antibody clears skin lesions of psoriasis resistant to treatment with methotrexate. Author(s): Ogilvie AL, Antoni C, Dechant C, Manger B, Kalden JR, Schuler G, Luftl M. Source: The British Journal of Dermatology. 2001 March; 144(3): 587-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11260020&dopt=Abstract
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Treatment of recalcitrant psoriasis with daclizumab. Author(s): Wohlrab J, Fischer M, Taube KM, Marsch WC. Source: The British Journal of Dermatology. 2001 January; 144(1): 209-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11167723&dopt=Abstract
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Treatment of severe psoriasis and psoriatic arthritis with leflunomide. Author(s): Reich K, Hummel KM, Beckmann I, Mossner R, Neumann C. Source: The British Journal of Dermatology. 2002 February; 146(2): 335-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11903256&dopt=Abstract
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Treatment of severe recalcitrant plaque psoriasis with single-dose intravenous tumour necrosis factor-alpha antibody (infliximab). Author(s): Chan JJ, Gebauer K. Source: The Australasian Journal of Dermatology. 2003 May; 44(2): 116-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12752184&dopt=Abstract
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Trends and developments in the pharmacological treatment of psoriasis. Author(s): Gniadecki R, Zachariae C, Calverley M. Source: Acta Dermato-Venereologica. 2002; 82(6): 401-10. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12575844&dopt=Abstract
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Trials, evidence, and the management of patients with psoriasis. Author(s): Rees JL. Source: Journal of the American Academy of Dermatology. 2003 January; 48(1): 135-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12522385&dopt=Abstract
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Tumoral enthesopathy in psoriasis. Author(s): Stevens KJ, Smith SL, Preston BJ, Deighton C. Source: Rheumatology (Oxford, England). 2001 March; 40(3): 342-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11285385&dopt=Abstract
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Turner's syndrome associated with psoriasis and alopecia areata. Author(s): Rosina P, Segalla G, Magnanini M, Chieregato C, Barba A. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2003 January; 17(1): 50-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12602969&dopt=Abstract
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Twice-daily vs. once-daily inpatient dithranol for psoriasis. Author(s): Kirkup ME, Sabroe RA, Kavanagh GM, Downs AM, Sansom JE, de Berker DA, Dunnill MG, Kennedy CT, Archer CB. Source: Clinical and Experimental Dermatology. 2002 November; 27(8): 695-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12472549&dopt=Abstract
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Ultrasonographic estimation of the size of spleen in children with psoriasis. Author(s): Pietrzak A, Dybiec E, Lecewicz-Torun B, Urban J, Wieczorek P. Source: Ann Univ Mariae Curie Sklodowska [med]. 1999; 54: 431-8. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11205805&dopt=Abstract
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Ultrastructural and biosynthetic characteristics of epidermal cells in patients with psoriasis treated with antiproliferative drugs. Author(s): Krinitsyna YM, Nepomnyashchikh GI, Aidagulova SV. Source: Bulletin of Experimental Biology and Medicine. 2001 August; 132(2): 797-802. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11713570&dopt=Abstract
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Ultrastructural characteristics of cell populations in the gastric and duodenal mucosa during psoriasis. Author(s): Khardikova SA, Nepomnyashchikh GI, Aidagulova SV, Lapii GA. Source: Bulletin of Experimental Biology and Medicine. 2002 November; 134(5): 489-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802460&dopt=Abstract
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Ultraviolet exposure as the main initiator of p53 mutations in basal cell carcinomas from psoralen and ultraviolet A-treated patients with psoriasis. Author(s): Seidl H, Kreimer-Erlacher H, Back B, Soyer HP, Hofler G, Kerl H, Wolf P. Source: The Journal of Investigative Dermatology. 2001 August; 117(2): 365-70. Erratum In: J Invest Dermatol 2001 December; 117(6): 1688. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11511317&dopt=Abstract
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Unilateral psoriasis: a case individualized by means of involucrin. Author(s): Ginarte M, Fernandez-Redondo V, Toribio J. Source: Cutis; Cutaneous Medicine for the Practitioner. 2000 March; 65(3): 167-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10738637&dopt=Abstract
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Unusual annular pustular psoriasis in a patient with type C hepatitis. Author(s): Yamamoto T, Otoyama K, Nishioka K. Source: The Journal of Dermatology. 2000 December; 27(12): 802-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11211799&dopt=Abstract
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Unusual palatal presentation of oral psoriasis. Author(s): Richardson LJ, Kratochvil FJ, Zieper MB. Source: Journal (Canadian Dental Association). 2000 February; 66(2): 80-2. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10730005&dopt=Abstract
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Update on psoriasis therapy: a perspective from the USA. Author(s): Koo J, Liao W. Source: Keio J Med. 2000 March; 49(1): 20-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10750377&dopt=Abstract
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Updates from the Third International Congress on Psoriasis: From Gene to Clinic, The Royal College of Physicians, London, U.K., 21-23 November 2002. Author(s): Camp RD. Source: The British Journal of Dermatology. 2003 May; 148(5): 878-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12786816&dopt=Abstract
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Up-regulated perforin expression of CD8+ blood lymphocytes in generalized nonanaphylactic drug eruptions and exacerbated psoriasis. Author(s): Behrendt C, Gollnick H, Bonnekoh B. Source: Eur J Dermatol. 2000 July-August; 10(5): 365-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10882944&dopt=Abstract
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Up-regulation of macrophage inflammatory protein-3 alpha/CCL20 and CC chemokine receptor 6 in psoriasis. Author(s): Homey B, Dieu-Nosjean MC, Wiesenborn A, Massacrier C, Pin JJ, Oldham E, Catron D, Buchanan ME, Muller A, deWaal Malefyt R, Deng G, Orozco R, Ruzicka T, Lehmann P, Lebecque S, Caux C, Zlotnik A. Source: Journal of Immunology (Baltimore, Md. : 1950). 2000 June 15; 164(12): 6621-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10843722&dopt=Abstract
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Upregulation of RANTES in psoriatic keratinocytes: a possible pathogenic mechanism for psoriasis. Author(s): Raychaudhuri SP, Jiang WY, Farber EM, Schall TJ, Ruff MR, Pert CB. Source: Acta Dermato-Venereologica. 1999 January; 79(1): 9-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10086850&dopt=Abstract
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Urinary adenosine and aminoimidazolecarboxamide excretion in methotrexatetreated patients with psoriasis. Author(s): Baggott JE, Morgan SL, Sams WM, Linden J. Source: Archives of Dermatology. 1999 July; 135(7): 813-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10411156&dopt=Abstract
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Urinary thymine dimers and 8-oxo-2'-deoxyguanosine in psoriasis. Author(s): Ahmad J, Cooke MS, Hussieni A, Evans MD, Patel K, Burd RM, Bleiker TO, Hutchinson PE, Lunec J. Source: Febs Letters. 1999 November 5; 460(3): 549-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10556533&dopt=Abstract
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Use of basiliximab as a cyclosporin-sparing agent in palmoplantar pustular psoriasis with myalgia as an adverse effect. Author(s): Bell HK, Parslew RA. Source: The British Journal of Dermatology. 2002 September; 147(3): 606-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12207613&dopt=Abstract
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Use of hydroxyurea in psoriasis. Author(s): Smith CH. Source: Clinical and Experimental Dermatology. 1999 January; 24(1): 2-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10233638&dopt=Abstract
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UV-B phototherapy clears psoriasis through local effects. Author(s): Dawe RS, Cameron H, Yule S, Man I, Ibbotson SH, Ferguson J. Source: Archives of Dermatology. 2002 August; 138(8): 1071-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12164745&dopt=Abstract
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Variations in the HCR (Pg8) gene are unlikely to be causal for familial psoriasis. Author(s): Chia NV, Stuart P, Nair RP, Henseler T, Jenisch S, Lim HW, Christophers E, Voorhees JJ, Elder JT. Source: The Journal of Investigative Dermatology. 2001 May; 116(5): 823-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11348479&dopt=Abstract
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Visual evoked potentials in patients with psoriasis vulgaris. Author(s): Grzybowski A, Grzybowski G, Druzdz A, Zaba R. Source: Documenta Ophthalmologica. Advances in Ophthalmology. 2001 November; 103(3): 187-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11824655&dopt=Abstract
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Vitamin D and scalp psoriasis. Author(s): Koo J. Source: Cutis; Cutaneous Medicine for the Practitioner. 2002 November; 70(5 Suppl): 214. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12467336&dopt=Abstract
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Vitamin D receptor genotypes are not associated with clinical response to calcipotriol in Korean psoriasis patients. Author(s): Lee DY, Park BS, Choi KH, Jeon JH, Cho KH, Song KY, Kim IG, Youn JI. Source: Archives of Dermatological Research. 2002 March; 294(1-2): 1-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12071154&dopt=Abstract
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Vitamin D receptor polymorphism is associated with psoriasis. Author(s): Park BS, Park JS, Lee DY, Youn JI, Kim IG. Source: The Journal of Investigative Dermatology. 1999 January; 112(1): 113-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9886274&dopt=Abstract
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Vitiligo following narrow-band TL-01 phototherapy for psoriasis. Author(s): Goodwin RG, Finlay AY, Anstey AV. Source: The British Journal of Dermatology. 2001 June; 144(6): 1264-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422056&dopt=Abstract
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VML 295 (LY-293111), a novel LTB4 antagonist, is not effective in the prevention of relapse in psoriasis. Author(s): Mommers JM, Van Rossum MM, Kooijmans-Otero ME, Parker GL, van de Kerkhof PC. Source: The British Journal of Dermatology. 2000 February; 142(2): 259-66. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10730758&dopt=Abstract
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What criteria do patients use when judging the effectiveness of psoriasis management? Author(s): Ersser SJ, Surridge H, Wiles A. Source: Journal of Evaluation in Clinical Practice. 2002 November; 8(4): 367-76. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12421386&dopt=Abstract
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What is the role of narrowband UVB in the treatment of psoriasis? Author(s): Ferguson J. Source: Photodermatology, Photoimmunology & Photomedicine. 2002 February; 18(1): 42-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11982921&dopt=Abstract
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What is the role of topical calcipotriol in the treatment of mild to moderate chronic plaque psoriasis? Author(s): Popescu CM, Popescu R. Source: Archives of Dermatology. 2000 December; 136(12): 1547-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11115169&dopt=Abstract
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What patients with psoriasis believe about their condition. Author(s): Lanigan SW. Source: Journal of the American Academy of Dermatology. 1999 August; 41(2 Pt 1): 2834. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10426908&dopt=Abstract
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What's new in psoriasis. Author(s): Christophers E. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2000 November; 14(6): 436. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11444259&dopt=Abstract
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What's your assessment? Psoriasis with steroid atrophy. Author(s): Bielan B. Source: Dermatology Nursing / Dermatology Nurses' Association. 2001 August; 13(4): 288, 318. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11917785&dopt=Abstract
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What's your assessment? Psoriasis. Author(s): Bielan B. Source: Dermatology Nursing / Dermatology Nurses' Association. 2001 April; 13(2): 139, 138. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11917308&dopt=Abstract
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Which T cells cause psoriasis? Author(s): Prinz JC. Source: Clinical and Experimental Dermatology. 1999 July; 24(4): 291-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10457134&dopt=Abstract
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Why do I have psoriasis? Author(s): Cox NH, Paterson WD. Source: The British Journal of Dermatology. 2003 January; 148(1): 169. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534615&dopt=Abstract
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Widespread plaque psoriasis responsive to mycophenolate mofetil. Author(s): Tong DW, Walder BK. Source: The Australasian Journal of Dermatology. 1999 August; 40(3): 135-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10439523&dopt=Abstract
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Xenon chloride ultraviolet B laser is more effective in treating psoriasis and in inducing T cell apoptosis than narrow-band ultraviolet B. Author(s): Novak Z, Bonis B, Baltas E, Ocsovszki I, Ignacz F, Dobozy A, Kemeny L. Source: Journal of Photochemistry and Photobiology. B, Biology. 2002 May; 67(1): 32-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12007465&dopt=Abstract
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CHAPTER 2. NUTRITION AND PSORIASIS Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and psoriasis.
Finding Nutrition Studies on Psoriasis The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail:
[email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “psoriasis” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.
7
Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.
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The following is a typical result when searching for recently indexed consumer information on psoriasis: •
Mahonia ointment in the treatment of Psoriasis. Source: Leigh, E. HerbalGram. Austin, TX : American Botanical Council and the Herb Research Foundation. Spring 1998. (42) page 17. 0899-5648
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Vitamin D and psoriasis. Author(s): Department of Biochemistry, University of California, Riverside 92521. Source: Lowe, K E Norman, A W Nutr-Revolume 1992 May; 50(5): 138-42 0029-6643
The following information is typical of that found when using the “Full IBIDS Database” to search for “psoriasis” (or a synonym): •
A clinical evaluation of tazarotene 0.1% gel, with and without a high- or mid-highpotency corticosteroid, in patients with stable plaque psoriasis. Author(s): Department of Dermatology, George Washington University, 2150 Pennsylvania Avenue NW, Washington, DC 20037, USA. Source: Green, Lawrence Sadoff, Wendy J-Cutan-Med-Surg. 2002 Mar-April; 6(2): 95-102 1203-4754
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A corticosteroid-induced flare of psoriasis. How to control or, better yet, avoid. Author(s): Northeastern Ohio Universities College of Medicine, Rootstown, USA.
[email protected] Source: Brodell, R T Williams, L Postgrad-Med. 1999 December; 106(7): 31-2 0032-5481
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A highly decreased binding of cyclic adenosine monophosphate to protein kinase A in erythrocyte membranes is specific for active psoriasis. Author(s): Department of Dermatology, Johannes Gutenberg University, Langenbeckstrasse 1, 55101 Mainz, Germany.
[email protected] Source: Schopf, R E Langendorf, Y Benz, R E Farber, L Benes, P J-Invest-Dermatol. 2002 July; 119(1): 160-5 0022-202X
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A review of the epidemiology of psoriasis vulgaris in the community. Author(s): University of Melbourne, Department of Medicine (Dermatology), St Vincent's Hospital, Fitzroy, Victoria, Australia. Source: Plunkett, A Marks, R Australas-J-Dermatol. 1998 November; 39(4): 225-32 00048380
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Acute methyl salicylate toxicity complicating herbal skin treatment for psoriasis. Author(s): Emergency Department, Royal Prince Alfred Hospital, Missenden Road, Camperdown, NSW, Australia.
[email protected] Source: Bell, A J Duggin, G Emerg-Med-(Fremantle). 2002 June; 14(2): 188-90 1441-0737
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Advances in experimental studies on treatment of psoriasis by traditional Chinese medicine. Author(s): Department of Dermatology, General Coal Hospital, Beijing, 100028. Source: Zhang, H Qu, X J-Tradit-Chin-Med. 2002 March; 22(1): 61-6 0254-6272
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Antiangiogenic properties of a novel shark cartilage extract: potential role in the treatment of psoriasis. Author(s): Les Laboratoires Aeterna, Ste-Foy, PQ, Canada. Source: Dupont, E Savard, P E Jourdain, C Juneau, C Thibodeau, A Ross, N Marenus, K Maes, D H Pelletier, G Sauder, D N J-Cutan-Med-Surg. 1998 January; 2(3): 146-52 12034754
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Arsenic keratosis and pigmentation accompanied by multiple Bowen's disease and genitourinary cancer in a psoriasis patient. Author(s): Department of Dermatology, Seoul National University College of Medicine, Korea. Source: Park, J Y Rim, J H Choe, Y B Youn, J I J-Dermatol. 2002 July; 29(7): 446-51 03852407
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Better patient compliance in psoriasis. Author(s): Section of Dermatology, Imperial College of Science, Technology & Medicine, Hammersmith Hospital, London. Source: Chu, T Practitioner. 2000 March; 244(1608): 238-42, 244 0032-6518
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Calcipotriol and betamethasone dipropionate (Dovobet, Daivobet): a new formulation for the treatment of psoriasis. Author(s): Department of Dermatology, Centre Hospitalier Universitaire de Quebec, Canada. Source: Poulin, Y Skin-Therapy-Lett. 2002 June; 7(6): 1-3 1201-5989
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Calcipotriol improves the efficacy of cyclosporine in the treatment of psoriasis vulgaris. Author(s): Institute of Dermatology, Ospedale di Cattinara, University of Trieste, Italy. Source: Kokelj, F Torsello, P Plozzer, C J-Eur-Acad-Dermatol-Venereol. 1998 March; 10(2): 143-6 0926-9959
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Calcipotriol ointment. A review of its use in the management of psoriasis. Author(s): Adis International Inc., Langhorne, Pennsylvania, USA.
[email protected] Source: Scott, L J Dunn, C J Goa, K L Am-J-Clin-Dermatol. 2001; 2(2): 95-120 1175-0561
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Chronic plaque psoriasis. Author(s): Ospedali Riuniti Bergamo, Bergamo, Italy. Source: Naldi, L Rzany, B Clin-Evid. 2002 June; (7): 1488-507 1462-3846
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Clinical trial of the efficacy and safety of oral etretinate with calcipotriol cream compared with etretinate alone in moderate-severe psoriasis. Author(s): Clinica Dermatologica, Universita, Modena, Italy. Source: Giannetti, A Coppini, M Bertazzoni, M G Califano, A Altieri, E Pazzaglia, A Lega, M Lombardo, M Pelfini, C Veller Fornasa, C Rabbiosi, G Cespa, M J-Eur-AcadDermatol-Venereol. 1999 September; 13(2): 91-5 0926-9959
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Clobetasol propionate followed by calcipotriol is superior to calcipotriol alone in topical treatment of psoriasis. Author(s): Sandvika Bad, Norway. Source: Austad, J Bjerke, J R Gjertsen, B T Helland, S Livden, J K Morken, T Mork, N J JEur-Acad-Dermatol-Venereol. 1998 July; 11(1): 19-24 0926-9959
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Coexistence of morphea and psoriasis responding to acitretin treatment. Author(s): Department of Dermatology, Kocaeli University, Faculty of Medicine, Izmit, Turkey. Source: Bilen, N Apaydin, R Ercin, C Harova, G Basdas, F Bayramgurler, D J-Eur-AcadDermatol-Venereol. 1999 September; 13(2): 113-7 0926-9959
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Combination therapy with low-dose etretinate and eicosapentaenoic acid for psoriasis vulgaris. Author(s): Department of Dermatology, Shiga University of Medical Science, Otsu, Japan. Source: Danno, K Sugie, N J-Dermatol. 1998 November; 25(11): 703-5 0385-2407
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Comparison of calcipotriol and coal tar in conjunction with sun exposure in chronic plaque psoriasis: a pilot study. Author(s): Department of Dermatology, Venereology and Leprology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. Source: Kaur, I Saraswat, A KuMarch, B J-Dermatol. 2001 August; 28(8): 448-50 03852407
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Detection of telomerase activity in psoriasis lesional skin and correlation with Ki-67 expression and suppression by retinoic acid. Author(s): Department of Dermatology, College of Medicine, Pusan National University, Pusan, Korea.
[email protected] Source: Jang, H S Oh, C K Jo, J H Kim, Y S Kwon, K S J-Korean-Med-Sci. 2001 October; 16(5): 623-9 1011-8934
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Differential expression of interferon gamma by mitogen-stimulated peripheral blood mononuclear cells among Kuwaiti psoriasis patients. Author(s): Department of Medical Laboratory Sciences, Faculty of Allied Health Sciences and Nursing, Kuwait University, Sulaibekhat, Kuwait. Source: Mahmoud, F Abul, H al Seleh, Q Morgan, G Haines, D al Ramly, M Burleson, J Kreutzer, D J-Dermatol. 1999 January; 26(1): 23-8 0385-2407
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Drug interactions in psoriasis: the pros and cons of combining topical psoriasis therapies. Author(s): Department of Dermatology, Mount Sinai School of Medicine, One Gustave Levy Place, New York, New York 10029, USA.
[email protected] Source: Endzweig Gribetz, C H Brady, C Lynde, C Sibbald, D Lebwohl, M J-Cutan-MedSurg. 2002 May-June; 6(3 Suppl): 12-6 1203-4754
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Effect of vitamin D3 on the increased expression of Bcl-xL in psoriasis. Author(s): Department of Dermatology, Tokyo Women's Medical University, 8-1, Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan. Source: Fukuya, Yasuko Higaki, Megumu Higaki, Yuko Kawashima, Makoto ArchDermatol-Res. 2002 February; 293(12): 620-5 0340-3696
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Effects of antipsoriatic therapies on hepatic microsomal enzyme activity in patients with psoriasis. Author(s): Department of Dermatology, Ruhr-University Bochum, St. Josef-Hospital, Gudrunstr. 56, D-44791 Bochum, Germany.
[email protected] Source: Brockmeyer, N H Fruhauf, S Mertins, L Barthel, B Goos, M Eur-J-Med-Res. 1998 August 18; 3(8): 361-6 0949-2321
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Effects of Mahonia aquifolium ointment on the expression of adhesion, proliferation, and activation markers in the skin of patients with psoriasis. Author(s): Universitats-Hautklinik Freiburg.
[email protected] Source: Augustin, M Andrees, U Grimme, H Schopf, E Simon, J ForschKomplementarmed. 1999 April; 6 Suppl 219-21 1021-7096
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Effects of topical calcipotriol on the expression of adhesion molecules in psoriasis. Author(s): 1st Dermatologic Clinic, University of Turin, Torino, Italy. Source: Savoia, P Novelli, M De Matteis, A Verrone, A Bernengo, M G J-Cutan-Pathol. 1998 February; 25(2): 89-94 0303-6987
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Efficacy of cyclosporine plus etretinate in the treatment of erythrodermic psoriasis (three case reports). Author(s): Institute of Dermatology, Ospedale di Cattinara, Trieste, Italy.
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Source: Kokelj, F Plozzer, C Torsello, P Trevisan, G J-Eur-Acad-Dermatol-Venereol. 1998 September; 11(2): 177-9 0926-9959 •
Eosinophils, pruritus and psoriasis: effects of treatment with etretinate or cyclosporin-A. Author(s): Department of Dermatology, Johannes Gutenberg University Mainz, Germany. Source: Schopf, R E Hultsch, T Lotz, J Brautigam, M J-Eur-Acad-Dermatol-Venereol. 1998 November; 11(3): 234-9 0926-9959
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Familial association of pseudohypoparathyroidism and psoriasis: case report. Author(s): Endocrinology and Metabolism Division, Department of Internal Medicine, Faculty of Medicine of Ribeirao Preto, Universidade de Sao Paulo, Avenida Bandeirantes 3900, Ribeirao Preto/SP, Brazil-CEP 14048-900. Source: Montenegro, Renan Magalhaes Jr Albuquerque de Paula, Francisco Jose Foss, Norma Tiraboshi Foss, Milton Cesar Sao-Paulo-Med-J. 2002 January 3; 120(1): 23-7 15163180
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Helping people to remain in control of their psoriasis. Author(s): Redbridge Healthcare Trust. Source: Watts, J Community-Nurse. 1998 August; 4(7): 19-21 1351-1416
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Induction of cutaneous lymphocyte-associated antigen expression by group A streptococcal antigens in psoriasis. Author(s): Department of Dermatology, St. Mary's Hospital, Paddington, London, UK.
[email protected] Source: Baker, B S Garioch, J J Hardman, C Powles, A Fry, L Arch-Dermatol-Res. 1997 November; 289(12): 671-6 0340-3696
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Interventions for guttate psoriasis. Author(s): Dermatology Centre, University of Manchester School of Medicine, Hope Hospital, Stott Lane, Eccles, Manchester, UK, M6 8HD.
[email protected] Source: Chalmers, R J O'Sullivan, T Owen, C M Griffiths, C E Cochrane-Database-SystRevolume 2000; (2): CD001213 1469-493X
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Management of guttate and generalized psoriasis vulgaris: prospective randomized study. Author(s): Department of Dermatology, Sts Cyrilus and Methodius University School of Medicine, Skopje, Republic of Macedonia. Source: Caca Biljanovska, N G V'lckova Laskoska, M T Croat-Med-J. 2002 December; 43(6): 707-12 0353-9504
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Management of psoriasis. Author(s): Monash Medical Centre, Victoria. Source: Cowen, P Aust-Fam-Physician. 2001 November; 30(11): 1033-7 0300-8495
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Narrowband UVB phototherapy for psoriasis: results with fixed increments by skin type (as opposed to percentage increments). Author(s): Dept. of Dermatology, College of Physicians & Surgeons of Columbia University, New York, NY, USA. Source: Halasz, C L Photodermatol-Photoimmunol-Photomed. 1999 April; 15(2): 81-4 0905-4383
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New topicals for mild and moderate psoriasis. Author(s): Peachtree Nurosurgery, Atlanta, Ga., USA. Source: Cooper, C W JAAPA. 1999 April; 12(4): 52-4, 57-60
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Novel therapeutic approaches to psoriasis. Author(s): Section of Dermatology, University of Manchester, Hope Hospital, Salford. Source: Griffiths, C E Hosp-Med. 1998 July; 59(7): 539-42 1462-3935
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Novel therapies for psoriasis. Author(s): Baylor University Medical Center, Dallas, Texas, USA.
[email protected] Source: Cather, Jennifer Menter, Alan Am-J-Clin-Dermatol. 2002; 3(3): 159-73 1175-0561
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Polymorphism of the vitamin D(3) receptor in patients with psoriasis. Author(s): Department of Dermatology, Dokkyo University School of Medicine, 880 Kitakobayashi, Mibu, Tochigi 321-0293, Japan. Source: Okita, H Ohtsuka, T Yamakage, A Yamazaki, S Arch-Dermatol-Res. 2002 July; 294(4): 159-62 0340-3696
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Psoriasis in children: a guide to its diagnosis and management. Author(s): Department of Dermatology, Western Infirmary, Glasgow, Scotland. Source: Leman, J Burden, D Paediatr-Drugs. 2001; 3(9): 673-80 1174-5878
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Psoriasis of the scalp. Diagnosis and management. Author(s): Department of Dermatology, University Hospital Nijmegen, Nijmegen, The Netherlands.
[email protected] Source: van de Kerkhof, P C Franssen, M E Am-J-Clin-Dermatol. 2001; 2(3): 159-65 11750561
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Retinoids for the treatment of psoriasis: outlook for the future. Author(s): Department of Dermatology, University Hospital, Geneva, Switzerland. Source: Kuenzli, S Saurat, J H Curr-Opin-Investig-Drugs. 2001 May; 2(5): 625-30 14724472
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Strategy in the optimization of medicinal plant preparations for treatment of psoriasis. Source: Korbely, I. Kiss, J. Kery, A. Plant-Med. Stuttgart, W. Ger. : Georg Thieme Verlag. December 1990. volume 56 (6) page 697. 0032-0943
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Tazarotene--a topical retinoid for psoriasis. Source: Anonymous Drug-Ther-Bull. 1999 June; 37(6): 47-8 0012-6543
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The efficacy of a new topical treatment for psoriasis: Mirak. Author(s): Department of Dermatology, University Hospital Nijmegen, The Netherlands.
[email protected] Source: Seyger, M M van de Kerkhof, P C van Vlijmen Willems, I M de Bakker, E S Zwiers, F de Jong, E M J-Eur-Acad-Dermatol-Venereol. 1998 July; 11(1): 13-8 0926-9959
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The fatty-acid spectrum in plasma and adipose tissue in patients with psoriasis. Source: Vahlquist, C Berne, B Boberg, M Michaelsson, G Vessby, B Arch-Dermatol-Res. 1985; 278(2): 114-9 0340-3696
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The SAPASI is valid and responsive to psoriasis disease severity changes in a multicenter clinical trial. Author(s): Department of Dermatology, Wake Forest University Medical Center, Winston-Salem, NC, USA. Source: Fleischer, A B Feldman, S R Dekle, C L J-Dermatol. 1999 April; 26(4): 210-5 03852407
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Topical agents for the treatment of psoriasis, past, present and future. Author(s): Division of Dermatology, University of Montreal Hospital Centre, Notre Dame Hospital, Montreal, Quebec, Canada.
[email protected]
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Source: Tremblay, J F Bissonnette, R J-Cutan-Med-Surg. 2002 May-June; 6(3 Suppl): 8-11 1203-4754 •
Topical tacalcitol treatment for psoriasis. Author(s): Department of Dermatology, Royal Lancaster Infirmary. Source: Harrison, P V Hosp-Med. 2000 June; 61(6): 402-5 1462-3935
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Topical tazarotene therapy for psoriasis, acne vulgaris, and photoaging. Author(s): Division of Dermatology, University of Western Ontario, London, Ontario, Canada. Source: Guenther, L C Skin-Therapy-Lett. 2002 March; 7(3): 1-4 1201-5989
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Traditional medicine as a source of new therapeutic agents against psoriasis. Author(s): Dipartimento di Scienze Botaniche, Universita di Palermo, Via Archirafi 38, Palermo, Italy. Source: Amenta, R Camarda, L Di Stefano, V Lentini, F Venza, F Fitoterapia. 2000 August; 71 Suppl 1: S13-20 0367-326X
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Treating psoriasis in primary care settings. Preserving quality of life is a primary--and possible--goal. Author(s): Dermatology Program, Veterans Affairs Medical Center, Bay Pines, Fla., USA. Source: Sinni McKeehen, B J Hazzard, E F Adv-Nurse-Pract. 2001 December; 9(12): 31-4, 74 1096-6293
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Treatment and management of psoriasis. Source: Rogers, S Ir-Med-J. 1999 Sep-October; 92(6): 391-2 0332-3102
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Treatment of psoriasis vulgaris with topical vitamin D analogue (calcipotriol): open multicenter study. Author(s): Department of Medical Services, Ministry of Public Health, Bangkok, Thailand. Source: Kullavanijaya, P Gritiyarangsan, P Huiprasert, P Leenutaphong, V J-Med-AssocThai. 1999 October; 82(10): 974-7 0125-2208
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Treatments for chronic palmoplantar pustular psoriasis. Author(s): Dermatology Centre, University of Manchester School of Medicine, Hope Hospital, Manchester, UK. Source: Marsland, A M Griffiths, C E Skin-Therapy-Lett. 2001 November; 6(12): 3-5 12015989
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Treatments of generalized pustular psoriasis: a multicenter study in Japan. Author(s): Department of Dermatology, Tokai University School of Medicine, Kanagawa, Japan. Source: Ozawa, A Ohkido, M Haruki, Y Kobayashi, H Ohkawara, A Ohno, Y Inaba, Y Ogawa, H J-Dermatol. 1999 March; 26(3): 141-9 0385-2407
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Ultrastructural and biosynthetic characteristics of epidermal cells in patients with psoriasis treated with antiproliferative drugs. Author(s): Laboratory of ultrastructural bases of Pathology, Institute of Regional Pathology and Pathomorphology, Siberian Division, Russian Academy of Medical Sciences, Novosibirsk.
[email protected] Source: Krinitsyna, Y M Nepomnyashchikh, G I Aidagulova, S V Bull-Exp-Biol-Med. 2001 August; 132(2): 797-802 0007-4888
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Update on psoriasis therapy: a perspective from the USA. Author(s): Department of Dermatology, University of California San Francisco Medical Center, USA. Source: Koo, J Liao, W Keio-J-Med. 2000 March; 49(1): 20-5 0022-9717
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Urinary excretion of glycosaminoglycans in psoriasis. Author(s): University Department of Dermatology, Royal Infirmary, Edinburgh, Scotland. Source: Priestley, G C Arch-Dermatol-Res. 1988; 280(2): 77-82 0340-3696
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Vitamin D receptor genotypes are not associated with clinical response to calcipotriol in Korean psoriasis patients. Author(s): Department of Dermatology, Seoul National University College of Medicine, Korea. Source: Lee, D Y Park, B S Choi, K H Jeon, J H Cho, K H Song, K Y Kim, I G Youn, J I Arch-Dermatol-Res. 2002 March; 294(1-2): 1-5 0340-3696
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Widespread plaque psoriasis responsive to mycophenolate mofetil. Author(s): Department of Dermatology, Prince of Wales Hospital, Randwick, New South Wales, Australia. Source: Tong, D W Walder, B K Australas-J-Dermatol. 1999 August; 40(3): 135-7 00048380
Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •
healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0
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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov
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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov
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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/
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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/
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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/
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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/
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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/
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Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html
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Google: http://directory.google.com/Top/Health/Nutrition/
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Healthnotes: http://www.healthnotes.com/
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Open Directory Project: http://dmoz.org/Health/Nutrition/
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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/
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WebMDHealth: http://my.webmd.com/nutrition
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
The following is a specific Web list relating to psoriasis; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
Vitamins Folic Acid Source: Healthnotes, Inc. www.healthnotes.com Pantothenic Acid Source: Integrative Medicine Communications; www.drkoop.com Vitamin A Source: Prima Communications, Inc.www.personalhealthzone.com Vitamin A Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10066,00.html Vitamin B complex Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,962,00.html Vitamin B5 (Pantothenic Acid) Source: Integrative Medicine Communications; www.drkoop.com Vitamin D Alternative names: Calciferol, Calcitrol, Cholecalciferol, Erocalciferol Source: Integrative Medicine Communications; www.drkoop.com
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Vitamin D Source: Prima Communications, Inc.www.personalhealthzone.com Vitamin D Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,905,00.html Vitamin E Source: Prima Communications, Inc.www.personalhealthzone.com •
Minerals Chromium Source: Prima Communications, Inc.www.personalhealthzone.com Folate Source: Prima Communications, Inc.www.personalhealthzone.com Quercetin Source: Integrative Medicine Communications; www.drkoop.com Retinol Source: Integrative Medicine Communications; www.drkoop.com Selenium Source: Integrative Medicine Communications; www.drkoop.com Selenium Source: Prima Communications, Inc.www.personalhealthzone.com Selenium Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10055,00.html Vitamin A (Retinol) Source: Integrative Medicine Communications; www.drkoop.com Zinc Source: Prima Communications, Inc.www.personalhealthzone.com Zinc Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10071,00.html Zinc/copper Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,938,00.html
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Food and Diet Barley Source: Healthnotes, Inc. www.healthnotes.com Burdock Alternative names: Arctium lappa Source: Healthnotes, Inc. www.healthnotes.com Burdock Source: Prima Communications, Inc.www.personalhealthzone.com Cartilage Alternative names: Shark Cartilage Source: Integrative Medicine Communications; www.drkoop.com Cartilage Source: Prima Communications, Inc.www.personalhealthzone.com Gluten-Free Diet Source: Healthnotes, Inc. www.healthnotes.com Omega-3 Fatty Acids Source: Integrative Medicine Communications; www.drkoop.com Omega-3 Fatty Acids Source: Integrative Medicine Communications; www.drkoop.com Omega-3 fatty acids Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,992,00.html Omega-6 fatty acids Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,1037,00.html Polyunsaturated Fats Source: Healthnotes, Inc. www.healthnotes.com Rye Source: Healthnotes, Inc. www.healthnotes.com Wheat Source: Healthnotes, Inc. www.healthnotes.com
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CHAPTER 3. ALTERNATIVE MEDICINE AND PSORIASIS Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to psoriasis. At the conclusion of this chapter, we will provide additional sources.
National Center for Complementary and Alternative Medicine The National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (http://nccam.nih.gov/) has created a link to the National Library of Medicine’s databases to facilitate research for articles that specifically relate to psoriasis and complementary medicine. To search the database, go to the following Web site: http://www.nlm.nih.gov/nccam/camonpubmed.html. Select “CAM on PubMed.” Enter “psoriasis” (or synonyms) into the search box. Click “Go.” The following references provide information on particular aspects of complementary and alternative medicine that are related to psoriasis: •
“Doctor fish” and psoriasis. Author(s): Undar L, Akpinar MA, Yanikoglu A. Source: Lancet. 1990 February 24; 335(8687): 470-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1968187&dopt=Abstract
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A Chinese cream (fu suo) for psoriasis. Author(s): Bonnetblanc JM, Marquet P. Source: Dermatology (Basel, Switzerland). 1996; 192(3): 294. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8726658&dopt=Abstract
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A comparison of bathwater and oral delivery of 8-methoxypsoralen in PUVA therapy for plaque psoriasis. Author(s): Cooper EJ, Herd RM, Priestley GC, Hunter JA.
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Source: Clinical and Experimental Dermatology. 2000 March; 25(2): 111-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10733632&dopt=Abstract •
A comparison of PUVA-etretinate and PUVA-placebo for palmoplantar pustular psoriasis. Author(s): Lawrence CM, Marks J, Parker S, Shuster S. Source: The British Journal of Dermatology. 1984 February; 110(2): 221-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6696838&dopt=Abstract
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A comparison of the effect of narrow-band ultraviolet B in the treatment of psoriasis after salt-water baths and after 8-methoxypsoralen baths. Author(s): Arnold WP, van Andel P, de Hoop D, de Jong-Tieben L, Visser-van Andel M. Source: The British Journal of Dermatology. 2001 August; 145(2): 352-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11531811&dopt=Abstract
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A controlled trial of acupuncture in psoriasis: no convincing effect. Author(s): Jerner B, Skogh M, Vahlquist A. Source: Acta Dermato-Venereologica. 1997 March; 77(2): 154-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9111831&dopt=Abstract
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A double-blind study comparing oleum horwathiensis with placebo in the treatment of psoriasis. Author(s): Lassus A, Forsstrom S. Source: J Int Med Res. 1991 March-April; 19(2): 137-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1864450&dopt=Abstract
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A double-blind, randomized, placebo-controlled trial of n-3 fatty acid based lipid infusion in acute, extended guttate psoriasis. Rapid improvement of clinical manifestations and changes in neutrophil leukotriene profile. Author(s): Grimminger F, Mayser P, Papavassilis C, Thomas M, Schlotzer E, Heuer KU, Fuhrer D, Hinsch KD, Walmrath D, Schill WB, et al. Source: Clin Investig. 1993 August; 71(8): 634-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8219661&dopt=Abstract
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A low-fat diet supplemented with dietary fish oil (Max-EPA) results in improvement of psoriasis and in formation of leukotriene B5. Author(s): Kragballe K, Fogh K. Source: Acta Dermato-Venereologica. 1989; 69(1): 23-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2563604&dopt=Abstract
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A pilot study of hypnosis in the treatment of patients with psoriasis. Author(s): Tausk F, Whitmore SE.
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Source: Psychotherapy and Psychosomatics. 1999; 68(4): 221-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10396014&dopt=Abstract •
A randomized controlled trial of narrowband ultraviolet B vs bath-psoralen plus ultraviolet A photochemotherapy for psoriasis. Author(s): Dawe RS, Cameron H, Yule S, Man I, Wainwright NJ, Ibbotson SH, Ferguson J. Source: The British Journal of Dermatology. 2003 June; 148(6): 1194-204. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828749&dopt=Abstract
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A survey of psoriasis patients in Japan from 1982 to 2001. Author(s): Kawada A, Tezuka T, Nakamizo Y, Kimura H, Nakagawa H, Ohkido M, Ozawa A, Ohkawara A, Kobayashi H, Harada S, Igarashi A; Japanese Society for Psoriasis Research. Source: Journal of Dermatological Science. 2003 February; 31(1): 59-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12615365&dopt=Abstract
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A systematic review of treatments for guttate psoriasis. Author(s): Chalmers RR, O'Sullivan T, Owen CC, Griffiths CC. Source: The British Journal of Dermatology. 2001 December; 145(6): 891-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11899141&dopt=Abstract
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A trial of oral zinc supplementation in psoriasis. Author(s): Burrows NP, Turnbull AJ, Punchard NA, Thompson RP, Jones RR. Source: Cutis; Cutaneous Medicine for the Practitioner. 1994 August; 54(2): 117-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7956335&dopt=Abstract
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Acupuncture treatment for psoriasis: a retrospective case report. Author(s): Liao SJ, Liao TA. Source: Acupuncture & Electro-Therapeutics Research. 1992 July-September; 17(3): 195208. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1357925&dopt=Abstract
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Acute contact dermatitis from a popular psoriasis remedy in Bulgaria. Author(s): Stransky L. Source: Contact Dermatitis. 1998 June; 38(6): 343. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9687040&dopt=Abstract
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Acute hepatitis induced by traditional Chinese herbs used in the treatment of psoriasis. Author(s): Verucchi G, Calza L, Attard L, Chiodo F.
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Source: Journal of Gastroenterology and Hepatology. 2002 December; 17(12): 1342-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12423285&dopt=Abstract •
Acute methyl salicylate toxicity complicating herbal skin treatment for psoriasis. Author(s): Bell AJ, Duggin G. Source: Emergency Medicine (Fremantle, W.A.). 2002 June; 14(2): 188-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12147116&dopt=Abstract
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Advances in experimental studies on treatment of psoriasis by traditional Chinese medicine. Author(s): Zhang H, Qu X. Source: J Tradit Chin Med. 2002 March; 22(1): 61-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11977526&dopt=Abstract
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Alternative therapies commonly used within a population of patients with psoriasis. Author(s): Fleischer AB Jr, Feldman SR, Rapp SR, Reboussin DM, Exum ML, Clark AR. Source: Cutis; Cutaneous Medicine for the Practitioner. 1996 September; 58(3): 216-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8886537&dopt=Abstract
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Alternative therapy for atopic dermatitis and psoriasis: patient-reported motivation, information source and effect. Author(s): Jensen P. Source: Acta Dermato-Venereologica. 1990; 70(5): 425-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1980978&dopt=Abstract
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Alternative treatment of psoriasis with balneotherapy using Leopoldine spa water. Author(s): Tsoureli-Nikita E, Menchini G, Ghersetich I, Hercogova J. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2002 May; 16(3): 260-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12195567&dopt=Abstract
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An hypothesis explaining the successful treatment of psoriasis with thermal biofeedback: a case report. Author(s): Goodman M. Source: Biofeedback Self Regul. 1994 December; 19(4): 347-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7880910&dopt=Abstract
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An update on common skin diseases. Acne, psoriasis, contact dermatitis, and warts. Author(s): Millikan LE, Shrum JP.
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Source: Postgraduate Medicine. 1992 May 1; 91(6): 96-8, 101-4, 107-10 Passim. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1533716&dopt=Abstract •
Antiangiogenic properties of a novel shark cartilage extract: potential role in the treatment of psoriasis. Author(s): Dupont E, Savard PE, Jourdain C, Juneau C, Thibodeau A, Ross N, Marenus K, Maes DH, Pelletier G, Sauder DN. Source: Journal of Cutaneous Medicine and Surgery. 1998 January; 2(3): 146-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9479080&dopt=Abstract
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Arsenic keratosis and pigmentation accompanied by multiple Bowen's disease and genitourinary cancer in a psoriasis patient. Author(s): Park JY, Rim JH, Choe YB, Youn JI. Source: The Journal of Dermatology. 2002 July; 29(7): 446-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12184646&dopt=Abstract
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Association of etretinate and fish oil in psoriasis therapy. Inhibition of hypertriglyceridemia resulting from retinoid therapy after fish oil supplementation. Author(s): Frati C, Bevilacqua L, Apostolico V. Source: Acta Derm Venereol Suppl (Stockh). 1994; 186: 151-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8073820&dopt=Abstract
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Balneo phototherapy for psoriasis. Modern application of an age-old treatment. Author(s): Mikula C. Source: Adv Nurse Pract. 2003 January; 11(1): 53-6. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12630261&dopt=Abstract
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Balneophototherapy of psoriasis: highly concentrated salt water versus tap water--a randomized, one-blind, right/left comparative study. Author(s): Gambichler T, Rapp S, Senger E, Altmeyer P, Hoffmann K. Source: Photodermatology, Photoimmunology & Photomedicine. 2001 February; 17(1): 22-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11169172&dopt=Abstract
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Balneo-phototherapy: a new holistic approach to treating psoriasis. Author(s): Mikula C. Source: Journal of the American Academy of Nurse Practitioners. 2003 June; 15(6): 253-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861891&dopt=Abstract
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Balneophototherapy--combined treatment of psoriasis vulgaris and atopic dermatitis with salt water baths and artificial ultraviolet radiation. Author(s): Gambichler T, Kuster W, Kreuter A, Altmeyer P, Hoffmann K.
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Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2000 September; 14(5): 425-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11305394&dopt=Abstract •
Balneotherapy of psoriasis in Lipova lazne. Author(s): Prokes P. Source: Acta Univ Carol [med] (Praha). 1986; 32(3-4): 255-8. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3434485&dopt=Abstract
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Bath PUVA: an effective treatment for psoriasis. Author(s): Fairlie C, Baldwin L, Vear L, Rogers C. Source: Dermatology Nursing / Dermatology Nurses' Association. 1998 August; 10(4): 285-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9849172&dopt=Abstract
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Bath-5-methoxypsoralen-UVA therapy for psoriasis. Author(s): Calzavara-Pinton PG, Zane C, Carlino A, De Panfilis G. Source: Journal of the American Academy of Dermatology. 1997 June; 36(6 Pt 1): 945-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9204060&dopt=Abstract
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Bathing for psoriasis in the Dead Sea. Author(s): Montgomery BJ. Source: Jama : the Journal of the American Medical Association. 1979 January 19; 241(3): 227-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=758522&dopt=Abstract
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Bath-photo-therapy with the thermal water of Comano: treatment of psoriasis. Author(s): Zumiani G, Zanoni M, Lo Brutto R, Cristofolini P, Tasin L. Source: Acta Derm Venereol Suppl (Stockh). 1989; 146: 122-3; Discussion 124. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2609852&dopt=Abstract
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Bath-water compared with oral delivery of 8-methoxypsoralen PUVA therapy for chronic plaque psoriasis. Author(s): Collins P, Rogers S. Source: The British Journal of Dermatology. 1992 October; 127(4): 392-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1419760&dopt=Abstract
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Bath-water delivery of 8-methoxypsoralen therapy for psoriasis. Author(s): Collins P, Rogers S. Source: Clinical and Experimental Dermatology. 1991 May; 16(3): 165-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1934565&dopt=Abstract
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Biofeedback and control of skin cell proliferation in psoriasis. Author(s): Benoit LJ, Harrell EH. Source: Psychological Reports. 1980 June; 46(3 Pt 1): 831-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7394097&dopt=Abstract
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Biofeedback and psychotherapeutic treatment of psoriasis: a brief report. Author(s): Hughes HH, England R, Goldsmith DA. Source: Psychological Reports. 1981 February; 48(1): 99-102. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7232633&dopt=Abstract
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Can psychotherapy help patients with psoriasis? Author(s): Price ML, Mottahedin I, Mayo PR. Source: Clinical and Experimental Dermatology. 1991 March; 16(2): 114-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2032371&dopt=Abstract
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Cancer incidence among Finnish psoriasis patients treated with 8-methoxypsoralen bath PUVA. Author(s): Hannuksela-Svahn A, Pukkala E, Koulu L, Jansen CT, Karvonen J. Source: Journal of the American Academy of Dermatology. 1999 May; 40(5 Pt 1): 694-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10321595&dopt=Abstract
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Chronic plaque psoriasis: an overview. Author(s): Jackson K. Source: Nursing Standard : Official Newspaper of the Royal College of Nursing. 2002 September 4-10; 16(51): 45-52; Quiz 54-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12271539&dopt=Abstract
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Climate therapy for psoriasis at the Dead Sea, Israel. Author(s): Azizi E, Kushelevsky AP, Avrach W, Schewach-Millet M. Source: Isr J Med Sci. 1982 February; 18(2): 267-70. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7068358&dopt=Abstract
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Climatotherapy at the Dead Sea is a remittive therapy for psoriasis: combined effects on epidermal and immunologic activation. Author(s): Hodak E, Gottlieb AB, Segal T, Politi Y, Maron L, Sulkes J, David M. Source: Journal of the American Academy of Dermatology. 2003 September; 49(3): 451-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12963909&dopt=Abstract
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Climatotherapy of psoriasis and hypertension in elderly patients at the Dead-Sea. Author(s): Kushelevsky AP, Harari M, Hristakieva E, Shani J.
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Source: Pharmacological Research : the Official Journal of the Italian Pharmacological Society. 1996 July-August; 34(1-2): 87-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8981562&dopt=Abstract •
Clinical and biological effects of balneotherapy with selenium-rich spa water in patients with psoriasis vulgaris. Author(s): Pinton J, Friden H, Kettaneh-Wold N, Wold S, Dreno B, Richard A, Bieber T. Source: The British Journal of Dermatology. 1995 August; 133(2): 344-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7547424&dopt=Abstract
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Clinical evaluation of a more rapid and sensitive Psoriasis Assessment Severity Score (PASS), and its comparison with the classic method of Psoriasis Area and Severity Index (PASI), before and after climatotherapy at the Dead-Sea. Author(s): Harari M, Shani J, Hristakieva E, Stanimirovic A, Seidl W, Burdo A. Source: International Journal of Dermatology. 2000 December; 39(12): 913-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11168660&dopt=Abstract
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Clinical trial and experimental study on treating psoriasis with camptothecine. Author(s): Lin XR, Huang TA, Yang CM, Tu CX, Yang GL. Source: Chin Med J (Engl). 1988 June; 101(6): 427-30. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3146474&dopt=Abstract
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Combination therapy with low-dose etretinate and eicosapentaenoic acid for psoriasis vulgaris. Author(s): Danno K, Sugie N. Source: The Journal of Dermatology. 1998 November; 25(11): 703-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9863281&dopt=Abstract
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Commercial tanning bed treatment is an effective psoriasis treatment: results from an uncontrolled clinical trial. Author(s): Fleischer AB Jr, Clark AR, Rapp SR, Reboussin DM, Feldman SR. Source: The Journal of Investigative Dermatology. 1997 August; 109(2): 170-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9242503&dopt=Abstract
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Comparison of heat delivery systems for hyperthermia treatment of psoriasis. Author(s): Orenberg EK, Noodleman FR, Koperski JA, Pounds D, Farber EM. Source: International Journal of Hyperthermia : the Official Journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group. 1986 JulySeptember; 2(3): 231-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3794419&dopt=Abstract
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Comparison of narrow-band (311 nm) UVB and broad-band UVA after oral or bathwater 8-methoxypsoralen in the treatment of psoriasis. Author(s): Ortel B, Perl S, Kinaciyan T, Calzavara-Pinton PG, Honigsmann H. Source: Journal of the American Academy of Dermatology. 1993 November; 29(5 Pt 1): 736-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8227546&dopt=Abstract
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Comparison of trioxsalen bath and oral methoxsalen PUVA in psoriasis. Author(s): Turjanmaa K, Salo H, Reunala T. Source: Acta Dermato-Venereologica. 1985; 65(1): 86-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2578716&dopt=Abstract
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Complement C3 proteins in psoriasis. Author(s): Acevedo F, Hammar H. Source: The British Journal of Dermatology. 1989 September; 121(3): 329-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2508741&dopt=Abstract
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Complementary therapy for psoriasis. Author(s): Capella GL, Finzi AF. Source: Dermatologic Therapy. 2003 June; 16(2): 164-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12919118&dopt=Abstract
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Contact dermatitis in psoriasis due to propolis. Author(s): Silvani S, Spettoli E, Stacul F, Tosti A. Source: Contact Dermatitis. 1997 July; 37(1): 48-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9255499&dopt=Abstract
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Cost-effectiveness of Dead-Sea climatotherapy and balneophototherapy of psoriasis. Author(s): Gambichler T, Altmeyer P, Hoffmann K. Source: International Journal of Dermatology. 2001 February; 40(2): 158-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11328403&dopt=Abstract
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Current treatment options in psoriasis. Author(s): Khachemoune A, Phillips TJ. Source: Hosp Pract (Off Ed). 2000 July 15; 35(7): 93-6, 101-4, 107. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10916507&dopt=Abstract
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Dead-Sea climatotherapy versus other modalities of treatment for psoriasis: comparative cost-effectiveness. Author(s): Shani J, Harari M, Hristakieva E, Seidl V, Bar-Giyora J.
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Source: International Journal of Dermatology. 1999 April; 38(4): 252-62. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10321939&dopt=Abstract •
Dealing with the disadvantaged: psoriasis. Author(s): Henley LA. Source: British Medical Journal (Clinical Research Ed.). 1981 June 6; 282(6279): 1851-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6786650&dopt=Abstract
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Delayed-type hypersensitivity to contact allergens in psoriasis. A clinical evaluation. Author(s): Heule F, Tahapary GJ, Bello CR, van Joost T. Source: Contact Dermatitis. 1998 February; 38(2): 78-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9506219&dopt=Abstract
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Determination of solar ultraviolet dose in the Dead Sea treatment of psoriasis. Author(s): Even-Paz Z, Efron D. Source: Isr Med Assoc J. 2003 February; 5(2): 87-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12674654&dopt=Abstract
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Dietary supplementation with a combination of n-3 and n-6 fatty acids (super gammaoil marine) improves psoriasis. Author(s): Kragballe K. Source: Acta Dermato-Venereologica. 1989; 69(3): 265-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2566241&dopt=Abstract
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Differences in efficacy between intention-to-treat and per-protocol analyses for patients with psoriasis vulgaris and atopic dermatitis: clinical and pharmacoeconomic implications. Author(s): Schiffner R, Schiffner-Rohe J, Gerstenhauer M, Hofstadter F, Landthaler M, Stolz W. Source: The British Journal of Dermatology. 2001 June; 144(6): 1154-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422035&dopt=Abstract
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Do dietary supplements of fish oils improve psoriasis? Author(s): Wilkinson DI. Source: Cutis; Cutaneous Medicine for the Practitioner. 1990 October; 46(4): 334-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2148141&dopt=Abstract
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Eczema, ichthyosis, psoriasis: conditions of cornification. Author(s): Burdette-Taylor SR. Source: Ostomy Wound Manage. 1995 August; 41(7): 36-8, 40, 42. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7662092&dopt=Abstract
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Effect of dietary supplementation with n-3 fatty acids on clinical manifestations of psoriasis. Author(s): Bjorneboe A, Smith AK, Bjorneboe GE, Thune PO, Drevon CA. Source: The British Journal of Dermatology. 1988 January; 118(1): 77-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2829958&dopt=Abstract
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Effect of dietary supplementation with very-long-chain n-3 fatty acids in patients with psoriasis. Author(s): Soyland E, Funk J, Rajka G, Sandberg M, Thune P, Rustad L, Helland S, Middelfart K, Odu S, Falk ES, et al. Source: The New England Journal of Medicine. 1993 June 24; 328(25): 1812-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8502270&dopt=Abstract
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Effect of fish oil supplementation on erythrocyte lipid pattern, malondialdehyde production and glutathione-peroxidase activity in psoriasis. Author(s): Corrocher R, Ferrari S, de Gironcoli M, Bassi A, Olivieri O, Guarini P, Stanzial A, Barba AL, Gregolini L. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 1989 February 15; 179(2): 121-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2920445&dopt=Abstract
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Effect of heliotherapy on skin and joint symptoms in psoriasis: a 6-month follow-up study. Author(s): Snellman E, Lauharanta J, Reunanen A, Jansen CT, Jyrkinen-Pakkasvirta T, Kallio M, Luoma J, Aromaa A, Waal J. Source: The British Journal of Dermatology. 1993 February; 128(2): 172-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8457451&dopt=Abstract
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Effect of heliotherapy on the cost of psoriasis. Author(s): Snellman E, Maljanen T, Aromaa A, Reunanen A, Jyrkinen-Pakkasvirta T, Luoma J. Source: The British Journal of Dermatology. 1998 February; 138(2): 288-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9602876&dopt=Abstract
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Effect of highly purified eicosapentaenoic acid on psoriasis. Author(s): Kojima T, Terano T, Tanabe E, Okamoto S, Tamura Y, Yoshida S. Source: Journal of the American Academy of Dermatology. 1989 July; 21(1): 150-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2545748&dopt=Abstract
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Effect of psoriasis heliotherapy on epidermal urocanic acid isomer concentrations. Author(s): Snellman E, Koulu L, Pasanen P, Lammintausta K, Neuvonen K, Ayras P, Jansen CT.
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Effect of regular consumption of oily fish compared with white fish on chronic plaque psoriasis. Author(s): Collier PM, Ursell A, Zaremba K, Payne CM, Staughton RC, Sanders T. Source: European Journal of Clinical Nutrition. 1993 April; 47(4): 251-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8491161&dopt=Abstract
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Effectiveness of relaxation and visualization techniques as an adjunct to phototherapy and photochemotherapy of psoriasis. Author(s): Benhard JD, Kristeller J, Kabat-Zinn J. Source: Journal of the American Academy of Dermatology. 1988 September; 19(3): 572-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3049703&dopt=Abstract
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Effects of dietary supplementation with eicosapentaenoic acid in patients with psoriasis. Author(s): Maurice PD, Allen BR, Barkley A, Stammers J. Source: Adv Prostaglandin Thromboxane Leukot Res. 1987; 17B: 647-50. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2823563&dopt=Abstract
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Effects of dietary supplementation with polyunsaturated ethyl ester lipids (Angiosan) in patients with psoriasis and psoriatic arthritis. Author(s): Lassus A, Dahlgren AL, Halpern MJ, Santalahti J, Happonen HP. Source: J Int Med Res. 1990 January-February; 18(1): 68-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2139859&dopt=Abstract
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Effects of Mahonia aquifolium ointment on the expression of adhesion, proliferation, and activation markers in the skin of patients with psoriasis. Author(s): Augustin M, Andrees U, Grimme H, Schopf E, Simon J. Source: Forschende Komplementarmedizin. 1999 April; 6 Suppl 2: 19-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10352377&dopt=Abstract
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Effects of Medical Resonance Therapy Music on patients with psoriasis and neurodermatitis--a pilot study. Author(s): Lazaroff I, Shimshoni R. Source: Integrative Physiological and Behavioral Science : the Official Journal of the Pavlovian Society. 2000 July-September; 35(3): 189-98. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11286371&dopt=Abstract
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Effects of psychologic intervention on psoriasis: a preliminary report. Author(s): Zachariae R, Oster H, Bjerring P, Kragballe K.
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Efficacy of bimolane in the Malassezia ovalis model of psoriasis. Author(s): Xu B, Noah PW, Skinner RB Jr, Bale G, Chesney TM, Rosenberg EW. Source: The Journal of Dermatology. 1991 December; 18(12): 707-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1806601&dopt=Abstract
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Evaluation of a multicentre study of synchronous application of narrowband ultraviolet B phototherapy (TL-01) and bathing in Dead Sea salt solution for psoriasis vulgaris. Author(s): Schiffner R, Schiffner-Rohe J, Wolfl G, Landthaler M, Glassl A, Walther T, Hofstadter F, Stolz W. Source: The British Journal of Dermatology. 2000 April; 142(4): 740-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10792225&dopt=Abstract
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Evening primrose oil and marine oil in the treatment of psoriasis. Author(s): Oliwiecki S, Burton JL. Source: Clinical and Experimental Dermatology. 1994 March; 19(2): 127-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8050140&dopt=Abstract
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Experience with psoriasis in a psychosomatic dermatology clinic. Author(s): Polenghi MM, Molinari E, Gala C, Guzzi R, Garutti C, Finzi AF. Source: Acta Derm Venereol Suppl (Stockh). 1994; 186: 65-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8073842&dopt=Abstract
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Fish oil supplementation results in decreased hypertriglyceridemia in patients with psoriasis undergoing etretinate or acitretin therapy. Author(s): Ashley JM, Lowe NJ, Borok ME, Alfin-Slater RB. Source: Journal of the American Academy of Dermatology. 1988 July; 19(1 Pt 1): 76-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2969924&dopt=Abstract
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Formation of DNA adducts in the skin of psoriasis patients, in human skin in organ culture, and in mouse skin and lung following topical application of coal-tar and juniper tar. Author(s): Schoket B, Horkay I, Kosa A, Paldeak L, Hewer A, Grover PL, Phillips DH. Source: The Journal of Investigative Dermatology. 1990 February; 94(2): 241-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2299199&dopt=Abstract
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High-dose topical calcipotriol in the treatment of extensive psoriasis vulgaris. Author(s): Bourke JF, Berth-Jones J, Iqbal SJ, Hutchinson PE.
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Highly purified omega-3-polyunsaturated fatty acids for topical treatment of psoriasis. Results of a double-blind, placebo-controlled multicentre study. Author(s): Henneicke-von Zepelin HH, Mrowietz U, Farber L, Bruck-Borchers K, Schober C, Huber J, Lutz G, Kohnen R, Christophers E, Welzel D. Source: The British Journal of Dermatology. 1993 December; 129(6): 713-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8286257&dopt=Abstract
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HLA system and therapy of psoriasis. Author(s): Zlatkov NB, Minev M, Dourmishev AL, Martinova F. Source: Dermatologica. 1983; 166(3): 156-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6852329&dopt=Abstract
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Improvement of psoriasis vulgaris after intralesional injections of 15hydroxyeicosatetraenoic acid (15-HETE). Author(s): Fogh K, Sogaard H, Herlin T, Kragballe K. Source: Journal of the American Academy of Dermatology. 1988 February; 18(2 Pt 1): 279-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3346412&dopt=Abstract
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Increased erythrocyte glutathione peroxidase activity in psoriatics consuming highselenium drinking water at the Dead-Sea Psoriasis Treatment Center. Author(s): Shani J, Livshitz T, Robberecht H, Van Grieken R, Rubinstein N, Even-Paz Z. Source: Pharmacol Res Commun. 1985 May; 17(5): 479-88. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4034629&dopt=Abstract
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Influence of a mindfulness meditation-based stress reduction intervention on rates of skin clearing in patients with moderate to severe psoriasis undergoing phototherapy (UVB) and photochemotherapy (PUVA). Author(s): Kabat-Zinn J, Wheeler E, Light T, Skillings A, Scharf MJ, Cropley TG, Hosmer D, Bernhard JD. Source: Psychosomatic Medicine. 1998 September-October; 60(5): 625-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9773769&dopt=Abstract
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Influence of water and salt solutions on UVB irradiation of normal skin and psoriasis. Author(s): Boer J, Schothorst AA, Boom B, Hermans J, Suurmond D. Source: Archives of Dermatological Research. 1982; 273(3-4): 247-59. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7165354&dopt=Abstract
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Intestinal permeability in patients with psoriasis. Author(s): Humbert P, Bidet A, Treffel P, Drobacheff C, Agache P. Source: Journal of Dermatological Science. 1991 July; 2(4): 324-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1911568&dopt=Abstract
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Kangal hot spring with fish and psoriasis treatment. Author(s): Ozcelik S, Polat HH, Akyol M, Yalcin AN, Ozcelik D, Marufihah M. Source: The Journal of Dermatology. 2000 June; 27(6): 386-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10920584&dopt=Abstract
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Know your organizations: the Psoriasis Association. Author(s): Henley L. Source: Health Visit. 1982 January; 55(1): 21. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6915913&dopt=Abstract
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Lack of consensus among experts on the choice of UV therapy for psoriasis. Author(s): Stern RS, Beer JZ, Mills DK. Source: Archives of Dermatology. 1999 October; 135(10): 1187-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10522665&dopt=Abstract
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Lesional elastase activity in psoriasis. Diagnostic and prognostic significance. Author(s): Wiedow O, Wiese F, Christophers E. Source: Archives of Dermatological Research. 1995; 287(7): 632-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8534125&dopt=Abstract
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Lithium-associated psoriasis and omega-3 fatty acids. Author(s): Akkerhuis GW, Nolen WA. Source: The American Journal of Psychiatry. 2003 July; 160(7): 1355. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12832259&dopt=Abstract
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Long-term administration of highly purified eicosapentaenoic acid provides improvement of psoriasis. Author(s): Kojima T, Terano T, Tanabe E, Okamoto S, Tamura Y, Yoshida S. Source: Dermatologica. 1991; 182(4): 225-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1884857&dopt=Abstract
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Long-term local trioxsalen photochemotherapy in psoriasis. Author(s): Vaatainen N, Hannuksela M, Karvonen J. Source: Dermatologica. 1981; 163(3): 229-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7286362&dopt=Abstract
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Long-term outcome of severe chronic plaque psoriasis following treatment with highdose topical calcipotriol. Author(s): Bleiker TO, Bourke JF, Mumford R, Hutchinson PE. Source: The British Journal of Dermatology. 1998 August; 139(2): 285-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9767244&dopt=Abstract
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Low prevalences of coronary heart disease (CHD), psoriasis, asthma and rheumatoid arthritis in Eskimos: are they caused by high dietary intake of eicosapentaenoic acid (EPA), a genetic variation of essential fatty acid (EFA) metabolism or a combination of both? Author(s): Horrobin DF. Source: Medical Hypotheses. 1987 April; 22(4): 421-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3035353&dopt=Abstract
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Low-dose narrow-band UVB phototherapy combined with topical therapy is effective in psoriasis and does not inhibit systemic T-cell activation. Author(s): de Rie MA, Out TA, Bos JD. Source: Dermatology (Basel, Switzerland). 1998; 196(4): 412-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9669117&dopt=Abstract
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Malignant tumours and psoriasis: climatotherapy at the Dead Sea. Author(s): Frentz G, Olsen JH, Avrach WW. Source: The British Journal of Dermatology. 1999 December; 141(6): 1088-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10606857&dopt=Abstract
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Management of psoriasis with Aloe vera extract in a hydrophilic cream: a placebocontrolled, double-blind study. Author(s): Syed TA, Ahmad SA, Holt AH, Ahmad SA, Ahmad SH, Afzal M. Source: Tropical Medicine & International Health : Tm & Ih. 1996 August; 1(4): 505-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8765459&dopt=Abstract
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Many patients with psoriasis use sunbeds. Author(s): Turner RJ, Farr PM, Walshaw D. Source: Bmj (Clinical Research Ed.). 1998 August 8; 317(7155): 412. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9694766&dopt=Abstract
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Melanosis coli: a consequence of “alternative therapy” for psoriasis. Author(s): Bertram PD. Source: The American Journal of Gastroenterology. 1993 June; 88(6): 971. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8503405&dopt=Abstract
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n-3 fatty acids in psoriasis. Author(s): Mayser P, Grimm H, Grimminger F.
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Neovastat (AE-941), an inhibitor of angiogenesis: Randomized phase I/II clinical trial results in patients with plaque psoriasis. Author(s): Sauder DN, Dekoven J, Champagne P, Croteau D, Dupont E. Source: Journal of the American Academy of Dermatology. 2002 October; 47(4): 535-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12271297&dopt=Abstract
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Neuroimmunologic aspects of psoriasis. Author(s): Raychaudhuri SP, Farber EM. Source: Cutis; Cutaneous Medicine for the Practitioner. 2000 November; 66(5): 357-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11107521&dopt=Abstract
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Neuropathogenesis and neuropharmacology of psoriasis. Author(s): Raychaudhuri SP, Rein G, Farber EM. Source: International Journal of Dermatology. 1995 October; 34(10): 685-93. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8537154&dopt=Abstract
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Non-aromatic naphthalane preparation; preliminary clinical study in the treatment of psoriasis vulgaris. Author(s): Alajbeg I, Krnjevic-Pezic G, Smeh-Skrbin A, Vrzogic P, Vucicevic-Boras V, Dobric I, Cekic-Arambasin A. Source: Journal of Pharmaceutical and Biomedical Analysis. 2001 December; 26(5-6): 801-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11600291&dopt=Abstract
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Observations on effect of Fructus Psoraleae injection in 800 cases of psoriasis. Author(s): Lu YT. Source: J Tradit Chin Med. 1983 September; 3(3): 229-30. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6556410&dopt=Abstract
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Omega-3 fatty acid-based lipid infusion in patients with chronic plaque psoriasis: results of a double-blind, randomized, placebo-controlled, multicenter trial. Author(s): Mayser P, Mrowietz U, Arenberger P, Bartak P, Buchvald J, Christophers E, Jablonska S, Salmhofer W, Schill WB, Kramer HJ, Schlotzer E, Mayer K, Seeger W, Grimminger F. Source: Journal of the American Academy of Dermatology. 1998 April; 38(4): 539-47. Erratum In: J Am Acad Dermatol 1998 September; 39(3): 421. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9555791&dopt=Abstract
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Phototherapy of psoriasis: comparative experience of different phototherapeutic approaches. Author(s): Karrer S, Eholzer C, Ackermann G, Landthaler M, Szeimies RM. Source: Dermatology (Basel, Switzerland). 2001; 202(2): 108-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11306830&dopt=Abstract
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Physical and psychologic measures are necessary to assess overall psoriasis severity. Author(s): Kirby B, Richards HL, Woo P, Hindle E, Main CJ, Griffiths CE. Source: Journal of the American Academy of Dermatology. 2001 July; 45(1): 72-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11423838&dopt=Abstract
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Physical illness and the family emotional system: psoriasis as a model. Author(s): Kerr ME. Source: Behavioral Medicine (Washington, D.C.). 1992 Fall; 18(3): 101-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1421744&dopt=Abstract
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Plasma levels of 8-methoxypsoralen after bath-PUVA for psoriasis: relationship to disease severity. Author(s): Gomez MI, Azana JM, Arranz I, Harto A, Ledo A. Source: The British Journal of Dermatology. 1995 July; 133(1): 37-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7669638&dopt=Abstract
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Preliminary report on the therapeutic effect of khellin in psoriasis. Author(s): Abdel-Fattah A, Aboul-Enein MN, Wassel G, El-Menshawi B. Source: Dermatologica. 1983; 167(2): 109-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6628802&dopt=Abstract
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Psoriasis and altered calcium metabolism: downregulated capacitative calcium influx and defective calcium-mediated cell signaling in cultured psoriatic keratinocytes. Author(s): Karvonen SL, Korkiamaki T, Yla-Outinen H, Nissinen M, Teerikangas H, Pummi K, Karvonen J, Peltonen J. Source: The Journal of Investigative Dermatology. 2000 April; 114(4): 693-700. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10733675&dopt=Abstract
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Psoriasis and contact allergy to propolis. Author(s): Angelini G, Vena GA, Meneghini CL. Source: Contact Dermatitis. 1987 October; 17(4): 251-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2962827&dopt=Abstract
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Psoriasis and the doctor fish. Author(s): Kurkcuoglu N, Oz G.
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Psoriasis in China. Author(s): Lin XR. Source: The Journal of Dermatology. 1993 December; 20(12): 746-55. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8120236&dopt=Abstract
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Psoriasis remission time at the Dead Sea. Author(s): Abels DJ, Harari M. Source: Journal of the American Academy of Dermatology. 2000 August; 43(2 Pt 1): 3256. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10906666&dopt=Abstract
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Psoriasis treatment at the Dead Sea: Second International Study Tour. Author(s): Abel EA, Barnes S, Le Vine MJ, Seidman DR, Wallk S. Source: Journal of the American Academy of Dermatology. 1988 August; 19(2 Pt 1): 3624. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3170803&dopt=Abstract
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Psoriasis treatment: bathing in a thermal lagoon combined with UVB, versus UVB treatment only. Author(s): Olafsson JH, Sigurgeirsson B, Palsdottir R. Source: Acta Dermato-Venereologica. 1996 May; 76(3): 228-30. Erratum In: Acta Derm Venereol 1997 May; 77(3): 253. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8800306&dopt=Abstract
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Psoriasis. Author(s): Blake J. Source: Prof Nurse. 2002 November; 18(3): 133-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12465536&dopt=Abstract
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Psoriasis: a stress-related disease. Author(s): Farber EM, Nall L. Source: Cutis; Cutaneous Medicine for the Practitioner. 1993 May; 51(5): 322-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8513683&dopt=Abstract
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Psoriasis: current concepts and new approaches to therapy. Author(s): Das UN, Vijaykumar K, Madhavi N, Suryaprabha P, Sravankumar G, Ramesh G, Koratkar R, Sagar PS, Padma M.
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Psoriasis--a dermatological enigma. Author(s): Zivkovic D. Source: Acta Med Croatica. 1998; 52(4-5): 199-202. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9988896&dopt=Abstract
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Psoriasis--a disease with no benefits. Author(s): Mangan P. Source: Nursing Standard : Official Newspaper of the Royal College of Nursing. 1990 April 11-17; 4(29): 25-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2109233&dopt=Abstract
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Psychological and psychophysiological aspects of psoriasis. Author(s): Ginsburg IH. Source: Dermatologic Clinics. 1995 October; 13(4): 793-804. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8785884&dopt=Abstract
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Psychological stress and psoriasis: experimental and prospective correlational studies. Author(s): Gaston L, Crombez JC, Lassonde M, Bernier-Buzzanga J, Hodgins S. Source: Acta Derm Venereol Suppl (Stockh). 1991; 156: 37-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2048373&dopt=Abstract
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PUVA therapy for psoriasis: comparison of oral and bath-water delivery of 8methoxypsoralen. Author(s): Lowe NJ, Weingarten D, Bourget T, Moy LS. Source: Journal of the American Academy of Dermatology. 1986 May; 14(5 Pt 1): 754-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3711379&dopt=Abstract
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Reduced density of T6-positive epidermal Langerhans' cells in uninvolved skin of patients with psoriasis. Author(s): Oxholm A, Oxholm P, Staberg B. Source: Acta Dermato-Venereologica. 1987; 67(1): 8-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2436422&dopt=Abstract
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Relaxation therapies in the treatment of psoriasis and possible pathophysiologic mechanisms. Author(s): Winchell SA, Watts RA.
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Source: Journal of the American Academy of Dermatology. 1988 January; 18(1 Pt 1): 1014. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3279078&dopt=Abstract •
Remarkable success of Chinese herbs in combination with a short course of low-dose narrow-band UVB phototherapy in severe recalcitrant plaque psoriasis. Author(s): Tjioe M, Gerritsen MJ, van de Kerkhof PC. Source: Acta Dermato-Venereologica. 2002; 82(4): 299-300. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12361138&dopt=Abstract
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Safety and effectiveness of an aggressive and individualized bath-PUVA regimen in the treatment of psoriasis. Author(s): Calzavara-Pinton PG, Ortel B, Honigsmann H, Zane C, De Panfilis G. Source: Dermatology (Basel, Switzerland). 1994; 189(3): 256-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7949478&dopt=Abstract
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Safety and efficacy of combined high-dose treatment with calcipotriol ointment and solution in patients with psoriasis. Author(s): Van de Kerkhof PC, Green C, Hamberg KJ, Hutchinson PE, Jensen JK, Kidson P, Kragballe K, Larsen FG, Munro CS, Tillman DM. Source: Dermatology (Basel, Switzerland). 2002; 204(3): 214-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12037450&dopt=Abstract
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Saline Spa water and UV-B for psoriasis. Author(s): Boer J. Source: Archives of Dermatology. 2002 July; 138(7): 979-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12071833&dopt=Abstract
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Saline spa water or combined water and UV-B for psoriasis vs conventional UV-B: lessons from the Salies de Bearn randomized study. Author(s): Leaute-Labreze C, Saillour F, Chene G, Cazenave C, Luxey-Bellocq ML, Sanciaume C, Toussaint JF, Taieb A. Source: Archives of Dermatology. 2001 August; 137(8): 1035-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11493096&dopt=Abstract
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Serum bromine levels in psoriasis. Author(s): Shani J, Barak S, Ram M, Levi D, Pfeifer Y, Schlesinger T, Avrach WW, Robberecht H, Van Grieken R. Source: Pharmacology. 1982; 25(6): 297-307. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7156179&dopt=Abstract
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Short-term methotrexate therapy in psoriasis: a study of 197 patients. Author(s): Kumar B, Saraswat A, Kaur I.
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Source: International Journal of Dermatology. 2002 July; 41(7): 444-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12121564&dopt=Abstract •
Simple chemiluminescence assays for free radicals in venous blood and serum samples: results in atopic, psoriasis, MCS and cancer patients. Author(s): Ionescu G, Merk M, Bradford R. Source: Forschende Komplementarmedizin. 1999 December; 6(6): 294-300. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10649000&dopt=Abstract
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Skin cancer and climatotherapy in psoriasis. Author(s): Even-Paz Z, Efron D. Source: The British Journal of Dermatology. 2001 January; 144(1): 202. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11167717&dopt=Abstract
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Skin cancer in patients with psoriasis-many intertwined risk factors. Author(s): Murphy GM. Source: The British Journal of Dermatology. 1999 December; 141(6): 1001-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10606842&dopt=Abstract
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Standard and innovative therapy of psoriasis. Author(s): Geilen CC, Orfanos CE. Source: Clin Exp Rheumatol. 2002 November-December; 20(6 Suppl 28): S81-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12463454&dopt=Abstract
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Stress and psoriasis. Author(s): Kantor SD. Source: Cutis; Cutaneous Medicine for the Practitioner. 1990 October; 46(4): 321-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2261790&dopt=Abstract
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Stress and psoriasis. Psychoneuroimmunologic mechanisms. Author(s): Farber EM, Rein G, Lanigan SW. Source: International Journal of Dermatology. 1991 January; 30(1): 8-12. Review. Erratum In: Int J Dermatol 1991 April; 30(4): 270. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1993574&dopt=Abstract
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Studies on tabellae indigo naturalis in treatment of psoriasis. Author(s): Yuan ZZ, Yuan X, Xu ZX. Source: J Tradit Chin Med. 1982 December; 2(4): 306. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6765729&dopt=Abstract
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Supervised four-week heliotherapy alleviates the long-term course of psoriasis. Author(s): Snellman E, Aromaa A, Jansen CT, Lauharanta J, Reunanen A, JyrkinenPakkasvirta T, Luoma J, Waal J. Source: Acta Dermato-Venereologica. 1993 October; 73(5): 388-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7904411&dopt=Abstract
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Systemic aspects of psoriasis. An integrative model based on intestinal etiology. Author(s): Mcmillin DL, Richards DG, Mein EA, Nelson CD. Source: Integr. Med. 2000 March 21; 2(2): 105-113. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10882884&dopt=Abstract
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The Blue Lagoon in Iceland and psoriasis. Author(s): Olafsson JH. Source: Clinics in Dermatology. 1996 November-December; 14(6): 647-51. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8960807&dopt=Abstract
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The cost of psoriasis treatment at the Dead Sea. Author(s): Weinrauch L. Source: International Journal of Dermatology. 1996 February; 35(2): 150-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8850054&dopt=Abstract
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The Dead Sea and psoriasis. Historical and geographic background. Author(s): Even-Paz Z, Shani J. Source: International Journal of Dermatology. 1989 January-February; 28(1): 1-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2645224&dopt=Abstract
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The effect of highly purified eicosapentaenoic acid in patients with psoriasis. Author(s): Terano T, Kojima T, Seya A, Tanabe E, Hirai A, Makuta H, Ozawa A, Fujita T, Tamura Y, Okamoto S, et al. Source: Adv Prostaglandin Thromboxane Leukot Res. 1989; 19: 610-3. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2546400&dopt=Abstract
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The effect of supplementation with selenium and vitamin E in psoriasis. Author(s): Fairris GM, Lloyd B, Hinks L, Perkins PJ, Clayton BE. Source: Annals of Clinical Biochemistry. 1989 January; 26 ( Pt 1): 83-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2735752&dopt=Abstract
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The effectiveness of modified ingram therapy compared with severity of psoriasis. Author(s): Youn JI, Kim BK, Suh DH.
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Source: The Journal of Dermatology. 1998 February; 25(2): 112-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9563279&dopt=Abstract •
The effects of dietary supplementation with fish oil in patients with psoriasis. Author(s): Maurice PD, Allen BR, Barkley AS, Cockbill SR, Stammers J, Bather PC. Source: The British Journal of Dermatology. 1987 November; 117(5): 599-606. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3689678&dopt=Abstract
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The efficacy of a new topical treatment for psoriasis: Mirak. Author(s): Seyger MM, van de Kerkhof PC, van Vlijmen-Willems IM, de Bakker ES, Zwiers F, de Jong EM. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 1998 July; 11(1): 13-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9731960&dopt=Abstract
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The fern Polypodium decumanum, used in the treatment of psoriasis, and its fatty acid constituents as inhibitors of leukotriene B4 formation. Author(s): Vasange-Tuominen M, Perera-Ivarsson P, Shen J, Bohlin L, Rolfsen W. Source: Prostaglandins, Leukotrienes, and Essential Fatty Acids. 1994 May; 50(5): 279-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8066104&dopt=Abstract
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The impact of psoriasis on psychosocial life domains. A review. Author(s): Wahl A. Source: Scandinavian Journal of Caring Sciences. 1997; 11(4): 243-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9505733&dopt=Abstract
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The role of psychoneuroimmunology in the pathogenesis of psoriasis. Author(s): Farber EM, Lanigan SW, Rein G. Source: Cutis; Cutaneous Medicine for the Practitioner. 1990 October; 46(4): 314-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2261789&dopt=Abstract
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The use of folic acid supplementation in psoriasis patients receiving methotrexate: a survey in the United Kingdom. Author(s): Kirby B, Lyon CC, Griffiths CE, Chalmers RJ. Source: Clinical and Experimental Dermatology. 2000 June; 25(4): 265-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10971481&dopt=Abstract
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Thymostimulin in treatment of psoriasis. Author(s): Pedragosa R, Vidal J. Source: Archives of Dermatology. 1986 June; 122(6): 624. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3717970&dopt=Abstract
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Topical camptothecine in treatment of psoriasis. Author(s): Lin XR, Huang T. Source: International Journal of Dermatology. 1988 September; 27(7): 475-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3220628&dopt=Abstract
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Topical podophyllotoxin in psoriasis vulgaris. Author(s): Wantke F, Fleischl G, Gotz M, Jarisch R. Source: Dermatology (Basel, Switzerland). 1993; 186(1): 79. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8435525&dopt=Abstract
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Total care of psoriasis. Author(s): Farber EM. Source: Cutis; Cutaneous Medicine for the Practitioner. 2000 November; 66(5): 318. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11107512&dopt=Abstract
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Traditional medicine as a source of new therapeutic agents against psoriasis. Author(s): Amenta R, Camarda L, Di Stefano V, Lentini F, Venza F. Source: Fitoterapia. 2000 August; 71 Suppl 1: S13-20. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10930708&dopt=Abstract
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Treatment of psoriasis at a Dead Sea dermatology clinic. Author(s): Abels DJ, Rose T, Bearman JE. Source: International Journal of Dermatology. 1995 February; 34(2): 134-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7737775&dopt=Abstract
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Treatment of psoriasis at the Dead Sea: why, how and when? Author(s): David M, Efron D, Hodak E, Even-Paz Z. Source: Isr Med Assoc J. 2000 March; 2(3): 232-4. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10774275&dopt=Abstract
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Treatment of psoriasis by cyclosporine and grapefruit juice. Author(s): Taniguchi S, Kobayashi H, Ishii M. Source: Archives of Dermatology. 1996 October; 132(10): 1249. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8859044&dopt=Abstract
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Treatment of psoriasis in the Nordic countries: a questionnaire survey from 5739 members of the psoriasis associations data from the Nordic Quality of Life Study. Author(s): Zachariae H, Zachariae R, Blomqvist K, Davidsson S, Molin L, Mork C, Sigurgeirsson B. Source: Acta Dermato-Venereologica. 2001 May; 81(2): 116-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11501648&dopt=Abstract
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Treatment of psoriasis with calcipotriene plus psoralen-UV-A-bath therapy. Author(s): Grundmann-Kollmann M, Behrens S, Krahn G, Leiter U, Ochsendorf F, Kaufmann R, Peter RU, Kerscher M. Source: Archives of Dermatology. 1999 July; 135(7): 861-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10411175&dopt=Abstract
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Treatment of psoriasis with polyethylene sheet bath PUVA. Author(s): Streit V, Wiedow O, Christophers E. Source: Journal of the American Academy of Dermatology. 1996 August; 35(2 Pt 1): 20810. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8708022&dopt=Abstract
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Trimethylpsoralen bath plus ultraviolet A combined with oral retinoid (etretinate) in the treatment of severe psoriasis. Author(s): Vaatainen N, Hollmen A, Fraki JE. Source: Journal of the American Academy of Dermatology. 1985 January; 12(1 Pt 1): 525. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3980803&dopt=Abstract
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Trioxsalen bath plus UVA effective and safe in the treatment of psoriasis. Author(s): Hannuksela M, Karvonen J. Source: The British Journal of Dermatology. 1978 December; 99(6): 703-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=737133&dopt=Abstract
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Trioxsalen bath plus UVA treatment of psoriasis. Plasma concentration of the drug and clinical results. Author(s): Salo OP, Lassus A, Taskinen J. Source: Acta Dermato-Venereologica. 1981; 61(6): 551-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6177169&dopt=Abstract
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Use of alternative medicine by patients with atopic dermatitis and psoriasis. Author(s): Jensen P. Source: Acta Dermato-Venereologica. 1990; 70(5): 421-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1980977&dopt=Abstract
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Use of alternative treatments by patients with psoriasis. Author(s): Clark CM, Mckay RA, Fortune DG, Griffiths CE. Source: The British Journal of General Practice : the Journal of the Royal College of General Practitioners. 1998 December; 48(437): 1873-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10198517&dopt=Abstract
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Use of common Chinese herbs in the treatment of psoriasis. Author(s): Tse TW.
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Source: Clinical and Experimental Dermatology. 2003 September; 28(5): 469-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12950329&dopt=Abstract •
Using aromatherapy in the management of psoriasis. Author(s): Walsh D. Source: Nursing Standard : Official Newspaper of the Royal College of Nursing. 1996 December 18; 11(13-15): 53-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9000946&dopt=Abstract
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Vindesine for psoriasis? Author(s): Hardi R, Slavik M. Source: Lancet. 1981 April 4; 1(8223): 773. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6110967&dopt=Abstract
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Vitamin B(12) cream containing avocado oil in the therapy of plaque psoriasis. Author(s): Stucker M, Memmel U, Hoffmann M, Hartung J, Altmeyer P. Source: Dermatology (Basel, Switzerland). 2001; 203(2): 141-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11586013&dopt=Abstract
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Willingness to pay and time trade-off: sensitive to changes of quality of life in psoriasis patients? Author(s): Schiffner R, Schiffner-Rohe J, Gerstenhauer M, Hofstadter F, Landthaler M, Stolz W. Source: The British Journal of Dermatology. 2003 June; 148(6): 1153-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828743&dopt=Abstract
Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •
Alternative Medicine Foundation, Inc.: http://www.herbmed.org/
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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
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Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMDHealth: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
The following is a specific Web list relating to psoriasis; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
General Overview Acne Source: Prima Communications, Inc.www.personalhealthzone.com Allergies and Sensitivities Source: Healthnotes, Inc. www.healthnotes.com Candidiasis Source: Integrative Medicine Communications; www.drkoop.com Dermatitis Source: Integrative Medicine Communications; www.drkoop.com Photodermatitis Source: Integrative Medicine Communications; www.drkoop.com Psoriasis Source: Healthnotes, Inc. www.healthnotes.com Psoriasis Source: Integrative Medicine Communications; www.drkoop.com Psoriasis Source: Prima Communications, Inc.www.personalhealthzone.com Sunburn Source: Integrative Medicine Communications; www.drkoop.com Yeast Infection Source: Integrative Medicine Communications; www.drkoop.com
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Alternative Therapy Acupuncture Source: Healthnotes, Inc. www.healthnotes.com Aromatherapy Source: Integrative Medicine Communications; www.drkoop.com
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Light therapy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,713,00.html Meditation Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,717,00.html Relaxation Techniques Source: Integrative Medicine Communications; www.drkoop.com •
Homeopathy Arsenicum album Source: Healthnotes, Inc. www.healthnotes.com Calcarea carbonica Source: Healthnotes, Inc. www.healthnotes.com Graphites Source: Healthnotes, Inc. www.healthnotes.com Mercurius solubilis Source: Healthnotes, Inc. www.healthnotes.com Mezereum Source: Healthnotes, Inc. www.healthnotes.com Petroleum Source: Healthnotes, Inc. www.healthnotes.com Rhus toxicodendron Source: Healthnotes, Inc. www.healthnotes.com Sepia Source: Healthnotes, Inc. www.healthnotes.com Staphysagria Source: Healthnotes, Inc. www.healthnotes.com Sulphur Source: Healthnotes, Inc. www.healthnotes.com
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Herbs and Supplements Adrenal Extract Source: Healthnotes, Inc. www.healthnotes.com
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ALA Source: Integrative Medicine Communications; www.drkoop.com Aloe Alternative names: Aloe vera L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Aloe Alternative names: Aloe vera, Aloe barbadensis Source: Healthnotes, Inc. www.healthnotes.com Aloe Alternative names: Aloe vera, Aloe barbadensis, Aloe ferox , Aloe Vera Source: Integrative Medicine Communications; www.drkoop.com Aloe Source: Prima Communications, Inc.www.personalhealthzone.com Aloe Vera Source: Integrative Medicine Communications; www.drkoop.com Aloe vera Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10001,00.html Alpha-Linolenic Acid (ALA) Source: Integrative Medicine Communications; www.drkoop.com Anthralin Source: Healthnotes, Inc. www.healthnotes.com Arnica Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,753,00.html Barberry Alternative names: Berberis vulgaris Source: Healthnotes, Inc. www.healthnotes.com Barberry Alternative names: Berberis vulgaris, Berberry Source: Integrative Medicine Communications; www.drkoop.com Berberis vulgaris Source: Integrative Medicine Communications; www.drkoop.com Berberry Source: Integrative Medicine Communications; www.drkoop.com
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Beta-Carotene Source: Prima Communications, Inc.www.personalhealthzone.com Beta-carotene Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10103,00.html Blue Flag Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Blue-green Algae Source: Integrative Medicine Communications; www.drkoop.com Brahmi Alternative names: Centella asiatica , Centella, March Pennywort, Indian Pennywort, Hydrocotyle, Brahmi (Sanskrit), Luei Gong Gen (Chinese)(Note: Gotu kola should not be confused with kola nut.) Source: Integrative Medicine Communications; www.drkoop.com Burdock Blend Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Calciferol Source: Integrative Medicine Communications; www.drkoop.com Calcitrol Source: Integrative Medicine Communications; www.drkoop.com Calendula Alternative names: Calendula officinalis L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Capsaicin Source: Integrative Medicine Communications; www.drkoop.com Capsicum frutescens Source: Integrative Medicine Communications; www.drkoop.com Cayenne Alternative names: Capsicum annuum, Capsicum frutescens Source: Healthnotes, Inc. www.healthnotes.com Cayenne Alternative names: Capsicum frutescens, Capsicum spp., Capsaicin, Chili Pepper, Red Pepper Source: Integrative Medicine Communications; www.drkoop.com Cayenne Source: WholeHealthMD.com, LLC. www.wholehealthmd.com
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Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,765,00.html Centella Alternative names: Gotu Kola; Centella asiatica (Linn.) Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Centella Source: Integrative Medicine Communications; www.drkoop.com Centella asiatica Alternative names: Centella asiatica , Centella, March Pennywort, Indian Pennywort, Hydrocotyle, Brahmi (Sanskrit), Luei Gong Gen (Chinese)(Note: Gotu kola should not be confused with kola nut.) Source: Integrative Medicine Communications; www.drkoop.com Chickweed Alternative names: Stellaria media Source: Healthnotes, Inc. www.healthnotes.com Chili Pepper Source: Integrative Medicine Communications; www.drkoop.com Cholecalciferol Source: Integrative Medicine Communications; www.drkoop.com Cleavers Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Coleus Alternative names: Coleus forskohlii Source: Healthnotes, Inc. www.healthnotes.com Coleus forskohlii Source: Prima Communications, Inc.www.personalhealthzone.com Corticosteroids Source: Healthnotes, Inc. www.healthnotes.com Docosahexaenoic Acid Source: Healthnotes, Inc. www.healthnotes.com Eicosapentaenoic Acid (EPA) Alternative names: EPA Source: Integrative Medicine Communications; www.drkoop.com EPA Alternative names: Eicosapentaenoic Acid (EPA) Source: Integrative Medicine Communications; www.drkoop.com
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Erocalciferol Source: Integrative Medicine Communications; www.drkoop.com Forskolin Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10025,00.html Fumaric Acid Source: Healthnotes, Inc. www.healthnotes.com German Chamomile Alternative names: Matricaria recutita Source: Integrative Medicine Communications; www.drkoop.com Glutamine Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10030,00.html Gotu Kola Alternative names: Centella asiatica , Centella, March Pennywort, Indian Pennywort, Hydrocotyle, Brahmi (Sanskrit), Luei Gong Gen (Chinese)(Note: Gotu kola should not be confused with kola nut.) Source: Integrative Medicine Communications; www.drkoop.com Grape seed extract Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,793,00.html Green-Lipped Mussel Source: Healthnotes, Inc. www.healthnotes.com Hydrocotyle Source: Integrative Medicine Communications; www.drkoop.com Indian Pennywort Source: Integrative Medicine Communications; www.drkoop.com Juniperus Alternative names: Juniper; Juniperus sp. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Licorice Source: Prima Communications, Inc.www.personalhealthzone.com Mahonia Alternative names: Mahonia aquifolium Source: Alternative Medicine Foundation, Inc. www.amfoundation.org
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Marsh Pennywort Alternative names: Centella asiatica , Centella, March Pennywort, Indian Pennywort, Hydrocotyle, Brahmi (Sanskrit), Luei Gong Gen (Chinese)(Note: Gotu kola should not be confused with kola nut.) Source: Integrative Medicine Communications; www.drkoop.com Matricaria recutita Source: Integrative Medicine Communications; www.drkoop.com Methotrexate Source: Healthnotes, Inc. www.healthnotes.com Methotrexate Alternative names: Rheumatrex Source: Prima Communications, Inc.www.personalhealthzone.com Milk Thistle Source: Prima Communications, Inc.www.personalhealthzone.com Milk thistle Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10044,00.html NAC (N-acetylcysteine) Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,809,00.html Oral Corticosteroids Source: Healthnotes, Inc. www.healthnotes.com Oregon Grape Alternative names: Berberis aquifolium Source: Healthnotes, Inc. www.healthnotes.com Organ Mountain Crape Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Pregnenolone Source: Healthnotes, Inc. www.healthnotes.com Red Clover Alternative names: Trifolium pratense Source: Healthnotes, Inc. www.healthnotes.com Red Clover Alternative names: Trifolium pratense, beebread, cow clover, cow grass, meadow clover, purple clover Source: Integrative Medicine Communications; www.drkoop.com
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Red Clover Source: Prima Communications, Inc.www.personalhealthzone.com Red Pepper Source: Integrative Medicine Communications; www.drkoop.com Sarsaparilla Alternative names: Smilax spp. Source: Healthnotes, Inc. www.healthnotes.com Sarsaparilla Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Shark Cartilage Source: Integrative Medicine Communications; www.drkoop.com Spirulina Alternative names: Blue-green Algae Source: Integrative Medicine Communications; www.drkoop.com Taurine Source: Prima Communications, Inc.www.personalhealthzone.com Topical Corticosteroids Source: Healthnotes, Inc. www.healthnotes.com Yellow Dock Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Zizyphus Alternative names: Jujube; Ziziphus sp. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 4. DISSERTATIONS ON PSORIASIS Overview In this chapter, we will give you a bibliography on recent dissertations relating to psoriasis. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “psoriasis” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on psoriasis, we have not necessarily excluded non-medical dissertations in this bibliography.
Dissertations on Psoriasis ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to psoriasis. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •
A Coping Skills Short-term Psychotherapy Group for Psoriasis Patients: Understanding and Coping with the Psychological and Physical Effects of Psoriasis by Dowling, Vickie Lynn; Psyd from Alliant International University, San Diego, 2002, 228 pages http://wwwlib.umi.com/dissertations/fullcit/3069405
•
Association of Hl-a17 and Hl-a13 with Guttate Psoriasis: the Autoimmune Reaction As a Mechanism of Differential Disease Susceptibility. by Williams, Robert Charles, Phd from The University of Michigan, 1976, 246 pages http://wwwlib.umi.com/dissertations/fullcit/7619274
•
Immunopathology of Human Skin: Adapting Recent Advances in Immunobiology to the Specialized Environment of the Skin (with Emphasis on Nk, Nk T-cells, and Psoriasis) by Bonish, Brian K. Phd from Loyola University of Chicago, 2003, 155 pages http://wwwlib.umi.com/dissertations/fullcit/3085067
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•
Studies on Vitamin a Signaling in Psoriasis: a Comparison between Normal and Lesional Keratinocytes by Karlsson, Teresa; Phd from Uppsala Universitet (sweden), 2002, 63 pages http://wwwlib.umi.com/dissertations/fullcit/f661121
•
The Asebia Mouse a New Animal Model Psoriasis by Brown, William Roy; Phd from University of Guelph (canada), 1983 http://wwwlib.umi.com/dissertations/fullcit/NK63428
Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.
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CHAPTER 5. CLINICAL TRIALS AND PSORIASIS Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning psoriasis.
Recent Trials on Psoriasis The following is a list of recent trials dedicated to psoriasis.8 Further information on a trial is available at the Web site indicated. •
Characterizing Serum Protein Patterns in Selected Skin Diseases Condition(s): Psoriasis; Cutaneous T-Cell Lymphoma; Healthy Study Status: This study is currently recruiting patients. Sponsor(s): National Cancer Institute (NCI) Purpose - Excerpt: The purpose of this study is to determine whether computer-aided analysis of proteins found in the blood can distinguish between the serum protein patterns in healthy patients versus patients with selected skin diseases, either psoriasis or cutaneous T cell lymphoma. It is hoped that the information obtained in this study will be useful in the development of improved methods for the diagnosis, prognosis, and treatment of diseases such as psoriasis and cutaneous T-cell lymphoma. Approximately 141 participants 18 years or older will be enrolled in this study, 47 for each of the study categories-healthy skin volunteers, patients with psoriasis, and patients with cutaneous T cell lymphoma. All participants will be examined by a dermatologist before being enrolled in the study. Each will fill out a questionnaire that details the participant's medical history and the general health of their skin. Investigators will then collect blood (20 cc) from each participant and analyze the serum for the presence of small proteins via a technique called mass spectroscopy. Participants enrolled through the Clinical Center of the National Institutes of Health for the express purposes of this protocol will be compensated $50 for their involvement in this study. Study Type: Observational Contact(s): see Web site below
8
These are listed at www.ClinicalTrials.gov.
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Web Site: http://clinicaltrials.gov/ct/show/NCT00063167 •
Conditioning, the Placebo Effect, and Psoriasis Condition(s): Psoriasis Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study uses the psychological principle known as classical conditioning to try to improve the standard treatment of psoriasis. Classical conditioning is a process of behavioral modification in which a person learns to connect a certain response-in this case, improvement of psoriasis-with a new action, or stimulusin this case, application of an inactive cream. The goal of this study is to show that people with psoriasis who are maintained on corticosteroid cream part of the time and an inactive (placebo) cream at other times will need a lower total amount of active medication over time than will people who are treated only with the active drug. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005922
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Serum Protein Patterns in Participants With Mycosis Fungoides/Cutaneous T-Cell Lymphoma, Psoriasis, or Normal Skin Condition(s): Cutaneous T-Cell Lymphoma; mycosis fungoides and Sezary syndrome Study Status: This study is currently recruiting patients. Sponsor(s): National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: The presence of specific serum proteins may allow a doctor to determine if a patient has mycosis fungoides/cutaneous T-cell lymphoma. PURPOSE: Pilot study to evaluate the effectiveness of analyzing blood proteins in detecting mycosis fungoides/cutaneous T-cell lymphoma. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00066664
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Study of Psoriatic Arthritis Condition(s): Psoriasis; Psoriatic Arthritis Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study will examine the genetic and immune factors involved in the cause and development of psoriatic arthritis-a disease of both the skin and joints. It will describe the medical features and natural course of the disease and determine participants' eligibility for experimental treatment protocols. Patients with known or suspected psoriatic arthritis 5 years of age and older and their relatives may enroll in this study. Patients will be evaluated with a medical history and physical examination,
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electrocardiogram, blood tests and X-rays. Additional procedures may include: 1. Leukapheresis-Collection of white blood cells for genetic analysis. Whole blood is collected through a needle placed in an arm vein. The blood circulates through a machine that separates it into its components. The plasma is removed and the cells are returned to the body through a second needle placed in the other arm. 2. Skin biopsyRemoval of a small skin sample for microscopic analysis. An area of skin is numbed with an anesthetic and one to three small circular portions (about 1/4 inch in diameter) are cut and removed. 3. Joint aspiration-Removal of a small sample of synovial fluid (lubricating joint fluid). An area of skin around the biopsy site is numbed with an anesthetic, and a needle is inserted into the joint to pull out a small fluid sample. 4. Synovial needle biopsy-Removal of a small sample of synovial tissue (tissue lining the joint). An area of skin around the biopsy site is numbed with an anesthetic and a large needle is inserted into the joint. A smaller needle attached to a syringe is then placed inside the larger needle and small pieces of synovial tissue are removed. 5. Genetic studies-Saliva and blood samples will be collected for gene testing. Saliva is collected by rinsing the mouth with a tablespoon of salt water and spitting into a test tube. Patients will be followed once or twice a year and may be evaluated for participation in an experimental treatment study. Participating relatives of patients will fill out a brief medical history questionnaire and provide a DNA sample (blood sample or tissue swab from the inside of the cheek). Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001420 •
To study the effects of CD25 and low dose Cyclosporin in the treatment of active Psoriasis vulgaris Condition(s): Psoriasis Study Status: This study is currently recruiting patients. Sponsor(s): Protein Design Labs Purpose - Excerpt: This study compares the efficacy and analyzes the cellular effects of anti-TAC (Daclizumab) and Cyclosporine in the treatment of psoriasis vulgaris. This is a three-armed study-Daclizumab alone, Cyclosporine alone, and the combination of both Daclizumab and Cyclosporine. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00050648
•
To study the use of Humanized CD25 in preventing the relapse of Psoriasis Vulgaris Condition(s): Psoriasis Study Status: This study is currently recruiting patients. Sponsor(s): Protein Design Labs Purpose - Excerpt: This study is designed to study disease relapse after NBUVB and how the administration of Daclizumab/placebo alters disease relapse. Phase(s): Phase I; Phase II
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Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00050661 •
A Controlled Trial of Intermittent Fludarabine for Psoriatic Arthritis Condition(s): Arthritis, Psoriatic; Psoriasis Study Status: This study is completed. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This is a placebo controlled study evaluating the role of fludarabine (a nucleoside analog targeting both resting and proliferating lymphocytes) in the treatment of moderate to severe psoriotic arthritis. Patients should have failed at least one disease modifying antirheumatic drug. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001422
•
A Pilot Study of Topical Antiflammin-2 for Psoriasis Condition(s): Psoriasis Study Status: This study is completed. Sponsor(s): National Cancer Institute (NCI) Purpose - Excerpt: This study is a pilot trial designed to evaluate topical antiflammin-2, a phospholipase A2 (PLA2) inhibitor, in the treatment of chronic plaque psoriasis. Antiflammin-2 in an ointment base, or the vehicle alone will each be applied four times per day to a single plaque in a randomized, double-blinded fashion. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001371
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A Study of Retrovir in the Treatment of Psoriasis in HIV-Positive Patients Condition(s): HIV Infections; Psoriasis Study Status: This study is completed. Sponsor(s): Glaxo Wellcome Purpose - Excerpt: To evaluate the feasibility of Retrovir (AZT) in the treatment of psoriasis in HIV antibody positive patients. Retrovir has been shown to be effective in the treatment of AIDS. In addition, the administration of AZT appears to have induced a remission of psoriasis in one case study. In light of AZT's antiviral activity and potential effectiveness as an agent for the treatment of psoriasis, this would be the most likely treatment for HIV positive, psoriatic patients whose disease progresses quickly. Study Type: Interventional Contact(s): see Web site below
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Web Site: http://clinicaltrials.gov/ct/show/NCT00002286 •
Assessment of Digital Imaging as a Tool for Diagnosing Psoriasis, Hand Rashes and Unusual Moles Condition(s): dermatitis; nevus; psoriasis Study Status: This study is completed. Sponsor(s): National Cancer Institute (NCI) Purpose - Excerpt: This study will evaluate whether digital photography is a reliable tool for diagnosing hand rashes, psoriasis and unusual moles. The findings will help determine if this method can be used in the National Health and Nutrition Examination survey (NHANES), which monitors disease in the United States. Employees of the National Institutes of Health 19 years and older may enroll in this study. Participants will complete a brief questionnaire that includes information on skin type, history of skin conditions (moles, cancer, rashes, psoriasis), and demographic information such as name, age and sex. They will be examined by a dermatologist, who will note in writing the appearance of any hand rashes, unusual moles, or psoriasis. If any areas suspicious for skin cancer are found, the participant will receive this information in writing, along with advice about where to go for treatment. A total of six photographs will then be taken of the participant's arms, legs, hands and back. The face will not be photographed, and the participants will not be identifiable. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005781
•
Micellar Paclitaxel to Treat Severe Psoriasis Condition(s): Psoriasis Study Status: This study is completed. Sponsor(s): National Cancer Institute (NCI) Purpose - Excerpt: This study will evaluate the safety and effectiveness of micellar paclitaxel for treating severe psoriasis. Paclitaxel in another formulation (Taxol) is approved by the Food and Drug Administration for use in patients with cancer. This drug can decrease growth of cancer cells and of new blood vessels. Because patients with psoriasis have an increase in skin cell and blood vessel growth, paclitaxel may also improve their condition. The dose of drug used in this study is much lower than those used to treat cancer patients and is expected to cause relatively few side effects. Patients 18 to 70 years of age with psoriasis lesions affecting at least 20% of their skin may be eligible for this study. Candidates will be screened with a history and physical examination, blood and urine tests, electrocardiogram, and possibly an exercise stress test. Participants will receive six intravenous (through a vein) infusions of paclitaxel over a 6-month period. Each infusion will take about 2 hours. Patients will stay in the clinic for observation for at least 1 hour before going home and will return to the clinic for follow-up examination and tests one week after each infusion. However, on weeks 0 and 8 visit will last for approximately 8 hours and will require a return to the clinic the following morning. Blood collection will be performed during the week 0 and 8 visits to determine how fast Micellar Paclitaxel is eliminated from your body. Approximately 2 teaspoons of blood will be taken prior to the infusion, twice during the infusion, and eight times during the 22 hours following the infusion for a total of eleven samples.
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These return visits will last approximately 1-2 hours. Patients will have the following procedures: 1. A skin biopsy (removal of a small tissue sample for microscopic examination) will be done at the first visit (week 0) and again at weeks 6, 14 and 22. The area of the biopsy will be numbed with an anesthetic, and a small circle of skin about the width of a pencil eraser and half as deep will be cut and lifted away. Stitches will be placed and removed 1 to 2 weeks later. 2. A history and physical examination will be done at every visit. Patients will be interviewed about changes in their skin condition and about treatment side effects and will be examined by a nurse or physician. 3. Blood and urine samples will be collected at frequent intervals (nearly every visit) to test for side effects. 4. Photographs of the skin will be taken at the first visit and at several later visits to document changes in psoriasis. 5. A blood sample will be drawn for genetic testing to look for gene changes in people with psoriasis. 6. An electrocardiogram will be taken at the last visit. This will be done at week 24 and compared to the screening EKG. 7. Gonadal toxicity monitoring will be started with all patients entered into the protocol as of May 2001. Blood will be drawn to measure Inhibit A for females and Inhibit B for males at weeks 0, 6, 14, and 22. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006276 •
Randomized Double-Blind Placebo-Controlled Trial Using Recombinant Human Interleukin-10 for Moderate-to-Severe Psoriasis Condition(s): Psoriasis Study Status: This study is completed. Sponsor(s): National Cancer Institute (NCI) Purpose - Excerpt: Several studies have documented an essential role for interleukin-10 (IL-10) in preventing prolonged and exaggerated immune responses to antigens and irritants. Psoriasis, a relatively common disease, is characterized by T cell-mediated inflammation in affected skin. In this study, the safety, tolerance, immunologic effects, and clinical activity of subcutaneous (SC) recombinant human (rh) IL-10 will be evaluated in patients with moderate-to-severe psoriasis. There will be 2 groups of patients, randomized to receive either 20 ug/kg rhIL-10 SC 3 times weekly (20 patients) or SC placebo (10 patients). This double-blind phase will continue for a total of 12 weeks and the principal evaluation will be the comparison between baseline and 12 week Psoriasis Area Severity Index (PASI) scores. Patients will come for an initial screening visit at day 0, and at weeks 1, 2, 4, 6, 8, and 12, with follow-up visits at weeks 16 and 20. All patients will be offered rhIL-10 at 12 weeks (following the blinded portion of the study protocol). Patients initially receiving active medication who wish to continue rhIL-10 therapy will be kept on the drug. This open-label portion of the study will continue for an additional 12 weeks. Patients continuing with active drug will be evaluated at weeks 14, 16, 20, and 24. Skin disease activity and toxicity will be assessed and recorded throughout the study. In addition, research studies will include functional assays to assess cytokine secretion and immunologic function of peripheral blood cells and immunohistochemical characterization of the inflammatory cells in skin. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below
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Web Site: http://clinicaltrials.gov/ct/show/NCT00001797 •
Research in Skin Inflammation Condition(s): Psoriasis Study Status: This study is completed. Sponsor(s): National Cancer Institute (NCI) Purpose - Excerpt: This study will examine the production of proteins called chemokines in inflammatory skin reactions. It is thought that chemokines attract or recruit white blood cells from the blood stream into the skin when there is a skin injury or infection, causing inflammation. This study will examine chemokine production in induced inflammatory reactions to try to gain a better understanding of how white blood cells are attracted to inflamed areas of the body. Healthy normal volunteers between 33 and 60 years old may be eligible for this study if they 1) have no history of chronic skin disease; 2) are not allergic to eggs; and 3) do not tend to form large irregular scars after trauma to the skin from, for example, cuts, scratches and surgical incisions. Candidates will be asked a short series of questions and have a limited skin examination. Participants will have 10 ml (2 tablespoons) of blood drawn from an arm vein at the start and end of the 5-day study and undergo the following procedures: 1. Day 1 - Participants receive an injection in the right upper arm of mumps antigen (a protein commonly used to tests for immunization against mumps) and an injection of "vehicle" (saline plus the preservatives thimerosal, glycine and formaldehyde) in the left upper arm. 2. Day 3 - Participants who develop a swelling from the mumps antigen larger than 5 mm wide will receive another injection of antigen in the right arm and another injection of vehicle in the left arm. Those whose swelling is not greater than 5 mm will be excluded from the study at this point. 3. Day 5 - All four injection sites, plus another site on the left upper arm will be biopsied. For this procedure the five injection areas are numbed with a local anesthetic. A punch biopsy instrument that resembles a small cookie cutter (about one-third the diameter of a dime) is inserted about one-fifth of an inch deep into the skin and the tissue is removed. Two stitches are used to close the wound. Antibiotic and bandages are applied for 5 days. Nine days after the biopsy the participant returns to NIH for removal of the stitches. New molecular biology techniques will be used to measure changes in chemokine production in the biopsied tissue. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00026741
•
Scalp Psoriasis Treatment with a Fiber Optic Comb Condition(s): Psoriasis Study Status: This study is completed. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This study will test the safety and effectiveness of a novel fiber optic device for treating scalp psoriasis with ultraviolet (UV-B) light. A effective treatment is not currently available for people with scalp psoriasis. Present methods for treating psoriasis with UV-B light cannot be used for the scalp because hair is usually blocking the light from reaching the affected skin. Our method overcomes this problem with the
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use of a comb that has optical fibers to deliver light directly to the skin. We will evaluate this device in a clinical setting and will use the results to tailor the design of the comb before producing it in large quantities. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00007293 •
Study of Topical Calcitriol in Children With Psoriasis Condition(s): Psoriasis Study Status: This study is completed. Sponsor(s): National Center for Research Resources (NCRR); Boston University School of Medicine Purpose - Excerpt: Objectives: I. Determine the therapeutic efficacy and safety of topical calcitriol in children with psoriasis. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006275
•
Study of Topical Calcitriol or Oral Calcitriol in Patients with Psoriasis Condition(s): Psoriasis Study Status: This study is suspended. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); Boston University School of Medicine Purpose - Excerpt: Objectives: I. Evaluate the long term safety and efficacy of orally administered calcitriol in patients with at least 5% of their body covered with psoriasis. II. Evaluate the long term safety and efficacy of topically administered calcitriol in patients with at least 5% of their body covered with psoriasis. III. Compare the topical calcitriol treatment to the oral calcitriol treatment in these patients. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004468
•
The Evaluation of Oral Acitretin in the Treatment of Psoriasis, Cutaneous Disorders of Keratinization, Multiple Basal Cell Carcinomas and Other Retinoid Responsive Diseases Condition(s): Basal Cell Carcinoma; Keratosis Palmaris et Plantaris; Psoriasis Study Status: This study is completed. Sponsor(s): National Cancer Institute (NCI) Purpose - Excerpt: This is a continuing study which evaluates the long-term safety and efficacy of oral acitretin in an open manner in the treatment of psoriasis, cutaneous disorders of keratinization, multiple basal cell carcinomas and other retinoid responsive diseases.
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Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005660 •
Treatment of Psoriasis Using Acitretin in HIV-Positive Patients Condition(s): HIV Infections; Psoriasis Study Status: This study is completed. Sponsor(s): Hoffmann-La Roche Purpose - Excerpt: To determine the efficacy of acitretin in the treatment of psoriasis in HIV/AIDS patients. Etretinate, a retinoid, has proven successful in the treatment of HIV-infected patients with psoriasis, but it has an elimination half-life of 100 days. Acitretin, a metabolite of etretinate, has a much shorter half-life of 2 to 3 days. Acitretin has proven effective in treating psoriasis in patients without HIV infection by reducing skin involvement and clearing of the condition, but it has not been thoroughly evaluated in HIV-infected patients. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00002143
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Treatment of Psoriasis with Parathyroid Hormone Condition(s): Plaque psoriasis Study Status: This study is completed. Sponsor(s): National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Purpose - Excerpt: This is a clinical study in two phases. The first phase compares the effect of an ointment containing parathyroid hormone (PTH) with the effect of a placebo ointment (inactive ointment without PTH) on psoriasis lesions. Neither the study participants nor the researchers will know who is receiving PTH ointment and who is receiving placebo until the end of this first study phase. The second phase is a study of the PTH ointment on large areas of psoriasis to find out how long the effects last. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00007306
Keeping Current on Clinical Trials The U.S. National Institutes of Health, through the National Library of Medicine, has developed ClinicalTrials.gov to provide current information about clinical research across the broadest number of diseases and conditions.
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The site was launched in February 2000 and currently contains approximately 5,700 clinical studies in over 59,000 locations worldwide, with most studies being conducted in the United States. ClinicalTrials.gov receives about 2 million hits per month and hosts approximately 5,400 visitors daily. To access this database, simply go to the Web site at http://www.clinicaltrials.gov/ and search by “psoriasis” (or synonyms). While ClinicalTrials.gov is the most comprehensive listing of NIH-supported clinical trials available, not all trials are in the database. The database is updated regularly, so clinical trials are continually being added. The following is a list of specialty databases affiliated with the National Institutes of Health that offer additional information on trials: •
For clinical studies at the Warren Grant Magnuson Clinical Center located in Bethesda, Maryland, visit their Web site: http://clinicalstudies.info.nih.gov/
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For clinical studies conducted at the Bayview Campus in Baltimore, Maryland, visit their Web site: http://www.jhbmc.jhu.edu/studies/index.html
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For cancer trials, visit the National Cancer Institute: http://cancertrials.nci.nih.gov/
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For eye-related trials, visit and search the Web page of the National Eye Institute: http://www.nei.nih.gov/neitrials/index.htm
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For heart, lung and blood trials, visit the Web page of the National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/studies/index.htm
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For trials on aging, visit and search the Web site of the National Institute on Aging: http://www.grc.nia.nih.gov/studies/index.htm
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For rare diseases, visit and search the Web site sponsored by the Office of Rare Diseases: http://ord.aspensys.com/asp/resources/rsch_trials.asp
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For alcoholism, visit the National Institute on Alcohol Abuse and Alcoholism: http://www.niaaa.nih.gov/intramural/Web_dicbr_hp/particip.htm
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For trials on infectious, immune, and allergic diseases, visit the site of the National Institute of Allergy and Infectious Diseases: http://www.niaid.nih.gov/clintrials/
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For trials on arthritis, musculoskeletal and skin diseases, visit newly revised site of the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health: http://www.niams.nih.gov/hi/studies/index.htm
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For hearing-related trials, visit the National Institute on Deafness and Other Communication Disorders: http://www.nidcd.nih.gov/health/clinical/index.htm
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For trials on diseases of the digestive system and kidneys, and diabetes, visit the National Institute of Diabetes and Digestive and Kidney Diseases: http://www.niddk.nih.gov/patient/patient.htm
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For drug abuse trials, visit and search the Web site sponsored by the National Institute on Drug Abuse: http://www.nida.nih.gov/CTN/Index.htm
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For trials on mental disorders, visit and search the Web site of the National Institute of Mental Health: http://www.nimh.nih.gov/studies/index.cfm
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For trials on neurological disorders and stroke, visit and search the Web site sponsored by the National Institute of Neurological Disorders and Stroke of the NIH: http://www.ninds.nih.gov/funding/funding_opportunities.htm#Clinical_Trials
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CHAPTER 6. PATENTS ON PSORIASIS Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.9 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “psoriasis” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on psoriasis, we have not necessarily excluded non-medical patents in this bibliography.
Patents on Psoriasis By performing a patent search focusing on psoriasis, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We
9Adapted
from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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will tell you how to obtain this information later in the chapter. The following is an example of the type of information that you can expect to obtain from a patent search on psoriasis: •
5-methoxy psoralen used to treat psoriasis Inventor(s): Goupil; Jean-Jacques (30 Avenue du President Wilson, 94230 Cachan, FR) Assignee(s): none reported Patent Number: 5,360,816 Date filed: May 4, 1992 Abstract: A pharmaceutical formulation comprising 5-methoxy psoralen, which is useful in the treatment of psoriasis and other skin disorders, is disclosed herein. 5-methoxy psoralen may be synthesized from phloroglucinol by a five step process which is also disclosed. Excerpt(s): It is known that certain furocoumarins, including psoralen and certain of its derivatives, exhibit a photo-dynamic activity which gives rise to photodermatitis. This dermatitis appears after oral or topical administration of the furocoumarins to a mammal and exposure to the sun or to ultra-violet rays. It has been found that the therapeutic activity of the psoralens is directly proportional to their phototoxicity. It has also been found that 8-methoxy-psoralen is useful in the treatment of psoriasis. This treatment is known and is generally carried out in the following fashion: 8-methoxypsoralen is administered orally followed several hours later by irradiation with ultraviolet A rays of large wavelength (360 nanometers) and high intensity. This treatment is carried out twice a week and the maximum dose of 8-methoxy-psoralen administered is on the order of 50 mmg. The results obtained are good in that an extensive "bleaching" of the psoriasis is obtained. The secondary effects observed are the appearance of erythemas, nausea, pruritis, and headache, which result from the toxicity of the product and the intense irradiation. In accordance with the present invention it has been discovered that, contrary to what might have been believed, another derivative of psoralen which is less phototoxic than 8-methoxy-psoralen and, therefore, less therapeutically active, displays a number of completely unexpected properties which make it much more suitable for therapeutic use and in particular more effective in the treatment of psoriasis. Web site: http://www.delphion.com/details?pn=US05360816__
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9-deazaguanines to treat psoriasis Inventor(s): Kostlan; Catherine R. (Ann Arbor, MI), Sircar; Jagadish C. (Ann Arbor, MI) Assignee(s): Warner-Lambert Company (Morris Plains, NJ) Patent Number: 5,061,707 Date filed: October 31, 1990 Abstract: The present invention is novel derivatives of pyrrolo[3,2-d]pyrimidines and pharmaceutical compositions and methods of use therefor. The derivatives are inhibitors of purine nucleoside phosphorylase selectively cytotoxic to T-cells but not to B-cells in the presence of 2'-deoxyguanosine and, therefore, are for use in the treatment of autoimmune diseases, gout, psoriasis or rejection of transplantation.
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Excerpt(s): Various purine derivatives are known including guanine derivatives having activity as inhibitors of purine nucleoside phosphoxylase (PNP-4) 767,202 filed Aug. 22, 1985, which is a continuation of U. S. Ser. No. 660,152 filed Oct. 12, 1984, now abandoned. Selected guanine derivatives previously known are also disclosed in the application. Therefore, U.S. Ser. No. 767,202 is incorporated herein by reference. The present invention also includes methods of manufacturing and a pharmaceutical composition for treating autoimmune diseases; such as arthritis, systemic lupus erythematosus, inflammatory bowel diseases, juvenile diabetes, myasthenia gravis, multiple sclerosis, gout and gouty arthritis, as well as psoriasis, viral infections, and cancer, or rejection of transplantation, comprising an immunomodulator or antirejection effective amount; such as a cytotoxic to T-cell amount, of a compound of the Formula I with a pharmaceutically acceptable carrier. Thus, the invention is also a method of treating an autoimmune disease, psoriasis, or rejection of transplantation as listed above comprising administering to a host, such as a mammal including a human suffering from an autoimmune disease or psoriasis or transplantation rejection advantageously affected by T-cell toxicity of the compounds of the present invention comprising administering an effective amount of a compound of the Formula I in unit dosage form. It is understood, an ordinarily skilled physician would begin treatment with a nontoxic and less than effective amount and increase the dose until the desired effect is obtained exercising care to administer an amount less than the amount toxic to the host of the disease. Under certain circumstances it may be necessary to protect either the N or O of intermediates in the above noted process with suitable protecting groups which are known. Introduction and removal of such suitable oxygen and nitrogen protecting groups are well known in the art of organic chemistry; see for example, (1) "Protective Groups in Organic Chemistry," J. F. W. McOmie, ed., (New York, 1973), pp 43ff, 95ff; (2) J. F. W. McOmie, Advances in Organic Chemistry, Vol. 3, 191-281 (1963); (3) R. A. Borssonas, Advances in Organic Chemistry, Vol. 3, 159-190 (1963); and (4) J. F. W. McOmie, Chem. & Ind., 603 (1979). Web site: http://www.delphion.com/details?pn=US05061707__ •
Acne and psoriasis treatment with retinoic acid analogs Inventor(s): Lee; Kwan-hua (San Francisco, CA) Assignee(s): The Regents of the University of California (Berkeley, CA) Patent Number: 3,934,028 Date filed: April 22, 1974 Abstract: Skin diseases resulting from abnormal metabolic processes, such as acne and psoriasis, are treated on a repetitive basis, either internally or topically, with a dermatologically sufficient amount of 11-(2',6',6'-trimethylcyclohex-1'-enyl-1')-5,9dimethylundeca-2,4,6,8,10-p entenoic acid or its physiologically acceptable salts to reduce the inflammation. The subject acid or its salts are found to provide remission of the dermatologically diseased condition, while avoiding side effects concommitant with the use of other analogous compounds. Excerpt(s): A wide variety of skin diseases are characterized by abnormal metabolic processes. Two classes of these conditions are the seborrheic dermatoses--which are typified by excessive secretion or disturbed quality of sebum, abnormal intercellular cement, and oily crusts or scales--and ichthyosiform dermatoses--which are typified by dry, scaly skin, abnormal thickening of epidermis, and rapid cell turnover in the skin. Specific diseases included in these broad categories include acne vulgaris (a seborrheic
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dermatosis) and psoriasis (an ichthyosiform dermatosis). Both of these conditions exhibit follicular keratin plugs. Other related conditions are ichthyosis vulgaris, senile hyperkeratosis, acanthosis, Derier's disease, keratoacanthomas, congenital ichthyosiform erythroderma, zosteriform keratosis, and lamellor ichthyosis. Because these diseases appear on the skin and are unsightly, satisfactory agents should have relatively rapid action in the remission of the condition. In addition, the reagents should not affect the skin adversely and may not be toxic at the levels employed or the manner in which it is applied. Of particular interest, is an agent which can be taken internally, acting in a systemic manner in combatting the abnormal metabolic process. Retinoic acid is found to be active in the remission of skin conditions, but has serious side effects. The retinoic acid when applied to the skin results in irritation and peeling of the skin, which is cosmetically undesirable. Because of the irritation, there is some discouragement of the user to employ the treatment. Web site: http://www.delphion.com/details?pn=US03934028__ •
Agent for preventing or treating psoriasis Inventor(s): Chiba; Ryoichi (Tokyo, JP) Assignee(s): Eisai Co., Ltd. (Tokyo, JP) Patent Number: 4,325,965 Date filed: October 20, 1980 Abstract: Psoriasis is treated with.delta.-tocopherol or ester thereof. Excerpt(s): The present invention relates to a method for treating psoriasis. More particularly, the present invention relates to a method for treating psoriasis with a composition containing.delta.-tocopherol or an ester thereof, as the effective ingredient. Psoriasis is chronic inflammatory keratodermia which causes clear erythema with silverwhite mica-like scales on the skin of a human being at various locations, such as at the elbow, knee, scalp, back and waist. This dermatitis is quite difficult to cure. Even if it is superficially cured once, it may soon return repeatedly. Psoriasis is a common dermatitis in countries in Europe and in America. Also in Japan, the number of psoriasis patients has recently increased rapidly. Web site: http://www.delphion.com/details?pn=US04325965__
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Animal model for psoriasis for the prevention and treatment of psoriasis in humans Inventor(s): Ehrhardt; Rolf (San Francisco, CA), Hong; Kenneth (El Cerrito, CA), Queen; Cary (Los Altos, CA) Assignee(s): Protein Design Labs, Inc. (Fremont, CA) Patent Number: 6,410,824 Date filed: December 8, 1999 Abstract: Methods and compositions are provided for the creation and screening of nonhuman animal models having many of the histologic characteristics of human psoriasis. Immunocompromised host animals are injected with a purified population of CD45Rb positive cells, which are tolerant of the host major histocompatibility antigens, but are mismatched at one or more minor antigens. The injected cells are stimulated with a proinflammatory cytokine, e.g. IL-12, and a polyclonal activating agent. The injected
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animals develop a chronic skin disorder that includes histological features observed in human psoriasis, e.g. rete pegs, severe acanthosis and infiltration of Th1 cells into the dermis. Excerpt(s): Psoriasis is a chronic skin disease, characterized by scaling and inflammation. Psoriasis affects 1.5 to 2 percent of the United States population, or almost 5 million people. It occurs in all age groups and about equally in men and women. People with psoriasis suffer discomfort, restricted motion of joints, and emotional distress. When psoriasis develops, patches of skin thicken, redden, and become covered with silvery scales, referred to as plaques. Psoriasis most often occurs on the elbows, knees, scalp, lower back, face, palms, and soles of the feet. The disease also may affect the fingernails, toenails, and the soft tissues inside the mouth and genitalia. About 10 percent of people with psoriasis have joint inflammation that produces symptoms of arthritis. When skin is wounded, a wound healing program is triggered, also known as regenerative maturation. Lesional psoriasis is characterized by cell growth in this alternate growth program. In many ways, psoriatic skin is similar to skin healing from a wound or reacting to a stimulus such as infection, where the keratinocytes switch from the normal growth program to regenerative maturation. Cells are created and pushed to the surface in as little as 2-4 days, and the skin cannot shed the cells fast enough. The excessive skin cells build up and form elevated, scaly lesions. The white scale (called "plaque") that usually covers the lesion is composed of dead skin cells, and the redness of the lesion is caused by increased blood supply to the area of rapidly dividing skin cells. The exact cause of psoriasis in humans is not known, although it is generally accepted that it has a genetic component, and a recent study has established that it has an autoimmune component. Whether a person actually develops psoriasis is hypothesized to depend on something "triggering" its appearance. Examples of potential "trigger factors" include systemic infections, injury to the skin (the Koebner phenomenon), vaccinations, certain medications, and intramuscular injections or oral steroid medications. Web site: http://www.delphion.com/details?pn=US06410824__ •
Antioxidant composition for the treatment of psoriasis and related diseases Inventor(s): Hersh; Theodore (Atlanta, GA) Assignee(s): Thione International, Inc. (Atlanta, GA) Patent Number: 6,011,067 Date filed: June 11, 1999 Abstract: The present invention deals with the combination of several synergistic antioxidants including enzymatic co-factors as adjuncts to therapy of desquamating inflammatory disorders, such as psoriasis. These topical compositions are aimed to neutralize free radical species generated by such inflammatory conditions which are responsible for certain clinical signs and symptoms. As such, damage to skin causing destruction of elastin and collagen tissues is reduced. The present synergistic antioxidants may be combined with anti-inflammatories, including corticosteroids, antimicrobials, including zinc pyrithione, and other preparations useful in the therapy of desquamating disorders as psoriasis, seborrhoeic dermatitis and related skin and scalp conditions. Excerpt(s): The present invention deals with the combination of several synergistic antioxidants including enzymatic co-factors as adjuncts to therapy of desquamating
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inflammatory disorders, such as psoriasis. These topical compositions are aimed to neutralize free radical species generated by such inflammatory conditions which are responsible for certain clinical signs and symptoms. As such, damage to skin causing destruction of elastin and collagen tissues is reduced. The present synergistic antioxidants may be combined with anti-inflammatories, including corticosteroids, antimicrobials, such as zinc pyrithione, and other preparations. The National Psoriasis Foundation estimates that there are more than six million Americans afflicted with psoriasis which is a chronic skin disorder. It is not contagious but its etiology is unknown. Most patients with psoriasis have several lesions confined to knees, elbows and scalp. Severe psoriasis affects larger areas such as the back, chest and legs and, not infrequently, the entire body. There are various types of psoriasis and thus there are a number of effective treatments or combinations, but not one that is specific or curative. The therapeutic armamentariun used to combat the symptoms of psoriasis, available both by prescription and over the counter, include corticosteroids, coal tar, bath solutions, including salts from the dead sea, retinoids, vitamin D3, occlusion therapy, cyclosporine and methotrexate to name a few. Psoralens have been used with ultraviolet A radiation, despite its known carcinogenic properties, much like that caused by sun damage. Ultraviolet B radiation has also been used successfully in some cases. Web site: http://www.delphion.com/details?pn=US06011067__ •
Azelastine and its salts used to combat psoriasis Inventor(s): Szelenyi; Istvan (Schwaig, DE), Molliere; Michael (Rutherford, NJ), Engel; Jurgen (Alzenau, DE) Assignee(s): Asta Pharma AG (DE) Patent Number: 5,110,814 Date filed: December 28, 1989 Abstract: The use of azelastine or its therapeutically acceptable salts and the preparation of a pharmaceutical composition for the treatment of inflammatory disorders and psoriasis disorders. Excerpt(s): The present invention relates of azelastine as an anti-inflammatory agent in the treatment of psoriasis and related disorders. The pharmaceutically active substance azelastine (chemical designation 4-(p-chloro-benyzl)-2-(hexahydro-1-methyl-1Hazepine-4-yl)-1-(2H)-phthalaz inone) is known to be useful in asthma prophylaxis and as an anti-allergic agent (see German Patent 21 64 058). In accordance with the present invention, it has been found that azelastine has anti-inflammatory effects which are useful in the treatment of psoriasis and disorders related thereto. The term psoriasis disorders is understood in the context of the invention as relating to skin disorders which are accompanied by hyperkeratoses, such as in particular psoriasis. The present invention also relates to the treatment of other inflammatory disorders, for example, the treatment of Colitis ulcerosa. Web site: http://www.delphion.com/details?pn=US05110814__
Patents 265
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Betamethasone- and hyaluronic acid-treated thin adhesive plaster for the treatment of psoriasis dermatitis and dermatosis Inventor(s): Rapaport; Irina (Rovio, CH), Donati; Elisabetta (Cavallasca, IT) Assignee(s): Altergon S.A. (Lugano, CH) Patent Number: 6,379,695 Date filed: October 22, 1999 Abstract: Thin adhesive plaster having a thickness lower than 500.mu.m for the treatment of psoriasis, dermatitis and dermatosis, comprising:a) a support comprising an outer layer in plastic film and an inner layer in woven or non-woven fabric having approximately the same size as the plastic film,b) an adhesive layer placed on the support inner layer having approximately the same size as the support comprising an adhesive matrix in the form of hydrogel, betamethasone or a pharmaceutically acceptable salt thereof and optionally hyaluronic acid or a pharmaceutically acceptable salt thereof,c) a protective plastic film contacted with the adhesive layer and removable immediately prior to use. Excerpt(s): The present invention refers to a plaster in the form of a thin film for the treatment of slight psoriasis, allergic dermatitis, and dermatosis. Corticosteroids are amply used in cases of eczema, dermatitis, contact dermatitis, psoriasis, etc., being remarkably efficacious for the treatment of skin diseases. However, prolonged treatments with said drugs cause untoward side effects at a systemic level, such as for example the suppression of the adrenocortical pituitary function, a phenomenon taking place even when corticosteroids are for external use and administered locally. Further side effects arising from a prolonged administration of corticosteroids consist in skin infections, such as for example acne. That is the reason why the hormone is administered locally at very low concentrations. Web site: http://www.delphion.com/details?pn=US06379695__
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Chemical entity (endipalene) in the treatment of psoriasis Inventor(s): Endrici; Giorgio (Via Brescia 2, 38100 Trento, IT) Assignee(s): none reported Patent Number: 6,291,534 Date filed: May 25, 2000 Abstract: In the literature, a correlation between the inhibition of 5-lipoxygenase and anti-inflammatory and immunomodulatory activity sufficient to effectively treat psoriasis, is known. It seems that, in particular, the excellent results can be obtained with lonapalene (6-chloro-2,3-dimethoxynaphthalendioldiacetate). However, the clinical use of lonapalene has not been successful most likely due to the significant number of side effects. With these considerations, after various studies, we have identified a molecule which we have patented with the name of endipalene, which seems to guarantee notable therapeutic results without side effects. Excerpt(s): My invention relates to the field of molecules with two aromatic condensed rings (naphtalenic rings) characterized by a good activity against inflammation through inhibitory actions in one or more passages of the "fall" of the arachidonic acid. Aromatics and compounds containing heteroatom-hetero atom bonds are the-same. Many of these are not selective 5-LO inhibitors. In vivo sistemic activity for many of
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these has been in general, disappointing, probably because of poor bioavailability caused by lipophilicity and metabolic instability (oxidation and conjugation of phenolic compounds). However, topically a number of agents have shown promise for skin inflammation, and best of all, lonapalene; (Batt D G., 5-LIPOXYGENASE INHIBITORS AND THEIR ANTI-INFLAMMATORY ACTIVITIES, PROGRESS IN MEDICINAL CHEMISTRY, 29:1-63, 1992). Web site: http://www.delphion.com/details?pn=US06291534__ •
Composition and method for treating psoriasis Inventor(s): Fredriksson; Torsten (Vasteras, SW) Assignee(s): Allergan Pharmaceuticals (Irvine, CA) Patent Number: 3,966,924 Date filed: November 13, 1974 Abstract: A composition and method for treating psoriasis in humans comprising the topical administration to a human suffering from psoriasis of an effective dose for treating psoriasis of a composition comprising from about 0.01 to about 5% of a corticosteroid and preferably a halogenated corticosteroid and from about 0.05 to about 10% of 5-fluorouracil together with a suitable topical carrier. Excerpt(s): The present invention relates to the therapeutic treatment of proliferationtype skin diseases. More particularly, the present invention relates to the use of corticosteroids in combination with 5-fluorouracil in the treatment of skin conditions such as psoriasis. Psoriasis is a common, chronic, relapsing disease of unknown etiology which consists of elevated, silvery, dry lesions which are known as plaques. Pathologically, there are three obvious changes associated with the disease: (1) increase in the rate of cell division of the epidermis, (2) striking increase in the thickness of the cornified epithelium, and (3) proliferation of the subepithelial capillaries. Corticosteroids and especially halogenated corticosteroids have been successfully used in the topical treatment of psoriasis to temporarily alleviate the signs and symptoms of the disease. This effect is probably due to influence on the nucleic acid metabolism of the epidermis. The effect, which is most striking when occlusive dressings are used, is now well documented and accepted. However, there are several disadvantages with this type of treatment: occlusion must go on for periods of up to 2-3 weeks before lesions are cleared; and the recurrence rate is high, that is, the lesions return within a few weeks to a few months after withdrawal of therapy. Web site: http://www.delphion.com/details?pn=US03966924__
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Composition and method for treatment of psoriasis Inventor(s): Noah; Patricia W. (Germantown, TN), Skinner, Jr. Robert B. (Memphis, TN), Rosenberg; E. William (Memphis, TN), Glenn; Thomas M. (Mobile, AL) Assignee(s): Panda Pharmaceuticals, L.L.C. (Memphis, TN), The University of Tennessee Research Corporation (Knoxville, TN) Patent Number: 5,990,100 Date filed: August 28, 1998
Patents 267
Abstract: Pharmaceutical compositions and methods for use in the treatment of psoriasis, having isopropyl myristate as a first active ingredient and a different antipsoriatic agent as a second active ingredient; preferably they are combined in the same pharmaceutical composition. Excerpt(s): This invention relates to pharmaceutical compositions and more particularly to pharmaceutical compositions and methods for use in the treatment of psoriasis. Psoriasis is a chronic skin disease or condition characterized by circumscribed red patches covered with white scales. Conventional treatment compositions include corticosteroid, calcipotriol, and retinoid creams. Coal tar, salicylic acid, zinc pyrithione, and anthralin compositions are also known. U.S. Pat. Nos. 4,513,011; 4,495,203; 4,507,321; 4,933,330; 4,847,257; 4,496,588; 4,981,681; and 4,518,789, the contents of which are incorporated herein by reference, disclose compositions for the treatment of psoriasis. See also U.S. FDA OTC Drug Monograph, Federal Register, Vol. 47, No. 233 (Dec. 3, 1982) pp. 54646-54684, the contents of which are incorporated by reference, which lists OTC compositions for treatment of psoriasis. Isopropyl myristate has been known as an excipient or vehicle for cosmetic creams and topical medicinals for many years, particularly where good absorption through the skin is desired. However, isopropyl myristate has not been known as an active ingredient or agent for the treatment of psoriasis. There is a need for a more effective composition and method for the treatment of psoriasis. Web site: http://www.delphion.com/details?pn=US05990100__ •
Composition and methods of paclitaxel for treating psoriasis Inventor(s): Hunter; William L. (Vancouver, CA) Assignee(s): Angiotech Pharmaceuticals, Inc. (Vancouver, CA) Patent Number: 6,515,016 Date filed: December 1, 1997 Abstract: The present invention provides methods for treating or preventing inflammatory diseases such as psoriasis or multiple sclerosis, comprising the step of delivering to the site of inflammation an anti-microtubule agent, or analogue or derivative thereof. Excerpt(s): The present invention relates generally to compositions and methods for treating or preventing inflammatory diseases. Inflammatory diseases, whether of a chronic or acute nature, represent a substantial problem in the healthcare industry. Briefly, chronic inflammation is considered to be inflammation of a prolonged duration (weeks or months) in which active inflammation, tissue destruction and attempts at healing are proceeding simultaneously (Robbins Pathological Basis of Disease by R. S. Cotran, V. Kumar, and S. L. Robbins, W. B. Saunders Co., p. 75, 1989). Although chronic inflammation can follow an acute inflammatory episode, it can also begin as an insidious process that progresses with time, for example, as a result of a persistent infection (e.g., tuberculosis, syphilis, fungal infection) which causes a delayed hypersensitivity reaction, prolonged exposure to endogenous (e.g., elevated plasma lipids) or exogenous (e.g., silica, asbestos, cigarette tar, surgical sutures) toxins, or, autoimmune reactions against the body's own tissues (e.g., rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, psoriasis). Chronic inflammatory diseases therefore, include many common medical conditions such as rheumatoid arthritis, restenosis, psoriasis, multiple sclerosis, surgical adhesions, tuberculosis, and
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chronic inflammatory lung diseases (e.g., asthma, pneumoconiosis, chronic obstructive pulmonary disease, nasal polyps and pulmonary fibrosis). Psoriasis is a common, chronic inflammatory skin disease characterized by raised, inflamed, thickened and scaly lesions, which itch, burn, sting and bleed easily. In approximately 10% of patients, psoriasis is accompanied by pronounced arthropathic symptoms that are similar to the changes seen in rheumatoid arthritis. Approximately 2 to 3% of the U.S. population suffers from psoriasis, with 250,000 new cases being diagnosed each year. Web site: http://www.delphion.com/details?pn=US06515016__ •
Composition for topical treatment of psoriasis and atopic dermatitis comprising a xanthine derivative Inventor(s): Eitan; Anat (Even Yehuah, IL), Cohen; Sasson (Tel-Aviv, IL), Nachman; Rachel (Tel-Aviv, IL) Assignee(s): Teva Pharmaceutical Industries, Ltd. (Jerusalem, IL), Ramot University for Applied Research and Industrial Development, Ltd. (Tel-Aviv, IL) Patent Number: 5,565,462 Date filed: June 21, 1994 Abstract: Use of a compound selected from the group consisting of pentoxifylline, propentofylline and torbafylline for topical treatment of psoriasis or atopic dermatitis and pharmaceutical compositions comprising them. Excerpt(s): This invention relates to topical pharmaceutical compositions for and a method of treating inflammatory and proliferative skin diseases such as psoriasis and atopic dermatitis. Psoriasis is a common chronic relapsing inflammatory skin disease which affects 1-3% of the population. It is characterised by the circumscribed scaling erythematous plaques of various sizes and forms which in some cases may extend to more than 50% of the skin area. The psoriatic condition is composed of two main processes: cellular hyperproliferation and inflammation. Despite extensive research the etiology of the disease is still unknown. Psoriasis is currently treated by a number of methods which include topical applications consisting of tar derivatives, steroids, vitamin D and its derivatives or vitamin A and its derivatives (J. P. Callen, Drug Therapy, April 1987, pp. 29-35). These therapies are only partially successful and may be accompanied by undesired side affects. Thus although steroids can be very effective, they are also frequently associated with side effects. Other therapies include phototherapy with or without concomitant systemic administration of psoralen derivatives. Additionally, systemic administration of steroids, methotrexate and cyclosporine have been used for treatment of severe cases of psoriasis. All of these therapies are associated with side effects. There is thus an urgent need for new effective, non-toxic therapeutics for psoriasis. Web site: http://www.delphion.com/details?pn=US05565462__
Patents 269
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Composition for treating and/or ameliorating the diseases of dandruff, seborrheic dermatitis, psoriasis and eczema and symptoms thereof Inventor(s): Khaiat; Alain (Singapore, SG), Hopkins; John (Newbury, GB), Ping; Elizabeth Wen (Shanghai, CN), Baker; Rex J. (Shanghai, CN), Manigbas; Noel D. (Muntinlupa, PH) Assignee(s): Johnson & Johnson Consumer Products, Inc. (Skillman, NJ) Patent Number: 6,333,027 Date filed: April 21, 2000 Abstract: A composition that is useful for treating and/or ameliorating the diseases of dandruff, seborrheic dermatitis, psoriasis, and eczema and/or the symptoms associated therewith, and is non-stinging to the eyes is disclosed. The composition contains from about 0.5 weight percent to about 16 weight percent of at least one amphoteric surfactant; from about 1 weight percent to about 10 weight percent of at least one anionic surfactant; from about 0.1 weight percent to about 10 weight percent of at least one non-ionic surfactant; and from about 0.1 percent to about 15 percent active ingredient selected from Undecylenamidopropylbetaine, Undecylenic Acid, and mixtures thereof. A method for treating and/or ameliorating the diseases of dandruff, seborrheic dermatitis, psoriasis, and eczema and/or the symptoms associated therewith including topically applying an effective amount of the composition to the area desired is also disclosed. Excerpt(s): The present invention relates to a composition that is useful for treating and/or ameliorating the disease of dandruff, seborrheic dermatitis, psoriasis And eczema and/or the symptoms associated therewith and has a low degree of ocular and skin irritation. More specifically, this invention is related to such compositions comprised of undecylenamidopropylbetaine and mixtures thereof with undecylenic acid which are suitable for such uses. It is well known that many surfactants used in shampoos are irritating to the eyes, which is of particular concern in shampoos used on infants and children. As a result, several less irritating surfactants have been developed. However, as children approach the age of puberty, hormonal changes associated with the development of scalp conditions normally associated with dandruff, such as scalp irritation and scaling, often occur. Unfortunately the active ingredients that are effective in treating such conditions are irritating to the eyes. For example, Undecylenic Acid, which is commercially available from Elf Atochem of France, and its betaine derivative, Undecylenamidopropylbetaine, which is commercially available from CECA-ATO of France under the tradename, "Amphoram U," are known as being useful for antidandruff properties in shampoos, but not without the disadvantage of eye irritancy. Therefore, there is a need for a shampoo formulation, which is not only suitable for use by children to effectively treat the skin conditions cited above, but also possesses a low degree of ocular and skin irritation. Web site: http://www.delphion.com/details?pn=US06333027__
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Composition for treating psoriasis vulgaris and a method for its preparation Inventor(s): Boncic; Ljubomir (11 Oktobar St. No. 7, 18310 Bela Palanka, YU) Assignee(s): none reported Patent Number: 4,740,372 Date filed: September 17, 1986
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Abstract: A composition for the treatment of psoriasis vulgaris, and a method for its preparation are described. The compound is made from the following ingredients: 6.alpha.,9.alpha.-difluoro-11.beta., 17.alpha.-dihidroxy-16.alpha.-methyl-21 trimethylacetoxy-1,4-pregnadiene-3,20 dione; (+)-17,21-dipropionyloxy-16.beta.-methyl-9.alpha.fluoro-prednisolone; salicylic acid; tetracycline chloride; gentamycin sulfate; neomycin sulfate; trypsin; chymotrypsin; and bismuth. A method for the preparations of this composition is also disclosed. In this method, 6.alpha.,9.alpha.-difluoro11.beta.,17.alpha.-dihidroxy-16.alpha.-methyl-2 1-trimethyl-acetoxy-1,4-pregnadiene3,20 dione and (+)-17,21-dipropionyloxy-16.beta.-methyl-9.alpha.-fluoroprednisolone are first mixed together under intensive agitation. Salicyclic acid, tetracycline chloride, gentamycin sulfate and neomycin sulfate are then added. Next, trypsin, chymotrypsin and bismuth are added. Finally, the preparation is mixed into a neutral cream, ointment, etc., at which time it is ready for use. This unique composition of ingredients acting together achieves excellant results in the treatment psoriasis vulgaris. Excerpt(s): This invention relates to a pharmaceutical composition for the treatment of psoriasis vulgaris. Psoriasis is characterized by pink or red lesions which are covered with silvery scales. These lesions are often found in the folds of the elbows and knees, the scalp and the genitoanal area. The condition is marked by accelerated turnover of the epidermal layer of the skin and consequential epidermal thickness. Psoriasis vulgaris is the common form of the disease. While normal epidermal turnover occurs every 25-30 days, in psoriatic skin it occurs approximately every 3-4 days. At this rate, the skin color is often affected, resulting in too much or too little pigmentation. Web site: http://www.delphion.com/details?pn=US04740372__ •
Compositions and delivery systems for the topical treatment of psoriasis and other conditions of the skin Inventor(s): Neigut; Stanley (10 Red Rowan La., Plymouth Meeting, PA 19462) Assignee(s): none reported Patent Number: 6,048,886 Date filed: September 30, 1999 Abstract: The invention provides compositions and methods for the application of those compositions in order to treat biological surfaces, especially the skin. The compositions contain a ubiquinone, may include other antioxidant agents (including melatonin), and may include an abrasive. The means of application may be by rubbing the composition into the skin, by means of a transdermal patch, or by rubbing the composition into the skin followed by application of a transdermal patch. The compositions and methods are useful for treating a variety of skin conditions, including psoriasis and hyperpigmentation, and may also be used for cosmetic purposes and the prevention of skin damage. Excerpt(s): The invention generally relates to the treatment of skin conditions such as psoriasis. In particular, the invention provides methods for treating skin, which is either damaged or undamaged, using compositions containing a ubiquinone and an abrasive, and for delivering compositions containing a ubiquinone by means of a transdermal patch. The skin provides an essential protective barrier against environmental challenges such as radiation, extremes of temperature, excessive dryness, invasion by infectious organisms, and many others. As such, the maintenance of the health of the skin is of great importance for the overall preservation of well-being. This maintenance
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includes both preventative skin care and attention to rapid and effective healing of pathological skin conditions. Much effort has been exerted in understanding the factors which promote healthy skin, especially those factors which are "naturally occurring", i.e. biological substances which are the components of the skin's endogenous protective and healing mechanisms. For example, it is known that the skin possesses an elaborate antioxidant defense system to deal with oxidative stress. Evidence for this is suggested by investigations of skin disorders such as Xeroderma pigmentosum, in which biopsies revealed an abnormally low level of activity of the enzyme catalase, which is involved in the defense against oxygen free radicals. Excessive exposure to environmental insults such as UV radiation can overwhelm the cutaneous antioxidant capacity, leading to oxidative damage and ultimately to skin cancer, immunosuppression, and premature skin aging. Web site: http://www.delphion.com/details?pn=US06048886__ •
Compositions and methods of treating psoriasis with vinyligs of desmethyl retinoic acid Inventor(s): Lee; Kwan-Hua (San Francisco, CA) Assignee(s): The Regents of the University of California (Berkeley, CA) Patent Number: 3,966,967 Date filed: October 29, 1974 Abstract: The C20 and C22 vinylogs of desmethyl retinoic acid have been found highly effective in promoting wound healing, in the treatment of acne, psoriasis and related skin disorders. The acid is applied to the site as a solution, ointment or powder. These acids are the most effective yet found for such purposes yet do not have some of the undesirable side effects of retinoic acid. Excerpt(s): In accordance with the present invention it has been found that certain desmethyl vinylogs of retinoic acid are highly effective in healing wounds and treating skin disorders such as psoriasis and acne. The mechanisms involved in the healing of acne and psoriasis are not understood but it has been found that the compounds of the present invention are highly effective in the treatment of these disorders. It has also been found that the compounds of the present invention are highly effective in wound healing. Inflammation and mucopolysaccharide synthesis are the two important features in the early stage of wound healing. The term "wound" as used in this application means any topical lesion such as a surgical incision, accidental wound or ulcer. Aspirin inhibits both features. The healing inhibitory action of aspirin and other inflammatory agents has been demonstrated. Vitamin A increases mucopolysaccharide synthesis and it also causes inflammation. The ability of vitamin A alone to promote healing and its effectiveness in reversing the healing retardation action of aspirin is known. Retinoic acid (the acid form of vitamin A) and its salts also have been found active compounds in promoting healing. Topical application of retinoic acid or its salts reverses the healing retardation action caused by oral administration of sodium salicylate, prednisone and other anti-inflammatory agents and topical application of salicylic acid or hydrocortisone. Topical application of retinoic acid and its salts promotes skin wound healing in rats and human beings. Retinoic acid has been used in the treatment of psoriasis, acne, and related dermatological conditions such as Darier's disease, ichthyosis, hyperkeratoses, pityriasis, and pseudofolliculitis of the beard. The exact mechanism of action of retinoic acid is unknown; however, the "normalizing" effect on keratinization that occurs is seen concomitantly with irritation which is
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characterized by redness and peeling of the skin. In fact, it is believed that retinoic acid may have to be irritating to be effective in acne. In psoriasis, the beneficial action of retinoic acid is limited by its irritant effect. Additionally, most of the other agents used to treat psoriasis--antimetabolites, tars, anthralin--are not used more frequently because of their potential for irritation. Web site: http://www.delphion.com/details?pn=US03966967__ •
Compositions and uses thereof in the diagnosis of psoriasis Inventor(s): Menter; Alan (Dallas, TX), Gaynor; Richard (Dallas, TX), Bowcock; Anne (Dallas, TX), Tomfohrde; James (Arlington, TX) Assignee(s): Board of Regents, Univ. of Texas System (Austin, TX) Patent Number: 5,811,233 Date filed: May 20, 1994 Abstract: A psoriasis susceptibility locus defined as among linked members within a family has been identified. The locus is linked to an intron of the interleukin enhancer binding factor gene in some families, while being linked to an interleukin 8 gene in other families demonstrating a familial linked form of psoriasis. The locus identified may be further defined as being located distal to genetic maker D17S784 of human chromosome 17q. This locus does not demonstrate linkage with DNA markers within flanking the HLA cluster of genes. A psoriasis susceptibility locus has also been observed close to the centromere of human chromosome 4. Both identified regions provide positive LOD scores with markers on chromosomes 17q and particularly 2 regions close to the ILF gene or the interleukin 8 gene. Methods of screening a family for psoriasis susceptibility using a defined familial psoriasis susceptibility locus are also disclosed. A cDNA capable of detecting a genetic polymorphism identifying the psoriasis susceptibility locus in families with a psoriasis afflicted member, and a process for preparing such a cDNA, are further disclosed. The molecular probes disclosed herein are also known to hybridize with the distal region of human chromosome 17q and with chromosome 4q, and therefore are useful for detecting a genetic lesion in chromosome 17q and 4q. A psoriasis gene related to familial forms of psoriasis is also disclosed. This gene maps to the distal end of human chromosome 17q and has close proximity or is within a gene encoding interleukin enhancer binding factor. Excerpt(s): The present invention relates generally to the field of molecular genetic tools for screening biological samples, as well as methods for using them in the mapping of chromosomes and in the diagnosis of disease. The invention also relates generally to the field of pharmaceutical compositions that include as an active agent preparations directed to a particular gene. More particularly, the invention concerns molecular genetic probes and methods of using them in detecting a genetic polymorphism associated with a familial psoriasis susceptibility locus in a human biological sample. Psoriasis is a chronic inflammatory dermatosis that affects.about.2% of the population. It is characterized by hyperproliferation of epidermal cells and inflammation resulting from infiltration of activated T helper cells and mononuclear cells and release of proinflammatory cytokines (Menter and Barker, 1991; Barker, 1991). It may also be associated with arthritis and can present as a severely inflammatory dermatosis in patients with acquired immunodeficiency syndrome (AIDS) (Duvic, 1990). The symptoms of psoriasis include sharply defined erythematous patches covered with a distinctive scale, hyperproliferation of the epidermis, incomplete differentiation of keratinocytes and dermal inflammation. Clinical variants of psoriasis include
Patents 273
erythroderma, seborrheic, inverse, guttate, and photosensitive psoriasis, pustular variants and Reiter's disease. The role of immunomodulation in psoriasis is supported by the pharmacological action of drugs such as cyclosporine. For example, inhibition of the synthesis of interleukin-2 prevents the proliferation of T cells and thus their release of cytokines. Mediators of inflammation play a role in the immunoregulation of psoriasis. Currently available methods for treatment include topical therapy, phototherapy, photochemotherapy and systemic therapy and provide, at best, only temporary relief. Topical glucocorticoids are most commonly prescribed as the initial treatment of psoriasis for their anti-inflammatory, antimitotic and antipruritic effects. However, their efficacy is often short term. Crude coal tar is a complex mixture of thousands of hydrocarbon compounds and affects psoriasis by enzyme inhibition and antimitotic action. Although effective, tar stains the skin and has an odor. Anthralin (dithranol) is used topically and inhibits enzyme metabolism and reduces epidermal mitotic turnover. Remission may last for weeks to months. Phototherapy and photochemotherapy entailing the administration of the photosensitizing drug methoxsalen are only temporarily effective, as psoriasis recurs months after this treatment is discontinued. This recurrence indicates that the therapy is palliative rather than curative. Long-term consequences are altered immunologic effects and an increased risk of carcinogenesis. Web site: http://www.delphion.com/details?pn=US05811233__ •
Compositions for and method of treatment for psoriasis Inventor(s): De Oliveira; Mariana (788 Adelaide Street West, Toronto, Ontario, CA) Assignee(s): none reported Patent Number: 6,403,654 Date filed: April 13, 2000 Abstract: Improved compositions for treating psoriasis, including a body wash composition, spray composition and cream composition and the use of these novel compositions in a system or method of treating psoriasis. Excerpt(s): This invention relates in general to a treatment for psoriasis and more particularly to a medication for treating psoriasis having three different formulations, a system for using the medication, and a method of medical treatment. Psoriasis is a skin disorder that includes the presence of small elevations of the skin that may be characterized as elevated red lesions, plaques or pustules on the skin which eventually result in silvery scales. These silvery scales and plaque are the result of accelerated epidermal proliferation and the metabolic activity and proliferation of capillaries in the dermal region and the invasion of the dermis and epidermis by inflammatory cells. More specifically, the capillaries in the dermal region become tortuous and dilated as well as suffering an inflammatory reaction causing the skin to redden. The exact mechanism which triggers the abnormal cell proliferation is not known, though it is believed there may be biochemical stimuli and environmental factors. The severity and course of psoriasis can vary greatly depending on the individual, but in general this chronic skin condition recurs throughout the life of the individual with varying intervals of one month to many years. Web site: http://www.delphion.com/details?pn=US06403654__
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Compositions for the treatment of psoriasis and their use Inventor(s): Whitefield; Martin (London, GB) Assignee(s): Diomed Developments Limited (GB) Patent Number: 5,817,675 Date filed: May 27, 1997 Abstract: 8-Hydroxyquinoline is useful in the topical treatment of inflammatory proliferative skin diseases, especially psoriasis. It should be applied from an essentially anhydrous vehicle. Excerpt(s): This invention relates to compositions for the topical treatment of inflammatory proliferative skin diseases, especially psoriasis, and their manufacture and use. Psoriasis is associated with the rapid turnover of skin cells (hyperproliferation) accompanied by a loss of differentiation so that silvery white scales form on the surface of the skin. Additionally, the capillaries become tortuous and dilated and an inflammatory reaction occurs, so that the skin reddens. The elevated silvery white scales on a contrasting red background produce the unsightly lesions characteristic of psoriasis. A number of methods are used for the topical treatment of psoriasis, but none is entirely satisfactory. Historically, the earliest form of therapy involved the use of coal tar derivatives. These are sometimes effective but are extremely messy. Subsequently, the use of dithranol (1,8-dihydroxy-9-anthrone) was developed. This substance is very effective, but it causes irritation of the skin and staining both of the skin and adjacent materials, which are disadvantages especially in home treatment. Topical corticosteroids have also been used. Although these are clean and convenient to use, they are only suppressive in action and therefore only provide short term relief of symptoms. In addition, psoriasis treated with corticosteroids tends to relapse in a more resistant form, so that more aggressive therapy is later required. Web site: http://www.delphion.com/details?pn=US05817675__
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Diphenylhexene composition for use in treating liver carcinoma and psoriasis Inventor(s): Metzler; Manfred (Im Speitel 23, D-76229 Karlsruhe, DE), Pechan; Reinhard (Elektrastr 36, D-81925 Munchen, DE) Assignee(s): none reported Patent Number: 5,650,445 Date filed: February 27, 1996 Abstract: The new compound 3,4-diphenyl-3-hexene has valuable pharmaceutical properties and is suitable for the treatment of diseases that are associated with degenerate cell growth in particular for the treatment of liver cancer and psoriasis. Excerpt(s): This application is a continuation of PCT/EP94/02837, filed Aug. 26, 1994, and designating the United States. The present invention concerns the new chemical compound diphenyl-3-hexene, a process for its production and its use as a therapeutic agent. Numerous diseases in humans are due to an uncontrolled growth of body cells. This disorder in proliferation can lead to a benign degeneration such as psoriasis vulgaris in the case of keratinocytes or.beta.-thalassaemia in the case of erythrocytes or even to a malignant degeneration such as in all forms of cancer. Web site: http://www.delphion.com/details?pn=US05650445__
Patents 275
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Furocoumarin for the photochemotherapy of psoriasis and related skin diseases Inventor(s): Carlassare; Francesco (Padua, IT), Rodighiero; Paolo (Padua, IT), Guiotto; Adriano (Padua, IT), Rodighiero; Giovanni (Padua, IT), Bordin; Franco (Padua, IT), Baccichetti; Francarosa (Padua, IT), Pastorini; Giovanni (Padua, IT), Vedaldi; Daniela (Padua, IT), Dall'Acqua; Francesco (Padua, IT) Assignee(s): Consiglio Nazionale delle Ricerche (Rome, IT) Patent Number: 4,312,883 Date filed: August 15, 1980 Abstract: A class of alkyl-substituted angular flurocoumarins, sometimes termed alkylangelicins, useful in the photochemotherapy of psoriasis and in other skin diseases characterized by cellular hyperproliferation or lack of skin pigmentation is disclosed for topical application or systemic administration. Compared with conventional psoralens the described compounds exhibit a lower risk of skin cancer, absence of phototoxicity problems anderithema to the patient so treated. One preferred compound is 5methylangelicin. Excerpt(s): The present invention relates to a furocoumarin for the photochemotherapy of psoriasis and of other skin diseases sensitive to this treatment, such skin diseases characterized by cellular hyperproliferation or by lack of skin pigmentation. The furocoumarins, widely diffused in the vegetable world, are well-known. They can be subdivided into two general groups: psoralens, or linear furocoumarins, and angelicins, or angular furocoumarins. A singular characterizing property of linear and angular furocoumarins is represented by their photosensitizing activity, which is evidenced on different biological substrata; such activity, as is known, obtained by the combined action of the furocoumarin and long-wave ultraviolet light (UV-A). The linear furocumarins (psoralens) are well known for their cutaneous photosensitizing activity. If, for example, the skin of a human or that of a guinea-pig is treated first with linear furocoumarins and successively irradiated with long wave ultraviolet light (UV-A), after a period of about 12-14 hours a cutaneous erythema appears and is followed by a dark pigmentation after some days. This property has already been exploited since 1948 by El Mofty employing a natural psoralen, xantotoxin (8-methoxypsoralen) which is extracted from an Egyptian plant, the Ammi Majus, for the treatment of leucodermin or vitiligo. See A. M. El Mofty, "Vitiligo and psoralens", edited by A, M. El Mofty, Pergamon Press, Oxford, 1968. The cure of this skin disease, which is characterized by the presence on the skin of white spots which do not resume their natural pigmentation even if exposed to the sunlight, is effected by treating these spots with a psoralen and successive exposure to UV-A light; this treatment restores the pigmentation. Web site: http://www.delphion.com/details?pn=US04312883__
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Herbal medication for the treatment of psoriasis Inventor(s): Jacob; George (7106 NW 11th Pl., Gainesville, FL 32605) Assignee(s): none reported Patent Number: 5,858,372 Date filed: September 12, 1997 Abstract: A pharmaceutical preparation for topical treatment of skin disorders, particularly psoriasis, comprising the ingredients of a latex extracted from the leaves of
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the Wrightia tinctoria R Br. plant, urea, and polyethylene glycol. The pharmaceutical preparation is also a hydrophilic ointment that is capable of delivering the active drugs without being greasy or irritating to the skin. Excerpt(s): Psoriasis is among the dermatoses having a poorly understood etiology. The ailment is a chronic skin disease usually occurring in early to middle age and affecting approximately 2% of the US population. Psoriasis is characterized by epidermal hyperplasia and a greatly accelerated rate of epidermal turnover. The lesions are characteristically dry, well demarcated, red, slightly raised and scaly. Gentle scraping of the lesion removes scales and produces many pinpoint bleeding sites, the so-called "Auspitz sign". The lesions are discrete or confluent erythromatous plaques and papules covered with white or silvery scales found on the extensor surfaces such as the elbows, knees, back and scalp. No part of the body is exempt. The lesions may be localized or generalized. The therapies of choice are generally limited to the topical application of fluorinated corticosteriods, keratolytics containing salicylates, coal tar, anthralin preparations and systemic therapy with corticosteroids and methotrexate. Methotrexate and drugs like it have severe side effects such as bone marrow depression and thus their therapeutic benefits must be weighed against potentially dangerous side effects. In addition, the formulations to be used are limited to the most common preparations such as, solutions, creams, and salves. Consequently, the manner of application for the dermatherapy is practically predetermined. Typically the only pharmaceutical forms in which the therapeutic agents are available are lipophilic preparations for local therapy, due to the high instability of the active ingredients against air, oxygen, water, and alkalis. The strongly fattening lipophilic preparations have relatively low storage stability. Such preparations are necessarily inconvenient to use because the hydrophobic preparations are difficult to wash off. Web site: http://www.delphion.com/details?pn=US05858372__ •
Infrared treatment for psoriasis Inventor(s): Horowitz; Jacob (10 Black Birch Rd., Scotch Plains, NJ 07076), Warshaw; Thelma G. (519 E. Broad St., Westfield, NJ 07090) Assignee(s): none reported Patent Number: 4,996,046 Date filed: November 24, 1989 Abstract: Psoriasis is treated with an infrared absorbing compound, preferably but not exclusively by occluding psoriatic lesions with a plastic film containing at least one compound which strongly absorbs infrared radiation in the range of from about 700 to about 1400 nanometers. The invention also includes a dressing for treating psoriasis incorporating one or more infrared blocking compounds. The infrared absorbing materials are preferably but not necessarily dispersed uniformly through a flexible carrier transparent to visible light, such as polyvinyl chloride (PVC) film or poly (methyl methacrylate) (PMMA) film, by known techniques of solution casting or dying. The materials can be used as the sole therapeutic agent, or as an adjunct to local and/or systemic treatments for psoriasis. Excerpt(s): The invention relates to the treatment of psoriasis and in particular to the use of infrared absorbing compounds in such treatment. In treating psoriasis, a dermatosis of yet unknown origin, the use of topical creams and salves, sometimes under plastic film dressings such as kitchen-wrap films, is common. We have discovered that
Patents 277
conventional occlusive dressings permit the escape of substantial amounts of energy via infrared radiation through the surface layers of psoriatic lesions, and that this energy leakage aggravates the disease and tends to counteract the effectiveness of conventional treatments. Such infrared energy leakage is typically found in psoriatic lesions but is absent in healthy skin. The use of materials that prevent such leakage has been found to have distinct therapeutic benefits, producing more rapid and more pronounced relief than is provided by conventional dressings, which freely transmit infrared radiation. Web site: http://www.delphion.com/details?pn=US04996046__ •
Local treatment of dandruff, seborrheic dermatitis, and psoriasis Inventor(s): Knoll; Donald W. (Waukesha, WI), Shelton; David L. (Racine County, WI), Szymczak; Thomas J. (Racine County, WI) Assignee(s): S. C. Johnson & Son, Inc. (Racine, WI) Patent Number: 4,822,604 Date filed: May 20, 1985 Abstract: A clear, therapeutic hair care composition is presented having a low pH and useful in the local treatment of dandruff, seborrheic dermatitis and psoriasis of the scalp which resists oxidative decomposition. The shampoo is comprised of a detergent shampoo base, a therapeutic amount of a keratolytic agent and a keratolytic stabilizing agent to stabilize the keratolytic agent against oxidative decoloration decomposition catalyzed by ultraviolet radiation exposure. The keratolytic agent is preferably a salicylate and preferably salicylic acid and the keratolytic stabilizing agent is a tertiary amine. Excerpt(s): This invention relates to a clear, therapeutic hair care composition having low pH for use in local treatment of dandruff, seborrheic dermatitis, and psoriasis of the scalp which resists decoloration due to oxidative decomposition. This invention further relates a clear, therapeutic hair care composition having low pH for use in local treatment of dandruff, seborrheic dermatitis, and psoriasis of the scalp which contains a detergent shampoo base, a therapeutic amount of keratolytic agents and keratolytic stabilizing agents in an amount sufficient to stabilize the keratolytic agents against decoloration decomposition from oxidation. This invention further relates to a method to create a clear, therapeutic hair care composition having low pH which resists decomposition due to oxidation. Web site: http://www.delphion.com/details?pn=US04822604__
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Lotion mixture and method of treating psoriasis Inventor(s): Tosti; Vittorio (Eagle Pharmaceuticals, 345F Central Ave., Bohemia, NY 11716) Assignee(s): none reported Patent Number: 4,981,681 Date filed: August 26, 1988 Abstract: A combination of ingredients consisting of a mixture of predetermined proportions of Purified Water, Methylparaben, Potassium Hydroxide, Hydrogenated Coconut Oil, Glycerine, Polysorbate 60, Polysorbate 80, Glyceryl Stearate (and) Laureth-
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23, White Wax, Stearic Acid, Cetyl Alcohol, PEG-40 Stearate, Glyceryl Stearate, Salicylic Acid, HQ Squalane, DL-Alpha Tocopherol Nicotinate, Isopropyl Myristate, EPA, Lecithin, Niacin, Vitamin B6, and Propylparaben, and said aforementioned ingredients having been found to constitute a safe method of treating psoriasis, consisting of the daily application on a person's skin on a daily bases of predetermined dosages of said ingredients. Excerpt(s): The present invention relates to a method for treating psoriasis and more particularly it relates to a method of treating psoriasis by systematic and periodic application of several selected ingredients including the active ingredient Salicylic Acid. A great number of people suffer from the chronic anguish of psoriasis. Irregularly shaped and slightly raised dull red blotches appear on the sufferer's skin. These characteristic patches of psoriasis are covered by grayish or silvery scales which, if scratched, will peel and flake off like dandruff The lesions of psoriasis, which in the early stages can be misdiagnosed as ringworm, may appear anywhere on the body, although psoriasis does afflict certain parts of the body more than others, such as the scalp (psoriasis of the scalp is often mistaken for dandruff), elbows, knees and the trunk of the body. The medical profession ascribes no definite cause to this embarrassing and unsightly disease, and no effective treatment has been offered. This vexatious scaling disease forces its sufferers to try everything in the dermatologist's chemical arsenal--tar, mercury, chrysarobin and phenol. These may bring some measure of transient relief, but recurrent outbreaks are the necessary outcome. In some instances, dermatologists even resort to X-ray therapy, which carries the obvious risk of dangerous side effects. Web site: http://www.delphion.com/details?pn=US04981681__ •
Medicament for psoriasis Inventor(s): Saijo; Taketoshi (Osaka, JP), Naka; Takehiko (Hyogo, JP) Assignee(s): Takeda Chemical Industries, Ltd. (Osaka, JP) Patent Number: 4,981,855 Date filed: August 1, 1989 Abstract: Disclosed is a method of using medicaments for psoriasis containing 3aminopyrazolo[3,4-d]pyrimidine compounds or their derivatives such as their salts and their glucuronides, which potently inhibit type III allergic reaction (reversed passive Arthus reaction). Excerpt(s): The present invention relates to medicaments for psoriasis containing 3aminopyrazolo[3,4-d]pyrimidine derivatives. On the other hand, 3-aminopyrazolo[3,4d]pyrimidine derivatives having a diuretic, vasodepressor, analgesic or antiinflammatory activity have been disclosed, for example, in Japanese Patent Unexamined Publication Nos. 53-31694 (1978), 60-126285 (1985) and 61-5082 (1986). However, a 3aminopyrazolo[3,4-d]pyrimidine derivative being effective to psoriasis has not been reported. Psoriasis is one of skin diseases recently increasing in Japan, and is expected to become common in the near future. However, its cause is not yet apparent, though various etiologies are proposed. For example, with respect to abnormalities in the control mechanism of cellular functions, there are observed a number of abnormalities in control in vivo such as (1) the sthenia of glucose utilization in carbohydrate metabolism, (2) serum lipoprotein hypometabolism in fat metabolism, (3) cacochymia through cyclooxygenase and an increase in the production of lipoxygenase metabolites thereby in arachidonic acid metabolism, (4) the activation of the enzyme in polyamine
Patents 279
synthesis and a rise in polyamine level in biological amine metabolism, (5) a remarkable reduction in adenylate cyclase activity and an increase in cyclic GMP, (6) the activation of various proteases and the inactivation of their inhibitors, (7) the activation of complement systems, (8) the activation of monocytes and polymorphonuclear leukocytes, and (9) abnormality in cell-mediated immunity. It is therefore very difficult to clarify its main cause. Further, nobody has yet succeeded in an attempt to produce psoriasis on experimental animals. These facts are obstacles to the development in studies on the etiology and treatment of psoriasis. Web site: http://www.delphion.com/details?pn=US04981855__ •
Medicinal skin cream for psoriasis and method Inventor(s): DeLuccia; Charles R. (2 Maple Ave., Rye, NH 03871) Assignee(s): none reported Patent Number: 4,131,652 Date filed: June 22, 1977 Abstract: A coactive mixture of acetohexamide and a steroid hormone in a cream base and method for the relief of psoriasis and related skin ailments. Excerpt(s): The present invention relates to medicinal skin creams and in particular to such a cream using acetohexamide as an active agent for the relief of psoriasis and related skin ailments. Psoriasis is a chronic skin disorder characterized by reddish elevated areas or epidermal plaques usually covered with silvery-white scales. Neither the cause nor a permanent cure are known at this time. Numerous methods of treatment have been devised and a large number of skin ointments developed and marketed for the relief of this ailment. The most successful ointments are believed to have been ointments utilizing various tars, steroid hormones and/or mercury. Tars generally produce an unpleasant odor and undesirable skin coloration while continuous use of mercury and/or steroid hormones frequently elicits undesired side effects. In accordance with the present invention it has been discovered that acetohexamide and a steroid hormone will coact so as to normally terminate the symptoms of psoriasis in an unusually short time. After original treatment in accordance with the invention, psoriasis symptoms either do not or are very slow in returning whereby further treatment is minimized and there are no undesirable side effects. The invention was discovered as a result of observing the reduction of psoriasis in a diabetic patient after commencing diabetic treatment with acetohexamide preparations administered internally. Web site: http://www.delphion.com/details?pn=US04131652__
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Method and apparatus for treating psoriasis using pulsed electromagnetic radiation Inventor(s): Eckhouse; Shimon (Haifa, IL), Kreindel; Michael (Haifa, IL) Assignee(s): ESC Medical Systems Ltd. (Yokneam, IL) Patent Number: 5,836,999 Date filed: September 28, 1995 Abstract: A method and apparatus for treating psoriasis includes a source of incoherent electromagnetic energy. The energy is directed to a region of tissue to be treated. The
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pulse duration and the number of pulses may be selected to control treatment parameters such as the heating of healthy tissue and the penetration depth of the energy to optimize the treatment. Also, the radiation may be filtered to control the radiation spectrum and penetration depth. The filtering may include attenuating an UV portion of the radiation spectrum and portions of the spectrum below a desired treatment bandwidth. A light guide for large or small spot sizes may be used to direct the light to the skin. A cooling gel is applied to the skin to be treated in another embodiment. The gel may be cooled either before or after it is applied to the skin. Excerpt(s): The present invention relates generally to a method and apparatus for treating psoriasis. More particularly, the invention relates to treating psoriasis by irradiating psoriatic plaques with visible and near infrared electromagnetic radiation. Psoriasis is a relatively common skin disease that appears in a few percent of the population. Prior art treatments of psoriatic plaques fall generally into two categories: the use of a topical drug (i.e., a drug that is applied to the skin externally) and the application of light to the psoriatic plaques. However, many of these prior art techniques have a common fundamental drawback: they offer relief to the patient for only a limited time. The topical drug treatment includes treatment by coal and wood tar dithranol and corticosteroids. These treatments produce acceptable results that last for no more than a few weeks. Detergent shampoos, salicylic acid ointments are also used, but they are also limited in their efficiency and the length of time of relief for the patient. Web site: http://www.delphion.com/details?pn=US05836999__ •
Method and composition for treating psoriasis Inventor(s): Collins; Jerry (401 Ocean Bluffs Blvd., #101, Jupiter, FL 33477) Assignee(s): none reported Patent Number: 5,444,092 Date filed: July 20, 1994 Abstract: A novel skin lotion consisting of a mixture of lye, oils, alcohol, coal tar, and menthol U.S.P. The mixture provides a cleansing lotion that readily treats psoriasis. When the mixture is applied to the skin, the lye provides a soap for cleansing and the base oil operates to soften and moisturize the skin. The use of a coal tar solution including alcohol penetrates the dermis of the skin to reduce inflammation. The addition of menthol U.S.P. helps cool the affected area and lessens itching. Excerpt(s): This invention relates to a method for treating psoriasis, namely, a treatment that provides for cleaning and soothing of affected areas to facilitate healing. Psoriasis is a chronic recurring disease of the skin characterized by the appearance of plaques, patches, or papules on the skin surface. Deletions are elevated above the skin surface and they are red to a reddish brown in color making them clearly distinguishable from the normal skin. Due to their slightly elevated status they can be easily scraped off leaving bleeding points. The extent of the disease may vary from a few lesions to a generalized involvement of most of the skin. Characteristically the portions of the body affected are the elbows, knees, scalp and chest. The cause of the disease is unknown but as a disease of the epidermis it is a major disability for nearly ten million persons in the United States alone. Since the cause of the disease is unknown, the treatment thereof remains the province of dermatologists. Web site: http://www.delphion.com/details?pn=US05444092__
Patents 281
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Method and composition for treating psoriasis Inventor(s): Mantynen; Philip R. (2515 Departure Bay Rd., Nanaimo, British Columbia, CA) Assignee(s): none reported Patent Number: 6,107,349 Date filed: April 16, 1998 Abstract: This invention pertains to the novel combination of Vitamin E, evening primrose oil and B-complex vitamins as a treatment for patients afflicted with psoriasis. It is postulated that the above compounds act synergistically to provide the cofactors required for normal skin production and repair in psoriatic patients. Excerpt(s): This invention pertains to the use of a novel composition comprising Vitamin E, evening primrose oil and B-complex vitamins for treatment of patients afflicted with psoriasis. It is postulated that the above compounds act synergistically to provide the cofactors required for normal skin production in psoriatic patients. The skin is the largest organ in the human body and is in a state of constant turnover. This is accomplished by the outward movement of the basal layer keratinocytes at a rate that varies with age, sex, position on the body and other conditions. Psoriasis, an affliction of the epidermis, is a common disorder present in approximately 6.4 million people in the United States according to the National Psoriasis Foundation. The frequency of the disease varies with race, age, skin location and other conditions. The characteristic feature of psoriasis is hyperproliferation of the keratinocytes, first described by Van Scott and Ekel.sup.1 There is evidence of significant shortening of the epidermal cell cycle (36 hours versus 311 hours for normal tissue) in the involved skin of patients with psoriasis. In addition there is a doubling of the proliferative cell population and it appears that in psoriatic skin 100% of the germinative cells of the epidermis enter the growth fraction, compared to 60 to 70% for normal skin of non-psoriatic patients. It is felt that as a result of these changes there is an increase in size and in cohesiveness of corneocytes.sup.2 Transplantation studies of normal and psoriatic human skin to congenitally athymic nude mice have found that, although epidermal proliferation remains above normal in the transplanted psoriatic skin, the absence of clinical lesions (erythema, induration and scaling) suggests that epidermal proliferation does not itself give rise to psoriasis. The fundamental cellular and metabolic defects underlying psoriasis are not well understood. Endothelial cells, mast cells and fibroblasts have been implicated in the pathogenesis of the disease.sup.3 Granulocytes are present in the spongioform microabscesses that constitute a hallmark of psoriasis and activation of isolated peripheral granulocytes correlates with disease severity. Web site: http://www.delphion.com/details?pn=US06107349__
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Method and composition for treating psoriasis Inventor(s): McLean; David I. (855 West 10th Avenue, Vancouver, B. C., CA), Burton; Albert F. (297 Rodello Street, Comox, B. C., CA) Assignee(s): none reported Patent Number: 5,217,962 Date filed: January 28, 1992
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Abstract: This invention pertains to the novel use of N-acetyl glucosamine as a cytoprotective agent for persons afflicted with psoriasis by restoring integrity and normal function of skin. A method of treating psoriasis in a human being comprising feeding the human being a therapeutic amount of N-acetyl glucosamine, or a pharmaceutically acceptable salt thereof, on a periodic basis. Excerpt(s): This invention pertains to the novel use of N-acetyl glucosamine as a cytoprotective agent for persons afflicted with psoriasis by restoring integrity and normal function of skin. The skin is the largest organ in the human body and the cells which form the three skin layers are in a constant state of growth, with the outer layer of dead tissue being constantly shed. Replacement of cells from underlying layers is accomplished by cell division and maturation, the cells moving outward constantly at a rate that varies with age, sex, and other conditions. An increased turnover of cells, where there is an increased rate of cell growth and cell death, is a common accompaniment of many conditions including injuries and disorders of various types. In the accompanying increased synthesis of all tissue components there is a strain placed upon the biosynthetic capacities of cells. A major component of the material which covers cells and occupies the spaces between them is glycosaminoglycans (GAG), which are by weight approximately half composed of amino sugars derived from N-acetyl glucosamine (NAG). In skin, about one-fifth of all the glucose utilized by the skin is destined for conversion to amino sugars. Web site: http://www.delphion.com/details?pn=US05217962__ •
Method and composition for treating psoriasis, seborrheic dermatitis and eczema Inventor(s): Smith; Lorraine J. (5801 E. 41st St., Suite 420, Tulsa, OK 74135), Smith; Steven A. (5801 E. 41st St., Suite 420, Tulsa, OK 74135) Assignee(s): none reported Patent Number: 5,681,593 Date filed: July 18, 1995 Abstract: Psoriasis, seborrheic dermatitis and eczema are treated by oral administration of inorganic nickel compound(s), with or without inorganic bromide(s). In an especially preferred embodiment, the nickel compound used to treat these diseases is NiBr.sub.2. Excerpt(s): Psoriasis is a chronic skin disorder that is proliferative in nature and widespread throughout the world, afflicting millions of humans and even domesticated animals having similar proliferative integument problems. The skin disorder is characterized by recurrent, elevated red lesions, plaques or rarely pustules on the skin. These plaques are the results of an excessively rapid growth and shedding of epidermal (skin) cells. No one knows what causes this abnormal cell proliferation. Its severity and course vary greatly from case to case, and also in the individual afflicted with the disease. Recurrences are almost the rule with intervals varying from one month to many years. One person may go through life with a single patch on the elbow, knee or scalp, while another will have repeated attacks of a generalized eruption or widespread chronic lesions lasting for years without remission. As discouraging as it may be, medical science and literature are replete with indications that patients exhibiting such lesions are destined for life to be "psoriatic." With all of the advances in medical science, no one knows what causes this abnormal cell proliferation. With some of it, it is felt that some type of biochemical stimulus triggers this abnormal cell growth. It is still unknown whether the origin of this biochemical malfunction resides in the skin, in the immune
Patents 283
system, in the white blood cells, or is possibly psycho-neural. It is known that certain environmental factors can "trigger" the initial appearance or worsening of psoriasis. Conversely, the symptoms can spontaneously clear for reasons scientists do not understand. Treatment of the psoriasis is aimed at clearing the lesions for as long as possible. This is what is meant by the term "remission" or "clearance." In any event, medical science has fairly well agreed that psoriasis is an heritable disease in which the specific defect seems to be unknown. For years there have been many attempts to treat the disease, and several topical and systemic treatments for psoriasis which inhibit cell division have been with limited success in clearing the skin for short periods of time. Yet, the reason why these treatments work is not yet clearly understood. Treatments which have been suggested in the art appear to be symptomatic and palliative. Lesions may disappear spontaneously or as a result of the therapy, but recurrences are likely. There is a tendency for each remedy gradually to lose its effectiveness or develop dangerous accumulative toxicity. Rarely, however, is the disease apparently cured, showing no evidence for years. Web site: http://www.delphion.com/details?pn=US05681593__ •
Method and compositions for treating psoriasis, eczema, seborrhea and arthritis Inventor(s): Smith; Steven A. (5801 E. 41st, Ste 200, Tulsa, OK 74135) Assignee(s): none reported Patent Number: 6,613,800 Date filed: December 3, 2001 Abstract: A method and composition for treating psoriasis, eczema, seborrheic dermatitis, and possibly arthritis. The present invention involves treatment of these conditions with an oral administration of a mixture comprised of three primary ingredients: fumaric acid and/or fumarate compounds, inorganic nickel compound(s) such as nickel sulfate, and inorganic bromide compound(s) such as potassium bromide. Excerpt(s): The present invention relates to a method and composition for treating psoriasis, eczema, seborrheic dermatitis, and possibly arthritis. More specifically, the present invention involves treatment of these conditions with an oral administration of a mixture of fumaric acid, inorganic nickel compound(s), and inorganic bromide(s). Psoriasis is a chronic skin disorder that proliferates in nature and is widespread throughout the world, afflicting millions of humans and even afflicting domesticated animals having similar proliferative integument problems. The skin disorder is characterized by recurrent, elevated red lesions, plaques and on rarely pustules on the skin. These plaques are the result of an excessively rapid growth and shedding of epidermal or skin cells. No one knows what causes this abnormal cell proliferation. Its severity and course vary greatly from case to case, and also vary in the individual afflicted with the disease. Recurrences are almost the rule with intervals varying from one month to many years. One person may go through life with a single patch on the elbow, knee or scalp, while another will have repeated attacks of a generalized eruption or widespread chronic lesions lasting for years without remission. As discouraging as it may be, medical science and literature are replete with indications that patients exhibiting such lesions are destined for life to be "psoriatic". With all of the advances in medical science, no one knows what causes this abnormal cell growth. With some of it, it is felt that some type of biochemical stimulus triggers this abnormal cell growth. It is still unknown whether the origin of this biochemical malfunction resides in the skin, in the immune system, in the white blood cells, or is possibly psycho-neural. It is know
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that certain environmental factors can "trigger" the initial appearance or worsening of psoriasis. Conversely, the symptoms can spontaneously clear for reasons scientists do not understand. Treatment of the psoriasis is aimed at clearing the lesions for as long as possible. This is what is meant by the term `remission" or "clearance". In any event, medical science has fairly well agreed that psoriasis is a heritable disease in which the specific defect seems to be unknown. Web site: http://www.delphion.com/details?pn=US06613800__ •
Method for alleviating psoriasis Inventor(s): Samuelsson; Bengt I. (Danderyd, SE), Voorhees; John J. (Ann Arbor, MI), Hamberg; Mats A. (Lidingo, SE), Hammarstrom; Sven R. (Djursholm, SE) Assignee(s): The Regents of the University of Michigan (Ann Arbor, MI) Patent Number: 4,181,725 Date filed: May 2, 1977 Abstract: Pharmaceutical compositions administered to humans and animals topically for treatment of proliferative skin diseases, primarily psoriasis. The composition comprises a pharmaceutical carrier with at least one active ingredient selected from the group consisting of para bromophenacyl bromide, alpha tocopherol, mepacrine, chloroquine, hydroxychloroquine, dibucaine, tetracaine, lidocaine, butacaine, procaine, ethylene diamine tetra acetic acid and ethylene glycol bis(.beta.-amino ethyl ether)-N-N' tetra acetic acid; the compositions may also include one or more unsaturated aliphatic compounds, a glucocorticoid and a prostaglandin. Excerpt(s): This invention relates to pharmaceutical compositions for application to the skin and to a method for the treatment of proliferative skin diseases. The compositions may be applied topically, and the treatment can be either therapeutic or prophylactic. Proliferative skin diseases are widespread throughout the world and afflict millions of humans and their domesticated animals. This invention provides a method for treatment of such diseases and pharmaceutical compositions which are useful in alleviating them. As used hereinafter in this specification and in the claims, the expression "proliferative skin diseases" means benign and proliferative skin diseases which are characterized by epidermal cell proliferation, or division, and may also be associated with incomplete tissue differentiation. Psoriasis is the most serious of the skin diseases with which this invention is concerned. Such diseases include: psoriasis, atopic dermatities, non-specific dermatitis, primary irritant contact dermatitis, allergic contact dermatitis, lamellar ichthyosis, epidermolytic hyperkeratosis, premalignant sun induced keratosis, non-malignant keratosis, and seborrheic dermatitis in humans and atopic dermatitis and mange in domesticated animals. Heretofore, proliferative skin diseases have been generally accepted by mankind as an ongoing evil having degrees of severity variable with time, with inherited skin traits and external factors but always have been recognized as unsightly, painful, morbid diseases. Over the history of mankind innumerable medicines and treatments have been proposed, tried and used with varying degrees of success. However, no treatment heretofor devised or pharmaceutical composition used has been entirely successful in the wide spectrum of specific diseases encompassed by the expression proliferative skin diseases. Web site: http://www.delphion.com/details?pn=US04181725__
Patents 285
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Method for suppressing immune response associated with psoriasis, contact dermatitis and diabetes mellitus Inventor(s): Dwyer; Donard S. (Shreveport, LA), Esenther; Kristin (Ashland, MA) Assignee(s): Procept, Inc. (Cambridge, MA) Patent Number: 5,489,441 Date filed: August 19, 1993 Abstract: This invention relates to the use of Ruthenium Red as an immunosuppressive agent to prevent or significantly reduce graft rejection in organ and bone marrow transplantation. Ruthenium Red can also be used as an immunosuppressant drug for T lymphocyte mediated autoimmune diseases, such as diabetes. Furthermore, Ruthenium Red may be useful in alleviating psoriasis and contact dermatitis. Excerpt(s): Replacement of defective or severely injured tissues and organs has been a medical objective as long as medicine has been practiced. Grafts from an individual to himself almost invariably succeed, and are especially important in the treatment of burn patients. Likewise, grafts between two genetically identical individuals almost invariably succeed. However, grafts between two genetically dissimilar individuals would not succeed without immunosuppressive drug therapies. The major reason for their failure is a T cell mediated immune response to cell-surface antigens that distinguish donor from host. Immunosuppressive agents are also indicated in the treatment of autoimmune diseases such as rheumatoid arthritis or type I diabetes mellitus. One particular condition worth mentioning here is psoriasis. This disease is characterized by erythematous patches of skin accompanied by discomfort and itching. Hyperplasia of the epidermis involving proliferation of keratinocytes is also a hallmark feature of psoriasis. An inflammatory component is suggested by: (i) the finding of lymphocytic infiltration of epidermis, and (ii) the fact that immunosuppressive agents such as cyclosporin and corticosteriods have beneficial effect on the disease. A number of drugs are currently being used or investigated for their immunosuppressive properties. Among these drugs, the most commonly used immunosuppressant is cyclosporin A. However, usage of cyclosporin has numerous side effects such as nephrotoxicity, hepatotoxicity and other central nervous system disorders. Thus, there is presently a need to investigate new immunosuppressive agents that are less toxic but equally as effective as those currently available. Web site: http://www.delphion.com/details?pn=US05489441__
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Method for the topical treatment of psoriasis Inventor(s): Perricone; Nicholas V. (350 Cosey Beach Ave., East Haven, CT 06512) Assignee(s): none reported Patent Number: 5,122,536 Date filed: October 12, 1989 Abstract: A method for the therapeutic treatment of psoriasis in which acsorbic acid, or a precursor or derivative thereof, is topically applied to the affected skin areas. Excerpt(s): The present invention relates to the skin disease known as psoriasis and, more particularly, to compositions and methods for the treatment of psoriasis. Psoriasis is without cure, and the course and remission of the disease are unpredictable, even capricious. Current therapeutic regimens include topical or intralesional application of
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corticosteroids, topical administration of anthralin or keratolytics, and use of tar and UV light on affected areas. These many treatments all have their benefits and drawbacks, and many factors must be considered in the choice of therapy. No single therapy is ideal, and it is rare for a patient not to be treated with several alternatives during the relapsing and remitting course of the disease. Whereas systematic treatment can induce prompt resolution of psoriatic lesions, suppression often requires ever-increasing doses, sometimes with toxic side effects, and tapering of therapy may result in rebound phenomena with extensions of lesions, possibly to exfoliation. Information representing the current state of the art with respect to psoriasis and its treatment can be found in, e.g., Lowe, Nicholas J., Practical Psoriasis Therapy, Year Book Medical Publishers, Chicago, 1986, pp. 11-13; Mier, Paul D., and van de Kerhof, Peter C. M., eds., Textbook of Psoriasis, Churchill Livingstone, New York, 1986, pp. 13-39, 167 et seq; and Wyngaarden, James B., and Smith, Lloyd H., Cecil's Textbook of Medicine, W. B. Saunders Co., Philadelphia, 1988, pp. 2326-2327. Web site: http://www.delphion.com/details?pn=US05122536__ •
Method for the treatment of psoriasis Inventor(s): Kallimanis; Georgios (16, Proteos St., Athens, GR) Assignee(s): none reported Patent Number: 4,857,554 Date filed: August 17, 1987 Abstract: Psoriasis in humans is treated by applying to the affected skin area 2-6 times a day an ointment containing ursolic acid and oleanolic acid in the weight ratio of 3:1 dispersed in a vaseline/lanolin carrier. An homogenous ointment may be prepared by dissolving the acids in ethyl ether, adding the carrier, warming until homogeneous and heating to remove the ether. Excerpt(s): Psoriasis is a chronic skin disease which progresses gradually, the main signs and symptoms of which are papulosquamous and itching. The present treatment of psoriasis is symptomatic and is based on the administration of steroids, antibiotics, keratolytics, antiseptics and in some cases cytostatic drugs. The treatment of posoriasis with the presently available drugs is considered satisfactory. The present invention relates to an improved composition for the treatment of psoriasis based on a mixture of ursolic acid and oleanolic acid in a weight ratio of 3:1, dissolved in a petroleum jelly/lanolin carrier, preferably containing propyl paraben and methyl paraben as preservatives. The invention also relates to the method for preparation of the composition and the method of treatment of psoriasis with the composition. A mixture of the oleanolic and ursolic acids is dissolved in the necessary quantity of ethyl ether. A mixture of the lanolin/petroleum jelly is added to the ether solution which is then warmed in order to dissolve the ingredients and form a homogeneous mixture. To this mixture, the necessary quantity of methyl paraben and propyl paraben, dissolved in a small quantity of ethyl alcohol, is added. The whole is warmed to to remove the ether. Web site: http://www.delphion.com/details?pn=US04857554__
Patents 287
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Method for the treatment of psoriasis and genital warts Inventor(s): Cheng; Yung-Chi (Woodbridge, CT), Chu; Chung K. (Athens, GA) Assignee(s): University of Georgia Research Foundation Inc. (Athens, GA), Yale University (New Haven, CT) Patent Number: 6,436,948 Date filed: March 3, 2000 Abstract: The present invention relates to the use of prodrug forms of (-)-(2S,4S)-1-(2hydroxymethyl-1,3-dioxolan-4-yl)cytosine to treat psoriasis, genital warts and other hyperproliferative keratinocyte diseases such as hyperkeratosis, ichthyosis, keratoderma or lichen planus. Excerpt(s): This invention is in the area of medicinal chemistry, and in particular is (-)(2S,4S)-1-(2-hydroxymethyl-1,3-dioxolan-4-yl)cytosine (also referred to as (-)-OddC) or its derivative, and its use to treat cancer in animals, including humans. A tumor is an unregulated, disorganized proliferation of cell growth. A tumor is malignant, or cancerous, if it has the properties of invasiveness and metastasis. Invasiveness refers to the tendency of a tumor to enter surrounding tissue, breaking through the basal laminas that define the boundaries of the tissues, thereby often entering the body's circulatory system. Metastasis refers to the tendency of a tumor to migrate to other areas of the body and establish areas of proliferation away from the site of initial appearance. Cancer is now the second leading cause of death in the United States. Over 8,000,000 persons in the United States have been diagnosed with cancer, with 1,208,000 new diagnoses expected in 1994. Over 500,000 people die annually from the disease in this country. Web site: http://www.delphion.com/details?pn=US06436948__
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Method for treating patients with psoriasis by administering substituted sulfonyl indenyl acetic acids, esters and alcohols Inventor(s): Skopinska-Rozewska; Ewa (Warsaw, PL), Piazza; Gary (Doylestown, PA), Pamukcu; Rifat (Spring House, PA) Assignee(s): Cell Pathways (Horsham, PA) Patent Number: 5,902,827 Date filed: April 17, 1998 Abstract: Substituted indenyl sulfonyl acetic acids, esters and alcohols are useful in the treatment of psoriasis. Excerpt(s): This invention relates to methods for treating psoriasis. Psoriasis is a chronic skin disorder that afflicts about 2 percent of the population. Classic psoriasis--called plaque psoriasis--commonly appears as inflamed swollen skin lesions covered with silvery white scale. Psoriasis can manifest itself in blistering (pustular psoriasis), severe sloughing of the skin (erythrodermic psoriasis), drop-like dotting (guttate psoriasis) or smooth inflamed lesions (inverse psoriasis). About 150,000 to 250,000 new cases of psoriasis are diagnosed each year. Psoriasis most commonly appears on the scalp, knees, elbows, hands and feet, but can affect any part of the skin. It can be very painful and psychologically devastating. The cause of the disease is unknown, though it is believed to have a genetic component, and may be an autoimmune skin disorder. There is no cure for psoriasis, presently, although there are various treatments with varying degrees of success. Current treatments can temporarily clear the plaques and significantly
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improve skin appearance. However, symptoms return once the therapies are discontinued. Thus, therapy must be resumed when the psoriasis returns. Web site: http://www.delphion.com/details?pn=US05902827__ •
Method for treating psoriasis Inventor(s): Hamberg; Mats A. (Lidingo, SE), Voorhees; John J. (Ann Arbor, MI), Hammarstrom; Sven R. (Djursholm, SE), Samuelsson; Bengt I. (Danderyd, SE) Assignee(s): The Regents of the University of Michigan (Ann Arbor, MI) Patent Number: 4,190,669 Date filed: May 2, 1977 Abstract: A process for the treatment of psoriasis comprising administering to humans or domesticated animals topically and/or systemically a composition comprising a pharmaceutical carrier and eicosa-5,8,11,14-tetraynoic acid, its congeners, and the lower alkyl esters thereof; in one preferred form of the invention the composition comprises a pharmaceutical carrier and 5,8,11 eicosatriynoic acid; in another preferred form of the invention the composition comprises a pharmaceutical carrier and at least one active compound selected from the groups eicosa-5,8,11,14-tetraynoic acid, its congeners and the lower alkyl esters thereof and at least one compound selected from the group consisting of PGE.sub.1, PGE.sub.2, PGE.sub.3 and the alkyl esters thereof containing from 1 to 8 carbon atoms inclusive, and 13,14-dihydro PGE.sub.1 and the alkyl esters thereof containing from 1 to 8 carbon atoms inclusive. Excerpt(s): This invention relates to pharmaceutical compositions for and a method of treating psoriasis. The compositions may be applied topically or by injection such that the composition enters the blood stream, or intralesionally or intradermally or subcutaneously or orally. The treatment may be either therapeutic or prophylactic. Psoriasis is well-known to afflict two to three percent of the earth's population and is considered by most to be one of man's most unsightly, painful, morbid diseases. Psoriasis is a complex disorder of many varieties and is not completely medically understood even though extensive research and effort has been expended in the attempt to determine and identify its cause and to provide a cure. It is known that the epidermis of a psoriasis patient is characterized by excessive cell proliferation, incomplete terminal differentiation and glycogen accumulation. Although many compositions and methods for alleviating psoriasis have been proposed and used, only certain of them have been successful; even those considered successful usually alleviated the disease only for temporary periods. There is still a need for improved compositions and methods for treating psoriasis. Previously existent compositions and treatments for psoriasis have provided in certain cases some remission of the original symptoms, or a temporary cure, but each composition or treatment heretofore known suffers from some defect to some degree. For a treatment to constitute a cure for psoriasis, it must be both safe and effective to cause an enduring remission of all the psoriasis lesions on the body to a degree such that they disappear and the skin assumes a normal appearance and is healthy and functional on a continuing basis. Alleviation of psoriasis to a degree less than a complete cure is useful and desirable because a treatment which accomplishes an alleviation in a seriously afflicted patient may be satisfactory to effect a substantially complete or permanent cure in a less seriously afflicted patient. Web site: http://www.delphion.com/details?pn=US04190669__
Patents 289
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Method for treating psoriasis Inventor(s): Reilly; Karen (Cranford, NJ), Abels; Robert I. (Westfield, NJ) Assignee(s): Amgen Inc. (Thousand Oaks, CA) Patent Number: 5,466,447 Date filed: April 21, 1994 Abstract: The present invention provides a therapeutic method of treating a human subject for psoriasis which comprises administering to the subject an effective psoriatic dermatosis-inhibiting amount of IL-2 and a pharmaceutically acceptable carrier. Excerpt(s): Psoriasis is a common chronic and recurrent disease characterized by hyperproliferation of the basal layer of the epidermis resulting in dry, wellcircumscribed, silvery-scaled maculopapules and plaques of various sizes. The lesions occur predominently on the elbows, knees, scalp, and trunk and microscopically show characteristic parakeratosis and elongation of rete ridges. General health is rarely affected, although psoriatic arthritis, a destructive form of arthritis in the fingers and toes which often closely resembles rheumatoid arthritis, may develop in some patients. Onset of psoriasis is usually gradual, however factors precipitating psoriatic eruptions include local trauma and occasionally severe sunburn, irritation, topical medications, chloroquine antimalarial therapy and withdrawal of systemic corticosteroids. 7. decreased to normal suppressor T-lymphocyte function. Web site: http://www.delphion.com/details?pn=US05466447__
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Method for treating psoriasis by externally administering to a patient a pharmaceutical composition containing active-type vitamin D Inventor(s): Suzuki; Yoshiki (Hino, JP), Makino; Yuji (Hino, JP), Aoyagi; Takashi (Sapporo, JP) Assignee(s): Teijin, Limited (Osaka, JP) Patent Number: 4,871,723 Date filed: November 21, 1986 Abstract: A process for treating psoriasis by externally applying to the skin of a warmblooded animal a composition comprising:(A) a pharmaceutically effective amount of an active-type vitamin D.sub.3,(B) a substantially water-free carrier containing the activetype vitamin D.sub.3 dissolved or uniformly dispersed therein, and(C) a solvent selected from fatty acid esters, higher alcohols with 10 or more carbons and propylene carbonate. Excerpt(s): This invention relates to a method of externally applying to the skin of a warm-blooded animal, a pharmaceutical composition for external use containing activetype vitamin D.sub.3. Active-type vitamins D.sub.3 such as 1.alpha.,25dihydroxycholecalciferol, 1.alpha.,24-dihydroxycholecalciferol and 1.alpha.hydroxycholecalciferol are hormones which promote absorption and transportation of calcium in the small intestine, regulate bone absorption and bone resorption in bones and suppress secretion of parathyroid hormone in the parathyroid (U.S. Pat. Nos. 3,901,928 and 4,022,891 and Tetrahedron Letters, 40, 4147, 1972). Hence, the active type vitamins D.sub.3 are used for the treatment of renal failure and osteomalacia in which active-type vitamins D.sub.3 are insufficient and absorption of calcium is reduced, osteoporosis which is a disease associated with abnormal bone metabolism, and rickets showing the insufficiency of vitamin D.sub.3 (Basic Research and Its Clinical
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Applications, 1099-1106, 1979). Recently, new pharmacological activities of the activetype vitamins D.sub.3 were found, and the possibility of using them as therapeutic agents for not only various diseases induced by abnormal metabolism of calcium but other diseases excepting bone disease has been studied. Web site: http://www.delphion.com/details?pn=US04871723__ •
Method for treating psoriasis using selected phosphorylase kinase inhibitor and additional compounds Inventor(s): Heng; Madalene C. Y. (17632 Vincennes St., Northridge, CA 91325) Assignee(s): none reported Patent Number: 5,925,376 Date filed: August 24, 1995 Abstract: An improved method of treating psoriasis involves controlling the enhanced proliferation and terminal differentiation of psoriatic epidermis through the activity of epidermal phosphorylase kinase. In general, the method involves contacting psoriatic epidermal cells with a combination of substances affecting the activity of phosphorylase kinase. The combination can be: (1) a calmodulin inhibitor together with a stimulator of cAMP-dependent protein kinase II, (2) a calmodulin inhibitor together with a calcium channel blocker; (3) a stimulator of cAMP-dependent protein kinase II together with a calcium channel blocker; or (4) a calmodulin inhibitor together with a calcium channel blocker and a stimulator of cAMP-dependent protein kinase II. Alternatively, a selective phosphorylase kinase inhibitor such as curcumin can be administered, alone or with an agent such as vitamin D.sub.3 or an analogue thereof, etretinate, diltiazem, or anthralin. The invention also includes pharmaceutical compositions. Excerpt(s): This application is directed to a method for combined therapy of psoriasis based on methods for decreasing the increased activity of phosphorylase kinase in psoriasis. Psoriasis is an inherited skin disease, the causal mechanisms of which are still unclear. However, the disease is believed to have a strong genetic basis. (H. Baker, "Psoriasis" in Textbook of Dermatology (A. Rook et al., eds., 4th ed., Blackwell Scientific Publications, Boston, 1986), vol. 2, pp. 1469-1532). In fact, this has been confirmed by recent findings from genetic studies of psoriatic families (G. Lomholt, "Psoriasis: Prevalence, Spontaneous Course, and Genetics" (Copenhagen, Denmark, GEC GAD, 1963); E. M. Farber et al., "Natural History of Psoriasis in 61 Twin Pairs," Arch. Dermatol. 109:207 (1974)), which suggest that at least two genes are implicated in the manifestation of psoriasis in predisposed individuals (J. T. Elder et al., "The Genetics of Psoriasis," Arch. Dermatol. 130:216-224 (1994)). One of these has been mapped to the short arm of the 6th chromosome (J. T. Elder et al. (1994), supra), and the other to the distal end of chromosome 17q (J. Tomfohrde et al., "Gene for Familial Psoriasis Susceptibility Mapped to the Distal End of Human Chromosome 17q," Science 264:11411145 (1994)). Chromosome 6 contain genes encoding not only class I and class II antigens of the major histocompatibility complex, but also class III (tumor necrosis factor-alpha ›TNF.alpha.! molecules (J. T. Elder et al. (1994), supra). The expression of TNF.alpha. and its receptors has been shown to be enhanced in psoriatic skin (M. Kristensen et al., "Localization of Tumor Necrosis Factor-Alpha (TNF.alpha.) and Its Receptors in Normal and Psoriatic Skin: Epidermal Cells Express the 55 kD but not the 75 kD TNF Receptor," Clin. Exp. Immun. 94:354-362 (1993)), pointing to the possible role of superantigens in precipitating the disease (M. C. Y. Heng et al., "Erythroderma Associated with Mixed Lymphocyte-Endothelial Cell Interaction and Staphylococcal aureus Infection," Br. J.
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Dermatol. 115:693-705 (1986); B. J. Nickoloff et al., "Activated Keratinocytes Present Bacterial-Derived Superantigens to T Lymphocytes: Relevance to Psoriasis," J. Dermatol. Sci. 6:127-133 (1993)). Current investigations suggest that TNF.alpha., through its capacity to influence the expression of the nuclear proto-oncoproteins, c-myc (J. X. Lin & J. Vilcek, "Tumor Necrosis Factor and Interleukin-1 Causes Rapid and Transient Stimulation of c-fos and c-myc mRNA in Fibroblasts," J. Biol. Chem. 262:11908-11911 (1987)) and c-fos (M. Hendriksson et al., "Phosphorylation Sites Mapping in the NTerminal Domain of c-myc Modulate its Transforming Potential," Oncogene 8:3199-3209 (11993)), which are known to be important in regulation of cell growth and differentiation (O. Baadsgaard et al., "UM4D4+ (CDw60) T Cells Are Compartmentalized in Psoriatic Skin and Release Lymphokines that Induce a Keratinocyte Phenotype Expressed in Psoriatic Skin Lesions," J. Invest. Dermatol. 95:275282 (1990)), may be important in increasing the gene expression of phosphorylase kinase. This hypothesis is consistent with current concepts involving the role of cytokines and proto-oncogenes in the phenotypic expression of psoriasis (J. T. Elder et al., "Protooncogene Expression in Normal and Psoriatic Skin," J. Invest. Dermatol. 94:1925 (1990); G. Sozzi et al., "A t(10.17) Translocation Creates the RET/PTC2 Chimeric Transforming Sequence in Papillary Thyroid Carcinoma," Genes, Chromosomes & Cancer 9:244-250 (1994)). It has been suggested that increased phosphorylase kinase activity may be due to defective regulation or presence of multiple copies of sequences encoding phosphorylase kinase in the genome of the psoriatic individual. This explanation is unlikely since, of the protein moieties under consideration, only the gene sequences encoding the regulatory subunit of cAMP-dependent protein kinase II has been mapped to the 17th chromosome (P. J. Barnard et al., "Mapping of the Phosphorylase Kinase Alpha Subunit Gene on the Mouse X Chromosome," Cytogenet. & Cell Genet. 53:91-94 (1990)). On the other hand, none of the phosphorylase kinase subunits have been mapped to chromosome 17. Instead, the alpha subunit of phosphorylase kinase has been mapped to the X chromosome, where it lies between the genes encoding the X-linked zinc finger protein and phosphoglycerate kinase genes (P. J. Williams et al., "Mapping of the Gene for X-Linked Liver Glycogenosis due to Phosphorylase Kinase Deficiency to Human Chromosome Region Xp22," Genomics 9:565-569 (1991); M. W. Kilimann, "Molecular Genetics of Phosphorylase Kinase: cDNA Cloning, Chromosomal Mapping and Isoform Structure," J. Inher. Metab. Dis. 13:435-441 (1990)); the.beta. subunit to chromosome 16 (T. A. Jones et al., "Localization of the Gene Encoding the Catalytic Gamma Subunit of Phosphorylase Kinase to Human Chromosome Bands 7p12-q21," Biochim. Biophys. Acta 1048:24-29 (1990)), and the catalytic (.gamma.) subunit to chromosome 7 (N. J. Lowe & H. B. Ridgeway, "Generalized Pustular Psoriasis Precipitated by Lithium," N. Eng. J. Med. 114:1788-1789 (1978)), and calmodulin (.delta.) subunit to chromosome 10. Aggravation of psoriasis by drugs which lower cAMP levels (M. C. Y. Heng & M. K. Heng, "Beta-Adrenoceptor Antagonist-Induced Psoriasiform Eruption," Int. J. Dermatol. 27:617-627 (1988); M. Sikorsia & J. F. Whitfield, "The Regulatory and Catalytic Subunits of Rat Liver Cyclic AMP-Dependent Protein Kinases Respond Differently to Thyroparathyroidectomy and 1.alpha., 25-Dihydroxyvitamin D3," Biochem. Biophys. Res. Commun. 129:766-772 (1985)) also supports cAMP-dependent protein kinase deficiency and defective deactivation of phosphorylase kinase as a basic mechanism in psoriasiform hyperplasia in psoriasis. Web site: http://www.delphion.com/details?pn=US05925376__
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Method for treating psoriasis with cytotoxic agents Inventor(s): Pearlman; Dale L. (21063 Christensen Dr., Cupertino, CA 95014) Assignee(s): none reported Patent Number: 4,853,388 Date filed: May 15, 1987 Abstract: A method for treating psoriasis comprising applying an effective amount of a cytotoxic drug dispersed in a pharmaceutically acceptable vehicle containing a penetrating solvent for the drug, the drug being applied to the skin area affected by the psoriasis without occlusion in pulses of from 1 to 3 applications per pulse, the pulses being applied at an interval of once every from 3 to 30 days and preferably at an interval of from 4 to 14 days. Optimally, the penetrating solvent is free from toxic effects, such as AZONE or similar substituted azacycloalkyl-2-ones, tertiary amine oxides, and the like. Excerpt(s): This invention relates to the therapeutic treatment of skin disorders such as psoriasis. In particular, this invention relates to an effective regimen for successfully treating psoriasis with a cytotoxic agent such as 5-fluorouracil in a penetrating solvent. Psoriasis is a chronic, hereditary, recurrent, papulosquamous dermatosis, the distinctive lesion of which is a vivid red macule, papule, or plaque covered almost to its edge by silvery lamellated scales. It usually involves the scalp and extensor surfaces of the limbs, especially the elbows, knees and shins. Traditional treatments of psoriasis have included daily or more frequent application of corticosteroids such as betamethasone acetate, betamethasone valerate, fluocinolone acetonide, fluocinolone acetonide acetate, and the like dissolved or suspended in an ointment, lotion, or glycol solvent to the affected area. Occlusive techniques such as wrapping cortiocoid treated areas with a moistureimpermeable wrapping such as a self-attracting plastic film such as polyvinylidene chloride film (SARAN) has been found to increase the effectiveness of the treatment. Penetrating solvents have been investigated for enhancing percutaneous absorption of these drugs in an effort to more successfully treat more resistive conditions. Web site: http://www.delphion.com/details?pn=US04853388__
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Method for treatment of psoriasis Inventor(s): Weber; Gerhard (Virchowstrasse 5, 8500 Nurnberg, DE) Assignee(s): none reported Patent Number: 4,382,921 Date filed: May 1, 1981 Abstract: A method for the treatment of psoriasis comprising administering an antipsoriasis effective amount of an antagonist of the growth hormone. Excerpt(s): This invention relates to a method for the treatment of psoriasis. Large segments of the population are affected by psoriasis. However, the cause of this disease is thus far unknown, see, for example, Brockhaus Encyclopedic Dictionary 1972, Vol. 15, Page 224. Generally, the treatments described in this reference include treatments with corticosteroids which can achieve a certain amount of a short term regression of the disease. This method as well as other methods known today have not produced a complete cure. I have discovered a method for the treatment of psoriasis which has achieved significant regression of the disease. My invention is based on the discovery that the cause of psoriasis is a persistence of the secretion of the human growth
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hormone, i.e., somatotropic hormone). Thus, the invention comprises the administration of an antagonist for the growth hormone in amounts effective to sufficiently antagonize the secretion of the hormone to normalize the psoriasis. Web site: http://www.delphion.com/details?pn=US04382921__ •
Method for treatment of psoriasis Inventor(s): Quarles; Ruth (1306 Karen Oval, Vienna, OH 44473) Assignee(s): none reported Patent Number: 5,776,920 Date filed: August 2, 1995 Abstract: A preparation containing salicylic acid, lactic acid and urea in a moisturizing base, which can be used for the topical treatment of psoriasis. Excerpt(s): This invention relates to a composition for the treatment of psoriasis, a process for preparing the composition, and a method of treating psoriasis using the composition. Psoriasis is a condition characterized by hyperproliferation of skin above an erythematous base. The disorder has a rapid turnover and greatly increased production of epidermal cells with lichenification and shedding. Dilated capillaries underlie these scales, producing the erythematous base. This multifactorial condition, known for remissions and recurrences, has no known cure. The disorder can affect any area of skin, but primarily affects the extensor surfaces of the knees, elbows, knuckles, scalp, and buttocks. Psoriasis is characterized by severe itching, scaling, bleeding with scratching and trauma, and infection. The disorder often results in severe embarrassment. Currently available treatments are generally directed towards reducing the rate of cell growth; keratolysis; anti-inflammatory action; inhibition of prostaglandin production; and inhibition of DNA synthesis. The most frequently used medications are corticosteroids, tar preparations, ultraviolet light treatments and systemic drugs. Web site: http://www.delphion.com/details?pn=US05776920__
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Method for treatment of psoriasis Inventor(s): Jaros; Apolonia (late of Bosna, YU), Miketin; Bronhilda (2019 E. 2nd St., Duluth, MN 55812) Assignee(s): none reported Patent Number: 6,316,001 Date filed: January 10, 2000 Abstract: This invention relates to the natural topical treatment of portions of skin of a person afflicted with psoriasis or other skin disorders such as dry skin, eczema, itchy skin, red skin, itchy eczema, inflamed skin, and/or cracked skin for the removal of itch and the restoration of the affected areas of skin to a normal condition. The natural treatment of a skin disorder initially involves formation of a natural ointment from the ingredients identified as chicken and hen herb; ruta herb; pure unsalted natural butter; and pure natural beeswax. The natural ointment is formed by combination of the ingredients which includes heating and stirring. The ointment is then applied twice daily to affected areas of skin until a natural cure of the skin disorder is obtained. Excerpt(s): The present invention relates to a topical composition for the treatment of psoriasis or other skin disorders such as dry skin, eczema, itchy skin, red skin, itchy
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eczema, inflamed skin, and/or cracked skin. Psoriasis is generally a skin disease evidenced by the presence of skin elevations and scales which may be silvery in appearance. Psoriasis in general is a disease which accelerates the epidermal proliferation and proliferation of capillaries in the dermal region. In addition, psoriasis frequently results in the evasion of the dermis and epidermis by inflammation of the affected cells. Areas of skin affected by psoriasis also frequently lose water significantly faster than normal healthy skin. The areas of skin affected by psoriasis therefore tend to have increased metabolic rates which in turn has a negative impact on tissue catabolism and potentially causes muscle wasting. Psoriasis as a chronic skin disease has been difficult to treat. Psoriasis may affect an individuals skin proximate to elbows, knees, trunk, and scalp. In the past, the treatment of psoriasis has included the use of various chemical agents including but not limited to dihydroxyanthralin, azarabine, colchicine, fluorouracil, methotrexate, methoxsalen, and the use of ultra-violet light. These methods have generally not provided satisfactory treatment of psoriasis for individuals. Web site: http://www.delphion.com/details?pn=US06316001__ •
Method for treatment of psoriasis, by omeprazole or related compounds Inventor(s): Hasselkus; Wolfgang (Rodental, DE) Assignee(s): Astra Aktiebolag (Sodertalje, SE) Patent Number: 5,714,505 Date filed: June 24, 1996 Abstract: A method for treatment of psoriasis is disclosed comprising administration of a therapeutically effective dosage of omeprazole. Excerpt(s): The present invention relates to a novel method of treating psoriasis. Psoriasis is a primary disease of the skin characterized by well-demarcated, inflammatory papules and plaques, which are typically covered by thickened scales. It is a disease of increased proliferation of epidermal cells, the precise cause of which is unknown. The incidence of psoriasis in e.g. the U.S. is about 2%. About 3% of whites and 1% of blacks are affected. Web site: http://www.delphion.com/details?pn=US05714505__
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Method of treating psoriasis Inventor(s): Johnson; Zelma M. (1574 Beupre, Madison Heights, MI 48071) Assignee(s): none reported Patent Number: 4,454,118 Date filed: December 9, 1981 Abstract: A cosmetic composition and a process for alleviating dry skin conditions of the hands, feet, cuticle, neck and facial areas and psoriasis comprising an admixture of lanolin, petrolatum and glycerine. Minor amounts of essential oils and other conditioners can be incorporated. Excerpt(s): This invention relates to cosmetic compositions and a process for alleviating dry skin conditions of the hands, feet, neck, cuticles and facial areas of the human body. More particularly, the invention relates to cosmetic compositions comprising an
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admixture of lanolin, petrolatum and glycerine. Yet, it will be appreciated that the expansion and growth of the prior art has devolved highly complex synthetic adjuvants for use in the formulations. Thus, organic surfactants, alcohols and the like are incorporated into the compositions of the prior art. The present invention, on the other hand, employs naturally occurring substances to achieve its purposes. Web site: http://www.delphion.com/details?pn=US04454118__ •
Method of treating psoriasis Inventor(s): McLaughlin; Julia (W. Roxbury, MA), Holick; Michael F. (Sudbury, MA) Assignee(s): The General Hospital Corporation (Boston, MA) Patent Number: 4,728,643 Date filed: November 2, 1984 Abstract: A method of treating psoriasis in a patient which comprises administering to said patient an effective amount of a vitamin D compound which is capable of stimulating the differentiation of cultured tumor cells or normal rodent or human fibroblasts or keratinocytes in vitro. Excerpt(s): The present invention relates to a novel method of treating psoriasis, a disease of the skin. The method comprises using vitamin D-related compounds. The disease is diagnosed by the presence of scaling erythematous on the scalp and extender aspects of the arms and legs; psoriatic lesions often are accentuated on the sites of repeated trauma, such as the elbows and knees. The papules or plaques of psoriasis often contain a silvery-white micaceous scale that is relatively easily removed in layers. There is a several fold increase in the normal number of the basal cells of the epidermis. This increase in the basal cell population reduces the turnover time of the epidermis from the normal 27 days to 3-4 days. This shortened interval leads to the consequence that normal events of call maturation or keratinization do not occur, and this failure of maturation is reflected by an array of abnormal morphologic and biochemical changes. Numerous cytologic, histologic, histochemical and biochemical alterations are now known to be the result, rather than the cause of the disease process. The only main fact known at this time about the fundamental cause of psoriasis is that the predisposition to its development is genetically transmitted. (This introduction is basically taken from Harrison's Principles of Internal Medicine, 10th Ed., Vol, 1, pp. 256 and 257). The treatment of psoriasis still remains the province of dermatologists. The most effective treatment in the control of localized psoriasis for most patients is the topical use of corticosteroids with a plastic wrap and ultraviolet light or sunlight exposures. On certain patients who have generalized psoriasis, it has been necessary to use a variety of systemic chemotherapeutic agents, especially methotrexate; the latter has the capacity to inhibit cell replication without a proportionate inhibition of cell function; i.e. keratinization. Photochemotherapy was introduced in 1974, in the so-called PUVA treatment. In this treatment, psoralen is administered two hours before total body irradiation with a special light system that emits predominantly long wave ultraviolet light. The light alone is ineffective in producing erythema or remission of psoriatic lesions; however, in the presence of one of the psoralens, the UV-A light becomes a potent photoactive agent and produces a remission of psoriatic lesions after several exposures. Photochemotherapy requires specialized knowledge and lighting systems delivering precisely measured amounts of ultraviolet light. Web site: http://www.delphion.com/details?pn=US04728643__
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Method of treating psoriasis Inventor(s): Cabezas; Orestes (10201 Fountainbleau Blvd., #205, Miami, FL 33172) Assignee(s): none reported Patent Number: 5,176,912 Date filed: January 29, 1991 Abstract: A method of treating psoriasis which includes subcutaneously injecting into the tissue of a person a dose of cc of a mixture composed of 0.1 milligrams histamine phosphate, 9.25 milligrams bacteriologic peptadase, 110.00 milligrams diprophylline, 4.0 milligrams chlorophenamine, about 0.1 milligram methyl paraben and propylparaben, about 0.2 milligrams sodium chloride, water and then observing the site for between one and three days to observe when the tissue surface at the site is no longer inflamed and is normal and, then, successively injecting 1 cc again and again with a similar observation interval for a period of about two weeks to develop a tolerance to the mixture; and thereafter, repeating the process of injecting every twenty-four hours to seventy-two hours with a 2 cc injection until the symptoms of the psoriasis condition disappear. Excerpt(s): The present invention relates to a series of treatments for the dermatological condition accompanied by pathological cell proliferation. Diseases accompanied by a pathological epidermal cell proliferation are relatively frequent and concern a substantial portion of the population. A main condition is known as psoriasis. Previous efforts to resolve symptoms of this disease include the method of U.S. Pat. No. 4,328,231 which teaches a topical application to the skin of a person with the disease; the method of U.S. Pat. No. 4,228,176, wherein a patient is administered an anti-inflammatory amount of Burimamide or a pharmaceutically acceptable salt thereof; the method of U.S. Pat. No. 3,212,970, wherein an antihistaminic component is utilized and injected intramuscularly; and the method of U.S. Pat. No. 3,904,766, wherein tolerance is induced to the drug, mechlorethamine hydrochloride, by intravenous injections over a three week period and, subsequently and periodically applying topically a composition of the chemical in an anhydrous pharmaceutically acceptable carrier. The present invention is of the discovery that a patient having the disease of psoriasis may enjoy a disappearance of the symptoms by, first, building a tolerance by subcutaneous injections of a medicine described below during a period of about two weeks with the successive injections spaced from one another by a period of about one to three days. The medicine is a solution sold under the commercial name Desensil. After the two week period of successive injections and the development of tolerance, the amount of the injections is increased from one cc to no more than two cc's per injection and the process is continued until the symptoms of the psoriasis condition disappear. Web site: http://www.delphion.com/details?pn=US05176912__
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Method of treating psoriasis Inventor(s): Sredni; Benjamin (Kfar Saba, IL), Albeck; Michael (Ramat Gan, IL) Assignee(s): Biomas Inc. (Tel Aviv, IL) Patent Number: 6,472,381 Date filed: October 12, 2001
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Abstract: The invention comprises the administration of an effective amount of a tellurium compound to a patients who is afflicted with psoriasis. The tellurium compound is administered either systemically or topically to one who is afflicted with psoriasis in an amount which is effective to alleviate the symptoms of psoriasis. Excerpt(s): Psoriasis is a well known condition which affects the skin of affected patients. The disease manifests itself as chronic, recurring silvery papules, scaling papules and plaques of various sizes. The condition may consist of one or two lesions or may be a widespread dermatosis with disabling arthritis or exfoliation. The cause is not known. Treatment in the prior art has comprised the use of lubricants, keratolytics, and topical corticosteroids. In severe disabling psoriasis, methotrexate may be used or PUVA (psoralens and high intensity ultraviolet light) masy be used. The applicant has discovered that the use of a tellurium compound will alleviate the symptoms of psoriasis. The invention comprises the administration of an effective amount of a tellurium compound to a patients who is afflicted with psoriasis. The tellurium compound is administered either systemically or topically to one who is afflicted with psoriasis in an amount which is effective to alleviate the symptoms of psoriasis. Web site: http://www.delphion.com/details?pn=US06472381__ •
Method of treating psoriasis of the nails and composition Inventor(s): Bernstein; Joel E. (615 Brierhill Rd., Deerfield, IL 60015) Assignee(s): none reported Patent Number: 4,250,164 Date filed: April 9, 1979 Abstract: An improved method of treating psoriasis of the nails comprising applying nail polish containing an anti-psoriasis effective amount of a topical steroid effective against psoriasis therein and composition useful in said method. Excerpt(s): Psoriasis is a chronic relapsing papulosquamous skin disease which can also affect nails. Nail involvement resembles a fungus infection with stippling, separation of the distal margin, nail loss, scales under the nail plate, thickening and discoloration and is seen in anywhere from ten to fifty percent of psoriasis patients. While there are a limited number of effective anti-psoriasis agents, it is far more difficult to treat psoriasis of the nails than that of the skin. Treatment of psoriasis (skin) can include daily removal of the scales by applying soap and water and scrubbing gently with a soft brush, followed by the application of a keratolytic ointment. Web site: http://www.delphion.com/details?pn=US04250164__
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Method of treating psoriasis using synthetic peptide compositions Inventor(s): Bridge; Peter (Washington, DC), Goodwin; Frederick K. (Chevy Chase, MD) Assignee(s): The United States of America as represented by the Secretary of the (Washington, DC) Patent Number: 5,248,667 Date filed: July 18, 1991
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Abstract: Peptides previously disclosed as useful for preventing HIV from binding to cell binding sites have now been shown to have thymoleptic qualities and to be useful for tretment of psoriasis in patients who lack antibodies against HIV. Excerpt(s): Peptides which inhibit binding of the human immunodeficiency virus (HIV) to receptor sites on the cell surface have now been shown to be useful as agents for treatment of mental disorders and psoriasis not associated with HIV infections. Compositions formulated for administration by sublingual or nasal route have proven particularly useful. have been disclosed by Pert, et al (U.S. patent application Ser. No. 07/048,148, abandoned). These short peptides inhibit binding of human immunodeficiency virus (HIV) to human cells by blocking receptor sites on the cell surface. The realization that viruses may exert cell and tissue tropism by attachment at highly specific sites on cell membrane receptors has encouraged investigators to seek agents which would bind at the viral receptor sites of cell membranes, thus preventing binding of a specific virus to these cells. A demonstration of specific receptor-mediated vaccinia virus infectivity being blocked by synthetic peptides has been previously demonstrated (Epstein et al, Nature 318:663-667). Web site: http://www.delphion.com/details?pn=US05248667__ •
Method of treating psoriasis, arthritis and reducing the toxicity of cancer chemotherapy Inventor(s): Batts; Donald Herman (Kalamazoo, MI), Ulrich; Roger G. (Gurnee, IL) Assignee(s): Pharmacia & Upjohn Company () Patent Number: 6,040,306 Date filed: November 10, 1998 Abstract: The present invention is a method of treating a person who has psoriasis or arthritis or reducing the toxicity of cancer chemotherapy which comprises administering to the patient an anti-psoriasis effective amount of an oxazolidinone, preferably (S)-N[[3-[3-fluoro-4-(4-morpholinyl)phenyl]-2-oxo-5-oxazolidinyl]methyl]a cetamide. Excerpt(s): The present invention is the use of known oxazolidinones to treat psoriasis, arthritis and to reduce the toxicity of cancer chemotherapy. U.S. Pat. Nos. 5,164,510, 5,231,188, 5,565,571, 5,652,238 and 5,688,792 all disclose various oxazolidinone antibiotics which are well known to those skilled in the art. Psoriasis is a well known condition, a proliferative disease of the skin of unknown etiology. It is not known, or believed, to have a microbiologic cause. Web site: http://www.delphion.com/details?pn=US06040306__
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Method of using IL-11 for treating psoriasis Inventor(s): Schendel; Paul (Wayland, MA), Keith; James (Andover, MA) Assignee(s): Genetics Institute, Inc. (Cambridge, MA) Patent Number: 5,958,401 Date filed: December 10, 1997 Abstract: Provided by the present invention are methods of treating psoriasis using IL11.
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Excerpt(s): The present invention relates generally to methods of treating disorders such as AIDS, arthritis (rheumatoid arthritis, osteoarthritis, spondyloarthropathies), antibiotic induced diarrheal diseases (Clostndium difficile), multiple sclerosis, osteoporosis, gingivitis, peptic ulcer disease, esophagitis, diabetes, retinitis, uveitis, reperfusion injury after myocardial infarction (MI), cerebral vascular accident (CVA), aphthous ulcers (oral), atherosclerosis (plaque rupture), prevention of tumor metastases, asthma, preeclampsia, acute pancreatitis, psoriasis, infertility and allergic disorders such as rhinitis, conjunctivitis, and urticaria. Inflammatory responses include a broad range of host reaction to a variety of insults, such as injury, infection, or rejection. It is the over production of mediators that is believed to be associated with a broad range of disorders, including AIDS, arthritis (rheumatoid arthritis, osteoarthritis, spondyloarthropathies), antibiotic induced diarrheal diseases (Clostfidium diffcile), multiple sclerosis, osteoporosis, gingivitis, peptic ulcer disease, esophagitis, diabetes, retinitis, uveitis, reperfusion injury after myocardial infarction (MI), cerebral vascular accident (CVA), aphthous ulcers (oral), atherosclerosis (plaque rupture), tumor metastases, asthma, preeclampsia, acute pancreatitis, psoriasis, infertility and allergic disorders such as rhinitis, conjunctivitis, and urticaria. These disorders and their symptoms are briefly summarized below. According to the methods of the present invention, IL-11 is administered to modulate the hosts' over reaction to insult thereby treating the following disorders. Web site: http://www.delphion.com/details?pn=US05958401__ •
Methods and compositions for the treatment of psoriasis Inventor(s): Foon; Kenneth A. (Lexington, KY), Chatterjee; Malaya (Lexington, KY) Assignee(s): University of Kentucky Research Foundation (Lexington, KY) Patent Number: 6,355,244 Date filed: November 16, 1998 Abstract: This invention provides methods of treating psoriasis which entail eliciting an immune response in an individual against an antigen aberrantly expressed in psoriatic tissue, such as a ganglioside, in an individual. The anti-ganglioside immune response is elicited by administration of an antigen such as a ganglioside, an anti-idiotype moiety for a ganglioside, or a polynucleotide encoding an anti-idiotype moiety. Also described is a strategy for developing additional compositions for psoriasis. The compositions elicit an immunological response against a target antigen present on psoriatic tissue, which in turn can be detected using antibody affinity-purified from the serum of the treated subject. The presence of the immunological response correlates positively with control or resolution of the psoriatic symptoms. Excerpt(s): Psoriasis is a chronic condition that affects as much as 2.6% of the population of the developed world. A recent survey reported by the National Psoriasis Foundation estimates that 6.4 million people suffers from psoriasis, of which about 500,000 is rated as severe. The annual patient cost for treating psoriasis is currently estimated at $1.6 to $3.2 billion. Every year, about 400 people are granted disability by the Social Security Administration, and another 400 people die from psoriasis-related causes. It is not known what causes psoriasis, although there is evidence of a genetic predisposition and an autoimmune etiology. Onset may be triggered by systemic infections such as strep throat, skin injury, vaccinations, and certain oral medications such as steroids. Subsequently, the immune system is thought to induce inflammation and excessive skin cell reproduction, which can be exacerbated by additional factors such as stress and diet.
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In normal skin, the time for a cell to move from the basal layer through the granular layer is 4-5 weeks. In psoriatic lesions, the time is decreased 7-10 fold because of a shortened cell cycle time, an increase in the absolute number of cells capable of proliferating, and an increased rate of division. T cell mediated immune responses appear to be responsible for the inflammation and hyperproliferation of keratinocytes. Neutrophils are found in psoriatic lesions, associated with increased levels of plasminogen activator. Psoriatic fibroblasts have increased levels of enzymes involved in collagen synthesis, secondary to expansion of the papillary dermis. Psoriatic plaques comprise HLA-DR positive keratinocytes and Langerhans cells, and activated T cells expressing elevated levels of IL-2 receptors. Web site: http://www.delphion.com/details?pn=US06355244__ •
Methods and compositions for treating psoriasis with retinoyl compounds Inventor(s): Yu; Ruey J. (4 Lindenwold Ave., Ambler, PA 19002), Van Scott; Eugene J. (1138 Sewell La., Rydal, PA 19046) Assignee(s): none reported Patent Number: 4,216,224 Date filed: September 22, 1978 Abstract: Compositions and methods for treating the symptoms of psoriasis consisting of topical application of a solution, gel, lotion, cream or ointment containing as a principal active ingredient one or more retinoyl compounds is disclosed. The active ingredient consists of one or more compounds which are retinoyl esters of a hydroxy acid, a hydroxy amide, or a hydroxy acid ester, or a retinoyl carbamic or thiocarbamic acid derivative. The composition of this invention may include a single member of the above active ingredients present in a total amount of from 0.01 to 5% by weight of the total composition, or a plurality thereof present in a preferred concentration of from 0.02 to 2% by weight of the total composition. Excerpt(s): Retinoic acid is known to be useful in the treatment of acne as disclosed in U.S. Pat. No. 3,729,568. In addition, in our previous U.S. Pat. No. 3,932,665 it was disclosed that retinal was useful in the treatment of acne without causing a worsening or irritation or peeling of the skin, a condition observed with the use of retinoic acid. In our above-identified U.S. patent application Ser. No. 869,351, filed Jan. 13, 1978, it was disclosed that alpha-hydroxyretinoic acids, alpha-ketoretinoic acid and mixtures thereof are useful in treating epithelial tissue that exhibits a disturbance in its keratinization. Said compounds were disclosed as active in the treatment of such conditions as dry skin, ichthyosis, dandruff, acne, psoriasis, eczema, mycosis fungoides, and even active in alleviating the symptoms of skin cancer. It has now been discovered that certain additional compounds broadly described as retinoyl derivatives are active in the treatment of psoriasis by topical application. The compounds of this invention have been found to be effective in alleviating the symptoms of psoriasis without causing unacceptable or painful skin irritation, burning or the like, and in addition, that the compounds of this invention are relatively non-toxic at the acceptable level of dosage for topical application. Web site: http://www.delphion.com/details?pn=US04216224__
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Methods and compounds for the treatment of immunologically-mediated psoriasis Inventor(s): Tan; Paul L. J. (Auckland, NZ), Watson; James D. (Auckland, NZ) Assignee(s): Genesis Research & Development Corp. (Auckland, NZ) Patent Number: 5,968,524 Date filed: December 23, 1997 Abstract: Methods for the treatment of skin disorders, including psoriasis, atopic dermatitis, allergic contact dermatitis, alopecia areata and skin cancers are provided, such methods comprising administering multiple doses of a composition having antigenic and/or adjuvant properties. Compositions which may be usefully employed in the inventive methods include inactivated M. vaccae cells, delipidated and deglycolipidated M. vaccae cells, M. vaccae culture filtrate and compounds present in or derived therefrom, together with combinations of such compositions. Excerpt(s): This invention relates generally to the treatment by vaccination or immunotherapy of skin disorders such as psoriasis, atopic dermatis, allergic contact dermatitis, alopecia areata, and the skin cancers basal cell carcinoma, squamous cell carcinoma and melanoma. In particular, the invention is related to the use of compounds which are present in or have been derived from Macobacterium vaccae (M. vaccae) or from the culture filtrate of M. vaccae. This invention deals with treatment of disorders of skin which appear to be associated with factors that influence the balance of thymus-derived (T) immune cells known as Th1 and Th2. These T cells are identified by their cytokine secretion phenotype. A common feature of treatment is the use of compounds prepared from M. vaccae which have immunomodulating properties that alter the balance of activities of these T cells as well as other immune cells. Psoriasis is a common, chronic inflammatory skin disease which can be associated with various forms of arthritis in a minority of patients. The defect in psoriasis appears to be overly rapid growth of keratinocytes and shedding of scales from the skin surface. Drug therapy is directed at slowing down this process. The disease may become manifest at any age. Spontaneous remission is relatively rare, and life-long treatment is usually necessary. Psoriasis produces chronic, scaling red patches on the skin surface. Psoriasis is a very visible disease, it frequently affects the face, scalp, trunk and limbs. The disease is emotionally and physically debilitating for the patient, detracting significantly from the quality of life. Between one and three million individuals in the United States have psoriasis with nearly a quarter million new cases occurring each year. Conservative estimates place the costs of psoriasis care in the United States currently at $248 million a year. Web site: http://www.delphion.com/details?pn=US05968524__
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Methods for the treatment of psoriasis and genital warts Inventor(s): Chu; Chung K. (Athens, GA), Cheng; Yung-Chi (Woodbridge, CT) Assignee(s): Yale University (New Haven, CT), The University of Georgia Research Foundation Center (Athens, GA) Patent Number: 6,063,787 Date filed: January 26, 1998
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Abstract: The present invention relates to the use of (-)-(2S,4S)-1-(2-hydroxymethyl-1,3dioxolan-4-yl) cytosine to treat psoriasis, genital warts and other hyperproliferative keratinocyte diseases such as hyperkeratosis, ichthyosis, keratoderma or lichen planus. Excerpt(s): This invention is in the area of medicinal chemistry, and in particular is (-)(2S,4S)-1-(2-hydroxymethyl-1,3-dioxolan-4-yl)cytosine (also referred to as (-)-OddC) or its derivative, and its use to treat cancer in animals, including humans. A tumor is an unregulated, disorganized proliferation of cell growth. A tumor is malignant, or cancerous, if it has the properties of invasiveness and metastasis. Invasiveness refers to the tendency of a tumor to enter surrounding tissue, breaking through the basal laminas that define the boundaries of the tissues, thereby often entering the body's circulatory system. Metastasis refers to the tendency of a tumor to migrate to other areas of the body and establish areas of proliferation away from the site of initial appearance. Cancer is now the second leading cause of death in the United States. Over 8,000,000 persons in the United States have been diagnosed with cancer, with 1,208,000 new diagnoses expected in 1994. Over 500,000 people die annually from the disease in this country. Web site: http://www.delphion.com/details?pn=US06063787__ •
Methods for treating psoriasis Inventor(s): Elslager; Edward F. (Ann Arbor, MI) Assignee(s): Warner-Lambert Company (Ann Arbor, MI) Patent Number: 4,391,809 Date filed: November 13, 1980 Abstract: Methods for treating psoriasis by administering 2,4-diamino-5-methyl-6[(3,4,5-trimethoxyanilino)methyl]-quinazoline, 2,4-diamino-5-chloro-6-[(3,4dichloroanilino)methyl]-quinazoline or a pharmaceutically acceptable acid-addition salt thereof. Excerpt(s): The present invention relates to methods for treating psoriasis in mammals, such as dogs, horses, sheep, etc., by administering 2,4-diamino-5-methyl-6-[(3,4,5trimethoxyanilino)methyl]quinazoline, 2,4-diamino-5-chloro-6-[(3,4dichloroanilino)methyl]quinazoline or a pharmaceutically acceptable acid-addition salt thereof. The term "pharmaceutically acceptable acid-addition salt" is intended to mean any salt form that is prepared from a relatively non-toxic acid, such as the hydrochloride, sulfate, phosphate, benzoate, acetate, citrate, tartrate, etc. In addition, 2,4-diamino-5-methyl-6-[(3,4,5-trimethoxyanilino)methyl]quinazoline, 2,4-diamino-5chloro-6-[(3,4-dichloroanilino)methyl]quinazoline and their pharmaceutically acceptable acid-addition salts can exist in anhydrous forms as well as in solvated (such as an acetate, hydrates, etc.) forms. In general, the hydrated forms and the solvated forms with pharmaceutically acceptable solvents are equivalent to the anhydrous or unsolvated form for the purposes of the invention and are intended to be within the scope of this invention. Web site: http://www.delphion.com/details?pn=US04391809__
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Methods of treating psoriasis employing substituted azaspiranes Inventor(s): Griswold; Don Edgar (North Wales, PA), Badger; Alison Mary (Bryn Mawr, PA) Assignee(s): AnorMED Inc. (Langley, CA) Patent Number: 5,981,538 Date filed: January 29, 1997 Abstract: Invented is a method of treatment of psoriasis in a mammal in need thereof which comprises administering to such mammal an effective amount of a substituted azaspirane. Excerpt(s): This invention relates to a method of treatment of psoriasis in a mammal in need thereof which comprises administering to such mammal an effective amount of a substituted azaspirane. Badger I does not disclose or claim the compounds of Formula I for the treatment of psoriasis. R.sup.3 and R.sup.4 are the same or different and are selected from hydrogen or straight chain alkyl having 1-3 carbon atoms; or R.sup.3 and R.sup.4 are joined together with the nitrogen atom to form a heterocyclic group having 5-8 atoms; or a pharmaceutically acceptable salt or hydrate or solvate thereof. Web site: http://www.delphion.com/details?pn=US05981538__
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Mouse model of psoriasis Inventor(s): Schon; Michael P. (Boston, MA), Parker; Christina M. (Newton Centre, MA) Assignee(s): Brigham & Women's Hospital, Inc. (Boston, MA) Patent Number: 5,945,576 Date filed: April 5, 1996 Abstract: Methods and compositions for preparing a mouse model of an inflammatory skin condition are disclosed. The methods involve administering donor lymphocytes to a recipient immune deficient mouse to induce the inflammatory skin response. The mouse models are useful for testing the efficacy of a therapeutic agent for treating the inflammatory skin condition. In particular, the mouse models are useful for screening therapeutic agents for treating human psoriasis. Excerpt(s): This invention relates to methods and compositions for preparing an animal model of an inflammatory skin condition. In particular, the invention relates to methods and compositions for preparing a murine model of psoriasis. Psoriasis is one of the most frequent skin diseases, affecting 1-3% of the Caucasian population worldwide (Barker, J. N. W. N., (1994), Bailliere's Clin. Rheumatol. 8, 429-437.). This complex disease is characterized by alterations in a variety of different cells. These include epidermal keratinocyte hyperproliferation and altered differentiation indicated by focal parakeratosis (cell nuclei in stratum corneum), aberrant expression of the hyperproliferation-associated keratin pair 6/16 (Stoler, A., et al., (1988), J. Cell Biol. 107, 427-446; Weiss, R. A., et al., (1984), J. Cell Biol. 98, 1397-1406), involucrin and filaggrin (Bernard, B. A. et al., (1986), Br. J. Dermatol. 114, 279-283; Dover, R. and Watt, F. M., (1987), J. Invest. Dermatol. 89, 349-352. Ishida-Yamamnoto, A. and Iizuka, H., (1995), J. Invest. Dermatol. 104, 391-395), and integrin adhesion molecules (VLA-3, 5 and 6,.alpha.sup.6.beta.sub.4) (Hertle, M. D., et al., (1992), J. Clin. Invest. 89, 1982-1901; Kellner, J., et al., (1992), Br. J. Dermatol. 125, 211-215). In addition, de-novo expression of major histocompatibility complex (MHC) class II and intercellular adhesion molecule-1
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(ICAM-1, CD54) by keratinocytes is observed (Barker, J. N. W. N., et al., (1990), J. Clin. Invest. 85, 605-608; Gottlieb, A. B., et al., (1986), J. Exp. Med. 164, 1013-1028; Griffiths, C. E. M., et al., (1989), J. Am. Acad. Dermatol. 20, 617-629; Nickoloff, B. J., et al., (1990), J. Invest. Dermatol. 94, 151S-157S; Veale, D., et al., (1995), Br. J. Deimatol. 132, 32-38). Endothelial cells also are hyperproliferative resulting in angiogenesis and dilation (Detmar, M., et al., (1994), J. Exp. Med. 180, 1141-1146; Goodfield, M., et al., (1994), Br. J. Dermatol. 131, 808-813; Malhotra, R., et al., (1989), Lab. Invest. 61, 162-168; Mordovtsev, V. N. and Albanova, V. I., (1989), Am. J. Dermatopathol. 11, 33-42) and express increased levels of ICAM-1, E-selectin (CD62E) and vascular cell adhesion molecule-1 (VCAM-1, CD106) (Das, P. K., et al., (1994), Acta Derm.Venereol. Supplementum 186, 21-22) as well as MHC class II (Bjerke, J. R., et al., (1988), Acta Derm. Venereol. 68, 306-311). Finally, a mixed leukocytic infiltrate is seen composed of activated T-lymphocytes which produce inflammatory cytokines (Ramirez-Bosca, A., et al., (1988), Br. J. Dermatol. 119, 587-595; Schlaak, J. F., et al., (1994), J. Invest. Dermatol. 102, 145-149), neutrophils within the dermis and formning Munro's microabscesses in the epidermis (Christophers, E., and Sterry, W. (1993). Psoriasis. In Dermatology in General Medicine, T. B. Fitzpatrick, A. Z. Eisen, K. Wolff, I. M. Freedberg and K. F. Austen, eds. (New York: McGraw-Hill, Inc.), pp. 489-514.), and an increased number of dermal mast cells (Brody, I., (1986), Upsala J. Med. Sci. 91, 1-16; Brody, I., (1984), J. Invest. Dermnatol. 82, 460-4; Rothe, M. J., et al., (1990), J. Am. Acad. Dermatol. 23, 615-24; Schubert, C. and Christophers, E., (1985), Arch. Dermatol. Res. 277, 352-358; Toruniowa, B. and Jablonska, S. (1988), Arch. Dermatol. Res. 280, 189-193; van de Kerkhof, P. C., et al., (1995), Skin Pharmacol. 8, 2529). Intracutaneous secretion of cytokines is thought to mediate some or all of the tissue alterations seen in psoriasis. These cytokines include tumor necrosis factor-.alpha. (TNF.alpha.) and interleukin-1 (IL-1) (Kupper, T. S., (1990), J. Clin. Invest. 86, 1783-1786); interferon-.gamma. (IFN.gamma.) (Barker, J. N. W. N., et al., (1991), J. Dermatol. Sci. 2, 106-111; Gottlieb, A. B., et al., (1988), J. Exp. Med. 167, 670-675; Livden, J. K., et al., (1989), Arch. Dermatol. Res. 281, 392-397), IL-6 (Castells-Rodellas, A., et al., (1992), Acta Derm.Venereol. 72, 165-168; Grossman, R. M., et al., (1989), Proc. Natl. Acad. Sci. USA 86, 6367-6371; Neuner, P., et al., (1991), J. Invest. Dermatol. 97,27-33), IL-8 (Barker, J. N., et al., (1991), Am. J. Pathol. 139, 869-876), vascular endothelial growth factor/vascular permeability factor (VEGF/VPF) (Detmar, M., et al., (1994), J. Exp. Med. 180, 1141-1146), and transforming growth factor-.alpha. (TGF.alpha.) (Elder, J. T., et al., (1989), Science 243, 811-814; Gottlieb, A. B., et al., (1988), J. Exp. Med. 167, 670-675; Prinz, J. C., et al., (1994), Eur. J. Immunol. 24, 593-598). Over the past decade, research into the pathophysiology of psoriasis has focused primarily on immunologic mechanisms and evidence is accumulating that this disease has an immunological basis. However, it has not been convincingly determined if the primary defect that results in psoriasis is an immunologic disorder or resides within the epithelium (Barker, J. N. W. N., (1994), Bailliere's Clin. Rheumatol. 8, 429-437; Christophers, E., and Sterry, W. (1993). Psoriasis. In Dermatology in General Medicine, T. B. Fitzpatrick, A. Z. Eisen, K. Wolff, I. M. Freedberg and K. F. Austen, eds. (New York: McGraw-Hill, Inc.), pp. 489-514). Abnormal immune regulation is suggested by the frequent association of psoriasis with the expression of certain MHC alleles including -B13, -B17, -Bw57 and -Cw6 (Russell, T. J., et al., (1972), N. Engl. J. Med. 287, 738-740; Tiilikainen, A., et al., (1980), J. Dermatol. 102, 179; Watson, W., et al., (1972), Arch. Dermatol. 105, 197-207; White, S. H., et al., (1972), N. Engl. J. Med. 287, 740-743), the improvement of psoriatic lesions by treatment with immunosuppressive agents such as cyclosporin A (Ellis, C. N., et al., (1986), J. Am. Med. Assoc. 256, 3110-3116; Mueller, W. and Herrmann, B., (1979), N. Engl. J. Med. 301, 555) and the lymphocyte-specific toxin DAB389 IL-2 (Gottlieb, J. L., et al., (1995), Nature Med. 1, 442-447), the possible linkage of a psoriasis susceptibility gene with a gene involved in IL-2 regulation (Tomfohrde, J., et al., (1994), Science 264, 1141-1145), and the
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failure of psoriasis to recur after bone marrow transplantation (Eedy, D. J., et al., (1990), Br. Med. J. 300, 908; Jowitt, S. N., et al., (1990), Br. Med. J. 300, 1398-1399). However, underlying epidermal and/or dermal defects are suggested by altered keratinocyte cell cycle and differentiation (Gelfant, S. (1982), Cell Tissue Kinet. 15, 393-397; Weinstein, G. D., et al., (1985), J. Invest. Dermatol. 84, 579-583), by aberrant expression of adhesion molecules by keratinocytes and endothelial cells (Das, P. K., et al., (1994), Acta Derm.Venereol. Supplementum 186, 21-22; Nickoloff, B. J., et al., (1990), J. Invest. Dermatol. 94, 151S-157S; Petzelbauer, P., et al., (1994), J. Invest. Dermatol. 103, 300-305; Veale, D., et al., (1995), Br. J. Dermatol. 132, 32-38; Wakita, H. and Takigawa, M., (1994), Arch. Dermatol. 130, 457-463), and by the abnormal expression of protooncogenes within keratinocytes (Elder, J. T., et al., (1990), J. Invest. Dermatol. 94, 19-25). Web site: http://www.delphion.com/details?pn=US05945576__ •
Nucleotides for topical treatment of psoriasis, and methods for using same Inventor(s): Hostetler; Karl Y. (14024 Rue St. Raphael, Del Mar, CA 92014) Assignee(s): none reported Patent Number: 5,654,286 Date filed: June 7, 1995 Abstract: Typical treatment of psoriasis and other diseases of skin cell hyperproliferation using pharmaceutical compositions containing mono-, di, and tri-phosphate esters of antiproliferative nucleoside analogs and related analogs, DNA chain-terminating dideoxynucleosides and other nucleoside analogs. The useful phosphate esters include phosphoramidates and phosphothiorates, as well as polyphosphates having C and S bridging atoms. Excerpt(s): The present invention relates to the topical treatment of psoriasis and other diseases caused by hyperproliferation of skin cells. Specifically, the invention relates to methods of treatment of psoriasis and other skin diseases with formulations containing phosphate esters of nucleoside analogs, antiproliferative nucleosides and DNA chainterminating dideoxynucleosides. Psoriasis is a benign disease of human skin generally characterized by plaques covered by thickened scales. The disease is caused by increased proliferation of epidermal cells of unknown cause. In normal skin the time required for a cell to move from the basal layer to the upper granular layer is about five weeks. In psoriasis, this time is only 6 to 9 days, partially due to an increase in the number of proliferating cells and an increase in the proportion of cells which are dividing (G. Grove, Int. J. Dermatol. 18:111, 1979). Approximately 2% of the population the United States have psoriasis, occurring in about 3% of caucasian Americans, in about 1% of African Americans, and rarely in native Americans. Epidermal hyperplasia associated with inflammation is characteristic of psoriatic skin. Skin biopsies of affected areas show hyperkeratosis with retention of nuclear fragments, increased proliferation with defective keratinization, and chronic inflammatory infiltrates. (E. A. Bauer, M. Tabas and J. B. Goslen, in Textbook of Internal Medicine, W. N. Kelly (ed.), 1989, pp 1042-1045). With increased cell proliferation, there is increased DNA synthesis in the affected tissue which has been the basis for assays for evaluating the efficacy of antipsoriasis agents. Web site: http://www.delphion.com/details?pn=US05654286__
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Oil containing 5-methoxypsoralen at a concentration of 60-100 ppm, and its use in treatment of psoriasis Inventor(s): Goupil; Jean Jacques (23 Quai Le Gallo, Boulogne, FR) Assignee(s): none reported Patent Number: 5,962,512 Date filed: September 8, 1995 Abstract: The invention relates to topically applied pharmaceutical compositions containing 5-methoxypsoralen in a concentration of 60 ppm to 100 ppm, and more particularly 65 to 95 ppm, and preferably 75 ppm, in a pharmaceutically acceptable oleaginous formula, as well as the use of these compositions in the treatment of psoriasis. Excerpt(s): The present invention has as its object pharmaceutical compositions intended for the topical treatment of psoriasis and other dermatoses, comprising 5methoxypsoralen (or 5-MOP) in a concentration of 60 ppm to 100 ppm, in a pharmaceutically acceptable oleaginous formulation. Psoriasis is a skin disease characterized by a hyperproliferation of keratinocytes and a disorder in their differentiation. An inflammation of the dermis also arises, with vascular and immunological changes involving an activation of T lymphocytes. Web site: http://www.delphion.com/details?pn=US05962512__
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Oral 1.alpha.-hydroxyprevitamin D in composition and method for treating psoriasis Inventor(s): Valliere; Charles R. (Madison, WI), Bishop; Charles W. (Verona, WI), Knutson; Joyce C. (Madison, WI) Assignee(s): Bone Care International, Inc. (Madison, WI) Patent Number: 6,147,064 Date filed: June 7, 1995 Abstract: Method of treating psoriasis by administering orally a 1.alpha.hydroxyprevitamin D. This previtamin D form treats psoriasis without significant risk of hypercalcemia associated with other oral dosing of vitamin D forms. The 1.alpha.hydroxyprevitamin is compounded into a pharmaceutical composition in combination with a pharmaceutically acceptable excipient. Excerpt(s): This invention relates to a method for increasing the blood level of active vitamin D compounds. More specifically, the invention relates to orally administering the 1.alpha.-hydroxylated previtamin form of vitamin D compounds in order to increase the blood level of the corresponding active vitamin D compound. Vitamin D is known to be important in the regulation of calcium metabolism in animals and man. See, Harrison's Principals of Internal Medicine: Part Eleven, "Disorders of Bone and Mineral Metabolism," Chapter 335, E. Braunwald et al., (eds.), McGraw-Hill, New York (1987) pp. 1860-1865. It is known that vitamin D.sub.3 must be hydroxylated in the carbon-1 and the carbon-25 position before it is activated, i.e., before it will produce a biological response. A similar metabolism appears to be required to activate the other forms of vitamin D, e.g., vitamin D.sub.2 and vitamin D.sub.4. As is generally understood and used herein, the term "vitamin D" is intended to include vitamins D.sub.3, D.sub.2, and D.sub.4. The term "activated vitamin D," as used herein, is intended to refer to vitamin D
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which has been hydroxylated in at least the carbon-1 position of the A ring, e.g., 1.alpha.-hydroxyvitamin D.sub.3. Web site: http://www.delphion.com/details?pn=US06147064__ •
Palladium complexes and methods for using same in the treatment of tumors or Psoriasis Inventor(s): Garnett; Merrill (178 W. Main St., East Islip, NY 11730) Assignee(s): none reported Patent Number: 5,463,093 Date filed: November 26, 1993 Abstract: Novel palladium complexes and pharmaceutical compositions comprising the same are provided. Such complexes comprise (palladium).sub.m (lipoic acid).sub.n, wherein m and n are each independently 1 or 2. A process for preparing such complexes is also disclosed. In addition, a method of treatment of tumors and a method of treatment of psoriasis comprising administering the pharmaceutical compositions of the present invention are provided. Excerpt(s): The present invention relates generally to novel palladium complexes and pharmaceutical compositions comprising same. In addition, a method for the preparation of novel palladium complexes is disclosed. Also disclosed is a method for the treatment of tumors comprising administering the novel palladium complexes of the present invention and a method for the treatment of psoriasis comprising administering the novel palladium complexes of the present invention. A number of researchers have studied the role that nucleic acids play in tumorigenesis. Although electron reduction of single nucleotides have been reported in, for example, Reichard, "From RNA to DNA, Why So Many Ribonucleotide Reductases?" Science 260:1773-1777 (Jun. 18, 1993); and Hamilton et al., "Cobamides and Ribonucleotide Reduction VII Cobalt(II)alamin as a Sensitive Probe for the Active Center of Ribonucleotide Reductase," Biochemistry 10(2):347-355 (1971), previous reviews of nucleic acids and their role in tumorigenesis make no mention of reactions or substances which result in the electron reduction of DNA or RNA. Townsend et al. (ed), Nucleic Acid Chemistry, Part 3, Wiley Interscience, New York (1986); Saenger, Principles of Nucleic Acid Structure, Springer-Verlag, New York (1984); Walker, "Nucleic Acids," Methods in Molecular Biology, vol. 2, Humana Press, Clifton, N.J. (1984); Grossman et al. (ed), "Nucleic Acids - part 1," Methods in Enzymology, vol. 65, Academic Press, New York (1980); Fasman (ed), "Nucleic Acids," Handbook of Biochemistry and Molecular Biology (3d), vol. 1, CRC Press, Cleveland, Ohio (1975); Blackburn et al. (ed), Nucleic Acids in Chemistry and Biology, IRL Press, Oxford Univ. Press (1990). The prevailing view of tumorigenesis today is that it may be treated by site-specific regulation, such as by a repressor protein, at proto-oncogene sites. Such proto-oncogene sites are different for each type of tumor being treated and an extensive effort is required in order to pursue this method of treatment for an individual patient. Web site: http://www.delphion.com/details?pn=US05463093__
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Peptides and methods against psoriasis Inventor(s): Brostoff; Steven W. (Carlsbad, CA), Chang; Jennie C. C. (San Marcos, CA), Carlo; Dennis J. (Rancho Santa Fe, CA) Assignee(s): The Immune Response Corporation (Carlsbad, CA) Patent Number: 6,413,516 Date filed: January 14, 1994 Abstract: This invention relates to methods of preventing or reducing the severity of psoriasis. In one embodiment, the method involves administering to the individual a peptide having substantially the sequence of a non-conserved region sequence of a T cell receptor, present on the surface of T cells mediating psoriasis or a fragment thereof, wherein the peptide or fragment is capable of causing an effect on the immune system to regulate the T cells. In particular, the T cell receptor has the V.beta. region-V.beta.3, V.beta.13.1 or V.beta.17. In another embodiment, the method involves gene therapy. The invention also relates to methods of diagnosing psoriasis by determining the presence of psoriasis predominant T cell receptors. Excerpt(s): This invention relates to the immune system and, more specifically, to methods of modifying pathological immune responses in psoriasis. Higher organisms are characterized by an immune system which protects them against invasion by potentially-deleterious substances or microorganisms. When a substance, termed an antigen, enters the body, and is recognized as foreign, the immune system mounts both an antibody-mediated response and a cell-mediated response. Cells of the immune system termed B lymphocytes, or B cells, produce antibodies that specifically recognize and bind to the foreign substance. Other lymphocytes termed T lymphocytes, or T cells, both effect and regulate the cell-mediated response resulting eventually in the elimination of the antigen. A variety of T cells are involved in the cell-mediated response. Some induce particular B cell clones to proliferate and produce antibodies specific for the antigen. Others recognize and destroy cells presenting foreign antigens on their surfaces. Certain T cells regulate the response by either stimulating or suppressing other cells. Web site: http://www.delphion.com/details?pn=US06413516__
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Pharmaceutical composition and method of treating psoriasis Inventor(s): O'Sullivan; Donncha (6 Greenfield Crescent, Donnybrook, Dublin 4, IE) Assignee(s): none reported Patent Number: 4,544,656 Date filed: May 23, 1983 Abstract: A method of treating psoriasis and similar or related ailments comprises applying to an affected skin area a therapeutically effective amount of at least one skincompatible zwitterionic aminosulfonic acid (ZASA) of the formulaRNR'SO.sub.3 Hwherein R is a straight or branched chain aliphatic radical, or RN is a substituted or unsubstituted nitrogen-containing heterocycle which may have one additional hetero atom; and R' is C.sub.2-4 straight or branched chain alkylene radical. A pharmaceutical composition is also provided, and comprises at least one ZASA of the above formula together with a pharmaceutically acceptable topical carrier or base.
Patents 309
Excerpt(s): This invention relates to a method of treating psoriasis, and to pharmaceutical compositions useful in such treatment. Psoriasis is a group of disfiguring and uncomfortable skin conditions for which physicians have long sought effective treatment methods. Its causes and etiology are very imperfectly understood. The term "psoriasis" as used in this specification designates not only the known five or six conditions commonly so designated in medical practice, but also, for the sake of simplicity in terminology, other related skin disorders namely the ichtyoses group, the dyskeratoses group and Dariers disease. The principal known compositions which have been used with greater or lesser success in the treatment of psoriasis belong to two groups: (1) coal tar products, (2) cortisone products. Group (1) compositions are variable and unpredictable in their effects, but their overall success in symptom alleviation has been small. Some of them cause undesirable skin discoloration. Group (2) compositions bring striking short-term benefit to sufferers, but are attended by well known undesirable side-effects which constitute a contraindication of extended periods of treatment. Web site: http://www.delphion.com/details?pn=US04544656__ •
Pharmaceutical compositions and use thereof in the treatment of psoriasis Inventor(s): Ishimaru; Hiroshi (Tokyo, JP), Hori; Kazuyoshi (Fuji, JP), Creaven; Patrick J. (Eggertsville, NY) Assignee(s): Health Research Inc. (Buffalo, NY) Patent Number: 5,342,613 Date filed: October 8, 1992 Abstract: A pharmaceuticl composition and a method for its use in the treatment of psoriasis are provided wherein the composition comprises tumor necrosis factor as an active ingredient and at least one pharmaceutically acceptable carrier, diluent or excipient. Excerpt(s): The present invention relates to pharmaceutical compositions for use in the treatment of psoriasis. More particularly, it relates to pharmaceutical compositions containing tumor necrosis factor or "TNF" as an active ingredient for treating psoriasis in humans. The invention also relates to a method for treating psoriasis by administering TNF in effective anti-psoriatic amounts to patients suffering from the disease. Psoriasis is a chronic skin disease long recognized for its peculiar clinical symptoms characterized by circumscribed red patches covered with white scales, and often accompanied by varying degrees of discomfort. It has been determined that the disease is not contagious; however, its cause and mechanism have not yet been elucidated. See, Kruger, G. G., "Psoriasis: Current Concepts of its Etiology and Pathogenesis", The Year Book of Dermatology (1981), edited by Dobson, R. L. and Thiers, B. H. Due to the characteristic formation of skin lesions and eruptions, psoriasis gives its victims an unfavorable psychological outlook on life. Among people in Western countries, about 2% of the total population suffer from the disease. Psoriasis is considered to be a pluricausal hereditary disease whose onset occurs due to the genetic makeup in the body, and which is stimulated by the action of various other factors, such as infection, drugs, food, climate and stress, any or all of which can trigger the genetic cause. Since it is known that psoriasis has a close relationship with a histocompatibility antigen (HLA) which exhibits polymorphism due to the variation of the HLA gene, it is clear that psoriasis is a hereditary disease.
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Web site: http://www.delphion.com/details?pn=US05342613__ •
Pharmaceutical material for the treatment of psoriasis Inventor(s): Petereit; Hans-Ulrich (Darmstadt, DE), Mueller; Josef (Lindenfels, DE) Assignee(s): Rohm Pharma GmbH (Weiterstadt, DE) Patent Number: 4,826,677 Date filed: April 2, 1987 Abstract: The invention relates to pharmaceutical materials for local and non-irritating therapy for psoriasis, containing antipsoriatic ingredients. The pharmaceutical material is a liquid preparation of film-forming polymers and antipsoriatic ingredients, with which the psoriasis affected skin area can be covered and treated in situ with a medicated film or foil formed at the treatment site. Dithranol and/or glucocorticoid in combination with keratolytically acting urea are preferred for use as antipsoriatic ingredients. Excerpt(s): The invention relates to a liquid pharmaceutical preparation for the local treatment of psoriasis containing known antipsoriatic active ingredients, in which the medicines therapeutically take effect from a film located on the affected skin area. In treating psoriasis, a dermatosis of yet unexplained origin, one is generally instructed to apply drugs topically such as salicylic acid, vitamin A-acid, glucocorticoids, and more recently with relatively good success, dithranol (1,8,9-anthracenetriol) or acyl derivatives thereof. The formulations to be used are limited to the most common preparations such as, for example, solutions, creams, and salves, in which the manner of application for the dermatherapy is practically predetermined. The use of the therapeutic preparations which generally contain some fat, such as dithranol-salicyclic acid vaseline, a paste-like preparation, are very time consuming for the patients and involve more difficult procedures. Large surface area applications can therefore be preformed only on inpatients, and involves soiling large amounts of laundry and clothing. By combining the use of urea and the application of dithranol, as according to EP-A No. 6,724, the psoriasis therapy is improved. Preparations of this kind, having for example 0.1% dithranol in a 17% urea salve base, are known, i.e., Psoradrate (see D.M. Wiliamson in Clin. Exp. Dermatol., vol. 8, pp. 287-290 (1983)). Urea, which is known for its keratolytic characteristics, disrupts the epidermis for a more rapid and therefore more effective penetration of the active drug. Web site: http://www.delphion.com/details?pn=US04826677__
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Potassium-containing composition useful in the treatment of acne, psoriasis and seborrhea Inventor(s): Goodwin; Gary (31 Brushwood Dr., Shirley, NY 11967-4009), Oge; Eray (11 Clamshell La., Northport, NY 11768) Assignee(s): none reported Patent Number: 5,955,067 Date filed: July 23, 1996 Abstract: A composition is disclosed which is useful in alleviating, at least in part, symptoms of acne vulgaris, psoriasis or seborrhea, which includes a potassium-based
Patents 311
compound a dermatologically acceptable base for the potassium-based compound, which is preferably a potassium salt, and which include potassium acetate, potassium aluminate, potassium arsenite solution, potassium bicarbonate, potassium bisulfate potassium bitartararte, potassium bromide, potassium carbonate, potassium chloride, potassium citrate, potassium gluconate, potassium glycerophosphate, potasium iodate, potassium iodide, potassium manganate, potassium permanganate, potassium phosphate monobasic potassium phosphate dibasic, potassium phosphate tribasic, potassium phosphite or a combination thereof. The composition is topically applied to the areas of a patient's skin which are afflicted with any of acne vulgaris, psoriasis or seborrhea. Excerpt(s): The present invention relates, generally to a composition containing potassium and its use for alleviating, at least in part, the symptons of acne, psoriasis and seborrhea, as well as a method for its use. More particularly, the present invention relates to a composition containing potassium, which is applied topically to a person's skin in area afflicted with acne, psoriasis or seborrhea for the purpose of reducing the effects of such skin ailments. Acne vulgaris is a common inflammatory pilosebaceous skin disease characterized by comedones, papules, pustules, inflamed nodules, superficial pus filled cysts and in extreme cases canalizing and deep inflamed sacks. Web site: http://www.delphion.com/details?pn=US05955067__ •
Procedure for obtaining the preparation for the treatment of the disease psoriasis: drug for the treatment of psoriasis and its application Inventor(s): Visnjic; Pero (Mose Pijade 3, 58300 Makarska, YU) Assignee(s): none reported Patent Number: 5,004,736 Date filed: June 23, 1989 Abstract: The invention refers to the obtaining of the preparation for the treatment of the skin disease psoriasis. The object of the invention is a medicinal agent based on two corticosteroids, salicylates and antibiotics which clear the skin from psoriasis effectively, the most quickly and without endangering the integrity of healthy organs and skin regions and relapses approximate to zero point. The procedure according to the invention consists of the preparation of emulsion consisting of previously sterilized oil phase and water, to which are then added solutions of the active ingredients in such a way that all the phases are completed according to the order principle of ingredient stability to specified temperatures. Excerpt(s): This invention relates to a composition for the treatment of psoriasis and methods for the manufacture and application of the composition. Skin diseases are as old as the human race and there has been an on-going search for curative agents. Plant extracts, as well as drugs of both organic and inorganic origin, have been used to treat these ailments. At the present time, over 2000 preparations exist to treat psoriasis. Most of these are based on corticosteroids or combinations of antibiotics and salicylates. The prior art compositions containing corticosteroids, however, cause negative, secondary effects such as skin necrosis and steroidal dermatitis. Secondary effects on the adrenal gland, e.g., adrenal gland suppression, have also been observed. Web site: http://www.delphion.com/details?pn=US05004736__
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Process for the treatment of psoriasis using typhoid vaccine Inventor(s): Catapano; Salvatore J. (66 S. Brush Dr., Valley Stream, NY 11580) Assignee(s): none reported Patent Number: 4,788,057 Date filed: October 2, 1987 Abstract: A method of treating a human patient to effect the remission of symptoms associated with psoriasis, which comprises parenterally administering, in multiple injections, to the patient typhoid vaccine in a therapeutically effective amount which is sufficient to provide immunostimulating activity. Excerpt(s): This invention relates to a process for treating psoriasis by administering multiple injections of typhoid vaccine. Psoriasis is a chronic skin disease marked by the development of red patches on various parts of the body including elbows, back, scalp, and the hairy side of the limbs, etc. The patches are usually covered with a white scale. The cause of the disease is unknown and [heretofore] the treatment has been unsatisfactory. J. E. Schmidt, M.D., Attorney's Dictionary of Medicine and Word Finder, Volume 3, page P-301 (1986). Typhoid vaccine is marketed by Wyeth Laboratories. Each c.c. contains not more than 1,000 million Salmonella Typhosa (Ty-2 strain) organisms, killed and suspended in buffered sodium chloride injection. The preservative is 0.5% phenol. It is described beginning at page 2209, Physicians'0 Desk Reference, Medical Economics Company (1987). Web site: http://www.delphion.com/details?pn=US04788057__
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Protease inhibitors for use in the treatment of psoriasis Inventor(s): Bunn; Clive Leighton (West Ryde, AU), Sharp; Phillip John (Glebe, AU) Assignee(s): Biotech Australia Pty Limited (Roseville, AU) Patent Number: 6,288,025 Date filed: August 5, 1999 Abstract: Psoriasis may be treated by topical administration of a urokinase inhibitor, such as PAI-2, or a combination of protease inhibitors, such as PAI-2 with other serine protease inhibitors and/or with protease inhibitors such as inhibitors of metalloproteinases, acid proteases, and thiol proteases. Excerpt(s): At the cellular level, psoriasis is characterized by a hyper proliferation of epidermal keratinocytes, accompanied by infiltration of T lymphocytes and other immune system cells, the latter giving rise to inflammation similar to that in autoimmnune diseases. The epidermal turnover time for a keratinocyte to travel from the basal cell layer to the stratum corneum normally is 14 days, during which the keratinocyte undergoes a complex series of changes in gene expression resulting in cell death--"terminal differentiation." In a psoriasis patient, the epidermal turnover time is 2 days, with marked increase in proliferation of keratinocytes, which are subsequently shed in a relative immature, or less differentiated, form. Currently, there is no long-term cure for psoriasis. Treatments include coal tar preparations (natural coal tar or the distillate anthralin), topical corticosteroids, mechanical treatments to remove scale, and antimetabolites such as methotrexate. The photosensitizing drug, psoralen, combined with long wavelength ultraviolet light (PUVA), and synthetic retinoids also are used. While mild to moderate cases can be treated somewhat effectively, more extensive cases
Patents 313
are difficult and tend to be resistant to either topical therapy or ultraviolet phototherapy. Moreover, systemic use of traditional antipsoriatic drugs, or prolonged use of topical steroids, can lead to undesirable side effects or rebound worsening of psoriasis. Genetic analysis indicates that at least some forms of psoriasis include an inherited component, and intense efforts are underway to locate "psoriasis susceptibility genes." The similarity to autoimmune diseases, and the increased incidence of HLA-13, HLA-17, HLA-Cw6, and HLA-DRw7 in affected individuals has focused attention on on immunomodulatory strategies and the development of new drugs which decrease T-cell activation or deplete activated T-cell pools. Research has been severely impeded, however, by the lack of an animal model which reflects all the diverse clinical and cellular changes present in psoriatic plaques. Web site: http://www.delphion.com/details?pn=US06288025__ •
Psoriasis medication and application for remission and/or cure of plaque psoriasis Inventor(s): Kessler; Kenneth D. (3020 St. Babette La., St. Charles, MO 63301) Assignee(s): none reported Patent Number: 5,898,034 Date filed: May 23, 1998 Abstract: A medication and application for the remission and/or cure of the disease of Psoriasis. Their are no other anti-fungal Psoriasis creams or medications of this type and style available on the market utilizing this form, format or application method. Excerpt(s): Psoriasis takes several forms: scaly, red patches of skin. Plaque Psoriasis have patches, which appear on the trunk and limbs, especially on the elbows, knees and the scalp; Postural Psoriasis has small pustules spread over the body; and Guttate Psoriasis, usually in children, is characterized by tear drop-shaped lesions. This unpredictable disease, which affects men and women equally, strikes people of all ages and can erupt anywhere on the body. Psoriasis lesions form when new skin cells are produced at a rapid rate. I spent many months in the McDonnell-Douglas (now BoeingMcDonnell) technical research library researching my Plaque Psoriasis problem. I have proven beyond a reasonable doubt that I had a fungal-yeast infection of a microbial nature, deep in my skin. This fungal-yeast infestation of my skin cells (May be referred to as Candida albicans) caused my skin cell reproductive cycle to be disrupted drastically. Normal skin reproduction rate is approximately every 28 days for a complete reproductive cycle. With Psoriasis, a three too 5-day cell reproduction rate is normal. Web site: http://www.delphion.com/details?pn=US05898034__
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Psoriasis treatment Inventor(s): Dubash; Darius D. (Pine Brook, NJ), Burnett; Debbie L. (Basking Ridge, NJ), Wong; Victor M. (Hackettstown, NJ), Ladas; Athanasios S. (Parsippany, NJ) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 5,747,064 Date filed: July 17, 1997
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Abstract: The present invention is directed to a topical composition for the treatment of psoriasis. The composition comprises a film forming agent, especially vinyl acetate crotonic acid copolymer a plasticizer, an aqueous alcoholic solution and an amount of alkali effective to prevent the gellation of the film forming agent. Excerpt(s): The present invention is directed to a topical composition for the treatment of psoriasis. Psoriasis is a skin disease marked by the presence of small elevations of the skin as well as silvery scales. In the area where scales have been shed, tiny bleeding points called "Auspitz sign" appear. The major pathophysiological events involved in the disease process are accelerated epidermal proliferation and metabolic activity, proliferation of capillaries in the dermal region, and invasion of the dermis and epidermis by inflammatory cells. Coal Tar and Salicylic Acid are the only two Category I drugs mentioned in the Final Monograph for dandruff, seborrheic and psoriatic drugs. There are a number of prescription products (different drug entities) that are also useful, e.g. Theophylline which arrests the proliferation of cells during the metaphase stage of cell division. Web site: http://www.delphion.com/details?pn=US05747064__ •
Psoriasis treatment Inventor(s): Boger; Robert S. (Lake Forest, IL), Crowley; Steven R. (Vernon Hills, IL) Assignee(s): Abbott Laboratories (Abbott Park, IL) Patent Number: 5,122,514 Date filed: April 9, 1991 Abstract: The present invention relates to the use of renin inhibitors and to renin inhibitor compositions for treatment of psoriasis. Excerpt(s): The present invention relates to the use of renin inhibitors and to renin inhibitor compositions for treatment of psoriasis. Psoriasis is a chronic skin disease which is known to be difficult to treat. Psoriasis is characterized by discrete and confluent, reddish, silvery-scaled maculopapules. These psoriatic lesions occur most often on the elbows, knees, trunk and scalp. Current treatment for psoriasis include the use of agents such as anthralin (dihydroxyanthralin), azarabine, colchicine, fluorouracil, methotrexate, methoxsalen (8-methoxypsoralen), resorcinol, retinoids (for example, retinoic acid), corticosteroids (for example, clobetasol propionate, trimcinolone acetonide and the like), cyclosporin, iodochlorhydroxyquin, salicyclic acid, vitamin D, dapsone, somatostatin, sulfur, tars and zinc oxide. Ultra-violet light treatment, alone or in combination with other agents such as psoralen (i.e., PUVA treatment), is also used to treat psoriasis. There are reports that the activity of the renin-angiotensin-aldosterone system is enhanced in patients with psoriasis (Ena, et al., Acta Cardiologica XL 199 (1985); Ryder, et al., Clin. Chem. Acta 153 143 (1985)). However, there is no established cause and effect relationship between the renin-angiotensin-aldosterone system and psoriasis. Web site: http://www.delphion.com/details?pn=US05122514__
Patents 315
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Psoriasis treatment with mycophenolic acid Inventor(s): Johnson; Irving S. (Indianapolis, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: RE29,465 Date filed: November 24, 1976 Abstract: Psoriasis is treated orally.[.and topically.]. with mycophenolic acid or its.beta.D-glucuronide. Excerpt(s): Psoriasis is a common chronic skin disease whose cause is unknown. It is characterized by persistent patches of redness covered with scales. The disease is in part determined by a genetically dominant trait. While it is absent at birth, it can begin at any age from childhood to extreme old age. Psoriasis does not, however, appear to be a communicable disease and there are no known causative factors for it in the environment. In the involved patches, the cells of the epidermis grow and multiply up to seven times faster than normal. The agents currently used for treatment of psoriasis include ultraviolet light, coal tar, ammoniated mercury, anthralin, and topical corticosteroids. Methotrexate has been used to treat psoriasis by systemic administration, but such treatment method is accompanied by all the side effects commonly encountered with its use for other conditions. Antimetabolite drugs such as aminopterin, thioguanine, and azaribine have also been used in treating this disease. Systemic corticosteroids or anti-malarial drugs such as chloroquin may aggravate psoriasis by mechanisms that are not understood. A low relative humdity also aggravates the disease, probably by allowing desiccation of the skin and irritation. It would, of course, be desirable to employ a topical treatment, for psoriasis, but according to Comaish and Juhlin, Arch. Dermatol. 100, 99 (1969) methotrexate, a drug of choice in severe cases, was not successful in treating psoriasis by the topical route. In fact, of the antimetabolite drugs, fluorouracil alone has been claimed to be effective in treating psoriasis by topical administration--see Z. Haut-Geschlechtskrankh 44, 361 (1969). Web site: http://www.delphion.com/details?pn=US0RE29465__
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Psoriasis treatment with polymer film Inventor(s): Ladas; Athanasios S. (Parsippany, NJ), Dubash; Darius D. (Pine Brook, NJ), Wong; Victor M. (Hackettstown, NJ), Burnett; Debbie L. (Basking Ridge, NJ) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 5,800,831 Date filed: April 1, 1996 Abstract: The present invention is directed to a topical composition for the treatment of psoriasis. The composition comprises a film forming agent, a plasticizer, an aqueous alcoholic solution and an amount of alkali effective to prevent the gellation of the film forming agent. Vinyl acetate crotonic acid copolymer and poly(vinyl)acetate are especially preferred film-forming agents. Excerpt(s): The present invention is directed to a topical composition for the treatment of psoriasis. Psoriasis is a skin disease marked by the presence of small elevations of the skin as well as silvery scales. In the area where scales have been shed, tiny bleeding points called "Auspitz sign" appear. The major pathophysiological events involved in the disease process are accelerated epidermal proliferation and metabolic activity,
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proliferation of capillaries in the dermal region, and invasion of the dermis and epidermis by inflammatory cells. Coal Tar and Salicylic Acid are the only two Category I drugs mentioned in the Final Monograph for dandruff, seborrheic and psoriatic drugs. There are a number of prescription products (different drug entities) that are also useful, e.g. Theophylline which arrests the proliferation of cells during the metaphase stage of cell division. Web site: http://www.delphion.com/details?pn=US05800831__ •
Psoriasis treatment with retinoic acid analogs Inventor(s): Lee; Kwan-Hua (San Francisco, CA) Assignee(s): The Regents of the University of California (Berkeley, CA) Patent Number: 4,021,573 Date filed: November 5, 1975 Abstract: Skin diseases resulting from abnormal metabolic processes, such as acne and psoriasis, are treated on a repetitive basis, either internally or topically, with a dermatologically sufficient amount of 11-(2',6',6'-trimethylcyclohex-1'-enyl-1')-5,9dimethylundeca-2,4,6,8,10-p entenoic acid or its physiologically acceptable salts to reduce the inflammation. The subject acid or its salts are found to provide remission of the dermatologically diseased condition, while avoiding side effects concommitant with the use of other analgous compounds. Excerpt(s): A wide variety of skin diseases are characterized by abnormal metabolic processes. Two classes of these conditions are the seborrheic dermatoses--which are typified by excessive secretion or disturbed quality of sebum, abnormal intercellular cement, and oily crusts or scales --and ichthyosiform dermatoses--which are typified by dry, scaly skin, abnormal thickening of epidermis, and rapid cell turnover in the skin. Specific diseases included in these broad categories include acne vulgaris (a seborrheic dermatosis) and psoriasis (an ichthyosiform dermatosis). Both of these conditions exhibit follicular keratin plugs. Other related conditions are ichthyosis vulgaris, senile hyperkeratosis, acanthosis, Derier's disease, keratoacanthomas, congenital ichthyosiform erythroderma, zosteriform keratosis, and lamellor ichthyosis. Because these diseases appear on the skin and are unsightly, satisfactory agents should have relatively rapid action in the remission of the condition. In addition, the reagents should not affect the skin adversely and may not be toxic at the levels employed or the manner in which it is applied. Of particular interest, is an agent which can be taken internally, acting in a systemic manner in combatting the abnormal metabolic process. Retinoic acid is found to be active in the remission of skin conditions, but has serious side effects. The retinoic acid when applied to the skin results in irritation and peeling of the skin, which is cosmetically undesirable. Because of the irritation, there is some discouragement of the user to employ the treatment. Web site: http://www.delphion.com/details?pn=US04021573__
Patents 317
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Pulsed infrared laser treatment of psoriasis Inventor(s): Holtz; James Z. (Livermore, CA), Grove; Robert E. (Pleasanton, CA) Assignee(s): Star Medical Technologies, Inc. (Pleasanton, CA) Patent Number: 5,527,350 Date filed: February 24, 1993 Abstract: A method for treating psoriasis with pulsed infrared laser illumination. A pulsed infrared diode laser having a wavelength of 800 nm and a pulse duration in the millisecond range selectively destroys abnormal blood vessels beneath psoriatic plaques at depths of up to one millimeter. Areas of approximately 0.5 cm.sup.2 are sequentially treated. Uniform illumination intensity at a wide range of penetration depths allows selective destruction of the blood vessels without damage to the surrounding tissue, causing the psoriatic lesions to heal. The method may be applied more generally to the treatment of other dermal vascular malformations. Excerpt(s): The invention relates generally to the treatment of psoriasis and more particularly to the use of a pulsed infrared laser source to treat psoriatic plaques. The majority of sufferers generally report lessened symptoms during the summer months, presumably due to increased exposure to sunlight. Ultraviolet B light, one component of sunlight, has been used in conjunction with topical ointments such as extracts of coal tar as a treatment strategy. A more elaborate technique, referred to as PUVA, involves ultraviolet A light in conjunction with oral psoralen compounds. During PUVA treatment, patients are exposed to ultraviolet A light in a box similar to a tanning booth after ingesting the psoralen drug. Relief is temporary and treatment must be repeated after several months. This treatment has recently been associated with significantly higher rates of skin cancer. Localized hyperthermia has also produced temporary clearing of psoriatic plaques. Several heat delivery systems have been investigated including infrared radiation from a sunlamp, ultrasound generation and hot water contact. Ultrasound hyperthermia provides the most uniform depthwise distribution of tissue heating. Web site: http://www.delphion.com/details?pn=US05527350__
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Salt mixture for the treatment of psoriasis Inventor(s): Biener; Hans F. (Heilman Strasse 21, 8000 Munich 71, DE) Assignee(s): none reported Patent Number: 4,943,432 Date filed: August 24, 1988 Abstract: A composition for the treatment of psoriasis and other skin diseases comprising a salt mixture of defined purity, which is applied to the diseased skin in solution or in gelled form. The composition may be characterized as composed primarily of a mixture of a magnesium halide, such as magnesium chloride, with mixed alkali and alkaline earth metal salts such as sodium and potassium chloride and/or bromide and calcium chloride or bromide. Other cations present in the mixture include strontium, aluminum, iron, lithium and zinc, and the anions include sulphate, hydrogen carbonate, borate, fluoride, silicate, iodide and carbonate. Excerpt(s): Between 2% and 3% of the populations of Europe and of the United States suffers from Psoriasis Vulgaris. Since a genetic defect is involved, no therapeutic
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method can assure a long term cure. All courses of treatment aim, therefore, at freedom from symptoms for the longest possible time, as a rule 6-12 months. Psoriasis, which according to experience, always recurs and which in particularly serious cases can even be life threatening, generally requires treating patients intermittently during their entire lifetime. The appearance of the disease in youth thus necessitates treatment spanning decades. Treatment risk increases with treatment length, since common substances such as cortico-steroids evidence cumulative long term side effects. This corresponds to years of ultraviolet radiation in cases of dermatosis and melanoma, the so-called light-induced cancer. The search for a natural risk-free treatment has, therefore, intensified in recent years. The most well known example is the Dead Sea bath treatment, which was known in antiquity. Dead Sea water contains about 26% by weight of mixed salts and solids. It is known from various studies, for example, E. Azizi et al, Israeli Journal of Medical Sciences, 18, p. 267 (1982) that in the treatment of psoriasis and other skin diseases an average of about 65% of patients given immersion treatments in Dead Sea water are rendered free of symptoms. In addition, 20% show an improvement such that in about 85% of the cases a positive effect is evident. Tests performed under my direction using solutions prepared by reconstituting salt mixtures obtained from Dead Sea salt deposits have exhibited approximately the same results. Web site: http://www.delphion.com/details?pn=US04943432__ •
Shampoo for treating seborrheic dermatitis, dandruff or psoriasis Inventor(s): Rapaport; Jeffrey (Fort Lee, NJ) Assignee(s): Dermatology Home Products, Inc. (Fort Lee, NJ) Patent Number: 5,730,965 Date filed: June 13, 1996 Abstract: A method is provided to treat and/or prevent seborrheic dermatitis of the scalp and other hair bearing areas, dandruff or psoriasis by topically applying to the skin and washing the skin in a shampoo containing an effective amount of a treatment composition containing chloroxylenol, preferably by daily application in a pharmaceutically acceptable vehicle at a concentration of from 0.1 to five (5) percent by weight, preferably about one (1) percent by weight. Excerpt(s): The present invention is directed to a method of treating seborrheic dermatitis of the scalp and other hair bearing areas, dandruff or psoriasis. Treatment of seborrheic dermatitis and dandruff has been discussed in the prior art. Among the most common treatment regimen is a shampoo with zinc pyrithione as an active ingredient, such as discussed in "Announcing Two improvements in Head & Shoulders.RTM.", a 1995 advertisement publication of Procter & Gamble, the manufacturer of Head & Shoulders.RTM. shampoo. Samuel L. Moschella, M.D. et al. in "Dermatology", in a chapter entitled "Papulosquamous Eruptions and Exfoliative Dermatitis" W. B. Saunders Company, Third Edition, pgs. 610-611, 1992 states that microbiological studies have revealed that skin conditions such as psoriasis are associated with increased numbers of Staphylococcus aureus bacteria, and that improvements in psoriatic skin lesions are noticed when topical and systemic antibiotics are administered. Web site: http://www.delphion.com/details?pn=US05730965__
Patents 319
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Short contact treatment of psoriasis with topical retinoids Inventor(s): Lebwohl; Mark G. (300 E. 85th St., New York, NY 10028), Bershad; Susan (2 Stonebridge Rd., Montclair, NJ 07042) Assignee(s): none reported Patent Number: 6,048,902 Date filed: February 12, 1999 Abstract: The present invention relates to a method of treating psoriasis using shortterm contact with a topically-applied retinoid composition. Excerpt(s): The present invention is directed to the treatment of psoriasis using topical retinoids. The retinoids are a family of compounds including vitamin A, retinoic acid (RA), related derivatives of these, and other compounds capable of binding to retinoic acid receptors (RAR). RA, which is a natural metabolite of vitamin A (retinol), is known as a potent modulator (i.e., an inhibitor or, to the contrary, a stimulator, depending on the nature of the cells treated) of the differentiation and proliferation of many normal or transformed cell types. All-trans-RA (tretinoin) acts on the differentiation and proliferation of cells by interacting with RARs contained in the cell nucleus. There are, to date, three identified subtypes of known RAR receptors, respectively termed RAR.alpha., -.beta., -.gamma. These receptors, after binding the RA ligand. interact with the promoter region of genes regulated by RA at specific response elements. To bind to the response elements, the RARs heterodimerize with another type of receptor designated as RXR. The natural ligand of RXRs is 9-cis-retinoic acid. Many retinoids are known and have been described to date. Generally, retinoids can be identified by their ability to bind RARs, either as all the RARs or selectively to an individual RAR class. Further, retinoids exhibit a diverse spectrum of activities. Among these is use as a topical therapeutic for treatment of skin conditions. Web site: http://www.delphion.com/details?pn=US06048902__
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Systemic treatment of psoriasis Inventor(s): Childress; Scott J. (Philadelphia, PA) Assignee(s): American Home Products Corporation (New York, NY) Patent Number: 4,006,250 Date filed: August 25, 1975 Abstract: A process for the treatment of psoriasis by systemic administration of 1-(2,6dihalobenzylideneamino)-3-hydroxyguanidines is disclosed. Excerpt(s): Psoriasis is a disease of the skin, whose etiology is unknown. The skin lesions associated with psoriasis may be described as dull red patches or plaques of scaly erythema. The scales are distinctive, having a slightly opalescent silvery appearance. The disease has a predilection for certain areas of the body; thus the scalp, the extensor surfaces of the extremeties (particularly at the elbows and knees), the back and the buttocks are most usually affected. However, the nails, eyebrows, axillae, umbilicus and anogenital regions are also frequent sites of involvement. To date, there has been no report of a complete and permanent cure for psoriasis, and although the several treatments of choice available afford temporary remission of the symptoms, recurrence is almost certain. Most treatments involve the topical application of steroid (e.g. the adrenocortical steroids) ointments and creams, and no clinically successful, long-term,
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systemic treatment for the disease is currently available. The compounds utilized in the process of the invention, substituted benzylideneamino-3-hydroxyguanidines and their pharmacologically acceptable acid addition salts, have previously been described in the literature. For example, U.S. Pat. No. 3,591,636 described the preparation of this class of compounds and discloses their utility as hypotensive agents and agrochemicals (i.e. antifungals and herbicides). In addition the preparation of the substituted benzaldehydes from which the benzylideneamino-3-hydroxyguanidines of the invention may be prepared is described in Chemical Abstracts, 26, 1271 (1931); 31, 3816 (1936). Web site: http://www.delphion.com/details?pn=US04006250__ •
Systemic treatment of psoriasis using certain salicylates Inventor(s): Diamond; Julius (Mountain Lakes, NJ) Assignee(s): Key Pharmaceuticals, Inc. (Miami, FL) Patent Number: 4,483,854 Date filed: April 12, 1983 Abstract: Psoriasis is systemically treated by the administration of a salicylate which is capable of inhibiting the endogenous lipoxygenase present in psoriatic plaque fluid without the inhibition of the cyclooxygenase enzyme. Excerpt(s): Psoriasis is systemically treated in accordance with this invention by introduction into the bloodstream of a salicylate which is capable of inhibiting the endogenous lipoxygenase present in psoriatic plaque fluid without inhibition of the cyclooxygenase enzyme. This invention includes both a method of treatment and a composition or dosage form suitable for administration to a patient suffering from psoriasis. High levels of arachidonic acid and 5-HETE are known to be associated with psoriasis, while levels of PGE.sub.2 are only slightly elevated. Thus, the cyclooxygenase pathway in psoriatic lesions is greatly inhibited, while 5-lipoxygenase and 12lipoxygenase pathways are encouraged. It appears that an inhibitor of cyclooxygenase is present in psoriatic lesions which causes the disposition of arachidonic acid to be redirected via the lipoxygenase pathway. The transformation of arachidonic acid to LTB.sub.4 and 5-HETE in the epidermis is catalyzed by the 5- and 12-lipoxygenases. Aspirin, the most widely prescribed and best known salicylate, acts to inhibit the cyclooxygenase pathway and will exacerbate psoriasis. In accordance with this invention a systemic treatment of psoriasis and dosage form for this treatment is provided by the use of certain salicylates, which I have found are relatively ineffective inhibitors of cyclooxygenase and thus have little inhibitory effect on the biosynthesis of PGE.sub.2. At the same time, however, the salicylates of this invention will inhibit the lipoxygenases and thereby interfere with the biotransformation of arachidonic acid to LTB.sub.4 and 5-HETE. Web site: http://www.delphion.com/details?pn=US04483854__
Patents 321
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Therapeutic agent for the external treatment of psoriasis, tinea and eczemas Inventor(s): Evers; Walter (Pinneberg, DE) Assignee(s): Pharmazeutische Fabrik Evers & Co. (Pinneberg, DE) Patent Number: 4,235,889 Date filed: April 25, 1979 Abstract: The subject of the invention is a pharmaceutical composition for the external treatment of psoriasis, tinea and eczemas, comprising coconut oil, palm kernel oil, an extract of Laurus nobilis (Linn.) and an emulsifier. Excerpt(s): The object of the present invention is to provide a pharmaceutical composition for the external treatment of psoriasis, tinea and eczemas, with which treatment on humans has proved very successful. Even "hopeless cases" have shown distinct healing. A further object of the invention is that the composition for topical application makes possible a therapy which is free from side effects. Therapeutic agents which are known for the external treatment of psoriasis, tinea and eczemas have not yet proved sufficiently effective, so that topical ointments based on tars have frequently been used in combination with an X-ray treatment. The subject of the invention is a pharmaceutical composition for topical application for the external treatment of psoriasis, tinea and eczemas, which comprises 30 to 50 percent by weight of coconut oil, 30 to 50 percent by weight of palm kernel oil, 5 to 15 percent by weight of laurel oil from Laurus nobilis (Linn.), and 5 to 15 percent by weight of an emulsifier, the percentages by weight summing up to 100 percent by weight. Web site: http://www.delphion.com/details?pn=US04235889__
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Therapeutic instrument for treating or relieving psoriasis, atopic dermatitis, articular rheumatism and/or cancer or preventing the progress of these diseases and method of utilization thereof Inventor(s): Morishige; Fukumi (Chiba, JP) Assignee(s): Morishige; Noritsugu (Omura, JP), Morishige; Fumie (Chiba, JP) Patent Number: 6,454,695 Date filed: August 3, 2000 Abstract: A therapeutic instrument for treating psoriasis, atopic dermatitis, articular rheumatism and/or cancer or preventing the progress thereof which includes a solid radiation source having a half-life within a range of from 20 to 1.41.times.10.sup.10 years and a radioactivity corresponding to a decay rate within a range of from 10 to 370 Becquerel/g and a solid material coating the same, characterized in that the solid material has a radiation face for radiating radial rays emitted from the radiation source. As the radiation source, use is made of, for example, monazite, while a cotton bag, Japan wax, etc. are usable as the solid coating material. Excerpt(s): The invention of the present application relates to a therapeutic instrument for treating psoriasis, atopic dermatitis, articular rheumatism and/or cancer or preventing the progress of these diseases. There has been at least carried out low dose irradiation of radial rays such as X-rays for treating psoriasis by means of radial rays (Hideo Irie, Radiation therapy respective for diseases, page 61, published by Kokuseido Shuppan K. K. (edition; Feb. 10, 1967)). However, the irradiated doses are divided into several low irradiation doses such as from 100 to 150 R (from 0.91 to 1.37 sieverts (Sv)
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(from 0.91 to 1.37 grays (Gy)). The total irradiation dose for several low irradiation doses becomes high such as, for example, 200 to 600 R (1.8 to 5.4 Sv (1.8 to 5.4 Gy)). Highly skilled technique is required for administering these radial rays. For atopic dermatitis, there is no known therapy that can be carried out safely by means of low dose irradiation of radial rays. Web site: http://www.delphion.com/details?pn=US06454695__ •
Therapeutical compositions against psoriasis Inventor(s): Horvath; Ferenc (Szalai Attila, HU) Assignee(s): Unipharma Co., Ltd. (Budapest, HU) Patent Number: 5,165,932 Date filed: September 15, 1989 Abstract: The invention relates to therapeutical compositions on medical herb basis for the treatment of psoriasis and the preparation of the same. A further object of the invention in the use of medical herbs as listed below in the treatment of psoriasis, rheumatism and asthmatic dyspnoea. The medical herbs used in the invention are as follows:Allium sativum /garlic/,Urtica dioica /common nettle/,Chelidonium majus /milkweed/,Veronica officinalis /veronica/,Calendula officinalis /calendula or marigold/,Achillea herba /millefolium/ /yarrow/,Fumaria officinalis /fumitory, earthgall/. Excerpt(s): The present invention relates to therapeutical compositions on medicinal herb basis for the treatment of psoriasis. An other object of the invention is the preparation of the said compositions. A further object of the invention is the use of the medicinal herbs as listed below in the treatment of psoriasis, rheumatism and asthmatic dyspnoea. Psoriasis constitutes one of the most common chronic skin diseases. Even nowdays the origin thereof has not been clarified, presumably it is based ona complex effect of various factors within the human organism. In pathological point of view it is a chronic dermatitis, with unnaturally high epithelial cell proliferation on the surface, and hyperaemia and dense lymphocita-infiltration on the corium side. Essentially, the disease may start in any period of life and exists for decades with periodic eruptions and/or permanent centres. Psoriasis most frequently occurs on the tensive surfaces of limbs, on hairy scalp and traumatic skin parts, respectively. A large number of methods have already been used for the treatment of psoriasis. B. Issekutz and L. Issekutz, Gyogyszerrendeles, Medicina, Budapest, 1979 gives a comprehensive review on the methods and materials used for the treatment of psoriasis. These treatments are, however, almost exclusively of symptomatic character only as no composition against psoriasis has been provided which would result in a total curative effect or at least in a suppression of the disease for a longer period, i.e. for some years. The literature suggest for the treatment of psoriasis e.g. vitamins B.sub.12 or A, different creams containing arsenic acid or arsenates, cooling ointments containing aluminum acetate, desquamatories with resorcine as active ingredient, lotions containing tallium acetate, as well as other compositions which contain salycilic acid or the derivatives thereof. The ointment Psoriasin contains 2,2'-dichlorodiethylsulfide/mustardgas/, the said ointment may be used, however, only once daily as a thin smear. The tar ointments have the disadvantage that only a part of the skin area may be treated once and even with a short contact period. The salycilic acid compositions serve for a desquamation of the skin surface and as such they are again of symptomatic effect only as the disease will not be terminated.
Patents 323
Web site: http://www.delphion.com/details?pn=US05165932__ •
Thiazolidine derivatives for the treatment of psoriasis Inventor(s): Kurtz; Theodore W. (Mill Valley, CA), Pershadsingh; Harrihar A. (Bakersfield, CA) Assignee(s): Bethesda Pharmaceuticals, Inc. (Mill Valley, CA) Patent Number: 5,824,694 Date filed: April 18, 1996 Abstract: A new medical use for certain thiazolidine derivatives is disclosed. Specifically, treatment of hyperproliferative epithelial cell conditions, such as psoriasis, by administration of thiazolidinediones or 5'-aryl substituted thiazolidine derivatives is described. Appropriate chemical structures, synthetic reactions, formulations, routes of administration and dosages are included. Excerpt(s): This invention relates to an additional medical use of thiazolidinediones, some of which are used in the treatment of diabetes and essential hypertension. These compounds are also useful for the treatment of psoriasis and other diseases including acne. Psoriasis is a disease which afflicts primarily the skin and produces raised, thickened, scaling, nonscarring lesions. The lesions are usually sharply demarcated erythematous papules covered with overlapping shiny scales. The scales are typically silvery or slightly opalescent. Involvement of the nails frequently occurs resulting in pitting, separation of the nail, thickening and discoloration. Arthritis is sometimes associated with psoriasis, and it may be crippling. Psoriasis afflicts about 1-2% of the United States population with about 200,000 new cases diagnosed annually. Some estimate that there are up to five million patients with psoriasis in the United States. Hyperproliferation of keratinocytes is a key feature of psoriasis along with epidermal inflammation and reduced differentiation of keratinocytes. Multiple mechanisms have been invoked to explain the keratinocyte hyperproliferation that characterizes psoriasis. However, no single mechanism has been definitively implicated. Activation of epidermal growth factor receptors, alterations in protein kinase C signal transduction pathways, and the attendant changes in intracellular calcium metabolism may play a role in psoriatic epidermal hyperplasia. Disordered cellular immunity has also been implicated in the pathogenesis of psoriasis. However, the exact mechanisms of keratinocyte hyperproliferation and epidermal inflammation remain unclear. Web site: http://www.delphion.com/details?pn=US05824694__
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Tin protoporphyrin and tin mesoporphyrin in the treatment of psoriasis Inventor(s): Emtestam; Lennart (Huddinge, SE), Kappas; Attallah (New York, NY), Drummond; George S. (New York, NY) Assignee(s): The Rockefeller University (New York, NY) Patent Number: 4,782,049 Date filed: December 2, 1987 Abstract: Use of tin protoporphyrin and tin mesoporphyrin together with ultraviolet light in the treatment of psoriasis.
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Excerpt(s): This invention relates to methods of treating humans afflicted with psoriasis by treatment with an antipsoriatic amount of tin protoporphyrin (SnPP) or tin mesoporphyrin (SnMP). Both SnPP and SnMP are known compounds. Their utility in the treatment of hyperbilirubinemia has been described by Drummond and Kappas. The utility of SnPP for this purpose is described in Proc. Nat. Acad. Sci. USA 78 6466-6470 (1981). The use of SnMP is described in commonly owned copending patent application Ser. No.: 715,515 filed Mar. 25, 1985 now U.S. Pat. No. 4,657,902. Clinically, psoriasis vulgaris is characterized by erythematous, scaling plaques that often begin in the extensor aspects of the body. It may be extremely widespread, with occasional total skin involvement. It is frequently distressing to the patient and occasionally life threatening. Web site: http://www.delphion.com/details?pn=US04782049__ •
Topical composition for the treatment of psoriasis and related skin disorders Inventor(s): Meisner; Lorraine Faxon (Madison, WI) Assignee(s): Bioderm, Inc. (Madison, WI) Patent Number: 6,440,465 Date filed: May 1, 2000 Abstract: Compositions and methods of use thereof for the treatment of psoriasis and related skin ailments are disclosed. The compositions include topical skin formulations of glucosamine in an emollient base such as moisturizing cream. In addition to glucosamine, the formulations may include keratolytic substances such as coal tar extract or salicylic acid. The formulations may also include glucosamine and antioxidant anti-inflammatory herbal extracts such as oleuropein and berberine in an emollient base. Excerpt(s): The present invention relates in general to the field of the treatment of psoriasis and related skin disorders, and more particularly to a non-toxic topical formulation that includes antioxidants and a pharmaceutically effective amount of an herbal extract for the treatment of psoriasis and related skin ailments. Without limiting the scope of the invention, its background is described in connection with disorders of the skin and, more particularly, to the general field of diseases that cause psoriasis, as an example. Psoriasis is a common skin disease characterized by hyperplasia of keratinocytes resulting in thickening of the epidermis and the presence of red scaly plaques. The lesions in this chronic disease typically are subject to remissions and exacerbations. There are several patterns, of which plaque psoriasis is the most common. Guttate psoriasis, with raindrop shaped lesions scattered on the trunk and limbs, is the most frequent form in children, while pustular psoriasis is usually localized to the palms and soles. The classical inflammatory lesions vary from discrete erythematous papules and plaques covered with silvery scales, to scaly itching patches that bleed when the scales are removed. Despite a voluminous scientific literature and numerous treatment strategies, there is still no effective treatment for psoriasis that is completely without side effects. Web site: http://www.delphion.com/details?pn=US06440465__
Patents 325
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Topical medicament for the treatment of psoriasis Inventor(s): Lipi; Ramon Efrain Vasquez (Lujan-Mendoza, AR) Assignee(s): Curacid America Corporation (Washington, DC) Patent Number: 6,383,499 Date filed: February 26, 2001 Abstract: A topical medicament for the treatment of psoriasis comprises metallic iodine, virgin wax, a variety of oils of animal and plant origin, camphor, chlorophyll and benzoic acid in a pharmaceutically acceptable emollient excipient base. Excerpt(s): The present invention relates to a topical medicament for treating psoriasis. Psoriasis is a common chronic skin disease whose cause is unknown. It is characterized by persistent patches of redness covered with scales. The disease is, in part, determined by a genetically dominant trait. While it is absent at birth, it can begin at any age from childhood to extreme old age. Psoriasis does not, however, appear to be a communicable disease and there are no known causative factors for it in the environment. In the involved patches, the cells of the epidermis grow and multiply many times faster than normal. The agents currently used for treatment of psoriasis include ultraviolet light, coal tar, ammoniated mercury, anthralin, and topical corticosteroids. Methotrexate has been used to treat psoriasis by systemic administration, but such treatment method is accompanied by all the side effects commonly encountered with its use for other conditions. Antimetabolite drugs such as aminopterin, thioguanine, and azaribine have also been used in treating this disease. Systemic corticosteroids or anti-malarial drugs such as chloroquine may aggravate psoriasis by mechanisms that are not understood. A low relative humidity also aggravates the disease, probably by allowing desiccation of the skin and irritation. Web site: http://www.delphion.com/details?pn=US06383499__
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Topical treatment of psoriasis Inventor(s): Albazi; Hermiz (4344 Moorpark Ave. #1, San Jose, CA 95117), Albazi; Rakhi (4344 Moorpark Ave. #1, San Jose, CA 95117) Assignee(s): none reported Patent Number: 6,153,197 Date filed: April 27, 1999 Abstract: A pharmaceutical composition for treatment of psoriasis is a mixture of garlic (Allium sativum) and seeds of the radish plant (Raphanus sativus) in dilute acetic acid, preferably in the form of white wine vinegar, which is pulverized and blended into a paste. For maximum potency, the composition is preferably prepared immediately before use from fresh ingredients in an amount sufficient for a single treatment. Alternatively, the composition may be prepared ahead of time and stored in a sealed, refrigerated container or otherwise preserved. In the method of treatment, the paste-like composition is applied topically directly to psoriatic plaques on the patient. The composition is allowed to dry on the patient's skin and is left in place for a period of approximately 24 to 72 hours, after which the composition is washed off. The composition is repeatedly applied at intervals of approximately one week over a three to six week period until the desired results are obtained. Typically, the patient's skin will begin to show signs of improvement after the first application of the composition and,
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after the course of the treatment, the plaque-like lesions will be replaced by healthy, normal skin. The method of treatment is effective on new cases of psoriasis and on longstanding intractable cases of psoriasis, which have not responded to other methods of treatment. Longterm follow-up of patients has shown relatively complete remission of the disease and restoration of normal skin growth for extended periods without recurring symptoms. Excerpt(s): The present invention relates to a composition and method for topical treatment of skin disorders, in particular, for the treatment of psoriasis. Psoriasis is a chronic skin disease long recognized for its peculiar clinical symptoms characterized by circumscribed red patches covered with white scales, and often accompanied by varying degrees of discomfort. It has been determined that the disease is not contagious; however, its cause and mechanism have not yet been elucidated. See, Kruger, G. G., "Psoriasis: Current Concepts of its Etiology and Pathogenesis", The Year Book of Dermatology (1981). Due to the characteristic formation of skin lesions and eruptions, psoriasis gives its victims an unfavorable psychological outlook on life. Among people in Western countries, about 2% of the total population suffer from the disease. Psoriasis is considered to be a pluricausal hereditary disease whose onset occurs due to the genetic makeup in the body, and which is stimulated by the action of various other factors, such as infection, drugs, food, climate and stress, any one of which can trigger the genetic cause. Since it is known that psoriasis has a close relationship with histocompatibility antigen (HLA) which exhibits polymorphism due to the variation of the HLA gene, it is clear that psoriasis is a hereditary disease. Web site: http://www.delphion.com/details?pn=US06153197__ •
Topical treatment of psoriasis with imidazole antibiotics Inventor(s): Rosenberg; E. William (Memphis, TN), Belew; Patricia W. (Germantown, TN) Assignee(s): University of Tennessee Research Corp. (Knoxville, TN) Patent Number: 4,569,935 Date filed: December 9, 1983 Abstract: A method is provided for treating psoriasis and seborrheic dermatitis in humans by topical application of an effective, lesion reducing amount of an imidazole antibiotic to affected areas. Excerpt(s): The present invention relates to methods for the treatment of skin disorders of seborrheic dermatitis and psoriasis and more particularly relates to topical treatment of those disorders by topical application of imidazole antibiotics to affected areas. Seborrheic dermatitis is a skin disorder characterized by lesions produced by an abnormal increase (>2.times.) in the production and shedding of epidermal cells from the skin, particularly in hairy areas, body folds, and in and behind the ears. Typically, the lesions have indefinite borders with an inflamed appearance and are covered by scales having a greasy appearance. Psoriasis is a skin disorder also characterized by lesions produced by an even greater abnormal increase (10-20.times.) in the production of shedding of epidermal cells from the skin. Typically, psoriasis lesions, which are welldefined and have a pink or dull red color, are covered with silvery scales. In addition, capillaries in the skin in affected areas undergo swelling. Web site: http://www.delphion.com/details?pn=US04569935__
Patents 327
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Transgenic animals as model of psoriasis Inventor(s): Watt; Fiona M. (London, GB), Carroll; Joseph M. (London, GB) Assignee(s): Imperial Cancer Research Technology Limited (London, GB) Patent Number: 6,187,993 Date filed: November 3, 1997 Abstract: A nucleic acid construct comprising a promoter capable of directing expression in the suprabasal cells of the epidermis and means to cause expression of an integrin subunit in the suprabasal cells. Preferably the means to cause expression of an integrin subunit is an integrin subunit coding sequence. A transgenic animal which expresses an.alpha. subunit and a.beta. subunit of integrin in the suprabasal cells of the epidermis and methods for making the transgenic animals. At least some of the transgenic animals are useful models of human disease, especially psoriasis. A method of treating psoriasis comprising administering to the patient a compound which modulates integrin function. Excerpt(s): The present invention relates to transgenic animals which can act as a model for a human disease state. In particular, the invention relates to transgenic mammals which can serve as a non-human model for psoriasis. Psoriasis is a skin condition that affects around 2% of the world's population and is characterized clinically by the presence of rounded, circumscribed, erythematous, dry, scaling patches of various sizes, covered by greyish white or silvery white, umbilicated and lamellar scales, which have a predilection for the exterior surfaces, nails, scalp, genitalia and lumbosacral region. Although in its mildest form it may merely be a nuisance which it is desirable to control for cosmetic reasons, in more severe forms it can lead to severe pustule and scab formation and may be associated with arthritis. Web site: http://www.delphion.com/details?pn=US06187993__
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Treatment of certain skin malignancies and pre-malignant skin lesions, herpes zoster and psoriasis Inventor(s): Miller; Daniel G. (Scarsdale, NY) Assignee(s): Exovir, Inc. (Great Neck, NY) Patent Number: 4,957,734 Date filed: July 6, 1987 Abstract: A composition consisting essentially of human leukocyte interferon and an antiviral surfactant, such as the non-ionic surfactant, nonylphenoxypolyethoxy ethanol, and a physiologically acceptable carrier therefor, has been found to be useful for the treatment of malignant and pre-malignant skin lesions and skin lesions associated with herpes zoster and psoriasis by topically administering or applying the composition to the affected skin area. Excerpt(s): This invention relates to a method for treatment of skin malignancies and pre-malignant skin lesions, including squamous cell carcinoma, basal cell carcinoma, actinic keratosis, and leukoplakia. This invention also relates to a method for treatment of psoriasis and herpes zoster. Basal cell carcinomas, which may appear as small, shiny, firm nodules or ulcerated crusted lesions on the skin, are generally treated by
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electrodesiccation and curettage, surgical excision or X-ray therapy. In about 5% of cases, recurrences occur. Such recurrences are treated typically with further excision or Moh's chemosurgery, i.e., microscopically controlled excision after chemical fixation of the tissue. Squamous cell carcinoma arises from the malpighian cells of the epithelium. The tumor generally begins as a small red papule or plaque with a scaly or crusted surface. Subsequently, it becomes nodular. Eventually, the lesion ulcerates and invades the underlying tissue. As with basal cell carcinoma, squamous cell carcinoma is heated with electrodesiccation and curettage, surgical excision or X-ray therapy. Web site: http://www.delphion.com/details?pn=US04957734__ •
Treatment of immunologically based disorders, specifically psoriasis Inventor(s): Golwyn; Daniel H. (P.O. Box 151408, Altamonte Springs, FL 32715-1408) Assignee(s): none reported Patent Number: 5,147,872 Date filed: June 19, 1990 Abstract: Methods and means for treating psoriasis, as well as Crohn's disease and other HLA-related disorders, to abate their symptoms, with a pharmaceutical diazepine having a component triazolo ring. HLA-related disorders amenable to such treatment include (i) persistent eruptive, granular, or ulcerative conditions of the skin, mouth, or gastrointestinal tract; and (ii) dibilitating inflammatory conditions of the circulatory, muscular, and nervous systems. This treatment alleviates abnormality or unbalance of patients' immune systems, such as an overabundance of natural killer cells and/or an abnormality of helper T-cell/suppressor T-cell ratio, and alleviates the self-cannibilism of the Koebner phenomenon, when present. Triazolobenzodiazepines, such as alprazolam or triazolam, and triazolothienodiazepines, such as etizolam, are examples of preferred treating compositions. Excerpt(s): This invention relates to treatment of psoriasis, as an example of human disorders such as have an apparently immunological basis defined as detailed below; it concerns especially alleviating the symptoms of patients having autoimmune system disorders, by treating them with certain drugs. Although sometimes such disorders may be alleviated more or less in one way or another, hitherto no readily effective treatment has been known for them individually, much less generally. Perhaps because of the lack of a recognized potentially successful treatment, many such disorders are deemed to be idiopathic. Indeed, insult may be added to injury, as unsympathetic persons characterize such patients as "mental" cases responsible--if only involuntarily--for their own condition or symptoms. A putatively more enlightened view is that such disorders are human leucocyte antigen (HLA) related, stemming from some unbalance or malfunction of the autoimmune system. Many are so classified by one or another medical authority. Several dozen, including all or most of those listed above, are so characterized in CECIL'S TEXTBOOK OF MEDICINE, edition of 1985, for example. Many of them exhibit the Koebner phenomenon, wherein bits of otherwise normal tissue released into the bloodstream of their host, as by some trauma, are erroneously treated as antigens by the host's autoimmune system, with resultant damage to tissues of such host. However, the present example is psoriasis, evident as an eruptive manifestation of the skin. Web site: http://www.delphion.com/details?pn=US05147872__
Patents 329
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Treatment of psoriasis Inventor(s): Wachter; Allan J. (9822 S. Grandview, Tempe, AZ 85284), Lezdey; John (976 Kingston Dr., Cherry Hill, NJ 08034) Assignee(s): none reported Patent Number: 5,190,917 Date filed: April 11, 1991 Abstract: A method for the prophylaxis or direct treatment of dermatitis including psoriasis which comprises administering to the site of the disease an effective amount of a corticosteroid and a company which inhibits mast cells or binds with their mediators. Excerpt(s): The present invention relates to a method and composition for treating a patient afflicted with psoriasis. More particularly, the present invention relates to the direct or prophylaxis treatment of psoriasis by topically administering synergistic amount of the combination of a compound which can inhibit mast cell proliferation or degranulation or bind with neutrophils, T-cells and their mediators, and a corticosteroid. The composition can also be used to treat chronic dermatitis, pruritis, contact dermatitis and palmoplentar eruptions. Psoriasis is an inflammatory skin condition whose cause is unknown. The condition involves thick scaling due to epidermal cell proliferation, cracking and bleeding. Mast cells have recently noted as being involved in psoriasis. Inflammation is a non-specific response of tissues to diverse stimuli or insults and results in release of a variety of materials at the site of inflammation that induce pain. It is now recognized that mast cells, neutrophils and Tcells are implicated in the pathophysiology of inflammatory skin conditions as well as in other physiological disorders. Mast cells provide the greatest source of histamines in acute inflammation, as well as chymases, after degranulation by IgE. Web site: http://www.delphion.com/details?pn=US05190917__
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Treatment of psoriasis and seborrheic dermatitis with imidazole antibiotics Inventor(s): Belew; Patricia W. (Germantown, TN), Rosenburg; E. William (Memphis, TN) Assignee(s): University of Tennessee Research Corporation (Knoxville, TN) Patent Number: 4,491,588 Date filed: March 17, 1983 Abstract: A method is provided for treating psoriasis and seborrheic dermatitis in humans by oral administration of an effective, lesion reducing, amount of an imidazole antibiotic. Excerpt(s): The present invention relates to methods for the clinical management of patients suffering with the skin diseases of psoriasis and seborrheic dermatitis. In particular, it provides for a new and safe treatment for those diseases by oral administration of imidazole antibiotics. Psoriasis is a skin disease of unknown cause that produces chronic, recurrent lesions which cause extreme emotional and physical discomfort to patients. Typically, the lesions of psoriasis are round, dry patches of varying size covered by abundant grayish-white scabs. The lesions may cover the entire body, though they are most frequently located around the scalp, body folds and nails. Seborrheic dermatitis is a common skin disease with clinical similarities to psoriasis.
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While suggestions have been made over the years that it may be related to microbial factors, its cause is also considered still unknown. Web site: http://www.delphion.com/details?pn=US04491588__ •
Treatment of psoriasis by ribofuranosylimidszolium-5-oleate
administration
of
4-carbamoyl-1-.beta.-D-
Inventor(s): Hori; Kazuyoshi (Hori, JP), Morishita; Masataka (Shizuoka, JP), Ishikawa; Hiroaki (Kanagawa, JP), Nagano; Kazuhiro (Hori, JP), Kawashima; Makoto (Tokyo, JP) Assignee(s): Asahi Kasei Kogyo Kabushiki Kaisha (Osaka, JP) Patent Number: 5,462,929 Date filed: April 11, 1994 Abstract: A composition for curing proliferative skin diseases containing 4-carbamoyl-1.beta.-D-ribofuranosyl-imidazolium 5-olate (mizoribine) as an active ingredient. It has a potent activity of inhibiting the growth of keratinocytes and an improved effect of curing psoriasis, so that it is useful for curing proliferative skin diseases. Further it has only an extremely reduced toxicity, is highly safe, and can be administered for long and perorally. Excerpt(s): The present invention relates to a composition for curing proliferative skin diseases containing 4-carbamoyl-1-.beta.-D-ribofuranosyl-imidazolium-5-olate as an active ingredient. 4-carbamoyl-1-.beta.-D-ribofuranosyl-imidazolium-5-olate (hereinafter sometimes designated as mizoribine) has an immunosuppressive activity and suppresses the rejection of the transplantation of an organ such as kidney. Mizoribine anhydrate crystal (bredinin. trade mark, tablet. Toyo Jozo Co.) has been applied as an immunosuppressant, which is prescribed for oral administration, with initial dose 2-3 mg/kg/day and maintenance dose 1-2mg/kg/day. A proliferative skin disease, especially psoriasis is a common chronic, squamous dermatosis, marked by exacerbations and remissions. It is characterized clinically by the presence of rounded, circumscribed, erythemtous, dry, scaling patches of various sizes, covered by grayish white or silvery white, umbilicated and lamellar scales. Central clearing and coalescence of the lesions produce a wide variety of clinical configurations, including annular or circinate, discoid or nummular, figurate, and gyrate arrangements. The most distinctive histological findings in well-developed psoriasis are characterized by proliferative and hypertrophic epidermis, disappearance of granular layer and promotion of parakeratosis, and migrating the leukocytes into epidermis and horny layer from edematous and elongated derml papilla, and resulted to form Munro microabscesses. Web site: http://www.delphion.com/details?pn=US05462929__ •
Treatment of psoriasis with 11-cis-retinoic acid Inventor(s): Braiman; Mark S. (Charlottesville, VA) Assignee(s): 4 Thought Technologies (Charlottesville, VA) Patent Number: 5,719,195 Date filed: May 5, 1995 Abstract: A particular uncommon isomer of retinoic acid (namely 11-cis-retinoic acid, or neotretinoin) is useful in treating conditions involving abnormal cellular differentiation
Patents 331
and hyperproliferation, such as psoriasis. A new method of synthesizing this isomer, in quantities that has allowed it to be compared therapeutically with the more commonly available all-trans and 13-cis isomers, is presented. As measured on the inventor's own psoriasis-affected skin, topical treatment with 11-cis-retinoic acid is much more efficacious in reducing symptoms and has substantially reduced side effects, as compared to topical treatment with the other isomers. A single application of a 0.001% neotretinoin cream to psoriasis lesions leads within 48 hours to substantial amelioration of associated dermatological symptoms, including itching, scaling, bleeding, and abnormal appearance. Continued application leads to complete remission, and replacement of lesions by skin that is indistinguishable from surrounding healthy tissue, without any noticeable irritation, erythema, or other problematic side effects. A less efficacious but more easily-implemented version of the same invention employs ultraviolet or blue-light irradiation of a commercially-available gel containing tretinoin as a means of effecting partial conversion of the tretinoin to neotretinoin, prior to application of the gel to psoriasis-affected areas of skin. Excerpt(s): The invention relates to methods using retinoids to treat conditions involving hyperproliferation and incomplete differentiation of cells, particularly skin conditions such as psoriasis. Differences in the biological activities of the various geometric isomers of retinoids were first noted by George Wald, who ascertained the primary role in the visual process of all-trans-retinaldehyde (which Wald and coworkers originally termed "retinene"). In the eye, retinene is the photoproduct of 11-cisretinaldehyde (which was originally termed "neo-b-retinene") when the latter is bound to visual pigment proteins such as rhodopsin ›2!. When dissolved in organic solvents, these geometric isomers of retinaldehyde are distinct and chemically stable, meaning that under most conditions the all-trans form and 11-cis forms are not rapidly interconverted except when exposed to blue or ultraviolet light. The all-trans- and 11-cis isomers of the corresponding acid (retinoic acid) are also stable and chemically distinct, as has been shown by their chromatographic separation from each other and from additional isomers such as: 7-cis; 9-cis; 13-cis; 9,13-dicis; and 11,13-dicis. As with retinaldehyde, these geometric isomers of retinoic acid can be interconverted upon absorption of ultraviolet light, and can subsequently be chromatographically separated from each other to yield the pure individual isomers. The separation methods, as well as the distinct spectroscopic properties of 9 of the resulting isomers of retinoic acid, are summarized in published work ›12!, which is incorporated herein by reference. Web site: http://www.delphion.com/details?pn=US05719195__ •
Treatment of psoriasis with 6-aminonicotinamide and thionicotinamide Inventor(s): Yu; Ruey J. (4400 Dexter St., Philadelphia, PA 19128), Van Scott; Eugene J. (1138 Sewell Lane, Rydal, PA 19046) Assignee(s): none reported Patent Number: 4,067,975 Date filed: August 4, 1975 Abstract: A treatment to alleviate the symptoms of psoriasis consisting of topical application of a cream, ointment or lotion containing as an active ingredient one or more of the following compounds: 6-aminonicotinamide, 6-carbamoylnicotinamide, 6chloronicotinamide, 6-dimethylaminonicotinamide, 6-formylaminonicotinamide, 6aminonicotinic acid, 6-aminonicotinic acid methyl ester, 6-hydroxy nicotinic acid, thionicotinamide, 2-aminopyrazinamide and 2-carbamoylpyrazinamide is disclosed.
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The therapeutic composition may include a single member of the above listed active ingredients present in a total amount of from 0.01 to 5 percent by weight of the total composition, or a plurality thereof present in a preferred concentration range of from 0.01 to 2 percent by weight of the total composition. Topical application of the therapeutic composition in a cream, ointment, or a water or alcohol solution has been found to achieve from substantial to complete remissions of psoriasis in humans. Excerpt(s): This invention relates to a treatment for psoriasis and specifically to a composition containing one or more compounds which have been found to be effective when topically applied, to improve and heal the skin lesions of psoriasis in humans. Psoriasis is a chronic disease, and remains a disfiguring and disabling cutaneous impairment to millions of persons. Its etiology is completely unknown, and therefore, prevention remains inconceivable. Therapy has necessarily been empiric, and has included the systemic use of antimitotic drugs such as methotrexate to induce remissions of the lesions. However, acute and chronic toxicity on tissues other than skin has discredited use of methotrexate. Therefore it is imperative that other means of therapy be found by external delivery of drugs so that toxicity is confined chiefly to the skin, or by the discovery of new drugs having nontoxic attributes. In our prior patent application entitled TREATMENT OF PSORIASIS, Ser. No. 371,516, filed June 19, 1973, now U.S. Pat. No. 3,904,766, we described and claimed the use of mechlorethamine hydrochloride ointment in the treatment of psoriasis by topical application. We also described that in an oil base the compound formed a stable composition. Web site: http://www.delphion.com/details?pn=US04067975__ •
Treatment of psoriasis with 6-substituted nicotinamides, 2-substituted pyrazinamides and closely related compounds Inventor(s): Yu; Ruey J. (4400 Dexter St., Philadelphia, PA 19128), Van Scott; Eugene J. (1138 Sewell La., Rydal, PA 19046) Assignee(s): none reported Patent Number: 4,141,977 Date filed: August 17, 1976 Abstract: A treatment to alleviate the symptoms of psoriasis consisting of topical application of a cream, ointment or lotion containing, as the principal active ingredient, one or more 6-substituted nicotinamides and or 2-substituted pyrazinamides is disclosed. The therapeutic composition may include a single member of the above active ingredients present in a total amount of from 0.01 to 5 percent by weight of the total composition, or a plurality thereof present in a preferred concentration range of from 0.02 to 2 percent by weight of the total composition. Topical application of the therapeutic composition in a cream, ointment, or a water or alcohol solution has been found to achieve from substantial to complete remissions of psoriasis in humans. Excerpt(s): This invention relates to a treatment for psoriasis and specifically to a composition containing one or more compounds which have been found to be effective when topically applied, to improve and heal the skin lesions of psoriasis in humans. Psoriasis is a chronic disease, and remains a disfiguring and disabling cutaneous impairment to millions of persons. Its etiology is completely unknown, and therefore prevention remains inconceivable. Therapy has necessarily been empiric, and has included the systemic use of antimitotic drugs such as methotrexate to induce remissions of the lesions. However, acute and chronic toxicity on tissues other than skin
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has discredited use of methotrexate. Therefore it is imperative that other means of therapy be found by external delivery of drugs so that toxicity is confined chiefly to the skin, or by the discovery of new drugs having nontoxic attributes. In our prior patent application entitled TREATMENT OF PSORIASIS, Ser. No. 371,516, filed June 19, 1973, now U.S. Pat. No. 3,904,766, we described and claimed the use of mechlorethamine hydrochloride ointment in the treatment of psoriasis by topical application. We also described that in an oil base the compound formed a stable composition. Web site: http://www.delphion.com/details?pn=US04141977__ •
Treatment of psoriasis with nicotinamide analogues Inventor(s): Yu; Ruey J. (4 Lindenwold Ave., Ambler, PA 19002), Van Scott; Eugene J. (1138 Sewell La., Rydal, PA 19046) Assignee(s): none reported Patent Number: 4,258,052 Date filed: February 5, 1979 Abstract: A treatment to alleviate the symptoms of psoriasis consisting of topical application of a cream, lotion, ointment or gel containing as the principal active ingredient one or more nicotinamide analogues is disclosed. The therapeutic composition may include a single member of the above active ingredients present in a total amount of from 0.01 to 5 percent by weight of the total composition or a plurality thereof present in a preferred concentration range of from 0.02 to 2 percent by weight of the total composition. Topical application of the therapeutic composition in a cream, ointment, lotion, water or gel has been found to achieve from substantial to complete remissions of psoriasis in humans. Excerpt(s): This application relates to a treatment of the symptoms of psoriasis and specifically to three classes of nicotinamide analogues found to be effective thereof. In our prior Patent Application Ser. No. 715,131 it was disclosed that certain 6-substituted nicotinamides and 2-substituted pyrazinamides were effective in treating the symptoms of psoriasis by topical application. In our parent case, U.S. Pat. No. 4,067,975, the use of 6-aminonicotinamide and thionicotinamide in compositions for the treatment of psoriasis was disclosed. It has now been discovered that many additional related compounds are also effective as will be subsequently described. 16. 6Diphenylphosphorylamino nicotinamide and its ester. Web site: http://www.delphion.com/details?pn=US04258052__
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Treatment of psoriasis, allergies and auto-immune disorders of the skin with cis-6hexadecenoic acid Inventor(s): Hoppe; Udo (Heidmuhlen, DE), Jacob; Jurgen (Hamburg, DE) Assignee(s): Beiersdorf AG (Hamburg, DE) Patent Number: 6,589,520 Date filed: April 17, 2000 Abstract: A method for the prophylaxes and treatment of psoriasis, allergies and autoimmune disorders of the skin, the treatment of sensitive skin, or a combination thereof, which comprises applying cis-6-hexadecenoic acid, or a salt or ester thereof.
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Excerpt(s): The invention relates to novel compounds of cis-6-hexadec-1-enoic acid or its derivatives. It is also called cis-hexadec-6-enoic acid or delta-6-hexadecenoic acid. Saturated and unsaturated fatty acids are constituents of the cell membrane of cells. The concentration of unsaturated fatty acids plays a part in the barrier properties of the skin and in the reactivity of cells in inflammatory processes. Thus it is already known to use cis-9-heptadecenoic acid for the treatment of psoriasis, allergies and auto-immune disorders (DE-A-4309512). Web site: http://www.delphion.com/details?pn=US06589520__ •
Ultraviolet emitting CeYMg aluminate fluorescent lamp phosphor for psoriasis treatment Inventor(s): Wolfe; Robert W. (Wysox, PA) Assignee(s): GTE Sylvania Incorporated (Stamford, CT) Patent Number: 4,153,572 Date filed: June 14, 1978 Abstract: This invention relates to a CeYMg Aluminate fluorescent lamp phosphor which emits ultraviolet radiation in a preferred region of the electromagnetic spectrum proven useful for the treatment of psoriasis. The phosphor in fluorescent lamps shows improved performance for this application over other phosphors known to the art. Excerpt(s): This invention relates to a cerium yttrium magnesium aluminate fluorescent lamp phosphor possessing the hexagonal magneto plumbite structure and to fluorescent lamps incorporating the phosphor. Philips Electronics and Associated Industries in British Pat. No. 1,452,083 disclosed an ultraviolet emitting fluorescent lamp phosphor having the composition CeMgAl.sub.11 O.sub.19 and the magneto plumbite structure. H.F. Ward of Thorn Industries, in British Patent 1,194,014 disclosed a phosphor having the composition CeAl.sub.11 O.sub.18 and the magnetoplumbite structure. Although CeAl.sub.11 O.sub.18 and CeMgAl.sub.11 O.sub.19 have similar crystal structures, incorporation of magnesium shifts the UV excited emission peak from about 460 nm in CeAl.sub.11 O.sub.19 to about 370 nm in CeMgAl.sub.11 O.sub.19. These phosphors are self-activated by the Ce.sup.3 + ion. The invention also includes fluorescent lamps incorporating the phosphor. Web site: http://www.delphion.com/details?pn=US04153572__
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Use of 1.alpha.-hydroxylated-19-nor-vitamin D compounds to treat psoriasis Inventor(s): DeLuca; Hector F. (Deerfield, WI) Assignee(s): Wisconsin Alumni Research Foundation (Madison, WI) Patent Number: 5,321,018 Date filed: November 20, 1992 Abstract: A novel use for 1.alpha.-hydroxylated-19-nor-vitamin D compounds to treat psoriasis inasmuch as these compounds when administered to humans are converted to a metabolite, such as a 1.alpha.,25-dihydroxylated compound, which metabolite in vitro will cause differentiation in a human cell line.
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Excerpt(s): The present invention relates to vitamin D compounds, and more particularly to the use of 1.alpha.-hydroxylated-19-nor-vitamin D compounds to treat psoriasis. The D vitamins are very important agents for the control of calcium and phosphate metabolism in animals and humans, and have long been used as dietary supplements and in clinical practice to assure proper bone growth and development. It is now known that the in vivo activity of these vitamins, specifically of vitamin D.sub.2 and D.sub.3, is dependent on metabolism to hydroxylated forms. Thus, vitamin D.sub.3 undergoes two successive hydroxylation reactions in vivo, leading first to 25hydroxyvitamin D.sub.3 and then to 1,25-dihydroxyvitamin D.sub.3 and the latter is indeed thought to be the compound responsible for the well-known beneficial effects of vitamin D.sub.3. Likewise, vitamin D.sub.2, which is commonly used as a dietary supplement, undergoes an analogous hydroxylation sequence to its active forms, being first converted to 25-hydroxyvitamin D.sub.2 (25--OH--D.sub.2) and then to 1,25dihydroxyvitamin D.sub.2 (1,25--(OH).sub.2 D.sub.2). These facts are well established and well known in the art (see, for example, Suda et al. Biochemistry 8, 3515 (1969) and Jones et al. Biochemistry 14, 1250 (1975)). Hollick, U.S. Pat. No. 4,728,643 discloses a method of treating psoriasis with vitamin D compounds which in vitro cause cell differentiation. However 1.alpha.-hydroxylated vitamin D compounds, i.e. those compounds having only a hydroxyl group at the carbon 1 position and initially lacking a hydroxyl group at the carbon 24 or 25 positions, are relatively inactive in causing cell differentiation in vitro. Additionally, it is also well known that 1.alpha.-hydroxylated compounds are rapidly converted in vivo to 1.alpha.,25-dihydroxy compounds, e.g. 1.alpha.-hydroxyvitamin D.sub.3 to 1.alpha.,25-dihydroxy-vitamin D.sub.3, or if the 25 carbon position is blocked to 1.alpha.,24-dihydroxy compounds. Hollick et al, Science, Vol. 190, pages 576-578 (1975) and Hollick et al, J. of Clinical Endocrinology & Metabolism, Vol. 44, pages 595-598 (1977). For example, in PCT patent application number PCT/DK89/00079 filed Apr. 7, 1989 and published Nov. 2, 1989 under number WO89/10351 there is disclosed numerous side chain homologated vitamin D compounds lacking the hydroxyl group at the carbon 25 position in the side chain. It is disclosed therein that such compounds are converted in vivo to active compounds having a hydroxyl group at the carbon 25 position by enzymatic hydroxylation, and may thus be used for the treatment of psoriasis. Thus, the human body can rapidly convert relatively inactive 1.alpha.-hydroxylated vitamin D compounds to metabolites highly active in causing cell differentiation. There has, however, been a failure in the art to recognize the ability of 1.alpha.-hydroxylated-19-nor-vitamin D compounds to treat malignancies such as psoriasis. Web site: http://www.delphion.com/details?pn=US05321018__ •
Use of calendula glycosides for the treatment of psoriasis Inventor(s): Anand; Chaman Lal (Glasgow, GB), Stimson; William Howard (Glasgow, GB), Habtemarium; Solomon (Glasgow, GB), Gray; Alexander Irvine (Glasgow, GB), Waterman; Peter George (Johnstone, GB) Assignee(s): University of Strathclyde (Glasglow, GB) Patent Number: 6,225,342 Date filed: May 21, 1998 Abstract: A method and compound for the treatment of disease involving hyperproliferation of dermis cells is provided. In particular, compounds isolated from the species of plants known as calendula have been found to be beneficial in the
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treatment of psoriasis. An extract of plant material obtained from calendula officinalis has been found to be advantageous as an active compound in medicaments for use in the treatment of psoriasis. Excerpt(s): The present invention relates to compounds, and plant extracts containing compounds which are indicated as having an inhibiting effect on cell proliferation. More specifically, the invention relates to glycosidic compounds derivable from Calendula species, the plant glycosides having a cytostatic effect on cells, and their use as cytostatic agents, in particular in the treatment of psoriasis. Crude Calendula plant extracts have been used in medicinal folklore for the treatment of several ailments for centuries. Such extracts have, for example, been used as or in anti-inflammatory medicaments and the like. International Patent application WO 91/15218 teaches a therapeutic composition against psoriasis comprising as active ingredient a solvent extract of at least six different herbs. This application teaches that marigold decoctions can be used against gastric and intestinal ulcers externally as well as for packing slowly healing wounds and ulcers. Nowhere is it stated that marigold extract is in fact used by itself as the active component in a therapeutical composition against psoriasis. Web site: http://www.delphion.com/details?pn=US06225342__ •
Use of Cis-9-heptadecenoic acid for treating psoriasis and allergies Inventor(s): Jacob; Jurgen (Hamburg, DE), Steckel; Friedhelm (Hamburg, DE), Degwert; Joachim (Tostedt, DE) Assignee(s): Beiersdorf AG (Hamburg, DE) Patent Number: 5,708,028 Date filed: September 20, 1995 Abstract: Cis-9-heptadecenoic acid or its salts can be used for the prophylaxis and treatment of psoriasis, allergies and autoimmune diseases. Excerpt(s): This application is a 371 of PCT/EP94/00941 Mar. 24, 1994. The invention relates to new uses of cis-9-heptadecenoic acid. Saturated and unsaturated fatty acids are constituents of the cell membrane of cells. The concentration of unsaturated fatty acids plays a role in the barrier properties of the skin and in the reactivity of calls in inflammatory processes. Web site: http://www.delphion.com/details?pn=US05708028__
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Use of hexadecylphosphocholine for the treatment of psoriasis Inventor(s): Unger; Clemens (Gottingen, DE), Eibl; Hansjorg (Bovenden, DE), Engel; Jurgen (Alzenau, DE) Assignee(s): Asta Pharma Aktiengesellschaft (DE) Patent Number: 5,290,769 Date filed: December 22, 1992 Abstract: The use of alkylphosphoric acid compounds of Formula IR--Y-PO.sub.2.sup.crclbar. --X--R.sub.1 Iwhere in Formula IR represents a saturated or unsaturated hydrocarbon radical with 12 to 24 carbon atoms or where R represents the group--CH.sub.2 --CHR.sub.3 --CH.sub.2 --Z--R.sub.4 and R.sub.3 is a C.sub.1 -C.sub.6 -
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alkoxy group or a C.sub.1 -C.sub.6 -alkoxymethyl group,Z represents oxygen or sulphur and R.sub.4 represents a C.sub.1 -C.sub.24 -alkyl radical,X is an oxygen atom, NH or NR.sub.2 and Y is an oxygen atom or NH, R.sub.1 is a C.sub.1 -C.sub.8 -alkyl group, or where R.sub.1 represents a C.sub.2 -C.sub.8 -alkyl group which is unsaturated and/or substituted by halogen, amino, C.sub.1 -C.sub.6 -alkylamino, di-C.sub.1 -C.sub.6 alkylamino, tri-C.sub.1 -C.sub.6 -alkylamino, hydroxy, carboxy, C.sub.3 -C.sub.8 cycloalkyl or phenyl for the preparation of a pharmaceutical composition for combating psoriasis disorders. Excerpt(s): for the treatment of psoriasis disorders. Alkylphosphoric acid compounds of Formula I are known substances having an anti-tumor effect. In accordance with the present invention, it has been found that compounds of Formula I and salts thereof with physiologically acceptable acids are effective against psoriasis and related disorders. Web site: http://www.delphion.com/details?pn=US05290769__ •
Use of trialkylsilyl-6-aminonicotinamides for the treatment of psoriasis Inventor(s): Zackheim; Herschel S. (Redwood City, CA), Pappo; Raphael (Redwood City, CA) Assignee(s): International Plant Research Institute, Inc. (San Carlos, CA) Patent Number: 4,385,052 Date filed: July 20, 1981 Abstract: The use of a composition for relieving the symptoms of psoriasis in humans is disclosed. The composition is an N-trialkylsilyl-substituted 6-aminonicotinamide. The composition is applied in a suitable pharmaceutical base, such as a cream or ointment, to the affected area of skin. Excerpt(s): This invention relates to the use of trialkylsilyl-6-aminonicotinamides for the treatment of psoriasis through topical application to improve and heal the skin lesions of psoriasis in humans. Psoriasis is a chronic disease, and remains a disfiguring and disabling cutaneous impairment to millions of persons. Its etiology is completely unknown, and therefore, prevention remains inconceivable. Therapy has necessarily been empiric, and has included the systemic use of anti-mitotic drugs such as methotrexate to induce remissions of the lesions. However, acute and chronic toxicity on tissues other than skin has discredited use of methotrexate. Therefore, it is imperative that other means of therapy be found for external delivery of drugs so that toxicity is confined chiefly to the skin, or by the discovery of new drugs having nontoxic attributes. U.S. Pat. No. 4,067,975 discloses the treatment of psoriasis with a family of 6-substituted nicotinamides, 6-substituted nicotinic acid and esters thereof and 2-substituted pyrazinamide or thionicotinamide. While such compounds have proven effective, their use must be accompanied by the application of Vitamin B.sub.3 to avoid possible hearing impairment in the patient. Web site: http://www.delphion.com/details?pn=US04385052__
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UV Radiation device for phototherapy of dermatoses, especially psoriasis Inventor(s): Mutzhas; Maximilian F. (Sonnenstr. 17, D-8000 Munchen 2, DE) Assignee(s): none reported Patent Number: 4,558,700 Date filed: July 18, 1983 Abstract: The invention relates to a UV radiation device for phototherapy of dermatoses, especially psoriasis, which produces UV radiation the radiation intensity E.sub.2 of which present in the effective area in the wavelength range below 300 nm is substantially less than the radiation intensity E.sub.1 in the wavelength range between 300 and 310 nm, the radiation dose being between 0.7 and 1.0 times the erythema threshold dose. Such a UV radiation device is distinguished by good therapeutic effectiveness and the avoidance of undesirable side effects. Excerpt(s): The invention relates to a UV radiation device for phototherapy of dermatoses, especially psoriasis. Approximately 2% of the population suffer from psoriasis, a flaking of the skin caused by a gene defect. A greatly increased rate of cell division (cell proliferation) in the basal layer of the epidermis gives rise to the flaky focus of the psoriasis which leads to severe physical and psychological effects. The object of psoriasis therapy is to cause the focus to recede in order to make the skin free of flakes and keep it in this condition. At present therapy takes the form of treatment by chemotherapy, photochemotherapy and phototherapy. Web site: http://www.delphion.com/details?pn=US04558700__
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Washable topical preparation for treating psoriasis Inventor(s): Roelz; Wolfgang (Langen-Neurott, DE), Mueller; Josef (Lindenfels, DE) Assignee(s): Rohm GmbH Chemische Fabrik (Darmstadt, DE) Patent Number: 4,769,390 Date filed: January 21, 1987 Abstract: A pharmaceutical preparation for topical treatment of skin disorders, particularly psoriasis, comprising active ingredients consisting essentially of combinations of 1,8,9-anthracenetriol, and/or derivatives thereof, and urea. The subject preparation is applied in an essentially water-free excipient. The preparation includes surfactants, which are ordinarily incompatible with the active ingredients. By the use of surfactant-urea combinations, surfactants can be incorporated into a stable, lipophilic pharmaceutical preparation, whereby after use the surfactants are liberated by the action of water, to form a readily washable emulsion system. The inventive preparation is advantageously used in the "short time" method of therapy of psoriasis. Excerpt(s): The present invention relates to pharmaceutical preparations for treating psoriasis comprising a combination of substances based on 1,8,9-anthracenetriol and urea. The preparations are particularly useful for treating psoriasis on the head and other hairy body parts, by the method of short-time therapy. Psoriasis is among the dermatoses having a poorly understood etiology. The therapies of choice are thus topical agents such as salicyclic acid, tars (pices var.), vitamin A acid, corticosteroids, etc. Sometimes, coal tar is used. Among the agents long used for treating psoriasis is 1,8,9-anthracenetriol (also called dithranol or Anthralin), and certain of its acyl derivatives, usually in preparations containing 0.1-5% by weight of this agent.
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Web site: http://www.delphion.com/details?pn=US04769390__
Patent Applications on Psoriasis As of December 2000, U.S. patent applications are open to public viewing.10 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to psoriasis: •
Anti-inflammatory and psoriasis treatment and protein kinase inhibition by hydroxyltilbenes and novel stilbene derivatives and analogues Inventor(s): Chen, Genhui; (Burnaby, CA), Hu, Kaiji; (Burnaby, CA), Li, Jianxiong; (Port Moody, CA), Zhu, Jiang; (Burnaby, CA), Webster, John M. (North Vancouver, CA) Correspondence: Pennie & Edmonds; 1155 Avenue of the Americas; New York; NY; 10036-2711; US Patent Application Number: 20030171429 Date filed: October 28, 2002 Abstract: Disclosed herein are compositions containing hydroxylstilbenes or their derivatives or analogues. The compositions are useful to inhibit protein kinease, and for the treatment of inflammatory diseases, including psoriasis, multiple sclerosis, rhumatoid arthritis, restinosis, inflammatory bowel disease, and inflammatory lung disease. They are also useful to treat surgical adhesions and graft rejection. Novel derivatives and analogues are also disclosed. Excerpt(s): The stilbenes isolated from Photorhabdus species bacteria are known to have antibiotic activity. See V. J. Paul, S. Frautschv, W. Fenical, and K. H. Nealson, Journal of Chemical Ecology, 7: 589-597 (1981), and K. Hu, J. Li, W. Wang, H. Wu, H. Lin and J. M. Webster, Canadian Journal of Microbiology. 44: 1072-1077 (1998). However, these compounds have not been shown to have other biological activity. A similar compound, resveratrol, has been disclosed as having cancer preventive (Jang et al. 1997) and protein kinase C inhibitory (Garcia-Garcia et. al., 1999) activities. There are many common conditions that cannot be treated successfully by antibiotics. Some of these are inflammatory diseases. The compounds of the invention possess specific antiinflammatory properties. Inflammatory diseases, whether of a chronic or acute nature, represent a substantial problem in the healthcare industry. Chronic inflammation is considered to be inflammation of a prolonged duration (weeks or months) in which active inflammation, tissue destruction and attempts at healing are proceeding simultaneously (Robbins Pathological Basis of Disease by R. S. Cotran, v. Kumar, and S. L. Robbins, W. B, Saunders Co., p. 75, 1989). Although chronic inflammation can follow an acute inflammatory episode, it can also begin as an insidious process that progresses with time, for example, as a result of a persistent infection (e.g., tuberculosis, syphilis, fungal infection) which causes a delayed hypersensitivity reaction, prolonged exposure to endogenous (e.g., elevated plasma lipids) or exogenous (e.g., silica, asbestos, cigarette tar, surgical sutures) toxins, or, autoimmune reactions against the body's own tissues (e.g., rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, psoriasis). Chronic inflammatory diseases therefore, include many common medical conditions such as rheumatoid arthritis, restenosis, psoriasis, multiple sclerosis, surgical adhesions,
10
This has been a common practice outside the United States prior to December 2000.
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tuberculosis, and chronic inflammatory lung and airway diseases (e.g., asthma, pneumoconiosis, chronic obstructive pulmonary disease, nasal polyps and pulmonary fibrosis). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
CD40 antagonists for use in treating psoriasis and other inflammatory skin conditions Inventor(s): Bos, J.D. (Heemstede, NL), Pasch, M. C. (Almere, NL), Thomas, David; (Houston, TX) Correspondence: TANOX, INC. 10301 STELLA LINK; HOUSTON; TX; 77025; US Patent Application Number: 20020031512 Date filed: April 19, 2001 Abstract: A method of treating psoriasis and other inflammatory conditions of the skin by administering anti-CD40 molecules, such as mAb 5D12, in an amount sufficient to inhibit the immunological activation of keratinocytes. These anti-CD40 molecules include antibodies, peptides, and other molecules. Excerpt(s): This application claims the benefit of priority of U.S. Provisional Application No. 60/198,174, filed Apr. 19, 2000, which is hereby incorporated by reference. The invention relates to CD40 antagonists for treating psoriasis and other inflammatory conditions of the skin. There are numerous skin conditions characterized by an increased immune response and/or abnormal antigen presentation in the dermis and epidermis. The physiologic mechanisms involved in the evolution of such inflammatory processes are poorly understood. However, it has become apparent that skin cells are important in the generation of a cutaneous inflammatory response (Kupper, "Immune and Inflammatory Processes in Cutaneous Tissues", J. Clin. Invest., 86, pp. 1783-89 (1990)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Chinese traditional medicines for psoriasis Inventor(s): Huang, Hsu-Shan; (Taipei, TW), Chen, Rong Fu; (Taipei, TW) Correspondence: DYKAS, SHAVER & NIPPER, LLP; P O BOX 877; BOISE; ID; 837010877; US Patent Application Number: 20030165533 Date filed: January 24, 2003 Abstract: The invention relates to disclose some Chinese formula for psoriasis. Whether treatment for psoriasis is targeted at both the hyperproliferative and inflammatory aspect of the topical therapy. Specially, the administration dosage is soft gel, cream, tincture and aerosol etc. topical dosages. Excerpt(s): This application is a Divisional of the utility application filed on Jan. 14, 2003 entitled Chinese traditional medicines for psoriasis with Ser. No. 10/050,060. The invention relates to disclose some Chinese formula for psoriasis. Whether treatment for psoriasis is targeted at both the hyperproliferative and inflammatory aspect of the topical therapy. Psoriasis is a widespread, inflammatory and scaling skin disease, which is characterized by abnormal keratinocyte proliferation and differentiation of the
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epidermis, accumulation of polymorphonuclear leukocytes in the skin. Dominant and interdependent features of psoriasis are epidermal hyperproliferation, disturbed keratinocyte differentiation, and inflammation of the dermis and epidermis. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Compositions and methods for diagnosing or treating psoriasis Inventor(s): Charmley, Patrick R. (Seattle, WA), Argonza-Barrett, Rhodora H. (Seattle, WA), Wang, Kai; (Bellevue, WA), Fitzgibbon, Matthew P. (Bellevue, WA), Smith, Ryan C. (Seattle, WA) Correspondence: CHRISTENSEN, O'CONNOR, JOHNSON, KINDNESS, PLLC; 1420 FIFTH AVENUE; SUITE 2800; SEATTLE; WA; 98101-2347; US Patent Application Number: 20020169127 Date filed: March 28, 2002 Abstract: The present invention provides nucleic acid molecules, polypeptides, antibodies and methods for the diagnosis and/or treatment of psoriasis. Excerpt(s): The application claims the benefit of U.S. Provisional Patent Application No. 60/280,514, filed Mar. 29, 2001, the benefit of which is hereby claimed under 35 U.S.C.sctn.119. The present invention relates generally to polynucleotides, proteins, antibodies and methods for the diagnosis of psoriasis, and/or the amelioration of the symptoms of psoriasis. Psoriasis is a chronic inflammatory dermatosis that affects about 2% of the Caucasian population. It is characterized by hyperproliferation of epidermal cells and inflammation resulting from infiltration of activated T-helper cells and mononuclear cells and release of pro-inflammatory cytokines (Menter and Barker, Lancet 338:231, 1991; Barker, Lancet 338:227 1991). It may also be associated with arthritis and can present as a severely inflammatory dermatosis in patients with acquired immunodeficiency syndrome (AIDS) (Duvic, J. Invest. Dermatol. 95:385 1990). The symptoms of psoriasis include sharply defined erythematous patches covered with a distinctive scale, hyperproliferation of the epidermis, incomplete differentiation of keratinocytes and dermal inflammation. Clinical variants of psoriasis include erythroderna, seborrheic, inverse, guttate, and photosensitive psoriasis, pustular variants and Reiter's disease. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Compositions and methods for treating psoriasis Inventor(s): Wang, Changyu; (El Cerrito, CA), Chu, Keting; (Burlingame, CA) Correspondence: Chiron Corporation; Intellectual Property, R338; P.O. Box 8097; Emeryville; CA; 94662-8097; US Patent Application Number: 20030165499 Date filed: January 23, 2003 Abstract: CD40 antagonists are used to prepare compositions, including pharmaceutical compositions, for treating autoimmune and neoplastic diseases in a mammal. The CD40 antagonist compositions are useful for reversing or substantially diminishing such autoimmune diseases as systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis and psoriasis.
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Excerpt(s): This application claims the benefit of Provisional Application No. 60/157,461, filed Oct. 4, 1999 which is incorporated herein by reference in its entirety. This invention relates to compositions for and methods of treating autoimmune and neoplastic diseases by administering one or more CD40 antagonist to a mammal. Psoriasis is one of the most prevalent, yet enigmatic, chronic, inflammatory skin disorders in humans, afflicting approximately 2% of the population. Despite intensive efforts to develop treatments, this autoimmune disease remains substantially refractory to therapy. Thus, there remains a critical need to identify new agents and methods for the treatment of psoriasis and other related autoimmune diseases. The compositions and methods of the present invention fulfill these and other related needs. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
COMPOSITIONS PSORIASIS
AND
METHODS
OF
PACLITAXEL
FOR
PREVENTING
Inventor(s): HUNTER, WILLIAM L. (VANCOUVER, CA) Correspondence: SEED INTELLECTUAL PROPERTY LAW GROUP PLLC; 701 FIFTH AVE; SUITE 6300; SEATTLE; WA; 98104-7092; US Patent Application Number: 20020037919 Date filed: December 1, 1997 Abstract: The present invention provides methods for treating or preventing inflammatory diseases such as psoriasis or multiple sclerosis, comprising the step of delivering to the site of inflammation an anti-microtubule agent, or analogue or derivative thereof. Excerpt(s): This application claims the benefit of Provisional Application No. 60/032,215, filed Dec. 2, 1996, and Provisional Application No. 60/063,087, filed Oct. 24, 1997, which applications are incorporated by reference in their entirety. The present invention relates generally to compositions and methods for treating or preventing inflammatory diseases. Inflammatory diseases, whether of a chronic or acute nature, represent a substantial problem in the healthcare industry. Briefly, chronic inflammation is considered to be inflammation of a prolonged duration (weeks or months) in which active inflammation, tissue destruction and attempts at healing are proceeding simultaneously (Robbins Pathological Basis ofDisease by R. S. Cotran, V. Kumar, and S. L. Robbins, W. B. Saunders Co., p. 75, 1989). Although chronic inflammation can follow an acute inflammatory episode, it can also begin as an insidious process that progresses with time, for example, as a result of a persistent infection (e.g., tuberculosis, syphilis, fungal infection) which causes a delayed hypersensitivity reaction, prolonged exposure to endogenous (e.g., elevated plasma lipids) or exogenous (e.g., silica, asbestos, cigarette tar, surgical sutures) toxins, or, autoimmune reactions against the body's own tissues (e.g., rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, psoriasis). Chronic inflammatory diseases therefore, include many common medical conditions such as rheumatoid arthritis, restenosis, psoriasis, multiple sclerosis, surgical adhesions, tuberculosis, and chronic inflammatory lung diseases (e.g., asthma, pneumoconiosis, chronic obstructive pulmonary disease, nasal polyps and pulmonary fibrosis). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Compositions, kits, and methods for identification, assessment, prevention, and therapy of psoriasis Inventor(s): Trepicchio, William L. (Andover, MA), Krueger, James G. (New York, NY), Oestreicher, Judith L. (Portsmouth, NH), Dorner, Andrew J. (Lexington, MA) Correspondence: LAHIVE & COCKFIELD; 28 STATE STREET; BOSTON; MA; 02109; US Patent Application Number: 20020037538 Date filed: May 9, 2001 Abstract: The invention relates to compositions, kits, and methods for detecting, characterizing, preventing, and treating psoriasis. A variety of markers are provided, wherein changes in the levels of expression of one or more of the markers is correlated with the presence of psoriasis. Excerpt(s): This application claims priority to U.S. Provisional Application No.: 60/203,087 filed on May 9, 2000, incorporated herein in it's entirety by this reference. Psoriasis is a chronic skin disorder characterized by thickened, erythematous, welldemarcated areas of skin covered by silvery scales. The extent of involvement ranges from isolated, small lesions confined to knees, elbows, and scalp, to the whole body surface. There are several clinical forms of psoriasis, ranging from stable plaque lesions to an unstable form typified by eruptive inflammatory lesions. Psoriasis is not a static disease: seasonal fluctuations, spontaneous remission, and physical and emotional wellbeing all affect the disease and hence its management. The disease is emotionally and physically debilitating for the subject, detracting significantly from the quality of life. Between one and three million individuals in the United States have psoriasis with nearly a quarter million new cases occurring each year. Conservative estimates place the costs of psoriasis care in the United States currently at $248 million a year. Psoriasis is characterized by hyper-proliferation and incomplete differentiation of epidermal keratinocytes. There are two major hypotheses concerning the pathogenesis of psoriasis. The first is that genetic factors determine abnormal proliferation of epidermal keratinocytes. The cells no longer respond normally to external stimuli such as those involved in maintaining epidermal homeostasis. Abnormal expression of cell membrane cytokine receptors or abnormal transmembrane signal transduction might underlie cell hyperproliferation. Inflammation associated with psoriasis is secondary to the release of pro-inflammatory molecules from hyperproliferative keratinocytes. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method for treatment of psoriasis Inventor(s): Jaros, Apolonia; (Bosna, YU), Miketin, Bronhilda; (Duluth, MN) Correspondence: VIDAS, ARRETT & STEINKRAUS, P.A. 6109 BLUE CIRCLE DRIVE; SUITE 2000; MINNETONKA; MN; 55343-9185; US Patent Application Number: 20010016212 Date filed: December 14, 2000 Abstract: This invention relates to the natural topical treatment of portions of skin of a person afflicted with psoriasis or other skin disorders such as dry skin, eczema, itchy skin, red skin, itchy eczema, inflamed skin, and/or cracked skin for the removal of itch and the restoration of the affected areas of skin to a normal condition. The natural
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treatment of a skin disorder initially involves formation of a natural ointment from the ingredients identified as chicken and hen herb; ruta herb; pure unsalted natural butter; and pure natural beeswax. The natural ointment is formed by combination of the ingredients which includes heating and stirring. The ointment is then applied twice daily to affected areas of skin until a natural cure of the skin disorder is obtained. Excerpt(s): This is a continuation-in-part patent application claiming priority to U.S. Utility patent application filed Jan. 10, 2000, application Ser. No. 09/480,745 entitled "Composition and Method for Treatment of Psoriasis". The present invention relates to a topical composition for the treatment of psoriasis or other skin disorders such as dry skin, eczema, itchy skin, red skin, itchy eczema, inflamed skin, and/or cracked skin. Psoriasis is generally a skin disease evidenced by the presence of skin elevations and scales which may be silvery in appearance. Psoriasis in general is a disease which accelerates the epidermal proliferation and proliferation of capillaries in the dermal region. In addition, psoriasis frequently results in the evasion of the dermis and epidermis by inflammation of the affected cells. Areas of skin affected by psoriasis also frequently lose water significantly faster than normal healthy skin. The areas of skin affected by psoriasis therefore tend to have increased metabolic rates which in turn has a negative impact on tissue catabolism and potentially causes muscle wasting. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method of testing for psoriasis vulgaris Inventor(s): Tamiya, Gen; (Kanagawa, JP), Inoko, Hidetoshi; (Kanagawa, JP) Correspondence: JANIS K. FRASER, PH.D., J.D. Fish & Richardson P.C. 225 Franklin Street; Boston; MA; 02110-2804; US Patent Application Number: 20030170652 Date filed: June 6, 2002 Abstract: By a detailed analysis of the sequences of the MHC S gene, SEEK1 gene, and HCR gene of Japanese patients with psoriasis and healthy individuals, it was demonstrated that some of the examined polymorphisms significantly correlate with psoriasis in the group of Japanese patients. Based on these correlations, it was demonstrated that psoriasis vulgaris can be detected by analyzing these gene polymorphisms in patients with psoriasis. Excerpt(s): This application is a continuation-in-part of PCT/JP00/08624, filed Dec. 6, 2000 which claims priority to Japanese Patent Application No. 11/346867, filed Dec. 6, 1999. The present invention relates to a method of testing for psoriasis vulgaris and DNA molecules used therefore. Psoriasis vulgaris (MIM 177900) is a skin disease characterized by inflammatory cell infiltration and hyperproliferation of epidermal cells. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method of treating psoriasis using anti-gamma interferon antibody Inventor(s): Hong, Kenneth; (El Cerrito, CA), Ehrhardt, Rolf; (San Francisco, CA) Correspondence: HOWREY SIMON ARNOLD & WHITE, LLP; BOX 34; 301 RAVENSWOOD AVE. MENLO PARK; CA; 94025; US Patent Application Number: 20030056233 Date filed: September 12, 2002 Abstract: Methods and compositions are provided for the creation and screening of nonhuman animal models having many of the histologic characteristics of human psoriasis. Immunocompromised host animals are injected with a purified population of CD45Rb positive cells, which are tolerant of the host major histocompatibility antigens, but are mismatched at one or more minor antigens. The injected cells are stimulated with a proinflammatory cytokine, e.g. IL-12, and a polyclonal activating agent. The injected animals develop a chronic skin disorder that includes histological features observed in human psoriasis, e.g. rete pegs, severe acanthosis and infiltration of Th1 cells into the dermis. Excerpt(s): Psoriasis is a chronic skin disease, characterized by scaling and inflammation. Psoriasis affects 1.5 to 2 percent of the United States population, or almost 5 million people. It occurs in all age groups and about equally in men and women. People with psoriasis suffer discomfort, restricted motion of joints, and emotional distress. When psoriasis develops, patches of skin thicken, redden, and become covered with silvery scales, referred to as plaques. Psoriasis most often occurs on the elbows, knees, scalp, lower back, face, palms, and soles of the feet. The disease also may affect the fingernails, toenails, and the soft tissues inside the mouth and genitalia. About 10 percent of people with psoriasis have joint inflammation that produces symptoms of arthritis. When skin is wounded, a wound healing program is triggered, also known as regenerative maturation. Lesional psoriasis is characterized by cell growth in this alternate growth program. In many ways, psoriatic skin is similar to skin healing from a wound or reacting to a stimulus such as infection, where the keratinocytes switch from the normal growth program to regenerative maturation. Cells are created and pushed to the surface in as little as 2-4 days, and the skin cannot shed the cells fast enough. The excessive skin cells build up and form elevated, scaly lesions. The white scale (called "plaque") that usually covers the lesion is composed of dead skin cells, and the redness of the lesion is caused by increased blood supply to the area of rapidly dividing skin cells. The exact cause of psoriasis in humans is not known, although it is generally accepted that it has a genetic component, and a recent study has established that it has an autoimmune component. Whether a person actually develops psoriasis is hypothesized to depend on something "triggering" its appearance. Examples of potential "trigger factors" include systemic infections, injury to the skin (the Koebner phenomenon), vaccinations, certain medications, and intramuscular injections or oral steroid medications. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method of treating psoriasis using anti-interleukin 12 antibody Inventor(s): Ehrhardt, Rolf; (San Francisco, CA), Queen, Cary; (Los Altos, CA), Hong, Kenneth; (El Cerrito, CA) Correspondence: HOWREY SIMON ARNOLD & WHITE, LLP; BOX 34; 301 RAVENSWOOD AVE. MENLO PARK; CA; 94025; US Patent Application Number: 20020194631 Date filed: March 26, 2002 Abstract: Methods and compositions are provided for the creation and screening of nonhuman animal models having many of the histologic characteristics of human psoriasis. Immunocompromised host animals are injected with a purified population of CD45Rb positive cells, which are tolerant of the host major histocompatibility antigens, but are mismatched at one or more minor antigens. The injected cells are stimulated with a proinflammatory cytokine, e.g. IL-12, and a polyclonal activating agent. The injected animals develop a chronic skin disorder that includes histological features observed in human psoriasis, e.g. rete pegs, severe acanthosis and infiltration of Th1 cells into the dermis. Excerpt(s): Psoriasis is a chronic skin disease, characterized by scaling and inflammation. Psoriasis affects 1.5 to 2 percent of the United States population, or almost 5 million people. It occurs in all age groups and about equally in men and women. People with psoriasis suffer discomfort, restricted motion of joints, and emotional distress. When psoriasis develops, patches of skin thicken, redden, and become covered with silvery scales, referred to as plaques. Psoriasis most often occurs on the elbows, knees, scalp, lower back, face, palms, and soles of the feet. The disease also may affect the fingernails, toenails, and the soft tissues inside the mouth and genitalia. About 10 percent of people with psoriasis have joint inflammation that produces symptoms of arthritis. When skin is wounded, a wound healing program is triggered, also known as regenerative maturation. Lesional psoriasis is characterized by cell growth in this alternate growth program. In many ways, psoriatic skin is similar to skin healing from a wound or reacting to a stimulus such as infection, where the keratinocytes switch o from the normal growth program to regenerative maturation. Cells are created and pushed to the surface in as little as 2-4 days, and the skin cannot shed the cells fast enough. The excessive skin cells build up and form elevated, scaly lesions. The white scale (called "plaque") that usually covers the lesion is composed of dead skin cells, and the redness of the lesion is caused by increased blood supply to the area of rapidly dividing skin cells. The exact cause of psoriasis in humans is not known, although it is generally accepted that it has a genetic component, and a recent study has established that it has an autoimmune component. Whether a person actually develops psoriasis is hypothesized to depend on something "triggering" its appearance. Examples of potential "trigger factors" include systemic infections, injury to the skin (the Koebner phenomenon), vaccinations, certain medications, and intramuscular injections or oral steroid medications. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Patents 347
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Methods and compositions for the treatment of psoriasis Inventor(s): Foon, Kenneth A. (Fremont, CA), Chatterjee, Malaya; (Fort Wright, KY) Correspondence: MORRISON & FOERSTER LLP; 755 PAGE MILL RD; PALO ALTO; CA; 94304-1018; US Patent Application Number: 20020150572 Date filed: November 20, 2001 Abstract: This invention provides methods of treating psoriasis which entail eliciting an immune response in an individual against an antigen aberrantly expressed in psoriatic tissue, such as a ganglioside, in an individual. The anti-ganglioside immune response is elicited by administration of an antigen such as a ganglioside, an anti-idiotype moiety for a ganglioside, or a polynucleotide encoding an anti-idiotype moiety. Also described is a strategy for developing additional compositions for psoriasis. The compositions elicit an immunological response against a target antigen present on psoriatic tissue, which in turn can be detected using antibody affinity-purified from the serum of the treated subject. The presence of the immunological response correlates positively with control or resolution of the psoriatic symptoms. Excerpt(s): This application claims the priority benefit of U.S. Provisional Patent Application No. 60/065,774, filed Nov. 17, 1997. The priority application is hereby incorporated herein by reference in its entirety. Psoriasis is a chronic condition that affects as much as 2.6% of the population of the developed world. A recent survey reported by the National Psoriasis Foundation estimates that 6.4 million people suffers from psoriasis, of which about 500,000 is rated as severe. The annual patient cost for treating psoriasis is currently estimated at $1.6 to $3.2 billion. Every year, about 400 people are granted disability by the Social Security Administration, and another 400 people die from psoriasis-related causes. It is not known what causes psoriasis, although there is evidence of a genetic predisposition and an autoimmune etiology. Onset may be triggered by systemic infections such as strep throat, skin injury, vaccinations, and certain oral medications such as steroids. Subsequently, the immune system is thought to induce inflammation and excessive skin cell reproduction, which can be exacerbated by additional factors such as stress and diet. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Mult-purpose skin balm including skin balm for psoriasis Inventor(s): Smith, Sadie N. (Chattanooga, TN) Correspondence: Sadie N. Smith; 5436 Winniespan Road; Chattanooga; TX; 37416; US Patent Application Number: 20020146440 Date filed: April 9, 2001 Abstract: The multi-purpose skin balm series is new to the art of skin healing, maintenance, and prevention in that each balm in the series is a compound of old products. Each ingredient in the series works to function in its own way but each action is enhanced when in combination. One will discover that indeed the whole is greater than the sum of its parts. In other words, 2+2=5. These products can offer much less healing time, greater pain control, and less cosmetic disfigurement in a wide range of conditions that affect the skin In and of itself the product is excellent, but when it is combined with the gold standard for each disease entity, injury, or surgical procedure it
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becomes a superb product. Skin Balm For Psoriasis is the flagship of this series. It was selected as such because of the millions of people world wide who afflicted by this chronic condition. Many have had little improvement in the past. Excerpt(s): Not applicable. This is a new use utility patent for a multi- purpose skin balm series produced by compounding already FDA approved drugs generally regarded as safe. Skin Balm For Psoriasis is the flagship product of this series. Treating damaged skin is a science and art that has always baffled healthcare professionals and individuals alike. The skin is the body's largest organ and a barrier and protector against harsh things in the environment. Injury and disease are always just around the corner waiting to destroy the skin's integrity. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Psoriasis patch Inventor(s): Nichols, Jane; (Bloomington, MN), Buseman, Teri; (Minnetonka, MN), Rolf, David; (Eden Prairie, MN), Brandwein, David; (New Brighton, MN), McWhorter, Daniel M. (Eagan, MN) Correspondence: SCHWEGMAN, LUNDBERG, WOESSNER & KLUTH, P.A. P.O. BOX 2938; MINNEAPOLIS; MN; 55402; US Patent Application Number: 20030077316 Date filed: April 2, 2001 Abstract: The present invention provides a water insoluble, protective, adhesive skin patch useful for treating or preventing psoriasis, dermatitis, and/or eczema. The adhesive patch includes a backing that is treated with a sizing agent (e.g., a fluorocarbon solution, a silicone-containing compound, or a combination thereof). The present invention also provides a method for treating or preventing at least one of psoriasis, dermatitis, and eczema in a mammal (e.g., human) and a method for exfoliating the skin surface of a mammal. Excerpt(s): Dermatitis is defined as an inflammation of the skin. Stedman's Medical Dictionary, 25.sup.th edition, pp.418-419, Williams & Wilkins, Baltimore. 1990. Among the types of dermatitis are contact dermatitis, atopic dermatitis (i.e., eczema), psoriasis, and seborrheic dermatitis. Stedman's Medical Dictionary, 25.sup.th edition, pp.418-419, Williams & Wilkins, Baltimore. 1990. The term eczema is used to describe all kinds of red, blistering, oozing, scaly, brownish, and itching skin conditions. (American Academy of Dermatology Website, www.aad.org/eczema.htm.) Examples include seborrheic eczema, nummular eczema, and allergic contact eczema. Eczema is also sometimes used to refer specifically to atopic dermatitis, which is a group of allergic or associated diseases that usually affect several members of a family. These families usually have allergies such as hay fever and asthma. Atopic dermatitis is very common throughout the world. Atopic dermatitis is typically recognized by an itching rash, along with a family history of allergies. (American Academy of Dermatology Website, www.aad.org/eczema.htm.) It affects about 10% of infants and 3% of the overall U.S. population. (American Academy of Dermatology Website, www.aad.org/eczema.htm.) The disease can occur at any age, but is most common in infants and young adults. The condition usually improves in childhood or sometime before the age of 25. In infancy, atopic dermatitis is evidenced by an itching, oozing, and crusting condition that tends to occur mainly on the face and scalp. (American Academy of Dermatology Website, www.aad.org/eczema.htm.) If the disease continues or occurs beyond infancy, the skin
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has less of a tendency to be red, blistering, oozing, and crusting. Instead, the lesions become dry, red to brown, and the skin may become scaly and thickened. An intense, almost unbearable itching can continue. Some patients scratch at their skin until it bleeds and crusts, which can lead to infection. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Substances for use in treating psoriasis Inventor(s): Napoli, Guido Di; (Collonge-Bellerive, CH) Correspondence: Clifford W. Browning, Woodard, Emhardt,; Naughton, Moriarty & McNett; Bank One Center/Tower; 111 Monument Circle, Suite 3700; Indianapolis; IN; 46204-5137; US Patent Application Number: 20020143057 Date filed: March 2, 2001 Abstract: It is disclosed the use of diacerein or a pharmaceutically acceptable derivative thereof for the manufacture of a pharmaceutical composition for the treatment of psoriasis or diseases associated therewith, such as psoriatic arthritis. Excerpt(s): This invention relates to substances for use in treating psoriasis and diseases associated therewith. Psoriasis is a heterogeneous, chronic inflammatory disease of the skin of unknown aetiology. The prevalence of psoriasis in the world population is estimated at around 2 to 3% and varies from minimal lesions of the elbows and knees to a large number of lesions scattered over the skin, with men and women being equally affected. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Synergetic composition for the treatment of psoriasis and other skin disorders and method therefor Inventor(s): Rivera, Carmelo; (Yauco, PR), Franco, Juan; (San Juan, PR), Carlo, Jaime; (Tampa, FL), Chinea, Nestor; (Bayamon, PR) Correspondence: EUGENIO J. TORRES; FERRAMAR BUILDING; SUITE 1; 1060 ASHFORD AVENUE; SAN JUAN; PR; 00907; US Patent Application Number: 20030185915 Date filed: March 28, 2002 Abstract: Synergetic compounded medication formula for the treatment of psoriasis, seborrhea, dermatitis, dandruff, eczema, acne, and other skin disorders. The present invention is to provide regenerative treatment of skin disorders recurrent in all areas of the body. The invention of this disclosure uses a well-known corticosteroid as an active ingredient, namely Triamcinolone acetonide, which when used in combination with a special formula is effective, easy to use, and less expensive than similar products available with a prescription in the market. A method for administering said composition to inhibit proliferation of psoriatic cell populations in the epidermis is disclosed Excerpt(s): The present invention relates generally to a composition and method for the topical treatment of psoriasis and other skin disorders and, more particularly, to a
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composition for the treatment of psoriasis comprising therapeutically effective doses of zinc pyrithione, triamcinolone acetonide, and polysorbate 80, incorporated into at least one suitable topical medication carrier, and combined, optionally, with anti-oxidants, anti-fungal, and/or anti-bacterial agents. Psoriasis is a condition in which cell proliferation is increased up to 10 times the normal rate for an individual. The skin is the largest portion of the human body which is comprised of cells within three skin layers. Each of the skin layers is in a constant state of growth with the outer layer being formed of predominantly dead tissue which is naturally being discarded at a normal rate. Replacement of cells from underlying layers is accomplished by cell division and maturation where cells move upwardly and outwardly at a rate which varies dependent upon the age, sex, and/or health of an individual. Psoriasis causes an increased turn over of cells, which in turn increases the rate of cell growth and cell death. This increased rate of cell growth and cell death may result in injuries and/or disorders which accompany the increased synthesis of all tissue components and further elevate the strain placed upon skin or other tissue and the bio-synthetic capabilities of the cells within the affected area. The word "psoriasis" comes from ancient Greece and means "to itch." Psoriasis is a chronic skin disease long recognized for its peculiar clinical symptoms characterized by circumscribed red patches covered with white scales, and often accompanied by varying degrees of discomfort. It has been estimated that psoriasis affects about 2 percent of the population in Western countries, 0.1 to 0.3 percent in the Far East and is rather rare in persons of the black race. Thus, psoriasis is one of the most common dermatologic diseases which, according to National Psoriasis Foundation's ("NPF's") estimates, affects more than 6.4 million people in the U.S. to some degree. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Topical composition for the treatment of psoriasis and related skin disorders Inventor(s): Meisner, Lorraine Faxon; (Madison, WI) Correspondence: Gardere Wynne Sewell LLP; Thanksgiving Tower; Suite 3000; 1601 Elm Street; Dallas; TX; 75201; US Patent Application Number: 20020164386 Date filed: June 28, 2002 Abstract: Compositions and methods of use thereof for the treatment of psoriasis and related skin ailments are disclosed. The compositions include topical skin formulations of glucosamine in an emollient base such as moisturizing cream. In addition to glucosamine, the formulations may include keratolytic substances such as coal tar extract or salicylic acid. The formulations may also include glucosamine and antioxidant anti-inflammatory herbal extracts such as oleuropein and berberine in an emollient base. Excerpt(s): The present invention relates in general to the field of the treatment of psoriasis and related skin disorders, and more particularly to a non-toxic topical formulation that includes antioxidants and a pharmaceutically effective amount of an herbal extract for the treatment of psoriasis and related skin ailments. Without limiting the scope of the invention, its background is described in connection with disorders of the skin and, more particularly, to the general field of diseases that cause psoriasis, as an example. Psoriasis is a common skin disease characterized by hyperplasia of keratinocytes resulting in thickening of the epidermis and the presence of red scaly plaques. The lesions in this chronic disease typically are subject to remissions and exacerbations. There are several patterns, of which plaque psoriasis is the most common.
Patents 351
Guttate psoriasis, with raindrop shaped lesions scattered on the trunk and limbs, is the most frequent form in children, while pustular psoriasis is usually localized to the palms and soles. The classical inflammatory lesions vary from discrete erythematous papules and plaques covered with silvery scales, to scaly itching patches that bleed when the scales are removed. Despite a voluminous scientific literature and numerous treatment strategies, there is still no effective treatment for psoriasis that is completely without side effects. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Topical treatment of psoriasis using neutralizing antibodies to IL-8 Inventor(s): Ye, George Q. W. (Mississauga, CA) Correspondence: VENABLE, BAETJER, HOWARD AND CIVILETTI, LLP; P.O. BOX 34385; WASHINGTON; DC; 20043-9998; US Patent Application Number: 20030077283 Date filed: September 21, 2001 Abstract: A method for treatment of psoriasis and other inflammatory skin conditions, comprising applying topically a composition containing as active ingredient an antibody neutralizing human Interleukin-8 (IL-8) biological activity together with a pharmaceutically acceptable carrier. The invention also includes a pharmaceutical composition for treating inflammatory skin conditions. The pharmaceutical composition includes antibodies that neutralize human Interleukin-8 (IL-8) biological activity. Excerpt(s): The invention relates to pharmaceutical compositions for topical application of mAb to treat psoriasis and other inflammatory skin conditions. Psoriasis is a common, noncontagious, chronic inflammatory disease of unknown cause. It is a worldwide disease and it's prevalence in the general population is nearly 3% for the people of the Faroe Islands and Denmark. Over 5 million people in the United States are afflicted with this disease (2% of the population). (2) Guttate Psoriasis: small, drop-like cots with some scale. Location: trunk, legs, arms. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Treating eczema and/or psoriasis Inventor(s): Cadwallader, Dianne; (Auckland, NZ), Meakin, Timothy David; (Auckland, NZ), Healtley, Craig Leonard; (Auckland, NZ) Correspondence: JACOBSON HOLMAN PLLC; 400 SEVENTH STREET N.W. SUITE 600; WASHINGTON; DC; 20004; US Patent Application Number: 20030153620 Date filed: February 12, 2003 Abstract: The treatment of humans or other mammals for eczema and/or psoriasis using dosage forms or compositions that include cetyl myristate alone or (in admixture or serially) both cetyl myristate and cetyl palmitate. Excerpt(s): The present invention relates to a method of treatment and/or prophylaxis of eczema and psoriasis. Eczema can be described as an inflammation of the skin where swelling, redness, itching or a burning sensation is present. Sometimes the first
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inflammation is felt, rather than seen, as it is immediately beneath the skin's surface. Eczema can also be seen as reddened spots, scales, crusts or blisters may also be present, either alone or in combination. It may take a mild form, or be more severe, as in the case of psoriasis. The present invention has surprisingly determined that the ingestion of cetyl myristate, and particularly cetyl myristate in conjunction with cetyl palmitate, provides an effective treatment of eczema and/or psoriasis. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Treatment of inflammatory diseases including psoriasis Inventor(s): Tao, Jing-Song; ( Vancouver, CA), Fazli, Ladan; (North Vancouver, CA), Hunt, David W.C. (Surrey, CA), Hannigan, Greg; (Toronto, CA), Dedhar, Shoukat; (Richmond, CA) Correspondence: PAMELA J. SHERWOOD; Bozicevic, Field and Francis LLP; Suite 200; 200 Middlefield Road; Menlo Park; CA; 94025; US Patent Application Number: 20020155179 Date filed: November 30, 2001 Abstract: Inhibitors of integrin-linked kinase (ILK) are used in the treatment of inflammatory disease, including cutaneous inflammatory diseases, such as psoriasis, scleroderma, systemic lupus erythematosus and atopic dermatitis. Excerpt(s): This application is a continuation-in-part of U.S. patent application Ser. No. 09/390,425, filed Sep. 3, 1999, which is a continuation of U.S. patent application Ser. No. 09/035,706, filed Mar. 5, 1998, now issued as U.S. Patent No. 6,001,622, which is a continuation-in-part of U.S. patent application Ser. No. 08/955,841 filed Oct. 21, 1997, now issued as U.S. Patent No. 6,013,782, which is a continuation-in-part of U.S. patent application Ser. No. 08/752,345, filed Nov. 19, 1996, now abandoned, which claims priority to provisional patent application no. 60/009,074, filed Dec. 21, 1995. The invention relates to the use of inhibitors of integrin-linked kinase (ILK) in the treatment of inflammatory diseases and autoimmune conditions such as psoriasis in which the immune system directly contributes to disease pathogenesis. Psoriasis is a chronic skin disease, characterized by scaling and inflammation. Psoriasis affects 1.5 to 2 percent of the United States population, or almost 5 million people. It occurs in all age groups and about equally in men and women. People with psoriasis suffer discomfort, restricted motion of joints, and emotional distress. When psoriasis develops, patches of skin thicken, redden, and become covered with silvery scales, referred to as plaques. Psoriasis most often occurs on the elbows, knees, scalp, lower back, face, palms, and soles of the feet. The disease also may affect the fingernails, toenails, and the soft tissues inside the mouth and genitalia. About 10 percent of people with psoriasis have joint inflammation that produces symptoms of arthritis. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Treatment of psoriasis Inventor(s): Thomasson, Holly Read; (Indianapolis, IN) Correspondence: ELI LILLY AND COMPANY; PATENT DIVISION; P.O. BOX 6288; INDIANAPOLIS; IN; 46206-6288; US Patent Application Number: 20030045585 Date filed: August 7, 2002 Abstract: Norepinephrine reuptake inhibitors are used to treat psoriasis. Excerpt(s): The invention belongs to the fields of pharmaceutical chemistry and dermatological medicine, and provides a method of treatment of the dermatological disorder known as psoriasis. Psoriasis is a chronic, painful skin disorder that affects more than 7 million Americans. With as many as 250,000 new cases occurring each year, psoriasis typically does not discriminate on the basis of the age or gender of its victims. The disorder occurs slightly more often in women than men, and it has been reported to present itself initially from birth to the age of 90 years. Psoriasis exacts a heavy societal burden in terms of both patient suffering and costs. Annual outpatient treatment of psoriasis was estimated in 1999 to be from $1.6 to $3.2 billion, with over 1.5 million patients seen annually for this disorder by U.S. physicians. Treatment options currently available to patients suffering from psoriasis include a variety of topical medications, phototherapies, and internal medications. Topical treatments include steroids, coal tar, anthralin, vitamin D3 and analogs, retinoids, and sunshine. Side effects associated with the use of these topical treatments include skin thinning, stretch marks, burns, irritation, and photosensitivity. The use of steroids may also lead to resistance, rendering subsequent steroid treatment ineffective. Phototherapy encompasses the medically supervised administration of ultraviolet light B or psoralen in combination with ultraviolet light A. Long term use of phototherapies may prematurely age the skin and increase the incidence of skin cancers. Internal medications, typically reserved for the most serious cases of psoriasis, include the administration methotrexate, oral retinoids, and cyclosporine. The use of methotrexate requires careful monitoring to avoid liver damage. Use of oral retinoids must be carefully controlled in women because of the potential for severe birth defects. This risk extends for years after the use of the drug has been terminated. Cyclosporine, an immunosuppresant, is reserved for patients that have failed other internal treatments, or for whom the other internal treatments are contraindicated. Rotating between therapies, and combinations of topical medications with phototherapies, have also been found to be useful regimens in the treatment of psoriasis. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Treatment of psoriasis with matrix metalloproteinase inhibitors Inventor(s): Fleischmajer, Raul; (Barnegat Light, NJ) Correspondence: BAKER & BOTTS; 30 ROCKEFELLER PLAZA; NEW YORK; NY; 10112 Patent Application Number: 20020198176 Date filed: July 29, 2002 Abstract: The present invention relates to methods of treating psoriasis by inhibiting one or more matrix metalloproteinase enzymes ("MMPs"). It is based, at least in part, on the
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discovery that the expression patterns of certain MMPs and related molecules are altered in patients suffering from psoriasis, relative to normal subjects. Certain expression patterns are altered even in unaffected skin of psoriasis-afflicted patients, although aberrancies are more pronounced in psoriatic lesions. In various non-limiting embodiments, the present invention provides for methods of treating psoriasis, including preventing the development of new psoriatic lesions, comprising administering, to subjects in need of such treatment, effective concentrations of compounds which inhibit the enzymatic activity of one or more MMP. Suitable inhibitors include tetracycline and its derivatives and various hydroxymate, carboxylic acid, and phosphonic acid derivatives. Therapy may comprise systemic and/or local administration of inhibitor. In additional embodiments, the present invention provides for methods of diagnosing MMP inhibitor responsive skin lesions, for evaluating the level of disease activity in a subject, and for transgenic animal and tissue culture models of psoriasis. Excerpt(s): This application claims priority to U.S. Provisional Patent Application No. 60/186,431, filed Mar. 2, 2000. The present invention relates to methods of treating psoriasis by inhibiting matrix metalloproteinase enzyme(s). It is based, at least in part, on the discovery that the expression of certain matrix metalloproteinase enzyme(s) is increased in the epidermis of patients suffering from psoriasis, and particularly increased in psoriatic skin lesions. Psoriasis is a chronic skin disease characterized by red scaly patches that usually affect the scalp, elbows and knees, although any part of the skin may be involved. At the cellular level, psoriasis is a benign proliferative disease of keratinocytes of unknown etiology. It has been estimated that psoriasis affects about 2 percent of the population in Western countries, 0.1 to 0.3 percent in the Far East and is rather rare in persons of the black race (Krueger et al., 1984, J. Am. Acad. Dermatol. 11:937-947; Yui-Yip, 1984, J. Am. Acad. Dermatol. 10:965-968). Although the disease appears to be inherited, its mode of transmission is not known and more than one genetic locus may be involved (Henseler, 1997, J. Am. Acad. Dermatol. 37:S1-11). Furthermore, the disease can be triggered or exacerbated by external factors such as trauma, infection and drugs. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Use of resveratrol for the treatment of exfoliative eczema, acne and psoriasis Inventor(s): Giannella, Attilio; (Codogno, IT), Pelliccia, Maria Teresa; (Avellino, IT), Giannella, Jenny; (Codogno, IT) Correspondence: YOUNG & THOMPSON; 745 SOUTH 23RD STREET 2ND FLOOR; ARLINGTON; VA; 22202 Patent Application Number: 20010056071 Date filed: March 22, 2001 Abstract: The use of resveratrol (3,4',5-trihydroxy-trans-stilbene) and derivatives thereof, for the preparation of medicaments for the treatment of exfoliative eczema, acne and psoriasis, topical pharmaceutical formulations containing resveratrol or derivatives thereof in combination with other active principles. Treatment consists in topical administrations of resveratrol at concentrations of 0.01 to 20%, in the form of lotions, creams or ointments, optionally in combination with other active principles such as melatonin, vitamins D, E and A and derivatives thereof, hormones, vegetable and/or animal extracts. Contrary to current therapies, the use of resveratrol has neither systemic nor topical effects during and after therapy.
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Excerpt(s): The present invention relates to the use of resveratrol (3,4',5-trihydroxytrans-stilbene) and derivatives thereof (esters, glycosides, 3'-oxyresveratrol), for the preparation of medicaments for the treatment of exfoliative eczema, acne and psoriasis. Resveratrol (3,4',5-trihydroxy-trans-stilbene), a phytoalexin produced by a number of vegetables under stress conditions, is one of the natural substances of vegetable origin at present arousing great interest in the pharmaceutical, cosmetic and nutritional fields, due to the important, established effects this molecule exerts in humans. In vitro and in vivo studies on resveratrol proved that the molecule: a) exerts protective action on the cardiovascular system, (Clin. Chim. Acta, 235:207, 1995) and decreases arteriosclerosis risks (Clin. Chim. Acta, 246:163, 1996); b) has vasal relaxing effect on the arteries (Gen. Pharm. 27:363, 1996); c) has antioxidant action which inhibits LDL cholesterol peroxidation (The Lancet, 341:1103, 1993); reduces oxidative stress (Neuroreport 8:1499, 1997); protects from the radical damage in cerebral ischemia (Chin. Pharm. Bull. 12:128, 1996); prevents the propagation of free radicals responsible for the molecular damage of the biological systems and for cell aging; d) modulates lipid synthesis, preventing the accumulation of cholesterol and fats in the liver, decreases the concentrations of blood triglycerids and of cholesterol in low-density LDL lipoproteins and reduces the atherogenic index (Chem Pharm. Bull. 30:1766, 1982); e) inhibits platelet aggregation, preventing the formation of thrombi (Int. J. Tiss. Reac. XVIII, 1, 1995; Thrombosis and Haemostasis, 76:818, 1996); f) inhibits the production of proatherogenic eicosanoids by platelets and neutrophils, exerting anti-inflammatory action (Biochem. Biophys. Acta, 834:275, 1985); g) inhibits protein-tyrosine kinase which modulates cell proliferation and differentiation and the signaling processes in the immune system cells, biological processes involved in the inflammatory response and in severe pathologies such as cancer, arteriosclerosis and psoriasis (J. Natural Products, 56:1805, 1993, Science 267:1782, 1995); h) has marked antimutagenic action, inhibiting the cell events connected with the initiation, promotion and progression of the tumor (Science 275:218, 1997, Anal. Biochem, 169:328, 1988, Proc. Natl. Acad. Sci USA, 91:3147, 1994, Proc. Natl. Acad. USA, 72:1848, 1975, Carcinogenesis, 8:541, 1987). The presence of resveratrol traces in red wines is believed to be the main cause of the beneficial nutritional effects thereof (Am, J. Enol. Vitic. 46:159, 1996, Clin. Chim. Acta, 246:183, 1996, Amer. J. Clin. Nutr., 55:1012, 1992). The poor concentrations of resveratrol in wine and in wine industry by-products have, until some time ago, remarkably restricted a wide use of this molecule in the pharmaceutical and nutritional fields. Recently, rhizomes of the Chinese plant Poligonum cuspidatum have been found to contain high amounts of resveratrol (more than about 400 times those in wine) thus inducing a strong commercial development of this molecule as alimentary supplement, in particular on the U.S. market. Lately, the actions of resveratrol for pharmacological or cosmetic use have been claimed (WO9959561; WO9958119; EP0773020; FR2766176; WO9904747). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Keeping Current In order to stay informed about patents and patent applications dealing with psoriasis, you can access the U.S. Patent Office archive via the Internet at the following Web address: http://www.uspto.gov/patft/index.html. You will see two broad options: (1) Issued Patent, and (2) Published Applications. To see a list of issued patents, perform the following steps: Under “Issued Patents,” click “Quick Search.” Then, type “psoriasis” (or synonyms) into the
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“Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on psoriasis. You can also use this procedure to view pending patent applications concerning psoriasis. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.
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CHAPTER 7. BOOKS ON PSORIASIS Overview This chapter provides bibliographic book references relating to psoriasis. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on psoriasis include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.
Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “psoriasis” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on psoriasis: •
Practical Psoriasis Therapy. Second Edition Source: St. Louis, MO: Mosby-Year Book, Inc. 1993. 322 p. Contact: Available from Mosby-Year Book, Inc., 11830 Westline Industrial Drive, St. Louis, MO 63416. Summary: This book for health professionals serves as a guide for physicians who manage patients with psoriasis. Chapters explain the differential diagnosis of psoriasis; describe the histopathology of psoriasis; discuss the selection of therapy for psoriasis patients; and examine the use of topical steroids and other topical agents, Coal tars, keratolytics, emollients, anthralin, phototherapy, psoralen ultraviolet A (PUVA) therapy, synthetic retinoids, systemic chemotherapy, and cyclosporine in the treatment of psoriasis. Chapters also discuss psoriasis day care centers and therapies for childhood psoriasis, scalp psoriasis, pustular psoriasis, exfoliative and erythrodermic psoriasis, nail psoriasis, and psoriatic arthritis. Appendices provide patients with information and
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instructions concerning topical therapies, topical corticosteroids, anthralin, ultraviolet phototherapy, home ultraviolet therapy, psoralen phototherapy, etretinate, methotrexate, cyclosporine, childhood psoriasis, and arthritic psoriasis. Numerous references, 22 figures, and 58 tables.
Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in Print). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “psoriasis” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “psoriasis” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “psoriasis” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •
A Practical Guide to Cyclosporin A in the Treatment of Psoriasis (International Congress and Symposium Series (ICSS)) by S. Shuster (Editor); ISBN: 1853151998; http://www.amazon.com/exec/obidos/ASIN/1853151998/icongroupinterna
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Aetiological Studies of Psoriasis: A Survey by Flemming Brandrup (1985); ISBN: 8774925067; http://www.amazon.com/exec/obidos/ASIN/8774925067/icongroupinterna
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Afectos Ocultos En. Psoriasis Asma Trastornos Re by Luis Chiozza (1991); ISBN: 9504000533; http://www.amazon.com/exec/obidos/ASIN/9504000533/icongroupinterna
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An Atlas of Psoriasis by Lionel Fry; ISBN: 1850704104; http://www.amazon.com/exec/obidos/ASIN/1850704104/icongroupinterna
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An Atlas of Psoriasis, Second Edition by Lionel Fry; ISBN: 1842142372; http://www.amazon.com/exec/obidos/ASIN/1842142372/icongroupinterna
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Analysing the Photochemotherapeutical Principle in the Treatment of Psoriasis by R. Roelandts (1990); ISBN: 9061863570; http://www.amazon.com/exec/obidos/ASIN/9061863570/icongroupinterna
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Arthritis, Rheumatism and Psoriasis (By Appointment Only) by Jan de Vries (2002); ISBN: 1840185589; http://www.amazon.com/exec/obidos/ASIN/1840185589/icongroupinterna
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Autoimmunity in Psoriasis by Ernst H. Beutner (Editor); ISBN: 0849354730; http://www.amazon.com/exec/obidos/ASIN/0849354730/icongroupinterna
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Autoradiographie : Unters. d. Zellproliferation bei Psoriasis vulgaris by Helmut Pullmann; ISBN: 3880400113; http://www.amazon.com/exec/obidos/ASIN/3880400113/icongroupinterna
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Beat Psoriasis: Simple and Effective Treatment-The Natural Way (Thorsons Health) by Sandra Gibbons; ISBN: 0722533578; http://www.amazon.com/exec/obidos/ASIN/0722533578/icongroupinterna
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Beat Psoriasis: The Natural Way by Sandra Gibbins, Sandra Gibbons; ISBN: 0722525869; http://www.amazon.com/exec/obidos/ASIN/0722525869/icongroupinterna
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Clinicians Guide Psoriasis by Marks; ISBN: 0412826909; http://www.amazon.com/exec/obidos/ASIN/0412826909/icongroupinterna
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Conquering Psoriasis: An Illustrated Guide to the Understanding and Control of Psoriasis by Eugene M. MD Farber, Lexie Nakk (2002); ISBN: 0969778155; http://www.amazon.com/exec/obidos/ASIN/0969778155/icongroupinterna
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Coping With Psoriasis. by Ronald Marks; ISBN: 0859696901; http://www.amazon.com/exec/obidos/ASIN/0859696901/icongroupinterna
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Coping with Psoriasis: A Patient's Guide to Treatment by David L. Cram M.D., et al; ISBN: 188603947X; http://www.amazon.com/exec/obidos/ASIN/188603947X/icongroupinterna
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Cyclosporin in Severe Psoriasis: The Italian Experience (Dermatology) by A.F. Finzi (Editor); ISBN: 3805558457; http://www.amazon.com/exec/obidos/ASIN/3805558457/icongroupinterna
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Diets to Help Psoriasis (Diets to Help) by Harry Clements ND DO, Roger Newman Turner (Editor); ISBN: 0722529295; http://www.amazon.com/exec/obidos/ASIN/0722529295/icongroupinterna
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Dr. John's Healing Psoriasis Cookbook.Plus! by John O. Pagano, Johanna Bayati (Editor) (2001); ISBN: 0962884715; http://www.amazon.com/exec/obidos/ASIN/0962884715/icongroupinterna
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Eczema and Psoriasis: How Your Diet Can Help (Nutritional Health Guide) by Stephen Terrass; ISBN: 0722531486; http://www.amazon.com/exec/obidos/ASIN/0722531486/icongroupinterna
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Handbook of Psoriasis by Charles Camisa (1998); ISBN: 0865425582; http://www.amazon.com/exec/obidos/ASIN/0865425582/icongroupinterna
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Healing Psoriasis: The Natural Alternative by John O. A. Pagano; ISBN: 0962884707; http://www.amazon.com/exec/obidos/ASIN/0962884707/icongroupinterna
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Herbs for Healthy Skin, Hair & Nails: Banish Eczema, Acne and Psoriasis With Healing Herbs That Cleanse and Tone to Body Inside and Out (Keats Good Herb Guide) by Brigitte Mars; ISBN: 0879838388; http://www.amazon.com/exec/obidos/ASIN/0879838388/icongroupinterna
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Hidden Affects in Somatic Disorders: Psychoanalytic Perspectives on Asthma, Psoriasis, Diabetes, Cerebrovascular Disease, and Other Disorders. by Luis A. Chiozza; ISBN: 1887841164; http://www.amazon.com/exec/obidos/ASIN/1887841164/icongroupinterna
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How I Overcame Psoriasis by Kent Trussell; ISBN: 1863512837; http://www.amazon.com/exec/obidos/ASIN/1863512837/icongroupinterna
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Key Advances in the Effective Management of Psoriasis by C. Griffiths (Editor) (2000); ISBN: 1853153990; http://www.amazon.com/exec/obidos/ASIN/1853153990/icongroupinterna
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Living with Psoriasis by Sandra Gibbons; ISBN: 0950831212; http://www.amazon.com/exec/obidos/ASIN/0950831212/icongroupinterna
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Managing Your Psoriasis by Nicholas J., M.D. Lowe (1993); ISBN: 0942361849; http://www.amazon.com/exec/obidos/ASIN/0942361849/icongroupinterna
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MarketLooks: The Global Market for Prescription Dermatitis, Seborrhea, and Psoriasis Drugs [DOWNLOAD: PDF] by MarketLooks - Kalorama Information
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(Author); ISBN: B000068IXD; http://www.amazon.com/exec/obidos/ASIN/B000068IXD/icongroupinterna •
Phg Psoriasis Pb; ISBN: 0356145018; http://www.amazon.com/exec/obidos/ASIN/0356145018/icongroupinterna
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Phototherapy Treatment Protocols: For Psoriasis and Other Phototherapy Responsive Dermatoses by Michael D. Zanolli, et al; ISBN: 1850709920; http://www.amazon.com/exec/obidos/ASIN/1850709920/icongroupinterna
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Pocket Guide to Psoriasis by Simon Davison, et al; ISBN: 0632052082; http://www.amazon.com/exec/obidos/ASIN/0632052082/icongroupinterna
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Practical Psoriasis Therapy by Nicholas J. Lowe (Editor); ISBN: 0801671817; http://www.amazon.com/exec/obidos/ASIN/0801671817/icongroupinterna
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Psoriasis by Ronald Marks; ISBN: 0668052805; http://www.amazon.com/exec/obidos/ASIN/0668052805/icongroupinterna
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Psoriasis by Charles Camisa; ISBN: 0865422478; http://www.amazon.com/exec/obidos/ASIN/0865422478/icongroupinterna
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PSORIASIS - PHG; ISBN: 090634820X; http://www.amazon.com/exec/obidos/ASIN/090634820X/icongroupinterna
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Psoriasis - pocketbook by Christopher E. M. Griffith, Brian Kiby (1999); ISBN: 185317873X; http://www.amazon.com/exec/obidos/ASIN/185317873X/icongroupinterna
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Psoriasis : proceedings of the second international symposium, Stanford University, 1976; ISBN: 0914316109; http://www.amazon.com/exec/obidos/ASIN/0914316109/icongroupinterna
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Psoriasis and Eczema (Clinical Handbook) by Lionel Fry (Editor); ISBN: 1854570021; http://www.amazon.com/exec/obidos/ASIN/1854570021/icongroupinterna
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Psoriasis at Your Fingertips (At Your Fingertips) by Tim Mitchell, Rebecca Penzer; ISBN: 1872362990; http://www.amazon.com/exec/obidos/ASIN/1872362990/icongroupinterna
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Psoriasis Fast Facts Series by Smith, et al; ISBN: 1899541985; http://www.amazon.com/exec/obidos/ASIN/1899541985/icongroupinterna
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Psoriasis, Healing from the Inside Out by Heather J. Ferris (1995); ISBN: 096937397X; http://www.amazon.com/exec/obidos/ASIN/096937397X/icongroupinterna
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Psoriasis: a patients guide by Nicholas Lowe (1998); ISBN: 1853175994; http://www.amazon.com/exec/obidos/ASIN/1853175994/icongroupinterna
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Psoriasis: A Practical Guide to Coping by Caroline Wilson; ISBN: 1852232129; http://www.amazon.com/exec/obidos/ASIN/1852232129/icongroupinterna
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Psoriasis: Cell Proliferation by N. A. Wright (Editor) (1983); ISBN: 0443029636; http://www.amazon.com/exec/obidos/ASIN/0443029636/icongroupinterna
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Psoriasis: Proceedings of the Fourth International Symposium by Nall Farber, Jacobs Morhenn; ISBN: 0444012125; http://www.amazon.com/exec/obidos/ASIN/0444012125/icongroupinterna
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Psoriasis: Proceedings of the Third International Symposium by Eugene Farber; ISBN: 0808914723; http://www.amazon.com/exec/obidos/ASIN/0808914723/icongroupinterna
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Psoriasis: The Real Way Out: A Self-Education Guide to Complete Natural Healing by Jerry G. Scott (2003); ISBN: 1550569589; http://www.amazon.com/exec/obidos/ASIN/1550569589/icongroupinterna
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Psoriasis: The Rowland Remedy by John Rowland; ISBN: 0713716762; http://www.amazon.com/exec/obidos/ASIN/0713716762/icongroupinterna
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Psoriasis: The Story of a Man by Gillette; ISBN: 0818021012; http://www.amazon.com/exec/obidos/ASIN/0818021012/icongroupinterna
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Psoriasis: The Struggle and the Triumph: A Healthy Transformation for Everyone Living with Psoriasis by Elliott Douglas Derzaph (2003); ISBN: 1410702162; http://www.amazon.com/exec/obidos/ASIN/1410702162/icongroupinterna
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Psoriasis: Third Edition Revised and Expanded by Henry H., Jr. Roenigk (Editor), Howard I. Maibach (Editor); ISBN: 0824701089; http://www.amazon.com/exec/obidos/ASIN/0824701089/icongroupinterna
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Psoriasis; proceedings; ISBN: 0804708010; http://www.amazon.com/exec/obidos/ASIN/0804708010/icongroupinterna
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Recent Advances in Psoriasis: The Role of the Immune System by Barbara S. Baker (2000); ISBN: 1860941206; http://www.amazon.com/exec/obidos/ASIN/1860941206/icongroupinterna
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Schuppen Flechte: Was Sie Schon Immer Uber Psoriasis Wissen Wollten by U. Mrowietz, G. Schmid Ott (2002); ISBN: 3805572883; http://www.amazon.com/exec/obidos/ASIN/3805572883/icongroupinterna
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Skin Care for Psoriasis by V.K. Dave (1997); ISBN: 187236263X; http://www.amazon.com/exec/obidos/ASIN/187236263X/icongroupinterna
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So You've Got Psoriasis, 2nd Edition by Richard Williams, et al; ISBN: 1853178217; http://www.amazon.com/exec/obidos/ASIN/1853178217/icongroupinterna
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Studies on Vitamin a Signaling in Psoriasis: A Comparison Between Normal and Lesional Keratinocytes (Comprehensive Summaries of Uppsala Dissertations from the Faculty of mediciNe, 1155) by Teresa Karlsson (2002); ISBN: 9155453171; http://www.amazon.com/exec/obidos/ASIN/9155453171/icongroupinterna
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Textbook of Psoriasis by P. C. M. Van De Kerkhof (Editor); ISBN: 0632051663; http://www.amazon.com/exec/obidos/ASIN/0632051663/icongroupinterna
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The 2002 Official Patient's Sourcebook on Psoriasis: A Revised and Updated Directory for the Internet Age by Icon Health Publications (2002); ISBN: 0597834059; http://www.amazon.com/exec/obidos/ASIN/0597834059/icongroupinterna
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The Chemotherapy of Psoriasis by H. Baden (Editor); ISBN: 0080298230; http://www.amazon.com/exec/obidos/ASIN/0080298230/icongroupinterna
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The Psoriasis & Eczema Solution: New Hope for Physical & Emotional Relief by Daniel A. Lobovits, et al (1999); ISBN: 1890819069; http://www.amazon.com/exec/obidos/ASIN/1890819069/icongroupinterna
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The Psoriasis Case: The Psoriasis Guide for the Millions Living With Psoriasis by Elliott D. Derzaph; ISBN: 0944214037; http://www.amazon.com/exec/obidos/ASIN/0944214037/icongroupinterna
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The Psoriasis Cure: A Drug-Free Guide to Stopping & Reversing the Symptoms of Psoriasis by Lisa Levan; ISBN: 0895299178; http://www.amazon.com/exec/obidos/ASIN/0895299178/icongroupinterna
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The Psoriasis Handbook by J. W. Psoriasis Fo Lewis (1996); ISBN: 0091809851; http://www.amazon.com/exec/obidos/ASIN/0091809851/icongroupinterna
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The Psoriasis Handbook: A Self-Help Guide by Muriel K. MacFarlane, L. E. Mills (Illustrator) (1995); ISBN: 1887053018; http://www.amazon.com/exec/obidos/ASIN/1887053018/icongroupinterna
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The U.S. Market and Developments Associated with Psoriasis [DOWNLOAD: PDF] by Kalorama Information (Author); ISBN: B00005RA1T; http://www.amazon.com/exec/obidos/ASIN/B00005RA1T/icongroupinterna
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Therapy of Moderate-To-Severe Psoriasis by Gerald D. Weinstein, Alice B. Gottlieb (2003); ISBN: 0824741161; http://www.amazon.com/exec/obidos/ASIN/0824741161/icongroupinterna
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Three Percent of Mankind Suffers from Psoriasis but Are Not Acquainted With Its Workings by Silvio Gaetti; ISBN: 9998959772; http://www.amazon.com/exec/obidos/ASIN/9998959772/icongroupinterna
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Understanding Psoriasis by A. Warin; ISBN: 1898205884; http://www.amazon.com/exec/obidos/ASIN/1898205884/icongroupinterna
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Understanding Skin Problems: Acne, Eczema, Psoriasis and Related Conditions by Linda Papadopoulos (Author), Carl Walker (Author); ISBN: 047084518X; http://www.amazon.com/exec/obidos/ASIN/047084518X/icongroupinterna
The National Library of Medicine Book Index The National Library of Medicine at the National Institutes of Health has a massive database of books published on healthcare and biomedicine. Go to the following Internet site, http://locatorplus.gov/, and then select “Search LOCATORplus.” Once you are in the search area, simply type “psoriasis” (or synonyms) into the search box, and select “books only.” From there, results can be sorted by publication date, author, or relevance. The following was recently catalogued by the National Library of Medicine:11 •
Blood lymphocyte subpopulations in some skin diseases: a study in alopecia areata, psoriasis and mycosis fungoides Author: Gu, Shao Qui.; Year: 1952; Stockholm: s.n., 1981; ISBN: 9172224096
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Histochemistry of the skin-psoriasis; a monograph on normal and parakeratotic epidermal keratinizatio with special reference to psoriasis and its treatment [by] A. Jarrett and R. I. C. Spearman. Author: Jarrett, A. (Arthur); Year: 1966; London, English Universities Press [1964]
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HLA antigens in psoriasis Author: Karvonen, Jaakko.; Year: 1957; Helsinki: [s.n.], 1976; ISBN: 9519907408
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In addition to LOCATORPlus, in collaboration with authors and publishers, the National Center for Biotechnology Information (NCBI) is currently adapting biomedical books for the Web. The books may be accessed in two ways: (1) by searching directly using any search term or phrase (in the same way as the bibliographic database PubMed), or (2) by following the links to PubMed abstracts. Each PubMed abstract has a "Books" button that displays a facsimile of the abstract in which some phrases are hypertext links. These phrases are also found in the books available at NCBI. Click on hyperlinked results in the list of books in which the phrase is found. Currently, the majority of the links are between the books and PubMed. In the future, more links will be created between the books and other types of information, such as gene and protein sequences and macromolecular structures. See http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Books.
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Importance of HLA-linked genes for the development of psoriasis and Author: Marcusson, Jan.; Year: 1964; Stockholm: [s.n., 1979?]
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Modern aspects of the responsible use of dithranol in psoriasis: proceedings of a meeting held at St. Pierre Hotel, Chepstow, 6th-7th April 1984 Author: Ponec, Maria.; Year: 1955; Tunbridge Wells, Kent, England: Research and Clinical Forums, [1984]
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New drugs used for nonapproved purposes (methotrexate for psoriasis). Hearings before a subcommittee of the Committee on Government Operations, House of Representatives, ninety-second Congress, first session, July 29 and 30, 1971. Author: United States. Congress. House. Committee on Government Operations.; Year: 1973; Washington, U. S. Govt. Print. Off., 1971
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Proceedings of the International Conference on Psoriasis Care: Gothenburg, August 28-31, 1983 Author: Swanbeck, Gunnar.; Year: 1970; Stockholm, Sweden: Almqvist; Wiksell International, 1984; ISBN: 9122006699
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Psoriasis from a prognostic and hereditary point of view. Author: Romanus, Torsten Kjellberg,; Year: 1968; Upsala, 1945
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Psoriasis therapy: January 1977 through October 1980, 299 citations in English Author: Abrams, Estelle J.; Year: 1955; [Bethesda, Md.]: U.S. Dept. of Health and Human Services, Public Health service, National Institutes of Health, [1980]
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Psoriasis, a guide to one of the commonest skin diseases Author: Marks, Ronald.; Year: 1951; New York: Arco Pub., 1981; ISBN: 0668052759 http://www.amazon.com/exec/obidos/ASIN/0668052759/icongroupinterna
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Psoriasis, prevalence, spontaneous course, and genetics: a census study on the prevalence of skin diseases on the Faroe Islands Author: Lomholt, Gunnar.; Year: 1953; Copenhagen: G.E.C. Gad, 1963
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Psoriasis, the disease and its treatment. Author: Shield Laboratories, Detroit.; Year: 1965; [Detroit, c1943]
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Psoriasis; compiled and edited by Edwin Sidi, Zenona W. Zagula-Mally, and Marc Hincky. Translation by Zenona W. Zagula-Mally. Author: Sidi, Edwin,; Year: 1972; Springfield, Ill., Thomas [c1968]
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Psoriasis; the prevalence in sex, age and occupational groups, in total populations in Sweden. Morphology, inheritance and association with other skin and rheumatic diseases. Author: Hellgren, Lars.; Year: 1973; Stockholm, Almqvist; Wiksell [1967]
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Rheumatoid arthritis and psoriasis vulgaris; internal and cutaneous manifestations of the permanent endoparasitism in the Homo sapiens, their common etiology, pathogenesis, and specific vaccine therapy. Author: Benedek, Tibor.; Year: 1967; [Ann Arbor, c1955]
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Second European Symposium on Psoriasis: Trieste, Italy, October 7-9, 1983 Author: Scarpa, Carmelo.; Year: 1969; Stockholm, Sweden: Distributed by Almqvist; Wiksell Periodical Co., 1984
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Textbook of psoriasis Author: Mier, Paul D.; Year: 1959; Edinburgh; New York: Churchill Livingstone, 1986; ISBN: 0443032106 http://www.amazon.com/exec/obidos/ASIN/0443032106/icongroupinterna
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The biology of psoriasis; an experimental study of the Koebner phenomenon. Author: Pedace, Francis Jos,; Year: 1973; [Minneapolis] 1966
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The treatment of psoriasis; alphosyl lotion and alphosyl lubricating cream. Author: Reed; Carnrick.; Year: 1971; Kenilworth, N. J. [1961]
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Chapters on Psoriasis In order to find chapters that specifically relate to psoriasis, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and psoriasis using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Book Chapter.” Type “psoriasis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on psoriasis: •
Chapter 48: Parapsoriasis Source: in Freedberg, I.M., et al., eds. Fitzpatrick's Dermatology in General Medicine. 5th ed., Vol. 1. New York, NY: McGraw-Hill. 1999. p. 546-553. Contact: Available from McGraw-Hill Customer Services. P.O. Box 548, Blacklick, OH 43004-0548. (800) 262-4729 or (877) 833-5524. Fax (614) 759-3749 or (614) 759-3641. E-mail:
[email protected]. PRICE: $395.00 plus shipping and handling. ISBN: 0070219435. Summary: This chapter provides health professionals with information on the incidence, diagnosis, etiopathogenesis, differential diagnosis, course, prognosis, and treatment of parapsoriasis. This group of disorders is characterized by a persistent, scaling, inflammatory eruption. Features that set the parapsoriasis group apart from other purely inflammatory dermatoses include the relation to malignant lymphoproliferative lesions and the coexistence or overlapping of entities in this group. The classification of parapsoriasis includes large plaque parapsoriasis (LPP), small plaque parapsoriasis (SPP), and pityriasis lichenoides. The peak incidence of LPP and SPP is in the fifth decade of life. The parapsoriasis group of diseases appear to be cutaneous T cell lymphoproliferative diseases. In some cases, LPP is a monoclonal proliferation of skinassociated lymphoid tissue T cells that have the capacity to move between the skin and extracutaneous sites. The chapter discusses the diagnosis of LPP and SPP in terms of clinical manifestations and histopathology. The differential diagnosis of LPP and SPP involves distinguishing LPP from SPP and mycosis fungoides and SPP from psoriasis. Both LPP and SPP may persist for years to decades with little change in clinical or histopathological appearance. Although LPP has the potential to become malignant, SPP is a clinically benign disorder. Treatment options for SPP include emollients, topical tar preparations, topical corticosteroids, and ultraviolet B (UVB) phototherapy. However, LPP requires more aggressive therapy, including high-potency topical corticosteroids with UVB phototherapy or psoralen and ultraviolet A. 10 figures, 2 tables, and 36 references.
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CHAPTER 8. MULTIMEDIA ON PSORIASIS Overview In this chapter, we show you how to keep current on multimedia sources of information on psoriasis. We start with sources that have been summarized by federal agencies, and then show you how to find bibliographic information catalogued by the National Library of Medicine.
Video Recordings An excellent source of multimedia information on psoriasis is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “psoriasis” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find video productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Videorecording (videotape, videocassette, etc.).” Type “psoriasis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on psoriasis: •
Vitamin D: Not Just for Bones Source: Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases, 1992, 60 minutes. Contact: WIN, 1 WIN WAY, Bethesda, MD 20892-3665. Summary: In this lecture, Dr. DeLuca discusses the major functions of Vitamin D in the body; studies demonstrating potential therapeutic uses for synthetic Vitamin D compounds; and his own laboratory's progress on developing several such compounds. According to Dr. DeLuca, Vitamin D is, in fact, not a vitamin but a prohormone that remains inactive until metabolized in the liver and the kidney. The principal active metabolite of Vitamin D, calcitrol, acts with parathyroid hormone (PTH) to regulate the blood calcium level. It also plays a role in building up bone and is an important regulator of intestinal calcium absorption. Disturbance of this regulatory mechanism can result in osteoporosis (brittle bones), as well as in several disorders characterized by a deficiency or an oversupply of calcium or PTH in the blood (hypo- and hypercalcemia;
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hypo-and hyperparathyroidism). Vitamin D deficiency results in rickets (soft, weak bones) and osteomalacia in adults. Dr. DeLuca discusses several clinical studies demonstrating an age-related decline in formation of the active Vitamin D metabolite in response to PTH. He describes research he is conducting to develop synthetic Vitamin D compounds that would stimulate bone formation in osteoporotic patients without producing hypercalcemia. He predicts that within a decade these compounds will be important contributors to the treatment of postmenopausal and age-related osteoporosis. Dr. DeLuca goes on to discuss evidence strongly suggesting that Vitamin D influences other biologic processes, including cellular differentiation and regulation of the immune system. Work is ongoing in his laboratory to develop Vitamin D "differentiation compounds" that may have a future role in cancer therapy. The lecture concludes with a discussion of other potential therapeutic uses for Vitamin D, including the treatment of In this l, renal osteodystropy (bone disease found with kidney failure), and infertility.
Bibliography: Multimedia on Psoriasis The National Library of Medicine is a rich source of information on healthcare-related multimedia productions including slides, computer software, and databases. To access the multimedia database, go to the following Web site: http://locatorplus.gov/. Select “Search LOCATORplus.” Once in the search area, simply type in psoriasis (or synonyms). Then, in the option box provided below the search box, select “Audiovisuals and Computer Files.” From there, you can choose to sort results by publication date, author, or relevance. The following multimedia has been indexed on psoriasis: •
Outpatient phototherapy for psoriasis and other skin diseases [videorecording] Source: with Lillian Freije and Jean Bolognia; Year: 1988; Format: Videorecording; Secaucus, N.J.: Network for Continuing Medical Education, c1988
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Psoriasis; Papulosquamous diseases; Atopic dermatitis; Common pediatric skin problems [videorecording] Source: produced for the Canadian Association of Professors of Dermatology by Roberta Ongley; Biomedical Communications, University of British Columbia; Year: 1993; Format: Videorecording; [Vancouver, B.C.]: The University, c1993
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Psoriasis [slide] Source: presented by David R. Harris, Eugene M. Farber and Marion B. Sulzberger; produced by the Institute for Dermatologic Communication and Education; Year: 1973; Format: Slide; San Francisco: The Institute, c1973
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Psoriasis [slide] Source: University of Michigan Medical Center, Dept. of Postgraduate Medicine and Health Professions Education, Independent Study Unit; Year: 1976; Format: Slide; Ann Arbor, Mich.: The University: [for loan and sale by its] Media Library, c1976
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Psoriasis [videorecording] Source: [presented by] Medical Video Library; co-produced by IMS, Faculty of Medicine, University of Toronto and Medical Productions and Associates; Year: 1989; Format: Videorecording; [Toronto, Ont.]: Burn-Shield, [1989]
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Psoriasis [videorecording]: A to Z Source: a presentation of Films for the Humanities & Sciences; ITN, Information Television Network; Year: 1997; Format: Videorecording; Princeton, N.J.: Films for the Humanities & Sciences, c1997
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Psoriasis [videorecording]: presentation, diagnosis, and therapy Source: a production of the Emory Medical Television Network; Year: 1990; Format: Videorecording; [Atlanta, Ga.]: Emory University, c1990
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Psoriasis [videorecording]. Year: 1999; Format: Videorecording; Carrollton, TX: HSTN, c1999
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Psoriasis education program [electronic resource] Source: Sandoz; Year: 1995; Format: Electronic resource; East Hanover, N.J.: Sandoz Pharmaceuticals Corp., c1995
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Psoriasis in the patient with HIV disease [videorecording] Source: Madeleine Duvic; Year: 1996; Format: Videorecording; Secaucus, N.J.: Network for Continuing Medical Education, c1996
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Recent advances in psoriasis therapy [videorecording] Source: with Nicholas J. Lowe; Year: 1986; Format: Videorecording; Secaucus, N.J.: Network for Continuing Medical Education, 1986
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CHAPTER 9. PERIODICALS AND NEWS ON PSORIASIS Overview In this chapter, we suggest a number of news sources and present various periodicals that cover psoriasis.
News Services and Press Releases One of the simplest ways of tracking press releases on psoriasis is to search the news wires. In the following sample of sources, we will briefly describe how to access each service. These services only post recent news intended for public viewing. PR Newswire To access the PR Newswire archive, simply go to http://www.prnewswire.com/. Select your country. Type “psoriasis” (or synonyms) into the search box. You will automatically receive information on relevant news releases posted within the last 30 days. The search results are shown by order of relevance. Reuters Health The Reuters’ Medical News and Health eLine databases can be very useful in exploring news archives relating to psoriasis. While some of the listed articles are free to view, others are available for purchase for a nominal fee. To access this archive, go to http://www.reutershealth.com/en/index.html and search by “psoriasis” (or synonyms). The following was recently listed in this archive for psoriasis: •
Retinoid use reduces skin cancer risk in PUVA-treated psoriasis patients Source: Reuters Industry Breifing Date: October 07, 2003 http://www.reutershealth.com/archive/2003/10/07/business/links/20031007clin006. html
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Biogen licenses psoriasis drug from Swiss company Source: Reuters Industry Breifing Date: October 01, 2003
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Genentech psoriasis drug backed by FDA panel Source: Reuters Industry Breifing Date: September 10, 2003
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FDA panel backs efalizumab for psoriasis Source: Reuters Medical News Date: September 10, 2003
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Genentech, Xoma Psoriasis drug effective-FDA staff Source: Reuters Health eLine Date: September 08, 2003
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Psoriasis drugs seem to work equally well Source: Reuters Health eLine Date: August 18, 2003
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Methotrexate and cyclosporine have similar efficacy in severe psoriasis Source: Reuters Industry Breifing Date: August 18, 2003
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Genentech unveils psoriasis drug data, approval expected this year Source: Reuters Medical News Date: July 28, 2003
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Genentech unveils psoriasis data, stock sets high Source: Reuters Industry Breifing Date: July 28, 2003
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Amgen submits psoriasis drug for marketing review Source: Reuters Industry Breifing Date: July 08, 2003
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Amgen submits Enbrel for psoriasis indication Source: Reuters Medical News Date: July 08, 2003
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Worrying may hamper psoriasis treatment: study Source: Reuters Health eLine Date: July 03, 2003
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Infliximab produces sustained improvement in plaque-type psoriasis Source: Reuters Industry Breifing Date: June 30, 2003
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Novel fusion protein can produces durable remission from psoriasis Source: Reuters Industry Breifing Date: June 16, 2003
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CellGate says topical cyclosporine effective for psoriasis in small study Source: Reuters Industry Breifing Date: May 02, 2003
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Galen inks deals on psoriasis treatments Source: Reuters Industry Breifing Date: April 02, 2003
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Drug maker says oral retinoid combats psoriasis Source: Reuters Health eLine Date: March 25, 2003
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Allergan's orally delivered tazarotene shows strong efficacy for psoriasis Source: Reuters Industry Breifing Date: March 25, 2003
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Biologic drugs seen helping hard-to-treat psoriasis Source: Reuters Health eLine Date: March 24, 2003
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Remicade demonstrates positive results in phase II psoriasis trial Source: Reuters Industry Breifing Date: March 21, 2003
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Genentech psoriasis drug effective in phase III studies Source: Reuters Industry Breifing Date: March 21, 2003
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Amgen's Enbrel demonstrates efficacy in phase III psoriasis study Source: Reuters Industry Breifing Date: March 21, 2003
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Angiotech's Paxceed clears phase I hurdle in psoriasis Source: Reuters Industry Breifing Date: March 19, 2003
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Isotechnika, Roche drug shows efficacy in phase II psoriasis trial Source: Reuters Industry Breifing Date: March 10, 2003
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Abbott starts new psoriasis trials for Humira Source: Reuters Industry Breifing Date: March 03, 2003
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Serono files for psoriasis drug approval in Europe Source: Reuters Industry Breifing Date: February 26, 2003
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Biogen psoriasis drug rejected in Europe Source: Reuters Industry Breifing Date: February 20, 2003
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New combination ointment shows superior anti-psoriasis activity Source: Reuters Industry Breifing Date: February 06, 2003
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Biogen gets US approval for new psoriasis drug Source: Reuters Industry Breifing Date: January 31, 2003
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Xoma psoriasis drug enters phase II for psoriatic arthritis Source: Reuters Industry Breifing Date: January 30, 2003
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Amgen arthritis drug effective against psoriasis Source: Reuters Industry Breifing Date: January 17, 2003
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Interleukin-10 ineffective in treating patients with psoriasis Source: Reuters Industry Breifing Date: December 09, 2002
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Injections hold promise for treating psoriasis Source: Reuters Health eLine Date: December 03, 2002
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Serono to carve out new drug business in psoriasis Source: Reuters Industry Breifing Date: December 02, 2002
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Interleukin-4 induces anti-inflammatory Th2 responses and improves psoriasis Source: Reuters Industry Breifing Date: December 02, 2002
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Phototherapy three times a week speeds plaque clearance in chronic psoriasis Source: Reuters Industry Breifing Date: November 07, 2002
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Connetics gets FDA approvable letter for Olux in non-scalp psoriasis Source: Reuters Industry Breifing Date: October 28, 2002
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Swede researchers apply for psoriasis gene patent Source: Reuters Health eLine Date: October 04, 2002
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Tropical daisy could help treat psoriasis: report Source: Reuters Health eLine Date: September 24, 2002
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Tropical daisy could help treat psoriasis Source: Reuters Industry Breifing Date: September 23, 2002
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Genmab cleared to start phase II psoriasis study Source: Reuters Industry Breifing Date: September 19, 2002
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Genentech, Xoma say psoriasis drug effective in confirmatory trial Source: Reuters Industry Breifing Date: September 17, 2002
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IDEC ends development of psoriasis drug on poor phase II results Source: Reuters Industry Breifing Date: September 05, 2002
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Genentech, Xoma rename psoriasis drug, present new data Source: Reuters Industry Breifing Date: August 02, 2002
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Infliximab may be helpful in psoriasis Source: Reuters Industry Breifing Date: July 30, 2002
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Psoriasis treatment effect persists for many years Source: Reuters Health eLine Date: July 09, 2002
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Carcinogenic effects of psoriasis treatment persists for many years Source: Reuters Medical News Date: July 08, 2002
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Biogen earns FDA advisors' backing for psoriasis therapy Source: Reuters Industry Breifing Date: May 23, 2002
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Genmab's HuMax-CD4 psoriasis drug shows long-term benefits Source: Reuters Industry Breifing Date: April 12, 2002 The NIH
Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine. Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name. Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “psoriasis” (or synonyms) into the search box, and click on “Search News.” As this service is technology oriented, you may wish to use it when searching for press releases covering diagnostic procedures or tests. Search Engines Medical news is also available in the news sections of commercial Internet search engines. See the health news page at Yahoo (http://dir.yahoo.com/Health/News_and_Media/), or
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you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “psoriasis” (or synonyms). If you know the name of a company that is relevant to psoriasis, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for the company name there. News items across various news sources are reported on indicated hyperlinks. Google offers a similar service at http://news.google.com/. BBC Covering news from a more European perspective, the British Broadcasting Corporation (BBC) allows the public free access to their news archive located at http://www.bbc.co.uk/. Search by “psoriasis” (or synonyms).
Newsletter Articles Use the Combined Health Information Database, and limit your search criteria to “newsletter articles.” Again, you will need to use the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter Article.” Type “psoriasis” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months. The following is a typical result when searching for newsletter articles on psoriasis: •
Cleaning Up After Psoriasis Source: Psoriasis Resource. 3(2): 8-9. July 2001. Contact: Available from National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (800) 723-9166 or (503) 244-7404. Fax (503) 245-0626. Email:
[email protected]. Website: www.psoriasis.org. PRICE: Contact NPF for current pricing. Summary: This newsletter article provides people who have psoriasis with information on cleaning up shedding scales and dealing with the mess created by psoriasis treatments. The article outlines tips for dealing with the problem of shedding scales and offers suggestions on keeping grease or cosmetic coverups off clothing, bedding, or towels. In addition, the article provides guidelines on avoiding stains when using anthralin and coal tar. Anthralin, a synthetic substitute for chrysarobin, stains the skin a brown or purple color, which will eventually fade, but it can permanently stain bathroom fixtures, clothing, towels, and bedding. Use of petrolatum may protect the skin around the lesions from staining, and a product called CuraStain will limit staining. Coal tar products work best when they can be left on the skin for several hours, but some products can stain. Staining of bedding can be minimized by wearing old clothing over affected skin, and allowing the product to dry before putting on clothing can be helpful. In addition, the article lists tips on removing blood stains from clothes or bedding.
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Keep an Eye on These Drugs: Possible Aggravators of Psoriasis Source: Psoriasis Resource. 3(2): 11. July 2001.
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Contact: Available from National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (800) 723-9166 or (503) 244-7404. Fax (503) 245-0626. Email:
[email protected]. Website: www.psoriasis.org. PRICE: Contact NPF for current pricing. Summary: This newsletter article provides people who have psoriasis with information on drugs that can worsen this condition. One such drug is lithium, which is used to treat manic depression and other psychiatric disorders and which aggravates psoriasis in about 50 percent of those who take it. However, several alternatives to lithium are available. Carbamazepine, which is sometimes prescribed for the same mood disorders as lithium, has no history of worsening psoriasis. Valproic acid is another anticonvulsant that has been used as an alternative to lithium. Other medications that can cause psoriasis to flare are antimalarials such as quinacrine, chloroquine, and hydroxychloroquine; Inderal; quinidine; and indomethacin. •
Nail Psoriasis: Always a Challenge Source: National Psoriasis Foundation Bulletin. 32(4): 9. July-August 2001. Contact: Available from National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (800) 723-9166 or (503) 244-7404. Fax (503) 245-0626. Email:
[email protected]. Website: www.psoriasis.org. PRICE: Contact NPF for current pricing. Summary: This newsletter article provides people who have psoriasis with information on effective therapies for this condition. Nail psoriasis is one of the most difficult and frustrating forms of psoriasis to treat. In a study of Tazorac, a prescription vitamin A derivative, 0.1 percent strength Tazorac gel improved pitting and onycholysis. Intralesional steroid injections are generally effective, but many people avoid them because they are commonly believed to be painful. However, if performed correctly, they should not be that uncomfortable. Severe nail psoriasis can be treated with the most potent psoriasis treatments, including psoralen plus ultraviolet A light and systemic medications such as methotrexate, oral retinoids, and cyclosporine. People who have psoriasis should be vigilant about getting a complete and accurate diagnosis because psoriasis of the nails can be difficult to distinguish from fungus of the nails. 1 figure.
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Interactions of Common Psoriasis Treatments Source: National Psoriasis Foundation Forum. 7(2): 6-7. Winter 2001. Contact: Available from National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (503) 244-7404 or (800) 723-9166. Fax: (503) 245-0626. Website: www.psoriasis.org. Summary: This newsletter article for patients discusses problems and benefits of combining psoriasis treatments. Many physicians ascribe to the idea that multiple therapies will be more effective. This idea can have unfortunate consequences. Drugs such as calcium channel blockers and antifungals used with cyclosporine interfere with the way cyclosporine metabolizes in the blood. Methotrexate (MTX) when combined with certain drugs, such as NSAIDS, may result in toxicity or death. Drugs used in combination with phototherapy often enhance the effect of the phototherapy treatment (PUVA or UVB), allowing the dosages of each to be reduced. Some drugs, such as cyclosporine, should not be used with PUVA as it may cause skin cancer. Topical medications must be used with care when combined with phototherapy. Tar may cause
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a phototoxic reaction whereas salicylic acid and thick white emollients block UV penetration. Interactions between topicals may prove deleterious. Calcipotriene deteriorates after mixing with salicylic acid and anthralin is oxidated after exposure to liquor carbonis detergens and coal tar. Salicylic acid does not affect anthralin nor does tar gel affect calcipotriene. Physicians should pay close attention to treatment interactions when treating their patients with psoriasis. Patients need to educate themselves about their treatments to avoid unfortunate outcomes. 6 references. •
Importance of Maintenance Therapy for Psoriasis Source: Pharmacy News. 10(1):13-14; March 1998. Contact: National Psoriasis Foundation, 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (503) 244-7404. (800) 723-9166. (503) 245-0626 (fax). Summary: This newsletter article for individuals with psoriasis discusses the need for maintenance therapy. Most patients cannot sustain a treatment-free remission, so continuing maintenance therapy is necessary. In addition, such therapy is needed to decrease the likelihood of a flare of psoriasis and to improve the quality of the life of the psoriasis patient. Maintenance agents for psoriasis include topical therapies, phototherapy, and systemic agents. Combinations of therapies may be used to maximize benefit and reduce side effects, and therapies may be rotated to avoid accumulating side effects. 5 photographs.
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Erasing Psoriasis Lesions Source: Pharmacy News. 10(1):1-3; March 1998. Contact: National Psoriasis Foundation, 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (503) 244-7404. (800) 723-9166. (503) 245-0626 (fax). Summary: This newsletter article for individuals with psoriasis offers advice for using cosmetic cover-ups to mask psoriasis lesions. Although the typical inflammation of psoriasis and guttate and inverse psoriasis can be masked with special cosmetics, using a masking agent on pustular or erythrodermic forms of psoriasis may cause stinging and redness. Before using a cosmetic cover-up, as much of the psoriasis scale as possible should be removed either through occlusion or hydration. Once the scales are removed, a cover-up can be applied with the fingertips, a make-up sponge, or an applicator. A special finishing powder may help keep the cover-up from smearing or rubbing off.
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Photodynamic Therapy Branches Out: Psoriasis, Alopecia Areata, Warts, and More Source: Dermatology Focus. 15(3):1,13-15; January 1997. Summary: This newsletter article for health professionals reports on the use of photodynamic therapy (PDT) in the treatment of various immunologic, dermatologic, and other conditions. The difference between PDT and cosmetic surgery is explained. The discovery of the principle of photodynamic action is discussed. First and second generation PDT agents are described. One of the most promising systemic agents is benzoporphyrin-derivative monoacid ring A (BPD). A promising topical photosensitizer is 5-aminolevulinic acid (ALA). Some research suggests that PDT, at certain lower dose photosensitizer/light combinations, targets activated T cells and may benefit conditions such as arthritis, psoriasis, and alopecia. Work with BPD and ALA in the treatment of psoriasis is highlighted. Evidence that suggests that topical ALA will be useful for treating alopecia areata is presented. In addition, other potential dermatologic applications of PDT are identified.
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Psoriasis Patients Try the Alternatives Source: Skin and Allergy News. 28(3):1,25; March 1997. Summary: This newsletter article for health professionals focuses on alternative methods of treating psoriasis. Current knowledge about the effectiveness of various nontraditional therapies used to treat psoriasis is presented. These therapies include exorex emulsion and cream, Skin-Cap, nonprescription tanning, Dead Sea clinics, and magnetic therapy. Although there is some evidence to indicate that psoriasis improves in some individuals who use these therapies, there is a lack of published data on their safety and efficacy. 2 photographs.
•
Glossary of Psoriasis-Related Terms Source: Pharmacy News. 6-7; November 1997. Contact: National Psoriasis Foundation, 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (503) 244-7404. (800) 723-9166. (503) 245-0626 (fax). Summary: This newsletter article for individuals with psoriasis presents a glossary of psoriasis-related terms to help them better express with their physician and explain psoriasis to others. Many terms are drugs or other modalities used to treat psoriasis. Other terms relate to the skin and various aspects of psoriasis.
•
Adverse Effects of Systemic Psoriasis Treatments: Retinoids Source: National Psoriasis Foundation Forum. 3(4): 6-7. Winter 1997. Contact: Available from National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (503) 244-7404. Fax (503) 245-0626. Summary: This newsletter article provides health professionals with information on the adverse effects of retinoids. Etretinate and acitretin are the two retinoids currently approved for the treatment of psoriasis in the United States. Although retinoids are highly effective in treating pustular and erythrodermic psoriasis and beneficial when combined with types of PUVA or UVB phototherapy, that is therapy using types of ultraviolet light, in treating plaque-type or guttate psoriasis, teratogenicity is a serious concern. Etretinate is not recommended for women of child bearing potential because of its long half life. Although acitretin has a much shorter half life than etretinate, it is converted to etretinate in the presence of ethanol. Isotretinoin is effective for pustular psoriasis, but it should not be used during pregnancy. Common side effects of retinoids include hair loss, failure to develop normal nail plates, chapped lips, dry skin, and elevated serum lipids. Despite these side effects, retinoids are among the safest systemic treatments available for psoriasis. 6 tables.
•
Adverse Effects of Systemic Psoriasis Treatments: Methotrexate Source: National Psoriasis Foundation Forum. 3(4): 4-5. Winter 1997. Contact: Available from National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (503) 244-7404. Fax (503) 245-0626. Summary: This newsletter article provides health professionals with information on the adverse effects of methotrexate, which is one of the most effective drugs available for treating psoriasis. The main adverse effect is hepatoxicity, as confirmed by various studies. Patients who are alcoholic, obese, or diabetic are at greater risk of developing cirrhosis of the liver when treated with methotrexate. Other side effects include bone
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marrow suppression, gastrointestinal and pulmonary toxicity, phototoxicity, and malignancy. Methotrexate also poses risks for conception and pregnancy, with miscarriages and birth defects occurring if it is taken during pregnancy. In addition, it may temporarily affect male fertility. 10 tables. •
Facial Lesions May Indicate Severe Psoriasis Source: Skin and Allergy News. 28(12): 12. December 1997. Summary: This newsletter article provides health professionals with information about the indicators of severe psoriasis. The occurrence of psoriasis on the cheeks, forehead, or chin is a tip-off that a patient will have a longer and more severe course of the disease. The article presents evidence that psoriasis involving the face carries with it a higher degree of treatment resistance, recurrence, and involvement of the rest of the body. First, psoriasis of the face is not common. Second, psoriasis of the face is more common in children than it is in adults. It is known that childhood psoriasis usually indicates a more severe course than adult onset of the disease. Third, studies show that patients who have severe psoriasis are likely to have it on the face. Fourth, atypical psoriasis on the face is seen more frequently in patients who are undergoing psoralen plus ultraviolet light A therapy. Last, patients who have photosensitive psoriasis are very likely to have facial lesions. The article also discusses the presence of the Koebner phenomenon as a marker for psoriasis severity.
•
Quality of Life Study Reveals New Demographics for Psoriasis Source: National Psoriasis Foundation Bulletin. 27(5):1,3; September/October 1996. Contact: National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (503)244-7404. Fax (503) 245-0626. Summary: This newsletter article for individuals with psoriasis presents findings from a recent epidemiologic study of psoriasis. Initially questionnaires were mailed to 50,000 households to obtain a statistically balanced distribution of individuals with psoriasis throughout the continental United States, and 33,411 questionnaires were returned. Respondents assessed their own disease severity and rated 22 factors related to the psychosocial aspects of psoriasis and 19 factors related to daily living. Findings related to the prevalence, incidence, treatment, and psychosocial impacts of psoriasis are highlighted.
•
Facial Skin Requires Gentle Psoriasis Treatments Source: National Psoriasis Foundation Bulletin. 27(5):4; September/October 1996. Contact: National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (503)244-7404. Fax (503)245-0626. Summary: This newsletter article for individuals with psoriasis discusses treatment of psoriasis that occurs on the face. Topical steroids must be used with caution on the face because they can thin already delicate skin. Dovonex is not recommended for the central face because it can be irritating, but it can be used around the hairline. Treating psoriasis on the eyelids may involve washing the lid margins and eye lashes with tap water and baby shampoo, applying emollients, and using special ophthalmic steroid medication if necessary. The relationship between seborrheic dermatitis and facial psoriasis is also discussed.
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Treating Psoriasis: A to Z Hits the Airwaves in April Source: National Psoriasis Foundation Bulletin. 27(2):1,3; March/April 1996. Contact: National Psoriasis Foundation, 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223. Summary: This newsletter article for health professionals, the general public, and individuals with psoriasis discusses the television debut of a show on psoriasis. The show explains the symptoms of psoriasis, discusses the therapies available to treat psoriasis, and provides guidelines for referring patients to psoriasis specialists. It also features patient interviews and information on the mission and services of the National Psoriasis Foundation ( NPF ). A tape of this program will be available to managed care health insurance organizations, physicians, and NPF members.
Academic Periodicals covering Psoriasis Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to psoriasis. In addition to these sources, you can search for articles covering psoriasis that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”
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APPENDICES
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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute12: •
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
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National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
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National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
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National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
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National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
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National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
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National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
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National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
12
These publications are typically written by one or more of the various NIH Institutes.
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National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
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National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
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National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
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National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
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National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
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National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
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National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
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National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
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National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
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National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
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National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
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National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
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National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
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Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
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National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
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National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
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Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
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Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.13 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:14 •
Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html
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HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
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NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
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Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
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Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
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Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
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Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
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Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
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Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
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Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
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MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
13
Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 14 See http://www.nlm.nih.gov/databases/databases.html.
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Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html
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Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html
The NLM Gateway15 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.16 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “psoriasis” (or synonyms) into the search box and click “Search.” The results will be presented in a tabular form, indicating the number of references in each database category. Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total
Items Found 20828 266 77 46 0 21217
HSTAT17 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.18 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.19 Simply search by “psoriasis” (or synonyms) at the following Web site: http://text.nlm.nih.gov.
15
Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.
16
The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH). 17 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 18 19
The HSTAT URL is http://hstat.nlm.nih.gov/.
Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations.
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Coffee Break: Tutorials for Biologists20 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.21 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.22 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.
Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •
CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.
•
Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.
The Genome Project and Psoriasis In the following section, we will discuss databases and references which relate to the Genome Project and psoriasis. Online Mendelian Inheritance in Man (OMIM) The Online Mendelian Inheritance in Man (OMIM) database is a catalog of human genes and genetic disorders authored and edited by Dr. Victor A. McKusick and his colleagues at Johns Hopkins and elsewhere. OMIM was developed for the World Wide Web by the National Center for Biotechnology Information (NCBI).23 The database contains textual information, pictures, and reference information. It also contains copious links to NCBI’s Entrez database of MEDLINE articles and sequence information. 20 Adapted 21
from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html.
The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 22 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process. 23 Adapted from http://www.ncbi.nlm.nih.gov/. Established in 1988 as a national resource for molecular biology information, NCBI creates public databases, conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information--all for the better understanding of molecular processes affecting human health and disease.
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To search the database, go to http://www.ncbi.nlm.nih.gov/Omim/searchomim.html. Type “psoriasis” (or synonyms) into the search box, and click “Submit Search.” If too many results appear, you can narrow the search by adding the word “clinical.” Each report will have additional links to related research and databases. In particular, the option “Database Links” will search across technical databases that offer an abundance of information. The following is an example of the results you can obtain from the OMIM for psoriasis: •
Mental Retardation Associated with Psoriasis Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?309480
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Psoriasis Susceptibility Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?177900
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Psoriasis Susceptibility 2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?602723
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Psoriasis Susceptibility 3 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?601454
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Psoriasis Susceptibility 4 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?603935
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Psoriasis Susceptibility 5 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?604316
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Psoriasis Susceptibility 6 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605364
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Psoriasis Susceptibility 7 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605606
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Psoriasis Susceptibility 9 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?607857 Genes and Disease (NCBI - Map)
The Genes and Disease database is produced by the National Center for Biotechnology Information of the National Library of Medicine at the National Institutes of Health. This Web site categorizes each disorder by system of the body. Go to http://www.ncbi.nlm.nih.gov/disease/, and browse the system pages to have a full view of important conditions linked to human genes. Since this site is regularly updated, you may wish to revisit it from time to time. The following systems and associated disorders are addressed: •
Cancer: Uncontrolled cell division. Examples: Breast and ovarian cancer, Burkitt lymphoma, chronic myeloid leukemia, colon cancer, lung cancer, malignant melanoma, multiple endocrine neoplasia, neurofibromatosis, p53 tumor suppressor, pancreatic cancer, prostate cancer, Ras oncogene, RB: retinoblastoma, von Hippel-Lindau syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Cancer.html
•
Immune System: Fights invaders. Examples: Asthma, autoimmune polyglandular syndrome, Crohn’s disease, DiGeorge syndrome, familial Mediterranean fever, immunodeficiency with Hyper-IgM, severe combined immunodeficiency. Web site: http://www.ncbi.nlm.nih.gov/disease/Immune.html
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•
Metabolism: Food and energy. Examples: Adreno-leukodystrophy, atherosclerosis, Best disease, Gaucher disease, glucose galactose malabsorption, gyrate atrophy, juvenile-onset diabetes, obesity, paroxysmal nocturnal hemoglobinuria, phenylketonuria, Refsum disease, Tangier disease, Tay-Sachs disease. Web site: http://www.ncbi.nlm.nih.gov/disease/Metabolism.html
•
Muscle and Bone: Movement and growth. Examples: Duchenne muscular dystrophy, Ellis-van Creveld syndrome, Marfan syndrome, myotonic dystrophy, spinal muscular atrophy. Web site: http://www.ncbi.nlm.nih.gov/disease/Muscle.html
•
Nervous System: Mind and body. Examples: Alzheimer disease, amyotrophic lateral sclerosis, Angelman syndrome, Charcot-Marie-Tooth disease, epilepsy, essential tremor, fragile X syndrome, Friedreich’s ataxia, Huntington disease, Niemann-Pick disease, Parkinson disease, Prader-Willi syndrome, Rett syndrome, spinocerebellar atrophy, Williams syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Brain.html
•
Signals: Cellular messages. Examples: Ataxia telangiectasia, Cockayne syndrome, glaucoma, male-patterned baldness, SRY: sex determination, tuberous sclerosis, Waardenburg syndrome, Werner syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Signals.html
•
Transporters: Pumps and channels. Examples: Cystic fibrosis, deafness, diastrophic dysplasia, Hemophilia A, long-QT syndrome, Menkes syndrome, Pendred syndrome, polycystic kidney disease, sickle cell anemia, Wilson’s disease, Zellweger syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Transporters.html Entrez
Entrez is a search and retrieval system that integrates several linked databases at the National Center for Biotechnology Information (NCBI). These databases include nucleotide sequences, protein sequences, macromolecular structures, whole genomes, and MEDLINE through PubMed. Entrez provides access to the following databases: •
3D Domains: Domains from Entrez Structure, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
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Books: Online books, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=books
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Genome: Complete genome assemblies, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Genome
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NCBI’s Protein Sequence Information Survey Results: Web site: http://www.ncbi.nlm.nih.gov/About/proteinsurvey/
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Nucleotide Sequence Database (Genbank): Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Nucleotide
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OMIM: Online Mendelian Inheritance in Man, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=OMIM
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PopSet: Population study data sets, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Popset
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ProbeSet: Gene Expression Omnibus (GEO), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
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Protein Sequence Database: Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Protein
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PubMed: Biomedical literature (PubMed), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
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Structure: Three-dimensional macromolecular structures, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Structure
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Taxonomy: Organisms in GenBank, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Taxonomy
To access the Entrez system at the National Center for Biotechnology Information, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=genome, and then select the database that you would like to search. The databases available are listed in the drop box next to “Search.” Enter “psoriasis” (or synonyms) into the search box and click “Go.” Jablonski’s Multiple Congenital Anomaly/Mental Retardation (MCA/MR) Syndromes Database24 This online resource has been developed to facilitate the identification and differentiation of syndromic entities. Special attention is given to the type of information that is usually limited or completely omitted in existing reference sources due to space limitations of the printed form. At http://www.nlm.nih.gov/mesh/jablonski/syndrome_toc/toc_a.html, you can search across syndromes using an alphabetical index. Search by keywords at http://www.nlm.nih.gov/mesh/jablonski/syndrome_db.html. The Genome Database25 Established at Johns Hopkins University in Baltimore, Maryland in 1990, the Genome Database (GDB) is the official central repository for genomic mapping data resulting from the Human Genome Initiative. In the spring of 1999, the Bioinformatics Supercomputing Centre (BiSC) at the Hospital for Sick Children in Toronto, Ontario assumed the management of GDB. The Human Genome Initiative is a worldwide research effort focusing on structural analysis of human DNA to determine the location and sequence of the estimated 100,000 human genes. In support of this project, GDB stores and curates data generated by researchers worldwide who are engaged in the mapping effort of the Human Genome Project (HGP). GDB’s mission is to provide scientists with an encyclopedia of the human genome which is continually revised and updated to reflect the current state of 24
Adapted from the National Library of Medicine: http://www.nlm.nih.gov/mesh/jablonski/about_syndrome.html. 25 Adapted from the Genome Database: http://gdbwww.gdb.org/gdb/aboutGDB.html - mission.
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scientific knowledge. Although GDB has historically focused on gene mapping, its focus will broaden as the Genome Project moves from mapping to sequence, and finally, to functional analysis. To access the GDB, simply go to the following hyperlink: http://www.gdb.org/. Search “All Biological Data” by “Keyword.” Type “psoriasis” (or synonyms) into the search box, and review the results. If more than one word is used in the search box, then separate each one with the word “and” or “or” (using “or” might be useful when using synonyms).
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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on psoriasis can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internet-based services that post them.
Patient Guideline Sources The remainder of this chapter directs you to sources which either publish or can help you find additional guidelines on topics related to psoriasis. Due to space limitations, these sources are listed in a concise manner. Do not hesitate to consult the following sources by either using the Internet hyperlink provided, or, in cases where the contact information is provided, contacting the publisher or author directly. The National Institutes of Health The NIH gateway to patients is located at http://health.nih.gov/. From this site, you can search across various sources and institutes, a number of which are summarized below. Topic Pages: MEDLINEplus The National Library of Medicine has created a vast and patient-oriented healthcare information portal called MEDLINEplus. Within this Internet-based system are “health topic pages” which list links to available materials relevant to psoriasis. To access this system, log on to http://www.nlm.nih.gov/medlineplus/healthtopics.html. From there you can either search using the alphabetical index or browse by broad topic areas. Recently, MEDLINEplus listed the following when searched for “psoriasis”:
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Guides on psoriasis Psoriasis http://www.nlm.nih.gov/medlineplus/psoriasis.html Psoriasis http://www.nlm.nih.gov/medlineplus/tutorials/psoriasisloader.html
•
Other guides Arthritis http://www.nlm.nih.gov/medlineplus/arthritis.html Nail Diseases http://www.nlm.nih.gov/medlineplus/naildiseases.html Skin Diseases http://www.nlm.nih.gov/medlineplus/skindiseases.html Vitiligo http://www.nlm.nih.gov/medlineplus/vitiligo.html
Within the health topic page dedicated to psoriasis, the following was listed: •
General/Overviews Psoriasis http://www.nlm.nih.gov/medlineplus/tutorials/psoriasisloader.html Psoriasis Source: National Women's Health Information Center http://www.4woman.gov/faq/psoriasis.htm Psoriasis FAQs Source: American Academy of Dermatology http://www.skincarephysicians.com/psoriasisnet/mythsANDfacts.htm
•
Diagnosis/Symptoms Skin Rashes and Other Changes: Self-Care Flowcharts Source: American Academy of Family Physicians http://familydoctor.org/flowcharts/545.html
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Treatment FDA Approves First Biologic Therapy for Psoriasis Source: Food and Drug Administration http://www.fda.gov/bbs/topics/ANSWERS/2003/ANS01194.html Methotrexate Source: American Academy of Family Physicians http://familydoctor.org/handouts/628.html New Laser/Light Therapies Hit the Mark in Treating Some Hard-to-Treat Skin Conditions Source: American Academy of Dermatology http://www.aad.org/PressReleases/hardtotreat.html
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New Treatments for Psoriasis Give Dermatologists More Choices Source: American Academy of Dermatology http://www.aad.org/PressReleases/psoriasis.html •
Specific Conditions/Aspects Psoriasis Treatment May Promote Skin Cancer Source: American Cancer Society http://www.cancer.org/docroot/nws/content/nws_1_1x_psoriasis_treatment_ma y_promote_skin_cancer.asp Psoriatic Arthritis Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=DS00476
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Children Juvenile Psoriatic Arthritis Source: Arthritis Foundation http://www.arthritis.org/conditions/diseasecenter/juvenilepsoriaticarthritis.asp Psoriasis: The “Dry Skin” Disease Source: American Academy of Dermatology http://www.aad.org/Kids/psoriasis.html
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Journals/Newsletters PsoriasisNet Update Source: American Academy of Dermatology http://www.skincarephysicians.com/psoriasisnet/update_current.htm
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Organizations American Academy of Dermatology http://www.aad.org/ National Institute of Arthritis and Musculoskeletal and Skin Diseases http://www.niams.nih.gov/ National Psoriasis Foundation http://www.psoriasis.org/
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Research New Laser Treatment Holds Promise for Millions of Americans with Psoriasis and Vitiligo Source: American Academy of Dermatology http://www.aad.org/PressReleases/psoriasisvit.html Psoriasis Causes Disability That Equals Other Major Medical Diseases Source: American Academy of Dermatology http://www.aad.org/PressReleases/psoriasis_causes_disability.html
You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the
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search box and click “Search.” This utility is similar to the NIH search utility, with the exception that it only includes materials that are linked within the MEDLINEplus system (mostly patient-oriented information). It also has the disadvantage of generating unstructured results. We recommend, therefore, that you use this method only if you have a very targeted search. The Combined Health Information Database (CHID) CHID Online is a reference tool that maintains a database directory of thousands of journal articles and patient education guidelines on psoriasis. CHID offers summaries that describe the guidelines available, including contact information and pricing. CHID’s general Web site is http://chid.nih.gov/. To search this database, go to http://chid.nih.gov/detail/detail.html. In particular, you can use the advanced search options to look up pamphlets, reports, brochures, and information kits. The following was recently posted in this archive: •
Understanding Psoriasis Source: Portland, OR: National Psoriasis Foundation. 2003. 15 p. Contact: Available from National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (800) 723-9166. Summary: This brochure discusses psoriasis, a chronic skin condition characterized by scaling and inflammation, affecting approximately 4.5 million adults in the United States. It is thought that psoriasis is an overreaction of the immune system that causes skin cells to grow too fast. The forms of the condition can be mild, moderate, or severe, and the plaques or lesions can appear on any part of the body but most often occur on the elbows, scalp, knees and torso. Plaque psoriasis is the most common form of psoriasis and is characterized by patches of raised, red, skin covered by a flaky white buildup. It is most often found on the elbows, knees, back, and scalp. Guttate psoriasis appears as small red dots on the arms, legs, and trunk. Erythrodermic, inverse, pustular, and psoriatic arthritis are other less common forms of the condition. Flaking and scaling are the most common symptoms of psoriasis. It can also make the skin itch, burn, bleed, or sting. Topical treatments for milder forms of psoriasis include anthralin, bath solutions, salicylic acid, tar, and steroids. Phototherapy is used to treat patients with moderate to severe forms of psoriasis or if topical therapy has proved ineffective. Systemic treatments such as cyclosporine, methotrexate, and oral retinoids are used for patients with severe cases of psoriasis. Biologics, a new class of systemic treatments, are made from proteins produced by living cells and are injected in patients with moderate to severe symptoms to block the immune system response. 3 figures.
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Biologic Therapies for Psoriasis and Psoriatic Artritis Source: National Psoriasis Foundation. 2003. 16 p. Contact: Available from National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (800) 723-9166. Website: www.psoriasis.org. Summary: This brochure discusses the use of Amevive, Enbrel, Raptiva, and Remicade to treat psoriasis and psoriatic arthritis. These drugs are biologic drugs, made from living human or animal proteins, and are used to treat moderate to severe psoriasis. They work by blocking the action of overactive immune cells. Amevive blocks and reduces the action of immune T cells. This drug is administered by a physician and injected into the muscles of a patient weekly for 12 weeks. Most patients experience a 75
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percent improvement in their psoriasis and after treatment maintain this improvement for 3.5 months. Minor side effects include sore throat, dizziness, cough, headache, nausea, itching, muscle aches, and chills. Serious but rare side effects of Amevive are lymphophenia, malignancies, and allergic reactons. Raptiva also works by blocking T cells and the migration of these cells into the skin. Raptiva is self-administered weekly under the skin. Patients experienced a 75 percent improvement in their psoriasis, but the drug must be taken continuously to maintain improvement. Side effects include headache, chills, pain, fever, and colds. Enbrel works by blocking tumor necrosis factoralpha. Enbrel is self-administered twice a week and must be taken continuously to maintain improvement. Patients with compromised immune systems, a past history of tuberculosis, or multiple sclerosis should not take Enbrel. The most common side effect of this medication is a reaction at the injection site. Remicade is a promising drug that also works by blocking tumor necrosis factor-alpha and is currently being tested in clinical trials. Based on studies, Remicade has provided patients with a 50 to 75 percent improvement in their symptoms. The initial treatment consists of three injections over six weeks given by a physician. Patients with compromised immune systems or active infections should not be given Remicade. Side effects include upper respiratory tract infections, rash, headache, pain, fatigue, fever, and muscle pain. These drugs are expensive and out-of-- pocket costs may occur depending upon the patient's health insurance coverage. Some of the drug manufacturers have programs to help patients work with their insurance and contact information is provided. •
Topical Treatments for Psoriasis Source: Portland, OR: National Psoriasis Foundation (NPF). 2002. 28 p. Contact: Available from National Psoriasis Foundation. P.O. Box 9009, Portland, OR 97207-9009. (800) 723-9166 Ext. 12 or (503) 244-7404. Fax (503) 245-0626. E-mail:
[email protected]. Website: www.psoriasis.org. PRICE: Contact NPF for current pricing. Summary: This brochure provides people who have psoriasis with information on the use of topical calcipotriene, tazarotene, anthralin, tar, and combination therapies in the treatment of this noncontagious, chronic skin disease. Calcipotriene (Dovonex) topical ointment, a vitamin D derivative, was approved in 1993 by the U.S. Food and Drug Administration for the treatment of mild to moderate psoriasis. Dovonex is also sold in cream and scalp solution formulations. All calcipotriene products, which come in 0.005 percent strength by prescription, are odorless and nonstaining. Tazarotene (Tazorac), available in topical gel and cream forms, was the first vitamin A derivative approved by the U.S. Food and Drug Administration for the treatment of plaque psoriasis. Tazorac gel is a water based emollient gel that is available in 0.05 percent and 0.1 percent formulations. Tazorac cream is also available in strengths of 0.05 percent and 0.1 percent. Anthralin, a synthetic substitute for chrysarobin, is very effective in treating plaque psoriasis. Short contact anthralin therapy is used for patients who have localized areas of psoriasis. Topical steroids are routinely used to treat psoriasis, and they can be very effective in controlling mild to moderate psoriasis lesions. Coal tar is the type of tar most commonly used to treat psoriasis. Nonprescription coal tar products are safe and effective at concentrations of 0.5 percent and 5 percent. Salicylic acid, which helps remove psoriasis scales, is available in many nonprescription topical forms. The brochure explains how these products work; how well they work; and how to use them on various parts of the body. In addition, the brochure identifies their common minor side effects and discusses the use of Dovonex, Tazorac, anthralin, and tar with other therapies. The brochure also includes information on the National Psoriasis Foundation.
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Handbook for Teens with Psoriasis Source: Portland, OR: National Psoriasis Foundation. 2001. 20 p. Contact: Available from National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (800) 723-9166 or (503) 244-7404. Fax (503) 245-0626. Email:
[email protected]. Website: www.psoriasis.org. PRICE: Contact NPF for current pricing. Summary: This illustrated booklet serves as an information source for adolescents living with psoriasis and uses a question and answer format to help them gain insight into the disease. The booklet begins by presenting facts about psoriasis, including what it is, who gets it, what causes it, and how it is treated. This is followed by a description of the types of psoriasis. The booklet then discusses types of psoriasis treatment such as topical agents, ultraviolet light therapies, and systemic medications; the role of the patient in treatment and treatment decisions; and the questions teens need to ask their doctor about psoriasis treatments. Other topics include the impact of psoriasis on self esteem, ways to cope with the emotional aspects of psoriasis, and guiding principles for coping with psoriasis. In addition, the booklet addresses lifestyle and social issues, including the impact of stress, chlorine, sunlight, body or ear piercing, and tattoos on psoriasis; the way to explain psoriasis to new friends or dates; the impact of psoriasis on an intimate relationship; and ways to cover up psoriasis.
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Young People and Psoriasis: Infancy Through Adolescence Source: Portland, OR: National Psoriasis Foundation. 1999. 20 p. Contact: National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (800) 723-9166 or (503) 244-7404. Fax (503) 245-0626. E-mail:
[email protected]. Website: www.psoriasis.org. Summary: This booklet for the general public and young people with psoriasis focuses on the special problems confronting infants, children, and adolescents who have psoriasis. It uses a question-and-answer format to explain what psoriasis is, who gets psoriasis, the different types of psoriasis, the cause of psoriasis, the role of infection and skin injury in psoriasis, the available treatments for psoriasis, and the role of the patient in treating psoriasis. In addition, the booklet answers questions frequently asked by parents or other care givers, offers practical advice for parents and adolescents, presents an interview with a pediatric dermatologist, and lists educational literature available from the National Psoriasis Foundation.
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Genital Psoriasis Source: Portland, OR: National Psoriasis Foundation. 1998. 12 p. Contact: Available from National Psoriasis Foundation. P.O. Box 9009, Portland, OR 97207-9009. (800) 723-9166 Ext. 12 or (503) 244-7404. Fax (503) 245-0626. E-mail:
[email protected]. Website: www.psoriasis.org. PRICE: $0.35 each plus shipping and handling; bulk orders available. Summary: This pamphlet provides people who have psoriasis with information on genital psoriasis. Although this type of psoriasis acts much the same as psoriasis elsewhere on the body, its location on or near the tender skin of the reproductive organs requires special treatment. The pamphlet presents methods of treating psoriasis on the pubis, the upper thighs, the creases between thigh and groin, the genitals, the anus and surrounding area, and the buttocks crease. Precautions on the use of ultraviolet light,
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topical vitamin D, and topical retinoids in treating genital psoriasis are presented. Other topics include relieving itching and getting a correct diagnosis. In addition, the pamphlet offers tips on dealing with genital psoriasis, presents a Bill of Rights for people who have psoriasis, provides information about the National Psoriasis Foundation (NPF), and lists NPF special services. •
Your Diet and Psoriasis: Does Nutrition Play a Role? Source: Portland, OR: National Psoriasis Foundation. 1998. 20 p. Contact: Available from National Psoriasis Foundation. P.O. Box 9009, Portland, OR 97207-9009. (800) 723-9166 Ext. 12 or (503) 244-7404. Fax (503) 245-0626. E-mail:
[email protected]. Website: www.psoriasis.org. PRICE: $0.35 each plus shipping and handling; bulk orders available. Summary: This pamphlet provides people who have psoriasis with information on the possible role of nutrition in treating it. Although there appears to be little statistical verification that manipulating diet is a valid treatment option, people who have psoriasis may want to consider changing or supplementing their diet if it seems to improve their condition and does not endanger their overall health. Guidelines on maintaining overall well being, are followed by research findings about psoriasis and diet, focusing on findings about the turkey diet, the low protein diet, starvation and weight loss, oral zinc, fish oil, evening primrose oil, lecithin, shark cartilage, and the Edgar Cayce regimen. Traditional Chinese medicine, herbal remedies, and vitamins and supplements are also discussed. In addition, the pamphlet recommends evaluating diet claims for psoriasis and offers advice on evaluating advertised claims for psoriasis cures and treatments. The pamphlet concludes with information on nutritional resources and on the National Psoriasis Foundation. 10 references.
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Specific Forms of Psoriasis: Pustular, Guttate, Inverse, Erythrodermic Source: Portland, OR: National Psoriasis Foundation. 1998. 12 p. Contact: Available from National Psoriasis Foundation. P.O. Box 9009, Portland, OR 97207-9009. (800) 723-9166 Ext. 12 or (503) 244-7404. Fax (503) 245-0626. E-mail:
[email protected]. Website: www.psoriasis.org. PRICE: $0.35 each plus shipping and handling; bulk orders available. Summary: This pamphlet provides people who have psoriasis with information on the triggers, characteristics, and treatment of its specific forms: guttate, pustular, generalized and localized pustular, inverse, and erythrodermic. Guttate psoriasis often starts in childhood or young adulthood. Guttate lesions are droplike and usually appear on the trunk and limbs. This form of psoriasis may resolve on its own, but bland ointments may be needed during the acute eruptive stage. Pustular psoriasis usually occurs in adults and is characterized by white pustules surrounded by red skin. Forms of pustular psoriasis include the von Zumbusch type, palmo-plantar pustulosis, and acrodermatitis continua of Hallopeau. Inverse psoriasis is found in the armpits, in the groin, under the breasts, and in other skin folds around the genitals and buttocks. Steroid creams and ointments are effective in treating this form. Erythrodermic psoriasis is a very inflammatory form characterized by periodic, widespread, fiery redness of the skin. Treatment may include medium potency topical steroids, moisturizers, oatmeal baths, bed rest, methotrexate, acitretin, or cyclosporin. In addition, the pamphlet provides information on the National Psoriasis Foundation (NPF) and special NPF services.
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Psoriasis on Specific Skin Sites Source: Portland, OR: National Psoriasis Foundation. 1998. 12 p. Contact: Available from National Psoriasis Foundation. P.O. Box 9009, Portland, OR 97207-9009. (800) 723-9166 Ext. 12 or (503) 244-7404. Fax (503) 245-0626. E-mail:
[email protected]. Website: www.psoriasis.org. PRICE: $0.35 each plus shipping and handling; bulk orders available. Summary: This pamphlet provides people who have psoriasis with information on treating specific skin sites, including the face, eyelids, eyes, ears, mouth, skin folds, hands, feet, palms, soles, and nails. The first method of treating facial psoriasis is with moisturizers and Vaseline. Mild topical steroids can be used intermittently. Other drugs and ultraviolet light can also be effective. Eyelid inflammation requires washing the lid margins and eyelashes with tap water and baby shampoo. Special ophthalmic steroid medication is used if scaling on the eyelid must be treated. Topical antibiotics are used to treat conjunctivitis, the most common type of interior eye involvement. Scale buildup that blocks the ear canal should be removed by a physician or by means of an over-thecounter ear cleaning kit. Treatment for oral psoriasis involves topical steroids designed to treat moist areas, while steroid creams and ointments are effective in treating psoriasis on skin folds. General measures for treating psoriasis on the hands and feet include emollients, mild soaps, and soap substitutes. Other methods are traditional topical therapy, psoralen plus ultraviolet light A (PUVA), and systemic therapies. Pustular psoriasis of the palms and soles is normally treated with topical agents; although PUVA or systemic therapies may be needed, as well. The major treatments for nails are topical therapy, intralesional injection of steroids, systemic therapy, and cosmetic repair. The pamphlet provides guidelines on nail care and concludes with information on the National Psoriasis Foundation.
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Scalp Psoriasis Source: Portland, OR: National Psoriasis Foundation. 1998. 20 p. Contact: Available from National Psoriasis Foundation. P.O. Box 9009, Portland, OR 97207-9009. (800) 723-9166 Ext. 12 or (503) 244-7404. Fax (503) 245-0626. E-mail:
[email protected]. Website: www.psoriasis.org. PRICE: $0.35 each plus shipping and handling; bulk orders available. Summary: This pamphlet provides people who have psoriasis with information on treating scalp psoriasis. This form, which can range from very mild to very severe, occurs in at least 50 percent of those who have psoriasis. Scalp psoriasis can sometimes cause hair loss, and scalp itching may be troublesome as well. Because there are many options, people need to select scalp treatments that are agreeable to them. The pamphlet discusses various medications in terms of their features and mode of application. Medications include tars, topical steroids, intralesional steroid scalp injections, anthralin, calcipotriene, tazarotene, antimicrobial therapy, ultraviolet light, medicated shampoos, and systemic medications. Specific considerations for treating the forehead, neck, and ears are presented. Other topics include softening and removing scales from psoriasis lesions before treating them and applying medications effectively. In addition, the pamphlet answers common questions about scalp psoriasis, presents a sample treatment regimen, lists some scalp psoriasis products, and concludes with information on the National Psoriasis Foundation.
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Overview of Psoriasis Treatments Source: Portland, OR: National Psoriasis Foundation. 1998. 20 p. Contact: National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (800) 723-9166 or (503) 244-7404. Fax (503) 245-0626. E-mail:
[email protected]. Website: www.psoriasis.org. Summary: This booklet for individuals with psoriasis presents an overview of options for treating psoriasis. Although a wide range of treatments are available, no psoriasis treatment is universally effective. Treatments can be divided into three categories: sunlight and topical agents, phototherapy, and systemic medications. Topical therapies include topical steroids, coal tar, anthralin, topical vitamin D, salicylic acid, tazarotene, occlusion therapy, moisturizer, bath solutions, nonprescription medications, and sunbathing. Phototherapy may involve exposure to ultraviolet light B or the use of psoralen and exposure to ultraviolet light A. Systemic medications include methotrexate, retinoids, sulfasalazine, and cyclosprorine. Therapies may be combined or rotated. In addition, the booklet provides some tips for taking care of the skin and lists educational literature available from the National Psoriasis Foundation. 1 figure and 1 photograph.
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Conception, Pregnancy, and Psoriasis Source: Portland, OR: National Psoriasis Foundation. 1996. 12 p. Contact: National Psoriasis Foundation, 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (503) 244-7404. (503) 245-0626 (fax). Summary: This booklet for individuals with psoriasis provides general information about psoriasis treatments during conception, pregnancy, and breast feeding. Treatments that should be avoided when trying to conceive a child include oral retinoids, photochemotherapy, methotrexate, and hydroxyurea. Treatments that are safe for pregnant women include some topical medications, phototherapy, and cyclosporine. Women with psoriasis who choose to breast fed should avoid application of topical steroids to the breasts, photochemotherapy, and systemic medications. In addition, the booklet presents information on the genetic aspects of psoriasis and lists educational literature available from the National Psoriasis Foundation.
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Nail Psoriasis: Recognition and Control Source: Schaumburg, IL: Council for Nail Disorders (CND). 1996. 6 p. Contact: Available from Council for Nail Disorders. 930 Meacham Road, Schaumburg, IL 60173. (847) 330-9830. PRICE: Single copy free. Summary: This pamphlet uses a question and answer format to provide people who have nail psoriasis with information on this condition. Psoriasis affects the nails in up to 50 percent of people with psoriasis of the skin. People who have psoriatic arthritis develop nail psoriasis more often than people who have psoriasis of the skin do. Pits of different shapes, sizes, and depths are the most common signs of nail psoriasis. Psoriatic patches under the nail may cause it to separate from the nail bed. In addition, the skin under the nail may thicken and appear silvery white, yellowish, or brown. Nail psoriasis is among the most difficult forms of psoriasis to treat, and options include topical medications, ultraviolet light, injection medications, and oral medications such as methotrexate and retinoids. The pamphlet offers suggestions for controlling nail psoriasis and provides information on the Council for Nail Disorders.
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Psoriasis: How It Makes You Feel Source: Portland, OR: National Psoriasis Foundation. 1996. 24 p. Contact: Available from National Psoriasis Foundation. P.O. Box 9009, Portland, OR 97207-9009. (800) 723-9166 Ext. 12 or (503) 244-7404. Fax (503) 245-0626. E-mail:
[email protected]. Website: www.psoriasis.org. PRICE: $0.35 each plus shipping and handling; bulk orders available. Summary: This pamphlet provides people who have psoriasis with information on the emotional impact of the disease. The way that people with psoriasis recognize and respond to their emotions may determine how successfully they cope. The pamphlet recommends that people with psoriasis allow themselves to feel angry, sad, and frustrated so that they can start to manage these feelings; recognize feelings as part of the process of learning to live with skin that looks different; talk about psoriasis; take responsibility for treatment choices; seek professional counseling if necessary; and educate themselves about the nature of psoriasis and learn to talk about it factually. The pamphlet then suggests a cognitive therapy strategy for dealing with experiences caused by distortion, disappointment, helplessness, and hopelessness. This is followed by questions and answers about the emotional aspects of living with psoriasis, a personal account, and the role of a person who wants to help someone with psoriasis. In addition, the pamphlet offers tips for people who have psoriasis and tips for others. The pamphlet concludes with information on the National Psoriasis Foundation.
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Psoriasis Source: Schaumburg, IL: American Academy of Dermatology. 1994. 4 p. Contact: Available from American Academy of Dermatology. P.O. Box 681069, Schaumburg, IL 60168-1069. (888) 462-3376 or (847) 330-0230. http://www.aad.org/index.html. PRICE: Single copy free; bulk prices available. Summary: This brochure for people with psoriasis uses a question and answer format to provide information about this persistent skin condition. It explains that in psoriasis, the skin becomes inflamed, producing red, thickened areas with silvery scales, usually on the scalp, elbows, knees, and lower back. The brochure discusses possible causes of psoriasis, including abnormal white cell function, infections, and certain medications. It describes the several types of psoriasis, how a diagnosis is made, and it details the many drug and nondrug treatments and therapeutic options available. 2 photographs.
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Psoriasis Research Source: Portland, OR: National Psoriasis Foundation. 1994. 16 p. Contact: Available from National Psoriasis Foundation. P.O. Box 9009, Portland, OR 97207-9009. (800) 723-9166 Ext. 12 or (503) 244-7404. Fax (503) 245-0626. E-mail:
[email protected]. Website: www.psoriasis.org. PRICE: $0.35 each plus shipping and handling; bulk orders available. Summary: This pamphlet provides people who have psoriasis with information on psoriasis research. The pamphlet begins with an overview of the disease and a discussion of different hypotheses about it. The role of the National Psoriasis Foundation (NPF) in this research is presented and a NPF research timeline is provided. In addition, the major directions of new psoriasis research are highlighted. Researchers are attempting to determine whether psoriasis is an autoimmune disease, so the immune system is receiving increased attention. Drugs that suppress the immune
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system are very effective in clearing psoriasis, which indicates that the immune system may have a key role in its development. Many researchers also believe that T cells, which alert the body to antigens and trigger defensive reactions, have a major role in mediating the expression of psoriasis. Further evidence of T cell involvement is the presence in plaques of cellular messengers, or cytokines, that T cells leave behind. In addition, high levels of interleukin-1, a proinflammatory cytokine manufactured by white blood cells, are found in psoriatic plaques. Researchers also believe that psoriasis is generally a genetically acquired disorder, so they are searching for the genetic defect responsible and the way to correct it. Research on other biochemical abnormalities associated with psoriasis is also being conducted. In addition, the pamphlet identifies funding sources for psoriasis research and concludes with information on the National Psoriasis Foundation. 1 figure. •
Skin Cancer Risks From Psoriasis Treatments Source: Portland, OR: National Psoriasis Foundation. 1994. 8 p. Contact: Available from National Psoriasis Foundation. P.O. Box 9009, Portland, OR 97207-9009. (800) 723-9166 Ext. 12 or (503) 244-7404. Fax (503) 245-0626. E-mail:
[email protected]. Website: www.psoriasis.org. PRICE: $0.35 each plus shipping and handling; bulk orders available. Summary: This pamphlet provides people who have psoriasis with information on the risk of skin cancer from common treatments. Treatments with the potential to increase the risk of skin cancer are exposing the skin to ultraviolet light B (UVB) or ultraviolet light A plus the drug psoralen (PUVA). Although UVB is an established carcinogen, long-term studies indicate that it is relatively safe at the low doses used for UVB phototherapy. Even for people treated with high levels of UVB, there seems to be little or no increased risk of skin cancer. The risk from PUVA is complicated by various environmental and genetic factors. Although PUVA has been identified as a carcinogen, the risk depends on the total dose. If there are no other complications, the risk becomes significant after a cumulative dose of over 150 to 160 treatments. Nonmelanoma skin cancers, such as basal cell carcinoma and squamous cell carcinoma, are the types directly associated with phototherapy. Actinic keratoses are precancerous lesions caused by overexposure to ultraviolet light. A type of skin damage known as photoaging may also occur from long-term exposure to ultraviolet light. The pamphlet describes the features of these skin conditions, and offers recommendations on using phototherapy, and concludes with information on the National Psoriasis Foundation.
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[Handout About Psoriasis] Source: Portland, OR: National Psoriasis Foundation. 2001. 2 p. Contact: Available from National Psoriasis Foundation. 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195. (800) 723-9166 or (503) 244-7404. Fax (503) 245-0626. Email:
[email protected]. Website: www.psoriasis.org. PRICE: Contact NPF for current pricing. Summary: This handout provides the general public with information on psoriasis. The handout serves as a way for young people who have psoriasis to educate adults about this chronic skin disease. The handout explains what psoriasis is and how adults can help a young person who has it. In addition, the handout presents some facts that adults should keep in mind when dealing with a child or teenager who has psoriasis. The handout identifies the National Psoriasis Foundation as a source of additional information.
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Questions About Psoriasis Source: American Family Physician. 61(3): 736. February 1, 2000. Contact: American Academy of Family Physicians. 11400 Tomahawk Creek Parkway, Leawood, KS 66211-2672. (800) 274-2237 or (913) 906-6000. E-mail:
[email protected]. Website: www.aafp.org. Summary: This journal article uses a question and answer format to provide people who have psoriasis with information on the causes and treatment of this disease. Psoriasis is a very common noncontagious skin disorder that causes large, thick, scaly red or purple patches on the skin. The exact cause of psoriasis is unknown. Anyone can get psoriasis, and the disease sometimes runs in families. Although there is no cure for psoriasis, it can be controlled with proper treatment. Options for treating psoriasis include keeping skin moisturized; using prescription creams, ointments, and lotions; taking oral medications; and undergoing ultraviolet light therapy. Exacerbating factors include stress, infections, and certain medications. The article includes sources of additional information about psoriasis.
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Help for Psoriasis Source: American Family Physician. 59(4): 964. February 1999. Contact: American Academy of Family Physicians. 11400 Tomahawk Creek Parkway, Leawood, KS 66211-2672. (800) 274-2237 or (913) 906-6000. E-mail:
[email protected]. Website: www.aafp.org. Summary: This journal article uses a question and answer format to provide people who have psoriasis with information on this skin condition, which causes red, silvery scales and flaky patches. The cause is unknown, and there is no cure. Although diagnosis is usually based on visual inspection of the skin, a biopsy may be needed in some cases. Mild psoriasis may not need any treatment or may be treated with materials available without a prescription, such as moisturizing creams and shampoos, ointments with salicylic acid, and preparations that contain coal tar. Prescription creams containing steroids are used for more severe cases. Other treatment options include phototherapy; light plus psoralen therapy; and drugs such as methotrexate, etretinate, acitretin, calcipotriene, and tazarotene.
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Questions and Answers About Psoriasis Source: Bethesda, MD: National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 1997. 9 p. Contact: Available from National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 1 AMS Circle, Bethesda, MD 20892-3675. (877) 226-4267 or (301) 495-4484. Fax (301) 718-6366. TTY (301) 565-2966. E-mail:
[email protected]. Website: www.niams.nih.gov. PRICE: 1 to 25 copies free. Order Number: AR-9791QA (fact sheet), or AR-97L QA (large print fact sheet). Summary: This fact sheet for people with psoriasis uses a question and answer format to provide information. This chronic skin disease is characterized by scaling and inflammation of the skin, and may be a disorder of the immune system. Various forms of psoriasis are discussed, as well as the many treatment options are available. Treatments can include exposure to sunlight; application of corticosteroids, calcipotriene ointment, coal tar, anthralin ointment, salicylic acid, and moisturizers; addition of oil to bath water; and other combinations of drug therapy and exposure to light. The fact sheet
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also discusses current research on the causes and treatments for psoriasis. It then refers the reader to a national voluntary health organization for additional information. Also available is a large print version of this fact sheet.
The National Guideline Clearinghouse™ The National Guideline Clearinghouse™ offers hundreds of evidence-based clinical practice guidelines published in the United States and other countries. You can search this site located at http://www.guideline.gov/ by using the keyword “psoriasis” (or synonyms). The following was recently posted: •
Psoriasis Source: Finnish Medical Society Duodecim - Professional Association; 2002 May 7; Various pagings http://www.guideline.gov/summary/summary.aspx?doc_id=3388&nbr=2614&a mp;string=psoriasis Healthfinder™
Healthfinder™ is sponsored by the U.S. Department of Health and Human Services and offers links to hundreds of other sites that contain healthcare information. This Web site is located at http://www.healthfinder.gov. Again, keyword searches can be used to find guidelines. The following was recently found in this database: •
FAQ - About Psoriasis Summary: Answers to the questions most often received from patients and the general public about this skin disorder. Source: National Psoriasis Foundation http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=2715
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PsoriasisNet Summary: Links to info about psoriasis and its treatment. Includes a glossary. Source: American Academy of Dermatology http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6381
•
Questions and Answers About Psoriasis Summary: This consumer health information fact sheet contains general information about psoriasis. Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=3778
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•
Retinoids Summary: In recent years new synthetic derivatives of Vitamin A (retinoids) have been developed for the treatment of various skin conditions, such as severe acne, sun spots, wrinkles, and psoriasis. Source: American Society For Dermatologic Surgery http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6748
•
Skincarephysicians.com Summary: An index to Web pages on psoriasis, eczema, aging skin, acne, melanoma, and actinic keratoses. Source: American Academy of Dermatology http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6380
•
What is Psoriasis? Summary: This consumer health information fact sheet provides basic information about this non-contagious skin disorder. Source: National Psoriasis Foundation http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=2714 The NIH Search Utility
The NIH search utility allows you to search for documents on over 100 selected Web sites that comprise the NIH-WEB-SPACE. Each of these servers is “crawled” and indexed on an ongoing basis. Your search will produce a list of various documents, all of which will relate in some way to psoriasis. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. NORD (The National Organization of Rare Disorders, Inc.) NORD provides an invaluable service to the public by publishing short yet comprehensive guidelines on over 1,000 diseases. NORD primarily focuses on rare diseases that might not be covered by the previously listed sources. NORD’s Web address is http://www.rarediseases.org/. A complete guide on psoriasis can be purchased from NORD for a nominal fee. PEDBASE Similar to NORD, PEDBASE covers relatively rare disorders, limited mainly to pediatric conditions. PEDBASE was designed by Dr. Alan Gandy. To access the database, which is
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more oriented to researchers than patients, you can view the current list of health topics covered at the following Web site: http://www.icondata.com/health/pedbase/pedlynx.htm. Additional Web Sources
A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/specific.htm
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Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
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Med Help International: http://www.medhelp.org/HealthTopics/A.html
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Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
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Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
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WebMDHealth: http://my.webmd.com/health_topics
Associations and Psoriasis The following is a list of associations that provide information on and resources relating to psoriasis: •
American Autoimmune Related Diseases Association, Inc Telephone: (586) 776-3900 Fax: (586) 776-3903 Email:
[email protected] Web Site: http://www.aarda.org/ Background: The American Autoimmune Related Diseases Association, Inc. (AARDA) is a national not-for-profit voluntary health agency dedicated to bringing a national focus to autoimmunity, a major cause of serious chronic diseases. The Association was founded for the purposes of supporting research to find a cure for autoimmune diseases and providing services to affected individuals. In addition, the Association s goals include increasing the public s awareness that autoimmunity is the cause of more than 80 serious chronic diseases; bringing national focus and collaborative effort among state and national voluntary health groups that represent autoimmune diseases; and serving as a national advocate for individuals and families affected by the physical, emotional, and financial effects of autoimmune disease. The American Autoimmune Related Diseases Association produces educational and support materials including fact sheets, brochures, pamphlets, and a newsletter entitled 'In Focus.'. Relevant area(s) of interest: Psoriasis
•
American Skin Association Telephone: (212) 753-8260 Toll-free: (800) 499-7546 Fax: (212) 688-6547
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Email:
[email protected] Web Site: None Background: The American Skin Association (ASA) is a national nonprofit organization dedicated to building a network of lay people to achieve more effective prevention, treatment, and cure of skin disorders. ASA programs include generating support for skin research and providing information and education to the public regarding the skin and its disorders. ASA's mission is to identify, promote, and support research in biology of the skin, stimulate the transfer of advances in the field to clinical care of dermatology patients, and educate the community regarding diseases, symptoms, and care of the skin. To meet this goal, the Association engages in fundraising to support research and develops local chapters throughout the country. Information on a wide spectrum of skin disorders is available including 'Your Newborn s Skin and the Sun,' 'Ultraviolet Index: What You Need To Know,' 'Outdoor Sports and Your Skin,' and 'Proper Skin Care Can Make Gardening a Bed of Roses.' Founded in 1987, ASA also publishes 'SkinFacts,' a quarterly newsletter. Relevant area(s) of interest: Psoriasis •
Canadian Psoriasis Foundation / La Fondation Canadienne du Psoriasis Telephone: (613) 728-4000 Toll-free: (800) 265-0926 Fax: (613) 728-8913 Email:
[email protected] Web Site: http://www.psoriasis.ca Background: The Canadian Psoriasis Foundation/La fondation canadienne du psoriasis is a not-for-profit voluntary health organization dedicated to promoting the health and improving the quality of life of Canadians affected by psoriasis through education, advocacy, service, and research. Psoriasis is a common, recurrent skin disorder characterized by thickened patches of reddish, inflamed skin and silvery or grayish, dry skin scaling due to abnormally rapid growth and turnover of skin cells. Although the exact underlying cause of psoriasis is unknown, the disease often appears to be familial. The Canadian Psoriasis Foundation was established in 1983 and currently has 16 chapters and approximately 1,300 members. The Foundation is committed to providing current information on psoriasis to inquirers including affected individuals, family members, health care professionals, and the general public; distributing educational literature to schools, libraries, hospitals, and clinics across Canada; publishing regular newsletters with feature articles on traditional and nontraditional psoriasis treatments; and conducting regular conferences and workshops. In addition, the organization provides referrals to dermatology facilities in Canada; promotes and supports research; promotes public and professional awareness of the disorder and the needs of affected individuals; and establishes and maintains local chapters in cities throughout Canada, providing a national communication network. The Foundation's educational materials include booklets, pamphlets on the various forms of psoriasis, a treatment series, and a quarterly newsletter entitled 'CPF Newsletter,' which includes information on new and existing treatments, research developments, and organizational activities on a national and local basis.
•
March of Dimes Birth Defects Foundation Telephone: (914) 428-7100 Toll-free: (888) 663-4637
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Fax: (914) 997-4763 Email:
[email protected] Web Site: http://www.marchofdimes.com Background: The March of Dimes Birth Defects Foundation is a national not-for-profit organization that was established in 1938. The mission of the Foundation is to improve the health of babies by preventing birth defects and infant mortality. The March of Dimes funds programs of research, community services, education, and advocacy. Educational programs that seek to prevent birth defects are important to the Foundation and to that end it also produces a wide variety of printed informational materials and videos. The Pregnancy and Newborn Health Education Center staffs trained health information specialists who provide researched information on pregnancy issues, complications and risks, newborn care, birth defects, genetic diseases and related topics as well as referrals to relevant organizations and support groups. Relevant area(s) of interest: Psoriasis •
National Psoriasis Foundation Telephone: (503) 244-7404 Toll-free: (800) 723-9166 Fax: (503) 245-0626 Email:
[email protected] Web Site: http://www.psoriasis.org/ Background: The National Psoriasis Foundation is a voluntary not-for-profit organization dedicated to providing support to, and improving the quality of life for, individuals with psoriasis, a chronic skin disorder; educating the public; and promoting and supporting research for psoriasis. Established in 1968 by affected individuals, physicians, and researchers, the National Psoriasis Foundation is committed to publishing the most current information on psoriasis and providing a forum for affected individuals to speak out. The organization promotes funding for psoriasis research and seeks to establish an alliance between affected people, the medical and scientific communities, and the pharmaceutical industry. The National Psoriasis Foundation promotes patient advocacy and legislation beneficial to affected individuals; provides appropriate referrals (e.g., to support groups); and offers a variety of educational materials. These materials include a regular newsletter and reports. Relevant area(s) of interest: Psoriasis
•
Psoriatic Arthropathy Alliance Telephone: (192) 367-2837 Fax: (192) 367-2837 Email:
[email protected] Web Site: http://www.paalliance.org Background: The Psoriatic Arthropathic Alliance (PAA) is a non-profit support and informational organization for individuals affected by psoriatic arthropathy (PA) and other related conditions. Psoriatic arthropathy is a rheumatoid-like arthritic condition that is associated with psoriasis of the skin or nails, and a negative rheumatoid arthritis (RA) serology laboratory test. The disorder is more common in females than males. The mission of the PAA is to provide support and information to individuals affected by PA. Established in 1993, the Alliance also monitors medical and health care services and
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supports research into the causes, prevention, and management of PA and related conditions. In addition, the group acts as a lobbyist for patient rights. Consisting of 1,000 members, the Alliance produces educational materials that are available to medical professionals, medical students, and the general public. PAA publishes a periodic newsletter and a journal and offers a networking service. Relevant area(s) of interest: Psoriasis
Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to psoriasis. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with psoriasis. The National Health Information Center (NHIC) The National Health Information Center (NHIC) offers a free referral service to help people find organizations that provide information about psoriasis. For more information, see the NHIC’s Web site at http://www.health.gov/NHIC/ or contact an information specialist by calling 1-800-336-4797. Directory of Health Organizations The Directory of Health Organizations, provided by the National Library of Medicine Specialized Information Services, is a comprehensive source of information on associations. The Directory of Health Organizations database can be accessed via the Internet at http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “psoriasis” (or a synonym), and you will receive information on all relevant organizations listed in the database. Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given the option to search by keyword or by browsing the subject list. When you have received your search results, click on the name of the organization for its description and contact information. The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “psoriasis”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop
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boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “psoriasis” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months. The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “psoriasis” (or a synonym) into the search box, and click “Submit Query.”
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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.
Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.26
Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.
Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of
26
Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.
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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)27: •
Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/
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Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)
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Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
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California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
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California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
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California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html
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California: Gateway Health Library (Sutter Gould Medical Foundation)
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California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
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California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
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California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
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California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
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California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
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California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
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California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
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California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
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Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
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Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
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Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
27
Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
Finding Medical Libraries 415
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Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
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Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm
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Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
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Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm
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Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp
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Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/
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Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm
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Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html
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Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/
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Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
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Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
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Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
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Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
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Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm
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Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html
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Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm
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Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
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Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
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Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
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Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
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Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html
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Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp
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Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp
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Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/
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Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
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Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
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Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
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Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
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Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
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Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
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Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
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Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
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Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html
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Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm
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Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
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Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
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National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
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National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/
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National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
Finding Medical Libraries 417
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Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
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New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
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New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
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New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
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New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
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New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
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New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html
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New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
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Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
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Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp
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Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/
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Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/
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Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml
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Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html
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Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html
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Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml
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Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
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Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
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Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/
418 Psoriasis
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South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp
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Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/
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Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/
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Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72
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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
•
MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
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Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
•
Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
•
On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
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Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
•
Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm
Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a). The NIH suggests the following Web sites in the ADAM Medical Encyclopedia when searching for information on psoriasis: •
Basic Guidelines for Psoriasis AIDS Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000594.htm Psoriasis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000434.htm Psoriasis - guttate Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000822.htm Psoriasis - resources Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002197.htm
•
Signs & Symptoms for Psoriasis Erythema Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003220.htm
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Eye burning, itching and discharge Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003034.htm Fatigue Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003088.htm Fever Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003090.htm Genital lesions (male) Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003221.htm Hypopigmentation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003224.htm Itching Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003217.htm Joint pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003261.htm Muscle aches Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003178.htm Nail abnormalities Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003247.htm Obesity Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003101.htm Onycholysis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003247.htm Papule Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003233.htm Patches Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003231.htm Patchy loss of skin color Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003224.htm Pruritus Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003217.htm Pustules Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003234.htm Rash Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003220.htm
Online Glossaries 421
Scales Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003226.htm Skin lesion Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003220.htm Skin lesions Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003220.htm Skin redness or inflammation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003220.htm Stress Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003211.htm Stria Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003287.htm Sunburn Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003227.htm Tearing, increased Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003036.htm •
Diagnostics and Tests for Psoriasis Biopsy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003416.htm HLA antigens Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003550.htm Hyperplasia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003441.htm Rheumatoid factor Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003548.htm Sedimentation rate Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003638.htm Skin biopsy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003840.htm X-ray Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003337.htm
•
Nutrition for Psoriasis Well-balanced diet Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002449.htm
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•
Background Topics for Psoriasis Aggravated by Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002227.htm Alcohol consumption Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001944.htm Analgesics Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002123.htm Burns Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000030.htm Chemotherapy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002324.htm Chronic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002312.htm Exercise Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001941.htm Inflammatory response Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000821.htm Insect bites Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000033.htm Intravenous Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002383.htm Phenol Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002903.htm Psoriasis - support group Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002197.htm Respiratory Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002290.htm Scales Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003226.htm Scaling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003226.htm Secondary infections Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002300.htm
Online Glossaries 423
Stress management Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001942.htm Support group Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002150.htm Systemic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002294.htm
Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •
Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical
•
MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html
•
Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/
•
Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
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PSORIASIS DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 6-Aminonicotinamide: A vitamin antagonist which has teratogenic effects. [NIH] Abdomen: That portion of the body that lies between the thorax and the pelvis. [NIH] Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Abdominal Pain: Sensation of discomfort, distress, or agony in the abdominal region. [NIH] Aberrant: Wandering or deviating from the usual or normal course. [EU] Abortion: 1. The premature expulsion from the uterus of the products of conception - of the embryo, or of a nonviable fetus. The four classic symptoms, usually present in each type of abortion, are uterine contractions, uterine haemorrhage, softening and dilatation of the cervix, and presentation or expulsion of all or part of the products of conception. 2. Premature stoppage of a natural or a pathological process. [EU] Acantholysis: Separation of the prickle cells of the stratum spinosum of the epidermis, resulting in atrophy of the prickle cell layer. It is seen in diseases such as pemphigus vulgaris (see pemphigus) and keratosis follicularis. [NIH] Acatalasia: A rare autosomal recessive disorder resulting from the absence of catalase activity. Though usually asymptomatic, a syndrome of oral ulcerations and gangrene may be present. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] Acetic Acids: Acetic acid and its derivatives which may be formed by substitution reactions. Mono- and di-substituted, as well as halogenated compounds have been synthesized. [NIH] Acetohexamide: A sulfonylurea hypoglycemic agent that is metabolized in the liver to 1hydrohexamide. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acetylcysteine: The N-acetyl derivative of cysteine. It is used as a mucolytic agent to reduce the viscosity of mucous secretions. It has also been shown to have antiviral effects in patients with HIV due to inhibition of viral stimulation by reactive oxygen intermediates. [NIH] Acetylgalactosamine: The N-acetyl derivative of galactosamine. [NIH] Acetylglucosamine: The N-acetyl derivative of glucosamine. [NIH] Acidity: The quality of being acid or sour; containing acid (hydrogen ions). [EU] Acitretin: An oral retinoid effective in the treatment of psoriasis. It is the major metabolite of etretinate with the advantage of a much shorter half-life when compared with etretinate. [NIH]
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Acne: A disorder of the skin marked by inflammation of oil glands and hair glands. [NIH] Acne Vulgaris: A chronic disorder of the pilosebaceous apparatus associated with an increase in sebum secretion. It is characterized by open comedones (blackheads), closed comedones (whiteheads), and pustular nodules. The cause is unknown, but heredity and age are predisposing factors. [NIH] Acquired Immunodeficiency Syndrome: An acquired defect of cellular immunity associated with infection by the human immunodeficiency virus (HIV), a CD4-positive Tlymphocyte count under 200 cells/microliter or less than 14% of total lymphocytes, and increased susceptibility to opportunistic infections and malignant neoplasms. Clinical manifestations also include emaciation (wasting) and dementia. These elements reflect criteria for AIDS as defined by the CDC in 1993. [NIH] Acrodermatitis: Inflammation involving the skin of the extremities, especially the hands and feet. Several forms are known, some idiopathic and some hereditary. The infantile form is called Gianotti-Crosti syndrome. [NIH] Acrylonitrile: A highly poisonous compound used widely in the manufacture of plastics, adhesives and synthetic rubber. [NIH] Actin: Essential component of the cell skeleton. [NIH] Actinic keratosis: A precancerous condition of thick, scaly patches of skin. Also called solar or senile keratosis. [NIH] Acute Disease: Disease having a short and relatively severe course. [NIH] Acute leukemia: A rapidly progressing cancer of the blood-forming tissue (bone marrow). [NIH]
Acute renal: A condition in which the kidneys suddenly stop working. In most cases, kidneys can recover from almost complete loss of function. [NIH] Acyl: Chemical signal used by bacteria to communicate. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adaptation: 1. The adjustment of an organism to its environment, or the process by which it enhances such fitness. 2. The normal ability of the eye to adjust itself to variations in the intensity of light; the adjustment to such variations. 3. The decline in the frequency of firing of a neuron, particularly of a receptor, under conditions of constant stimulation. 4. In dentistry, (a) the proper fitting of a denture, (b) the degree of proximity and interlocking of restorative material to a tooth preparation, (c) the exact adjustment of bands to teeth. 5. In microbiology, the adjustment of bacterial physiology to a new environment. [EU] Adenine: A purine base and a fundamental unit of adenine nucleotides. [NIH] Adenocarcinoma: A malignant epithelial tumor with a glandular organization. [NIH] Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adenosine Deaminase: An enzyme that catalyzes the hydrolysis of adenosine to inosine with the elimination of ammonia. Since there are wide tissue and species variations in the enzyme, it has been used as a tool in the study of human and animal genetics and in medical diagnosis. EC 3.5.4.4. [NIH] Adenosine Monophosphate: Adenylic acid. Adenine nucleotide containing one phosphate group esterified to the sugar moiety in the 2'-, 3'-, or 5'-position. [NIH] Adenylate Cyclase: An enzyme of the lyase class that catalyzes the formation of cyclic AMP
Dictionary 427
and pyrophosphate from ATP. EC 4.6.1.1. [NIH] Adhesions: Pathological processes consisting of the union of the opposing surfaces of a wound. [NIH] Adipose Tissue: Connective tissue composed of fat cells lodged in the meshes of areolar tissue. [NIH] Adjunctive Therapy: Another treatment used together with the primary treatment. Its purpose is to assist the primary treatment. [NIH] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH] Adjuvant: A substance which aids another, such as an auxiliary remedy; in immunology, nonspecific stimulator (e.g., BCG vaccine) of the immune response. [EU] Adolescence: The period of life beginning with the appearance of secondary sex characteristics and terminating with the cessation of somatic growth. The years usually referred to as adolescence lie between 13 and 18 years of age. [NIH] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Aerosol: A solution of a drug which can be atomized into a fine mist for inhalation therapy. [EU]
Aetiology: Study of the causes of disease. [EU] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Affinity Chromatography: In affinity chromatography, a ligand attached to a column binds specifically to the molecule to be purified. [NIH] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]
Age Groups: Persons classified by age from birth (infant, newborn) to octogenarians and older (aged, 80 and over). [NIH] Age of Onset: The age or period of life at which a disease or the initial symptoms or
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manifestations of a disease appear in an individual. [NIH] Aged, 80 and Over: A person 80 years of age and older. [NIH] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Agranulocytosis: A decrease in the number of granulocytes (basophils, eosinophils, and neutrophils). [NIH] Agrochemicals: Chemicals used in agriculture. These include pesticides, fumigants, fertilizers, plant hormones, steroids, antibiotics, mycotoxins, etc. [NIH] Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Aldosterone: (11 beta)-11,21-Dihydroxy-3,20-dioxopregn-4-en-18-al. A hormone secreted by the adrenal cortex that functions in the regulation of electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU] Alkaline: Having the reactions of an alkali. [EU] Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Some alkaloids have been shown to work against cancer. [NIH] Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Allergen: An antigenic substance capable of producing immediate-type hypersensitivity (allergy). [EU] Allergic Rhinitis: Inflammation of the nasal mucous membrane associated with hay fever; fits may be provoked by substances in the working environment. [NIH] Allogeneic: Taken from different individuals of the same species. [NIH] Allogeneic bone marrow transplantation: A procedure in which a person receives stem cells, the cells from which all blood cells develop, from a compatible, though not genetically identical, donor. [NIH] Allograft: An organ or tissue transplant between two humans. [NIH] Alloys: A mixture of metallic elements or compounds with other metallic or metalloid elements in varying proportions. [NIH] Allylamine: Possesses an unusual and selective cytotoxicity for vascular smooth muscle cells in dogs and rats. Useful for experiments dealing with arterial injury, myocardial fibrosis or cardiac decompensation. [NIH]
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Alopecia: Absence of hair from areas where it is normally present. [NIH] Alpha Particles: Positively charged particles composed of two protons and two neutrons, i.e., helium nuclei, emitted during disintegration of very heavy isotopes; a beam of alpha particles or an alpha ray has very strong ionizing power, but weak penetrability. [NIH] Alpha-1: A protein with the property of inactivating proteolytic enzymes such as leucocyte collagenase and elastase. [NIH] Alpha-helix: One of the secondary element of protein. [NIH] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Alternative Splicing: A process whereby multiple protein isoforms are generated from a single gene. Alternative splicing involves the splicing together of nonconsecutive exons during the processing of some, but not all, transcripts of the gene. Thus a particular exon may be connected to any one of several alternative exons to form messenger RNA. The alternative forms produce proteins in which one part is common while the other part is different. [NIH] Aluminum: A metallic element that has the atomic number 13, atomic symbol Al, and atomic weight 26.98. [NIH] Alveolar Process: The thickest and spongiest part of the maxilla and mandible hollowed out into deep cavities for the teeth. [NIH] Alveoli: Tiny air sacs at the end of the bronchioles in the lungs. [NIH] Amber: A yellowish fossil resin, the gum of several species of coniferous trees, found in the alluvial deposits of northeastern Germany. It is used in molecular biology in the analysis of organic matter fossilized in amber. [NIH] Ameliorating: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Amine: An organic compound containing nitrogen; any member of a group of chemical compounds formed from ammonia by replacement of one or more of the hydrogen atoms by organic (hydrocarbon) radicals. The amines are distinguished as primary, secondary, and tertiary, according to whether one, two, or three hydrogen atoms are replaced. The amines include allylamine, amylamine, ethylamine, methylamine, phenylamine, propylamine, and many other compounds. [EU] Amino acid: Any organic compound containing an amino (-NH2 and a carboxyl (- COOH) group. The 20 a-amino acids listed in the accompanying table are the amino acids from which proteins are synthesized by formation of peptide bonds during ribosomal translation of messenger RNA; all except glycine, which is not optically active, have the L configuration. Other amino acids occurring in proteins, such as hydroxyproline in collagen, are formed by posttranslational enzymatic modification of amino acids residues in polypeptide chains. There are also several important amino acids, such as the neurotransmitter y-aminobutyric acid, that have no relation to proteins. Abbreviated AA. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Aminolevulinic Acid: A compound produced from succinyl-CoA and glycine as an intermediate in heme synthesis. [NIH]
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Aminopterin: N-(4-(((2,4-Diamino-6-pteridinyl)methyl)amino)benzoyl)-L-glutamic acid. A folic acid derivative used as a rodenticide that has been shown to be teratogenic. [NIH] Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH] Anabolic: Relating to, characterized by, or promoting anabolism. [EU] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Anal: Having to do with the anus, which is the posterior opening of the large bowel. [NIH] Analgesic: An agent that alleviates pain without causing loss of consciousness. [EU] Analog: In chemistry, a substance that is similar, but not identical, to another. [NIH] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] Anaphase: The third phase of cell division, in which the chromatids separate and migrate to opposite poles of the spindle. [NIH] Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anaplasia: Loss of structural differentiation and useful function of neoplastic cells. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Androgens: A class of sex hormones associated with the development and maintenance of the secondary male sex characteristics, sperm induction, and sexual differentiation. In addition to increasing virility and libido, they also increase nitrogen and water retention and stimulate skeletal growth. [NIH] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anergy: Absence of immune response to particular substances. [NIH] Anesthesia: A state characterized by loss of feeling or sensation. This depression of nerve function is usually the result of pharmacologic action and is induced to allow performance of surgery or other painful procedures. [NIH] Angina: Chest pain that originates in the heart. [NIH] Angiogenesis: Blood vessel formation. Tumor angiogenesis is the growth of blood vessels from surrounding tissue to a solid tumor. This is caused by the release of chemicals by the tumor. [NIH] Angiogenesis Factor: Substance causing proliferation of new blood vessels. It is found in tissues with high metabolic requirements, such as the retina, and in certain cancers. The factor is also released by hypoxic macrophages at the edges or outer surfaces of wounds and initiates revascularization in wound healing. [NIH] Angiogenesis inhibitor: A substance that may prevent the formation of blood vessels. In anticancer therapy, an angiogenesis inhibitor prevents the growth of blood vessels from surrounding tissue to a solid tumor. [NIH] Angiotensinogen: An alpha-globulin of which a fragment of 14 amino acids is converted by
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renin to angiotensin I, the inactive precursor of angiotensin II. It is a member of the serpin superfamily. [NIH] Anhydrous: Deprived or destitute of water. [EU] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Anionic: Pertaining to or containing an anion. [EU] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Ankle: That part of the lower limb directly above the foot. [NIH] Annealing: The spontaneous alignment of two single DNA strands to form a double helix. [NIH]
Anode: Electrode held at a positive potential with respect to a cathode. [NIH] Anogenital: Pertaining to the anus and external genitals. [EU] Anomalies: Birth defects; abnormalities. [NIH] Anorexia: Lack or loss of appetite for food. Appetite is psychologic, dependent on memory and associations. Anorexia can be brought about by unattractive food, surroundings, or company. [NIH] Antagonism: Interference with, or inhibition of, the growth of a living organism by another living organism, due either to creation of unfavorable conditions (e. g. exhaustion of food supplies) or to production of a specific antibiotic substance (e. g. penicillin). [NIH] Anthelmintic: An agent that is destructive to worms. [EU] Anthralin: An anti-inflammatory anthracene derivative used for the treatment of dermatoses, especially psoriasis. It may cause folliculitis. [NIH] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]
Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Antibody Affinity: A measure of the binding strength between antibody and a simple hapten or antigen determinant. It depends on the closeness of stereochemical fit between antibody combining sites and antigen determinants, on the size of the area of contact between them, and on the distribution of charged and hydrophobic groups. It includes the concept of "avidity," which refers to the strength of the antigen-antibody bond after formation of reversible complexes. [NIH] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Anticonvulsant: An agent that prevents or relieves convulsions. [EU]
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Antidepressant: A drug used to treat depression. [NIH] Antidote: A remedy for counteracting a poison. [EU] Antifungal: Destructive to fungi, or suppressing their reproduction or growth; effective against fungal infections. [EU] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Antigen-presenting cell: APC. A cell that shows antigen on its surface to other cells of the immune system. This is an important part of an immune response. [NIH] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antimetabolite: A chemical that is very similar to one required in a normal biochemical reaction in cells. Antimetabolites can stop or slow down the reaction. [NIH] Antimicrobial: Killing microorganisms, or suppressing their multiplication or growth. [EU] Antimycotic: Suppressing the growth of fungi. [EU] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antiproliferative: Counteracting a process of proliferation. [EU] Antipruritic: Relieving or preventing itching. [EU] Antiseptic: A substance that inhibits the growth and development of microorganisms without necessarily killing them. [EU] Antiserum: The blood serum obtained from an animal after it has been immunized with a particular antigen. It will contain antibodies which are specific for that antigen as well as antibodies specific for any other antigen with which the animal has previously been immunized. [NIH] Antispasmodic: An agent that relieves spasm. [EU] Antitumour: Counteracting tumour formation. [EU] Antiviral: Destroying viruses or suppressing their replication. [EU] Anuria: Inability to form or excrete urine. [NIH] Anus: The opening of the rectum to the outside of the body. [NIH] Apolipoproteins: The protein components of lipoproteins which remain after the lipids to which the proteins are bound have been removed. They play an important role in lipid transport and metabolism. [NIH]
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Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Approximate: Approximal [EU] Aqueous: Having to do with water. [NIH] Arachidonate 15-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 15-hydroperoxyarachidonate (15-HPETE) which is rapidly converted to 15-hydroxy5,8,11,13-eicosatetraenoate (15-HETE). The 15-hydroperoxides are preferentially formed in neutrophils and lymphocytes. EC 1.13.11.33. [NIH] Arachidonate Lipoxygenases: Enzymes catalyzing the oxidation of arachidonic acid to hydroperoxyarachidonates (HPETES). These products are then rapidly converted by a peroxidase to hydroxyeicosatetraenoic acids (HETES). The positional specificity of the enzyme reaction varies from tissue to tissue. The final lipoxygenase pathway leads to the leukotrienes. EC 1.13.11.- . [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Aromatic: Having a spicy odour. [EU] Arsenates: Inorganic or organic salts and esters of arsenic acid. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arteriolar: Pertaining to or resembling arterioles. [EU] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Arteriolosclerosis: Sclerosis and thickening of the walls of the smaller arteries (arterioles). Hyaline arteriolosclerosis, in which there is homogeneous pink hyaline thickening of the arteriolar walls, is associated with benign nephrosclerosis. Hyperplastic arteriolosclerosis, in which there is a concentric thickening with progressive narrowing of the lumina may be associated with malignant hypertension, nephrosclerosis, and scleroderma. [EU] Arteriosclerosis: Thickening and loss of elasticity of arterial walls. Atherosclerosis is the most common form of arteriosclerosis and involves lipid deposition and thickening of the intimal cell layers within arteries. Additional forms of arteriosclerosis involve calcification of the media of muscular arteries (Monkeberg medial calcific sclerosis) and thickening of the walls of small arteries or arterioles due to cell proliferation or hyaline deposition (arteriolosclerosis). [NIH] Arteriovenous: Both arterial and venous; pertaining to or affecting an artery and a vein. [EU] Arteriovenous Fistula: An abnormal communication between an artery and a vein. [NIH] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Arthropathy: Any joint disease. [EU]
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Articular: Of or pertaining to a joint. [EU] Artifacts: Any visible result of a procedure which is caused by the procedure itself and not by the entity being analyzed. Common examples include histological structures introduced by tissue processing, radiographic images of structures that are not naturally present in living tissue, and products of chemical reactions that occur during analysis. [NIH] Asbestos: Fibrous incombustible mineral composed of magnesium and calcium silicates with or without other elements. It is relatively inert chemically and used in thermal insulation and fireproofing. Inhalation of dust causes asbestosis and later lung and gastrointestinal neoplasms. [NIH] Asbestosis: A lung disorder caused by constant inhalation of asbestos particles. [NIH] Aseptic: Free from infection or septic material; sterile. [EU] Aspiration: The act of inhaling. [NIH] Aspirin: A drug that reduces pain, fever, inflammation, and blood clotting. Aspirin belongs to the family of drugs called nonsteroidal anti-inflammatory agents. It is also being studied in cancer prevention. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Astringents: Agents, usually topical, that cause the contraction of tissues for the control of bleeding or secretions. [NIH] Astrocytes: The largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the blood brain barrier. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with microglia) respond to injury. Astrocytes have high- affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitter, but their role in signaling (as in many other functions) is not well understood. [NIH] Asymptomatic: Having no signs or symptoms of disease. [NIH] Ataxia: Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharnyx, larnyx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or peripheral nerve diseases. Motor ataxia may be associated with cerebellar diseases; cerebral cortex diseases; thalamic diseases; basal ganglia diseases; injury to the red nucleus; and other conditions. [NIH] Atopic: Pertaining to an atopen or to atopy; allergic. [EU] Atopic Eczema: Generic term for acute or chronic inflammatory conditions of the skin, typically erythematous, edematous, papular, vesicular, and crusting; often accompanied by sensations of itching and burning. [NIH] Atrial: Pertaining to an atrium. [EU] Atrioventricular: Pertaining to an atrium of the heart and to a ventricle. [EU] Atrium: A chamber; used in anatomical nomenclature to designate a chamber affording entrance to another structure or organ. Usually used alone to designate an atrium of the heart. [EU] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH]
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Attenuation: Reduction of transmitted sound energy or its electrical equivalent. [NIH] Atypical: Irregular; not conformable to the type; in microbiology, applied specifically to strains of unusual type. [EU] Auditory: Pertaining to the sense of hearing. [EU] Autacoids: A chemically diverse group of substances produced by various tissues in the body that cause slow contraction of smooth muscle; they have other intense but varied pharmacologic activities. [NIH] Autoantibodies: Antibodies that react with self-antigens (autoantigens) of the organism that produced them. [NIH] Autoantigens: Endogenous tissue constituents that have the ability to interact with autoantibodies and cause an immune response. [NIH] Autodigestion: Autolysis; a condition found in disease of the stomach: the stomach wall is digested by the gastric juice. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autoimmunity: Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by autoimmune diseases. [NIH] Autologous: Taken from an individual's own tissues, cells, or DNA. [NIH] Autonomic: Self-controlling; functionally independent. [EU] Autonomic Nervous System: The enteric, parasympathetic, and sympathetic nervous systems taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the central nervous system, especially the hypothalamus and the solitary nucleus, which receive information relayed from visceral afferents; these and related central and sensory structures are sometimes (but not here) considered to be part of the autonomic nervous system itself. [NIH] Avidity: The strength of the interaction of an antiserum with a multivalent antigen. [NIH] Axonal: Condition associated with metabolic derangement of the entire neuron and is manifest by degeneration of the distal portion of the nerve fiber. [NIH] Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacterial Physiology: Physiological processes and activities of bacteria. [NIH] Bacterial toxin: A toxic substance, made by bacteria, that can be modified to kill specific tumor cells without harming normal cells. [NIH] Bactericidal: Substance lethal to bacteria; substance capable of killing bacteria. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Barbiturate: A drug with sedative and hypnotic effects. Barbiturates have been used as
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sedatives and anesthetics, and they have been used to treat the convulsions associated with epilepsy. [NIH] Basal cell carcinoma: A type of skin cancer that arises from the basal cells, small round cells found in the lower part (or base) of the epidermis, the outer layer of the skin. [NIH] Basal cells: Small, round cells found in the lower part (or base) of the epidermis, the outer layer of the skin. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Basal Ganglia Diseases: Diseases of the basal ganglia including the putamen; globus pallidus; claustrum; amygdala; and caudate nucleus. Dyskinesias (most notably involuntary movements and alterations of the rate of movement) represent the primary clinical manifestations of these disorders. Common etiologies include cerebrovascular disease; neurodegenerative diseases; and craniocerebral trauma. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Base Sequence: The sequence of purines and pyrimidines in nucleic acids and polynucleotides. It is also called nucleotide or nucleoside sequence. [NIH] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its subdivisions is the basal (basement) lamina. [NIH] Basophils: Granular leukocytes characterized by a relatively pale-staining, lobate nucleus and cytoplasm containing coarse dark-staining granules of variable size and stainable by basic dyes. [NIH] Baths: The immersion or washing of the body or any of its parts in water or other medium for cleansing or medical treatment. It includes bathing for personal hygiene as well as for medical purposes with the addition of therapeutic agents, such as alkalines, antiseptics, oil, etc. [NIH] Bed Rest: Confinement of an individual to bed for therapeutic or experimental reasons. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]
Benzoic Acid: A fungistatic compound that is widely used as a food preservative. It is conjugated to glycine in the liver and excreted as hippuric acid. [NIH] Berberine: An alkaloid from Hydrastis canadensis L., Berberidaceae. It is also found in many other plants. It is relatively toxic parenterally, but has been used orally for various parasitic and fungal infections and as antidiarrheal. [NIH] Beta 2-Microglobulin: An 11 kDa protein associated with the outer membrane of many cells including lymphocytes. It is the small subunit of the MHC class I molecule. Association with beta 2-microglobulin is generally required for the transport of class I heavy chains from the endoplasmic reticulum to the cell surface. Beta 2-microglobulin is present in small amounts in serum, csf, and urine of normal people, and to a much greater degree in the urine and plasma of patients with tubular proteinemia, renal failure, or kidney transplants. [NIH] Beta-Thromboglobulin: A platelet-specific protein which is released when platelets aggregate. Elevated plasma levels have been reported after deep venous thrombosis, preeclampsia, myocardial infarction with mural thrombosis, and myeloproliferative disorders.
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Measurement of beta-thromboglobulin in biological fluids by radioimmunoassay is used for the diagnosis and assessment of progress of thromboembolic disorders. [NIH] Bilateral: Affecting both the right and left side of body. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile duct: A tube through which bile passes in and out of the liver. [NIH] Bile Pigments: Pigments that give a characteristic color to bile including: bilirubin, biliverdine, and bilicyanin. [NIH] Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [NIH] Biliary Tract: The gallbladder and its ducts. [NIH] Bilirubin: A bile pigment that is a degradation product of heme. [NIH] Binding Sites: The reactive parts of a macromolecule that directly participate in its specific combination with another molecule. [NIH] Bioavailability: The degree to which a drug or other substance becomes available to the target tissue after administration. [EU] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biogenesis: The origin of life. It includes studies of the potential basis for life in organic compounds but excludes studies of the development of altered forms of life through mutation and natural selection, which is evolution. [NIH] Biological response modifier: BRM. A substance that stimulates the body's response to infection and disease. [NIH] Biological therapy: Treatment to stimulate or restore the ability of the immune system to fight infection and disease. Also used to lessen side effects that may be caused by some cancer treatments. Also known as immunotherapy, biotherapy, or biological response modifier (BRM) therapy. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Biotransformation: The chemical alteration of an exogenous substance by or in a biological system. The alteration may inactivate the compound or it may result in the production of an active metabolite of an inactive parent compound. The alteration may be either nonsynthetic (oxidation-reduction, hydrolysis) or synthetic (glucuronide formation, sulfate conjugation, acetylation, methylation). This also includes metabolic detoxication and clearance. [NIH] Bismuth: A metallic element that has the atomic symbol Bi, atomic number 83 and atomic weight 208.98. [NIH] Bladder: The organ that stores urine. [NIH] Blastocyst: The mammalian embryo in the post-morula stage in which a fluid-filled cavity, enclosed primarily by trophoblast, contains an inner cell mass which becomes the
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embryonic disc. [NIH] Blister: Visible accumulations of fluid within or beneath the epidermis. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Coagulation Factors: Endogenous substances, usually proteins, that are involved in the blood coagulation process. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood Proteins: Proteins that are present in blood serum, including serum albumin, blood coagulation factors, and many other types of proteins. [NIH] Blood Stains: Antigenic characteristics and DNA fingerprint patterns identified from blood stains. Their primary value is in criminal cases. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [NIH]
Body Fluids: Liquid components of living organisms. [NIH] Bone Density: The amount of mineral per square centimeter of bone. This is the definition used in clinical practice. Actual bone density would be expressed in grams per milliliter. It is most frequently measured by photon absorptiometry or x-ray computed tomography. [NIH] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bone Marrow Cells: Cells contained in the bone marrow including fat cells, stromal cells, megakaryocytes, and the immediate precursors of most blood cells. [NIH] Bone Marrow Transplantation: The transference of bone marrow from one human or animal to another. [NIH] Bone Resorption: Bone loss due to osteoclastic activity. [NIH] Boron: A trace element with the atomic symbol B, atomic number 5, and atomic weight 10.81. Boron-10, an isotope of boron, is used as a neutron absorber in boron neutron capture therapy. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Bowel Movement: Body wastes passed through the rectum and anus. [NIH] Brachytherapy: A collective term for interstitial, intracavity, and surface radiotherapy. It uses small sealed or partly-sealed sources that may be placed on or near the body surface or within a natural body cavity or implanted directly into the tissues. [NIH]
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Bradykinin: A nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from mast cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter. [NIH] Brain Stem: The part of the brain that connects the cerebral hemispheres with the spinal cord. It consists of the mesencephalon, pons, and medulla oblongata. [NIH] Branch: Most commonly used for branches of nerves, but applied also to other structures. [NIH]
Breakdown: A physical, metal, or nervous collapse. [NIH] Broadband: A wide frequency range. Sound whose energy is distributed over a broad range of frequency (generally, more than one octave). [NIH] Broad-spectrum: Effective against a wide range of microorganisms; said of an antibiotic. [EU] Bromine: A halogen with the atomic symbol Br, atomic number 36, and atomic weight 79.904. It is a volatile reddish-brown liquid that gives off suffocating vapors, is corrosive to the skin, and may cause severe gastroenteritis if ingested. [NIH] Bronchi: The larger air passages of the lungs arising from the terminal bifurcation of the trachea. [NIH] Bronchial: Pertaining to one or more bronchi. [EU] Bronchioles: The tiny branches of air tubes in the lungs. [NIH] Bronchitis: Inflammation (swelling and reddening) of the bronchi. [NIH] Bronchoconstriction: Diminution of the caliber of a bronchus physiologically or as a result of pharmacological intervention. [NIH] Bronchus: A large air passage that leads from the trachea (windpipe) to the lung. [NIH] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] Buccal mucosa: The inner lining of the cheeks and lips. [NIH] Bullous: Pertaining to or characterized by bullae. [EU] Bupivacaine: A widely used local anesthetic agent. [NIH] Bupropion: A unicyclic, aminoketone antidepressant. The mechanism of its therapeutic actions is not well understood, but it does appear to block dopamine uptake. The hydrochloride is available as an aid to smoking cessation treatment. [NIH] Burns: Injuries to tissues caused by contact with heat, steam, chemicals (burns, chemical), electricity (burns, electric), or the like. [NIH] Burns, Electric: Burns produced by contact with electric current or from a sudden discharge of electricity. [NIH] Caffeine: A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes smooth muscle, stimulates cardiac muscle, stimulates diuresis, and appears to be useful in the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide phosphodiesterases, antagonism of adenosine receptors, and modulation of intracellular calcium handling. [NIH] Calcifediol: The major circulating metabolite of vitamin D3 produced in the liver and the
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best indicator of the body's vitamin D stores. It is effective in the treatment of rickets and osteomalacia, both in azotemic and non-azotemic patients. Calcifediol also has mineralizing properties. [NIH] Calcification: Deposits of calcium in the tissues of the breast. Calcification in the breast can be seen on a mammogram, but cannot be detected by touch. There are two types of breast calcification, macrocalcification and microcalcification. Macrocalcifications are large deposits and are usually not related to cancer. Microcalcifications are specks of calcium that may be found in an area of rapidly dividing cells. Many microcalcifications clustered together may be a sign of cancer. [NIH] Calcineurin: A calcium- and calmodulin-binding protein present in highest concentrations in the central nervous system. Calcineurin is composed of two subunits. A catalytic subunit, calcineurin A, and a regulatory subunit, calcineurin B, with molecular weights of about 60 kD and 19 kD, respectively. Calcineurin has been shown to dephosphorylate a number of phosphoproteins including histones, myosin light chain, and the regulatory subunit of cAMP-dependent protein kinase. It is involved in the regulation of signal transduction and is the target of an important class of immunophilin-immunosuppressive drug complexes in T-lymphocytes that act by inhibiting T-cell activation. EC 3.1.3.-. [NIH] Calcinosis: Pathologic deposition of calcium salts in tissues. [NIH] Calcitonin: A peptide hormone that lowers calcium concentration in the blood. In humans, it is released by thyroid cells and acts to decrease the formation and absorptive activity of osteoclasts. Its role in regulating plasma calcium is much greater in children and in certain diseases than in normal adults. [NIH] Calcitonin Gene-Related Peptide: Calcitonin gene-related peptide. A 37-amino acid peptide derived from the calcitonin gene. It occurs as a result of alternative processing of mRNA from the calcitonin gene. The neuropeptide is widely distributed in neural tissue of the brain, gut, perivascular nerves, and other tissue. The peptide produces multiple biological effects and has both circulatory and neurotransmitter modes of action. In particular, it is a potent endogenous vasodilator. [NIH] Calcitriol: The physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (calcifediol). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calcium channel blocker: A drug used to relax the blood vessel and heart muscle, causing pressure inside blood vessels to drop. It also can regulate heart rhythm. [NIH] Calcium Channel Blockers: A class of drugs that act by selective inhibition of calcium influx through cell membranes or on the release and binding of calcium in intracellular pools. Since they are inducers of vascular and other smooth muscle relaxation, they are used in the drug therapy of hypertension and cerebrovascular spasms, as myocardial protective agents, and in the relaxation of uterine spasms. [NIH] Calcium Chloride: A salt used to replenish calcium levels, as an acid-producing diuretic, and as an antidote for magnesium poisoning. [NIH]
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Calculi: An abnormal concretion occurring mostly in the urinary and biliary tracts, usually composed of mineral salts. Also called stones. [NIH] Calendula: Genus of annuals in the family Asteraceae that contains carotenoids, essential oils (oils, volatile), flavonoids, mucilage, saponins, and sterols. It is used both topically and internally. [NIH] Callus: A callosity or hard, thick skin; the bone-like reparative substance that is formed round the edges and fragments of broken bone. [NIH] Calmodulin: A heat-stable, low-molecular-weight activator protein found mainly in the brain and heart. The binding of calcium ions to this protein allows this protein to bind to cyclic nucleotide phosphodiesterases and to adenyl cyclase with subsequent activation. Thereby this protein modulates cyclic AMP and cyclic GMP levels. [NIH] Camphor: A bicyclic monoterpene ketone found widely in plant (primarily the camphor tree, Cinnamomum camphora). Natural camphor is used topically as a skin antipruritic and as an anti-infective agent. [NIH] Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU] Capsaicin: Cytotoxic alkaloid from various species of Capsicum (pepper, paprika), of the Solanaceae. [NIH] Capsules: Hard or soft soluble containers used for the oral administration of medicine. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carboxy: Cannabinoid. [NIH] Carcinogen: Any substance that causes cancer. [NIH] Carcinogenesis: The process by which normal cells are transformed into cancer cells. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]
Cardiac: Having to do with the heart. [NIH] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular Abnormalities: Congenital structural abnormalities of the cardiovascular system. [NIH] Cardiovascular disease: Any abnormal condition characterized by dysfunction of the heart and blood vessels. CVD includes atherosclerosis (especially coronary heart disease, which can lead to heart attacks), cerebrovascular disease (e.g., stroke), and hypertension (high blood pressure). [NIH] Cardiovascular System: The heart and the blood vessels by which blood is pumped and circulated through the body. [NIH] Carotene: The general name for a group of pigments found in green, yellow, and leafy
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vegetables, and yellow fruits. The pigments are fat-soluble, unsaturated aliphatic hydrocarbons functioning as provitamins and are converted to vitamin A through enzymatic processes in the intestinal wall. [NIH] Carotenoids: Substance found in yellow and orange fruits and vegetables and in dark green, leafy vegetables. May reduce the risk of developing cancer. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Case series: A group or series of case reports involving patients who were given similar treatment. Reports of case series usually contain detailed information about the individual patients. This includes demographic information (for example, age, gender, ethnic origin) and information on diagnosis, treatment, response to treatment, and follow-up after treatment. [NIH] Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group. [NIH] Catabolism: Any destructive metabolic process by which organisms convert substances into excreted compounds. [EU] Catalase: An oxidoreductase that catalyzes the conversion of hydrogen peroxide to water and oxygen. It is present in many animal cells. A deficiency of this enzyme results in acatalasia. EC 1.11.1.6. [NIH] Catecholamine: A group of chemical substances manufactured by the adrenal medulla and secreted during physiological stress. [NIH] Cathode: An electrode, usually an incandescent filament of tungsten, which emits electrons in an X-ray tube. [NIH] Cations: Postively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis. [NIH] Cauda Equina: The lower part of the spinal cord consisting of the lumbar, sacral, and coccygeal nerve roots. [NIH] Causal: Pertaining to a cause; directed against a cause. [EU] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Caustic: An escharotic or corrosive agent. Called also cauterant. [EU] Caveolae: Endocytic/exocytic cell membrane structures rich in glycosphingolipids, cholesterol, and lipid-anchored membrane proteins that function in endocytosis (potocytosis), transcytosis, and signal transduction. Caveolae assume various shapes from open pits to closed vesicles. Caveolar coats are composed of caveolins. [NIH] Caveolins: The main structural proteins of caveolae. Several distinct genes for caveolins have been identified. [NIH] Celiac Disease: A disease characterized by intestinal malabsorption and precipitated by gluten-containing foods. The intestinal mucosa shows loss of villous structure. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Adhesion: Adherence of cells to surfaces or to other cells. [NIH] Cell Aging: The decrease in the cell's ability to proliferate with the passing of time. Each cell
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is programmed for a certain number of cell divisions and at the end of that time proliferation halts. The cell enters a quiescent state after which it experiences cell death via the process of apoptosis. [NIH] Cell Communication: Any of several ways in which living cells of an organism communicate with one another, whether by direct contact between cells or by means of chemical signals carried by neurotransmitter substances, hormones, and cyclic AMP. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell Division: The fission of a cell. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell Membrane Structures: Structures which are part of the cell membrane or have cell membrane as a major part of their structure. [NIH] Cell motility: The ability of a cell to move. [NIH] Cell Movement: The movement of cells from one location to another. [NIH] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Cell Size: The physical dimensions of a cell. It refers mainly to changes in dimensions correlated with physiological or pathological changes in cells. [NIH] Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. [NIH] Cell Transplantation: Transference of cells within an individual, between individuals of the same species, or between individuals of different species. [NIH] Cellular adhesion: The close adherence (bonding) to adjoining cell surfaces. [NIH] Cellulose: A polysaccharide with glucose units linked as in cellobiose. It is the chief constituent of plant fibers, cotton being the purest natural form of the substance. As a raw material, it forms the basis for many derivatives used in chromatography, ion exchange materials, explosives manufacturing, and pharmaceutical preparations. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Central Nervous System Infections: Pathogenic infections of the brain, spinal cord, and meninges. DNA virus infections; RNA virus infections; bacterial infections; mycoplasma infections; Spirochaetales infections; fungal infections; protozoan infections; helminthiasis; and prion diseases may involve the central nervous system as a primary or secondary process. [NIH] Centrifugation: A method of separating organelles or large molecules that relies upon differential sedimentation through a preformed density gradient under the influence of a gravitational field generated in a centrifuge. [NIH]
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Centromere: The clear constricted portion of the chromosome at which the chromatids are joined and by which the chromosome is attached to the spindle during cell division. [NIH] Cerebellar: Pertaining to the cerebellum. [EU] Cerebellum: Part of the metencephalon that lies in the posterior cranial fossa behind the brain stem. It is concerned with the coordination of movement. [NIH] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral Cortex: The thin layer of gray matter on the surface of the cerebral hemisphere that develops from the telencephalon and folds into gyri. It reaches its highest development in man and is responsible for intellectual faculties and higher mental functions. [NIH] Cerebrospinal: Pertaining to the brain and spinal cord. [EU] Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] Cerium: An element of the rare earth family of metals. It has the atomic symbol Ce, atomic number 58, and atomic weight 140.12. Cerium is a malleable metal used in industrial applications. [NIH] Cervix: The lower, narrow end of the uterus that forms a canal between the uterus and vagina. [NIH] Chaperonins: A class of sequence-related molecular chaperones found in bacteria, mitochondria, and plastids. Chaperonins are abundant constitutive proteins that increase in amount after stresses such as heat shock, bacterial infection of macrophages, and an increase in the cellular content of unfolded proteins. Bacterial chaperonins are major immunogens in human bacterial infections because of their accumulation during the stress of infection. Two members of this class of chaperones are chaperonin 10 and chaperonin 60. [NIH] Character: In current usage, approximately equivalent to personality. The sum of the relatively fixed personality traits and habitual modes of response of an individual. [NIH] Chemokines: Class of pro-inflammatory cytokines that have the ability to attract and activate leukocytes. They can be divided into at least three structural branches: C (chemokines, C), CC (chemokines, CC), and CXC (chemokines, CXC), according to variations in a shared cysteine motif. [NIH] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chemotaxis: The movement of cells or organisms toward or away from a substance in response to its concentration gradient. [NIH] Chemotherapeutic agent: A drug used to treat cancer. [NIH] Chemotherapy: Treatment with anticancer drugs. [NIH] Child Development: The continuous sequential physiological and psychological maturing of the child from birth up to but not including adolescence. It includes healthy responses to situations, but does not include growth in stature or size (= growth). [NIH] Chimera: An individual that contains cell populations derived from different zygotes. [NIH]
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Chin: The anatomical frontal portion of the mandible, also known as the mentum, that contains the line of fusion of the two separate halves of the mandible (symphysis menti). This line of fusion divides inferiorly to enclose a triangular area called the mental protuberance. On each side, inferior to the second premolar tooth, is the mental foramen for the passage of blood vessels and a nerve. [NIH] Chlorine: A greenish-yellow, diatomic gas that is a member of the halogen family of elements. It has the atomic symbol Cl, atomic number 17, and atomic weight 70.906. It is a powerful irritant that can cause fatal pulmonary edema. Chlorine is used in manufacturing, as a reagent in synthetic chemistry, for water purification, and in the production of chlorinated lime, which is used in fabric bleaching. [NIH] Chlorophyll: Porphyrin derivatives containing magnesium that act to convert light energy in photosynthetic organisms. [NIH] Chloroquine: The prototypical antimalarial agent with a mechanism that is not well understood. It has also been used to treat rheumatoid arthritis, systemic lupus erythematosus, and in the systemic therapy of amebic liver abscesses. [NIH] Cholangitis: Inflammation of a bile duct. [NIH] Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Cholesterol Esters: Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis. [NIH] Chondrocytes: Polymorphic cells that form cartilage. [NIH] Chorioallantoic membrane: The membrane in hen's eggs that helps chicken embryos get enough oxygen and calcium for development. The calcium comes from the egg shell. [NIH] Chorioretinitis: Inflammation of the choroid in which the sensory retina becomes edematous and opaque. The inflammatory cells and exudate may burst through the sensory retina to cloud the vitreous body. [NIH] Choroid: The thin, highly vascular membrane covering most of the posterior of the eye between the retina and sclera. [NIH] Chromaffin System: The cells of the body which stain with chromium salts. They occur along the sympathetic nerves, in the adrenal gland, and in various other organs. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chromosome Segregation: The orderly segregation of chromosomes during meiosis or mitosis. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic granulocytic leukemia: A slowly progressing disease in which too many white blood cells are made in the bone marrow. Also called chronic myelogenous leukemia or chronic myeloid leukemia. [NIH] Chronic leukemia: A slowly progressing cancer of the blood-forming tissues. [NIH] Chronic myelogenous leukemia: CML. A slowly progressing disease in which too many
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white blood cells are made in the bone marrow. Also called chronic myeloid leukemia or chronic granulocytic leukemia. [NIH] Chronic Obstructive Pulmonary Disease: Collective term for chronic bronchitis and emphysema. [NIH] Chronic renal: Slow and progressive loss of kidney function over several years, often resulting in end-stage renal disease. People with end-stage renal disease need dialysis or transplantation to replace the work of the kidneys. [NIH] Chylomicrons: A class of lipoproteins that carry dietary cholesterol and triglycerides from the small intestines to the tissues. [NIH] Chymotrypsin: A serine endopeptidase secreted by the pancreas as its zymogen, chymotrypsinogen and carried in the pancreatic juice to the duodenum where it is activated by trypsin. It selectively cleaves aromatic amino acids on the carboxyl side. [NIH] Circulatory system: The system that contains the heart and the blood vessels and moves blood throughout the body. This system helps tissues get enough oxygen and nutrients, and it helps them get rid of waste products. The lymph system, which connects with the blood system, is often considered part of the circulatory system. [NIH] Cirrhosis: A type of chronic, progressive liver disease. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Clamp: A u-shaped steel rod used with a pin or wire for skeletal traction in the treatment of certain fractures. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [NIH]
Clinical Protocols: Precise and detailed plans for the study of a medical or biomedical problem and/or plans for a regimen of therapy. [NIH] Clinical study: A research study in which patients receive treatment in a clinic or other medical facility. Reports of clinical studies can contain results for single patients (case reports) or many patients (case series or clinical trials). [NIH] Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Clobetasol: Topical corticosteroid that is absorbed faster than fluocinonide. It is used in psoriasis, but may cause marked adrenocortical suppression. [NIH] Clone: The term "clone" has acquired a new meaning. It is applied specifically to the bits of inserted foreign DNA in the hybrid molecules of the population. Each inserted segment originally resided in the DNA of a complex genome amid millions of other DNA segment. [NIH]
Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA molecules. [NIH] Clot Retraction: Retraction of a clot resulting from contraction of platelet pseudopods attached to fibrin strands that is dependent on the contractile protein thrombosthenin. Used as a measure of platelet function. [NIH] Coagulation: 1. The process of clot formation. 2. In colloid chemistry, the solidification of a sol into a gelatinous mass; an alteration of a disperse phase or of a dissolved solid which
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causes the separation of the system into a liquid phase and an insoluble mass called the clot or curd. Coagulation is usually irreversible. 3. In surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation and photocoagulation. [EU] Coal: A natural fuel formed by partial decomposition of vegetable matter under certain environmental conditions. [NIH] Coal Tar: A by-product of the destructive distillation of coal used as a topical antieczematic. It is an antipruritic and keratoplastic agent used also in the treatment of psoriasis and other skin conditions. Occupational exposure to soots, tars, and certain mineral oils is known to be carcinogenic according to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985) (Merck Index, 11th ed). [NIH] Cod Liver Oil: Oil obtained from fresh livers of the cod family, Gadidae. It is a source of vitamins A and D. [NIH] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Cognition: Intellectual or mental process whereby an organism becomes aware of or obtains knowledge. [NIH] Cognitive Therapy: A direct form of psychotherapy based on the interpretation of situations (cognitive structure of experiences) that determine how an individual feels and behaves. It is based on the premise that cognition, the process of acquiring knowledge and forming beliefs, is a primary determinant of mood and behavior. The therapy uses behavioral and verbal techniques to identify and correct negative thinking that is at the root of the aberrant behavior. [NIH] Colchicine: A major alkaloid from Colchicum autumnale L. and found also in other Colchicum species. Its primary therapeutic use is in the treatment of gout, but it has been used also in the therapy of familial Mediterranean fever (periodic disease). [NIH] Colitis: Inflammation of the colon. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Collagen disease: A term previously used to describe chronic diseases of the connective tissue (e.g., rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis), but now is thought to be more appropriate for diseases associated with defects in collagen, which is a component of the connective tissue. [NIH] Collapse: 1. A state of extreme prostration and depression, with failure of circulation. 2. Abnormal falling in of the walls of any part of organ. [EU] Colloidal: Of the nature of a colloid. [EU] Colon: The long, coiled, tubelike organ that removes water from digested food. The remaining material, solid waste called stool, moves through the colon to the rectum and leaves the body through the anus. [NIH] Colorectal: Having to do with the colon or the rectum. [NIH] Colorectal Cancer: Cancer that occurs in the colon (large intestine) or the rectum (the end of the large intestine). A number of digestive diseases may increase a person's risk of colorectal
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cancer, including polyposis and Zollinger-Ellison Syndrome. [NIH] Combination Therapy: Association of 3 drugs to treat AIDS (AZT + DDC or DDI + protease inhibitor). [NIH] Communicable disease: A disease that can be transmitted by contact between persons. [NIH] Community Health Centers: Facilities which administer the delivery of health care services to people living in a community or neighborhood. [NIH] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complement Activation: The sequential activation of serum components C1 through C9, initiated by an erythrocyte-antibody complex or by microbial polysaccharides and properdin, and producing an inflammatory response. [NIH] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complete remission: The disappearance of all signs of cancer. Also called a complete response. [NIH] Complete response: The disappearance of all signs of cancer in response to treatment. This does not always mean the cancer has been cured. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and
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theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Concomitant: Accompanying; accessory; joined with another. [EU] Cone: One of the special retinal receptor elements which are presumed to be primarily concerned with perception of light and color stimuli when the eye is adapted to light. [NIH] Congestion: Excessive or abnormal accumulation of blood in a part. [EU] Conjugated: Acting or operating as if joined; simultaneous. [EU] Conjugation: 1. The act of joining together or the state of being conjugated. 2. A sexual process seen in bacteria, ciliate protozoa, and certain fungi in which nuclear material is exchanged during the temporary fusion of two cells (conjugants). In bacterial genetics a form of sexual reproduction in which a donor bacterium (male) contributes some, or all, of its DNA (in the form of a replicated set) to a recipient (female) which then incorporates differing genetic information into its own chromosome by recombination and passes the recombined set on to its progeny by replication. In ciliate protozoa, two conjugants of separate mating types exchange micronuclear material and then separate, each now being a fertilized cell. In certain fungi, the process involves fusion of two gametes, resulting in union of their nuclei and formation of a zygote. 3. In chemistry, the joining together of two compounds to produce another compound, such as the combination of a toxic product with some substance in the body to form a detoxified product, which is then eliminated. [EU] Conjunctiva: The mucous membrane that lines the inner surface of the eyelids and the anterior part of the sclera. [NIH] Conjunctivitis: Inflammation of the conjunctiva, generally consisting of conjunctival hyperaemia associated with a discharge. [EU] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue Cells: A group of cells that includes fibroblasts, cartilage cells, adipocytes, smooth muscle cells, and bone cells. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Constipation: Infrequent or difficult evacuation of feces. [NIH] Constitutional: 1. Affecting the whole constitution of the body; not local. 2. Pertaining to the constitution. [EU] Constriction: The act of constricting. [NIH] Constriction, Pathologic: The condition of an anatomical structure's being constricted beyond normal dimensions. [NIH] Consultation: A deliberation between two or more physicians concerning the diagnosis and the proper method of treatment in a case. [NIH] Consumption: Pulmonary tuberculosis. [NIH] Contact dermatitis: Inflammation of the skin with varying degrees of erythema, edema and vesinculation resulting from cutaneous contact with a foreign substance or other exposure. [NIH]
Contraception: Use of agents, devices, methods, or procedures which diminish the
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likelihood of or prevent conception. [NIH] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Contrast Media: Substances used in radiography that allow visualization of certain tissues. [NIH]
Controlled clinical trial: A clinical study that includes a comparison (control) group. The comparison group receives a placebo, another treatment, or no treatment at all. [NIH] Controlled study: An experiment or clinical trial that includes a comparison (control) group. [NIH]
Conventional therapy: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional treatment. [NIH] Conventional treatment: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional therapy. [NIH] Convulsions: A general term referring to sudden and often violent motor activity of cerebral or brainstem origin. Convulsions may also occur in the absence of an electrical cerebral discharge (e.g., in response to hypotension). [NIH] Coordination: Muscular or motor regulation or the harmonious cooperation of muscles or groups of muscles, in a complex action or series of actions. [NIH] Cor: The muscular organ that maintains the circulation of the blood. c. adiposum a heart that has undergone fatty degeneration or that has an accumulation of fat around it; called also fat or fatty, heart. c. arteriosum the left side of the heart, so called because it contains oxygenated (arterial) blood. c. biloculare a congenital anomaly characterized by failure of formation of the atrial and ventricular septums, the heart having only two chambers, a single atrium and a single ventricle, and a common atrioventricular valve. c. bovinum (L. 'ox heart') a greatly enlarged heart due to a hypertrophied left ventricle; called also c. taurinum and bucardia. c. dextrum (L. 'right heart') the right atrium and ventricle. c. hirsutum, c. villosum. c. mobile (obs.) an abnormally movable heart. c. pendulum a heart so movable that it seems to be hanging by the great blood vessels. c. pseudotriloculare biatriatum a congenital cardiac anomaly in which the heart functions as a three-chambered heart because of tricuspid atresia, the right ventricle being extremely small or rudimentary and the right atrium greatly dilated. Blood passes from the right to the left atrium and thence disease due to pulmonary hypertension secondary to disease of the lung, or its blood vessels, with hypertrophy of the right ventricle. [EU] Coreceptors: Invariant receptor of the helper T-cells. [NIH] Cornea: The transparent part of the eye that covers the iris and the pupil and allows light to enter the inside. [NIH] Corneum: The superficial layer of the epidermis containing keratinized cells. [NIH] Coronary: Encircling in the manner of a crown; a term applied to vessels; nerves, ligaments, etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH]
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Corpus: The body of the uterus. [NIH] Corpus Luteum: The yellow glandular mass formed in the ovary by an ovarian follicle that has ruptured and discharged its ovum. [NIH] Corpuscle: A small mass or body; a sensory nerve end bulb; a cell, especially that of the blood or the lymph. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Corticosteroid: Any of the steroids elaborated by the adrenal cortex (excluding the sex hormones of adrenal origin) in response to the release of corticotrophin (adrenocorticotropic hormone) by the pituitary gland, to any of the synthetic equivalents of these steroids, or to angiotensin II. They are divided, according to their predominant biological activity, into three major groups: glucocorticoids, chiefly influencing carbohydrate, fat, and protein metabolism; mineralocorticoids, affecting the regulation of electrolyte and water balance; and C19 androgens. Some corticosteroids exhibit both types of activity in varying degrees, and others exert only one type of effect. The corticosteroids are used clinically for hormonal replacement therapy, for suppression of ACTH secretion by the anterior pituitary, as antineoplastic, antiallergic, and anti-inflammatory agents, and to suppress the immune response. Called also adrenocortical hormone and corticoid. [EU] Cortisone: A natural steroid hormone produced in the adrenal gland. It can also be made in the laboratory. Cortisone reduces swelling and can suppress immune responses. [NIH] Cowpox: A mild, eruptive skin disease of milk cows caused by cowpox virus, with lesions occurring principally on the udder and teats. Human infection may occur while milking an infected animal. [NIH] Cowpox Virus: A species of orthopoxvirus that is the etiologic agent of cowpox. It is closely related to but antigenically different from vaccina virus. [NIH] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Craniocerebral Trauma: Traumatic injuries involving the cranium and intracranial structures (i.e., brain; cranial nerves; meninges; and other structures). Injuries may be classified by whether or not the skull is penetrated (i.e., penetrating vs. nonpenetrating) or whether there is an associated hemorrhage. [NIH] Criterion: A standard by which something may be judged. [EU] Crossing-over: The exchange of corresponding segments between chromatids of homologous chromosomes during meiosia, forming a chiasma. [NIH] CSF: Cerebrospinal fluid. The fluid flowing around the brain and spinal cord. CSF is produced in the ventricles of the brain. [NIH] Culture Media: Any liquid or solid preparation made specifically for the growth, storage, or transport of microorganisms or other types of cells. The variety of media that exist allow for the culturing of specific microorganisms and cell types, such as differential media, selective media, test media, and defined media. Solid media consist of liquid media that have been solidified with an agent such as agar or gelatin. [NIH] Cultured cells: Animal or human cells that are grown in the laboratory. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Curcumin: A dye obtained from tumeric, the powdered root of Curcuma longa Linn. It is used in the preparation of curcuma paper and the detection of boron. Curcumin appears to
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possess a spectrum of pharmacological properties, due primarily to its inhibitory effects on metabolic enzymes. [NIH] Curettage: Removal of tissue with a curette, a spoon-shaped instrument with a sharp edge. [NIH]
Curette: A spoon-shaped instrument with a sharp edge. [NIH] Cutaneous: Having to do with the skin. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cyclin: Molecule that regulates the cell cycle. [NIH] Cyclosporine: A drug used to help reduce the risk of rejection of organ and bone marrow transplants by the body. It is also used in clinical trials to make cancer cells more sensitive to anticancer drugs. [NIH] Cyst: A sac or capsule filled with fluid. [NIH] Cysteinyl: Enzyme released by the cell at a crucial stage in apoptosis in order to shred all cellular proteins. [NIH] Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, . New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytokinesis: Division of the rest of cell. [NIH] Cytomegalovirus: A genus of the family Herpesviridae, subfamily Betaherpesvirinae, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytosine: A pyrimidine base that is a fundamental unit of nucleic acids. [NIH] Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytostatic: An agent that suppresses cell growth and multiplication. [EU] Cytotoxic: Cell-killing. [NIH] Daclizumab: A monoclonal antibody that is being studied for treatment of adult T-cell leukemia. Also called dacliximab. Monoclonal antibodies are laboratory-produced substances that can locate and bind to cancer cells. [NIH] Day Care: Institutional health care of patients during the day. The patients return home at night. [NIH]
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Deamination: The removal of an amino group (NH2) from a chemical compound. [NIH] Decarboxylation: The removal of a carboxyl group, usually in the form of carbon dioxide, from a chemical compound. [NIH] Decidua: The epithelial lining of the endometrium that is formed before the fertilized ovum reaches the uterus. The fertilized ovum embeds in the decidua. If the ovum is not fertilized, the decidua is shed during menstruation. [NIH] Defense Mechanisms: Unconscious process used by an individual or a group of individuals in order to cope with impulses, feelings or ideas which are not acceptable at their conscious level; various types include reaction formation, projection and self reversal. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Delivery of Health Care: The concept concerned with all aspects of providing and distributing health services to a patient population. [NIH] Dementia: An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness. [NIH] Denaturation: Rupture of the hydrogen bonds by heating a DNA solution and then cooling it rapidly causes the two complementary strands to separate. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Dendritic: 1. Branched like a tree. 2. Pertaining to or possessing dendrites. [EU] Dendritic cell: A special type of antigen-presenting cell (APC) that activates T lymphocytes. [NIH]
Denileukin diftitox: A substance used to treat cutaneous T-cell lymphoma when other treatments have not worked. [NIH] Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Deoxyguanosine: A nucleoside consisting of the base guanine and the sugar deoxyribose. [NIH]
Depigmentation: Removal or loss of pigment, especially melanin. [EU] Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Depressive Disorder: An affective disorder manifested by either a dysphoric mood or loss of interest or pleasure in usual activities. The mood disturbance is prominent and relatively persistent. [NIH] Dermal: Pertaining to or coming from the skin. [NIH] Dermatitis: Any inflammation of the skin. [NIH] Dermatitis, Allergic Contact: A contact dermatitis due to allergic sensitization to various substances. These substances subsequently produce inflammatory reactions in the skin of those who have acquired hypersensitivity to them as a result of prior exposure. [NIH] Dermatitis, Contact: A type of acute or chronic skin reaction in which sensitivity is
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manifested by reactivity to materials or substances coming in contact with the skin. It may involve allergic or non-allergic mechanisms. [NIH] Dermatitis, Irritant: A non-allergic contact dermatitis caused by prolonged exposure to irritants and not explained by delayed hypersensitivity mechanisms. [NIH] Dermatologist: A doctor who specializes in the diagnosis and treatment of skin problems. [NIH]
Dermatology: A medical specialty concerned with the skin, its structure, functions, diseases, and treatment. [NIH] Dermatosis: Any skin disease, especially one not characterized by inflammation. [EU] Dermis: A layer of vascular connective tissue underneath the epidermis. The surface of the dermis contains sensitive papillae. Embedded in or beneath the dermis are sweat glands, hair follicles, and sebaceous glands. [NIH] DES: Diethylstilbestrol. A synthetic hormone that was prescribed from the early 1940s until 1971 to help women with complications of pregnancy. DES has been linked to an increased risk of clear cell carcinoma of the vagina in daughters of women who used DES. DES may also increase the risk of breast cancer in women who used DES. [NIH] Desensitization: The prevention or reduction of immediate hypersensitivity reactions by administration of graded doses of allergen; called also hyposensitization and immunotherapy. [EU] Desiccation: Removal of moisture from a substance (chemical, food, tissue, etc.). [NIH] Desquamation: The shedding of epithelial elements, chiefly of the skin, in scales or small sheets; exfoliation. [EU] Detergents: Purifying or cleansing agents, usually salts of long-chain aliphatic bases or acids, that exert cleansing (oil-dissolving) and antimicrobial effects through a surface action that depends on possessing both hydrophilic and hydrophobic properties. [NIH] Detoxification: Treatment designed to free an addict from his drug habit. [EU] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diabetic Retinopathy: Retinopathy associated with diabetes mellitus, which may be of the background type, progressively characterized by microaneurysms, interretinal punctuate macular edema, or of the proliferative type, characterized by neovascularization of the retina and optic disk, which may project into the vitreous, proliferation of fibrous tissue, vitreous hemorrhage, and retinal detachment. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diarrhoea: Abnormal frequency and liquidity of faecal discharges. [EU] Diastolic: Of or pertaining to the diastole. [EU] Dideoxynucleosides: Nucleosides that have two hydroxy groups removed from the sugar moiety. The majority of these compounds have broad-spectrum antiretroviral activity due to their action as antimetabolites. The nucleosides are phosphorylated intracellularly to their 5'triphosphates and act as chain-terminating inhibitors of viral reverse transcription. [NIH] Diflucortolone: A topical glucocorticoid used in various dermatoses. It is absorbed through the skin, bound to plasma albumin, and may cause adrenal suppression. It is also administered as the valerate. [NIH]
Dictionary 455
Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digestive system: The organs that take in food and turn it into products that the body can use to stay healthy. Waste products the body cannot use leave the body through bowel movements. The digestive system includes the salivary glands, mouth, esophagus, stomach, liver, pancreas, gallbladder, small and large intestines, and rectum. [NIH] Digestive tract: The organs through which food passes when food is eaten. These organs are the mouth, esophagus, stomach, small and large intestines, and rectum. [NIH] Digital photography: A type of photography in which images can be viewed on a computer screen. [NIH] Dihydrotestosterone: Anabolic agent. [NIH] Dihydroxy: AMPA/Kainate antagonist. [NIH] Dilatation: The act of dilating. [NIH] Dilation: A process by which the pupil is temporarily enlarged with special eye drops (mydriatic); allows the eye care specialist to better view the inside of the eye. [NIH] Diltiazem: A benzothiazepine derivative with vasodilating action due to its antagonism of the actions of the calcium ion in membrane functions. It is also teratogenic. [NIH] Diploid: Having two sets of chromosomes. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Discoid: Shaped like a disk. [EU] Discrete: Made up of separate parts or characterized by lesions which do not become blended; not running together; separate. [NIH] Disinfectant: An agent that disinfects; applied particularly to agents used on inanimate objects. [EU] Disposition: A tendency either physical or mental toward certain diseases. [EU] Dissection: Cutting up of an organism for study. [NIH] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Dizziness: An imprecise term which may refer to a sense of spatial disorientation, motion of the environment, or lightheadedness. [NIH] Domesticated: Species in which the evolutionary process has been influenced by humans to meet their needs. [NIH] Dominance: In genetics, the full phenotypic expression of a gene in both heterozygotes and homozygotes. [EU] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate
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precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Dorsal: 1. Pertaining to the back or to any dorsum. 2. Denoting a position more toward the back surface than some other object of reference; same as posterior in human anatomy; superior in the anatomy of quadrupeds. [EU] Dosage Forms: Completed forms of the pharmaceutical preparation in which prescribed doses of medication are included. They are designed to resist action by gastric fluids, prevent vomiting and nausea, reduce or alleviate the undesirable taste and smells associated with oral administration, achieve a high concentration of drug at target site, or produce a delayed or long-acting drug effect. They include capsules, liniments, ointments, pharmaceutical solutions, powders, tablets, etc. [NIH] Double-blind: Pertaining to a clinical trial or other experiment in which neither the subject nor the person administering treatment knows which treatment any particular subject is receiving. [EU] Double-blinded: A clinical trial in which neither the medical staff nor the person knows which of several possible therapies the person is receiving. [NIH] Doxycycline: A synthetic tetracycline derivative with a range of antimicrobial activity and mode of action similar to that of tetracycline, but more effective against many species. Animal studies suggest that it may cause less tooth staining than other tetracyclines. [NIH] Drive: A state of internal activity of an organism that is a necessary condition before a given stimulus will elicit a class of responses; e.g., a certain level of hunger (drive) must be present before food will elicit an eating response. [NIH] Dross: Residue remaining in an opium pipe which has been smoked; contains 50 % of the morphine present in the original drug. [NIH] Drug Approval: Process that is gone through in order for a drug to receive approval by a government regulatory agency. This includes any required pre-clinical or clinical testing, review, submission, and evaluation of the applications and test results, and post-marketing surveillance of the drug. [NIH] Drug Design: The molecular designing of drugs for specific purposes (such as DNAbinding, enzyme inhibition, anti-cancer efficacy, etc.) based on knowledge of molecular properties such as activity of functional groups, molecular geometry, and electronic structure, and also on information cataloged on analogous molecules. Drug design is generally computer-assisted molecular modeling and does not include pharmacokinetics, dosage analysis, or drug administration analysis. [NIH] Drug Eruptions: Adverse cutaneous reactions caused by ingestion, parenteral use, or local application of a drug. These may assume various morphologic patterns and produce various types of lesions. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH] Duct: A tube through which body fluids pass. [NIH] Duodenum: The first part of the small intestine. [NIH]
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Dura mater: The outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain and spinal cord; called also pachymeninx. [EU] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [NIH] Dyspnea: Difficult or labored breathing. [NIH] Dyspnoea: Difficult or laboured breathing. [EU] Dystrophy: Any disorder arising from defective or faulty nutrition, especially the muscular dystrophies. [EU] Eclampsia: Onset of convulsions or coma in a previously diagnosed pre-eclamptic patient. [NIH]
Ectopic: Pertaining to or characterized by ectopia. [EU] Eczema: A pruritic papulovesicular dermatitis occurring as a reaction to many endogenous and exogenous agents (Dorland, 27th ed). [NIH] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Effector cell: A cell that performs a specific function in response to a stimulus; usually used to describe cells in the immune system. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Eicosanoids: A class of oxygenated, endogenous, unsaturated fatty acids derived from arachidonic acid. They include prostaglandins, leukotrienes, thromboxanes, and hydroxyeicosatetraenoic acid compounds (HETE). They are hormone-like substances that act near the site of synthesis without altering functions throughout the body. [NIH] Elastic: Susceptible of resisting and recovering from stretching, compression or distortion applied by a force. [EU] Elasticity: Resistance and recovery from distortion of shape. [NIH] Elastin: The protein that gives flexibility to tissues. [NIH] Elective: Subject to the choice or decision of the patient or physician; applied to procedures that are advantageous to the patient but not urgent. [EU] Electrocardiogram: Measurement of electrical activity during heartbeats. [NIH] Electrocoagulation: Electrosurgical procedures used to treat hemorrhage (e.g., bleeding ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. [NIH] Electrode: Component of the pacing system which is at the distal end of the lead. It is the interface with living cardiac tissue across which the stimulus is transmitted. [NIH] Electrodesiccation: The drying of tissue by a high-frequency electric current applied with a needle-shaped electrode. [NIH] Electrolysis: Destruction by passage of a galvanic electric current, as in disintegration of a chemical compound in solution. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electrophoresis: An electrochemical process in which macromolecules or colloidal particles with a net electric charge migrate in a solution under the influence of an electric current. [NIH]
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Emaciation: Clinical manifestation of excessive leanness usually caused by disease or a lack of nutrition. [NIH] Embolus: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Embryogenesis: The process of embryo or embryoid formation, whether by sexual (zygotic) or asexual means. In asexual embryogenesis embryoids arise directly from the explant or on intermediary callus tissue. In some cases they arise from individual cells (somatic cell embryoge). [NIH] Emollient: Softening or soothing; called also malactic. [EU] Emphysema: A pathological accumulation of air in tissues or organs. [NIH] Empiric: Empirical; depending upon experience or observation alone, without using scientific method or theory. [EU] Emulsion: A preparation of one liquid distributed in small globules throughout the body of a second liquid. The dispersed liquid is the discontinuous phase, and the dispersion medium is the continuous phase. When oil is the dispersed liquid and an aqueous solution is the continuous phase, it is known as an oil-in-water emulsion, whereas when water or aqueous solution is the dispersed phase and oil or oleaginous substance is the continuous phase, it is known as a water-in-oil emulsion. Pharmaceutical emulsions for which official standards have been promulgated include cod liver oil emulsion, cod liver oil emulsion with malt, liquid petrolatum emulsion, and phenolphthalein in liquid petrolatum emulsion. [EU] Enamel: A very hard whitish substance which covers the dentine of the anatomical crown of a tooth. [NIH] Encapsulated: Confined to a specific, localized area and surrounded by a thin layer of tissue. [NIH]
Encephalitis: Inflammation of the brain due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see encephalitis, viral) are a relatively frequent cause of this condition. [NIH] Encephalomyelitis: A general term indicating inflammation of the brain and spinal cord, often used to indicate an infectious process, but also applicable to a variety of autoimmune and toxic-metabolic conditions. There is significant overlap regarding the usage of this term and encephalitis in the literature. [NIH] Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] Endocrine Glands: Ductless glands that secrete substances which are released directly into the circulation and which influence metabolism and other body functions. [NIH] Endocrine System: The system of glands that release their secretions (hormones) directly into the circulatory system. In addition to the endocrine glands, included are the chromaffin system and the neurosecretory systems. [NIH] Endocytosis: Cellular uptake of extracellular materials within membrane-limited vacuoles or microvesicles. Endosomes play a central role in endocytosis. [NIH] Endoderm: The inner of the three germ layers of the embryo. [NIH] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH]
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Endometrial: Having to do with the endometrium (the layer of tissue that lines the uterus). [NIH]
Endometrium: The layer of tissue that lines the uterus. [NIH] Endopeptidases: A subclass of peptide hydrolases. They are classified primarily by their catalytic mechanism. Specificity is used only for identification of individual enzymes. They comprise the serine endopeptidases, EC 3.4.21; cysteine endopeptidases, EC 3.4.22; aspartic endopeptidases, EC 3.4.23, metalloendopeptidases, EC 3.4.24; and a group of enzymes yet to be assigned to any of the above sub-classes, EC 3.4.99. EC 3.4.-. [NIH] Endostatin: A drug that is being studied for its ability to prevent the growth of new blood vessels into a solid tumor. Endostatin belongs to the family of drugs called angiogenesis inhibitors. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium, Lymphatic: Unbroken cellular lining (intima) of the lymph vessels (e.g., the high endothelial lymphatic venules). It is more permeable than vascular endothelium, lacking selective absorption and functioning mainly to remove plasma proteins that have filtered through the capillaries into the tissue spaces. [NIH] Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components from interstitium to lumen; this function has been most intensively studied in the blood capillaries. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxin: Toxin from cell walls of bacteria. [NIH] End-stage renal: Total chronic kidney failure. When the kidneys fail, the body retains fluid and harmful wastes build up. A person with ESRD needs treatment to replace the work of the failed kidneys. [NIH] Enhancer: Transcriptional element in the virus genome. [NIH] Enteropeptidase: A specialized proteolytic enzyme secreted by intestinal cells. It converts trypsinogen into its active form trypsin by removing the N-terminal peptide. EC 3.4.21.9. [NIH]
Environmental Exposure: The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]
Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Eosinophil: A polymorphonuclear leucocyte with large eosinophilic granules in its cytoplasm, which plays a role in hypersensitivity reactions. [NIH] Eosinophilia: Abnormal increase in eosinophils in the blood, tissues or organs. [NIH] Eosinophilic: A condition found primarily in grinding workers caused by a reaction of the pulmonary tissue, in particular the eosinophilic cells, to dust that has entered the lung. [NIH]
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Epidemic: Occurring suddenly in numbers clearly in excess of normal expectancy; said especially of infectious diseases but applied also to any disease, injury, or other healthrelated event occurring in such outbreaks. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU] Epidermal Growth Factor: A 6 kD polypeptide growth factor initially discovered in mouse submaxillary glands. Human epidermal growth factor was originally isolated from urine based on its ability to inhibit gastric secretion and called urogastrone. epidermal growth factor exerts a wide variety of biological effects including the promotion of proliferation and differentiation of mesenchymal and epithelial cells. [NIH] Epidermal growth factor receptor: EGFR. The protein found on the surface of some cells and to which epidermal growth factor binds, causing the cells to divide. It is found at abnormally high levels on the surface of many types of cancer cells, so these cells may divide excessively in the presence of epidermal growth factor. Also known as ErbB1 or HER1. [NIH] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epidermoid carcinoma: A type of cancer in which the cells are flat and look like fish scales. Also called squamous cell carcinoma. [NIH] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epistasis: The degree of dominance exerted by one gene on the expression of a non-allelic gene. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Epitope: A molecule or portion of a molecule capable of binding to the combining site of an antibody. For every given antigenic determinant, the body can construct a variety of antibody-combining sites, some of which fit almost perfectly, and others which barely fit. [NIH]
Erythema: Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes. [NIH] Erythrocyte Membrane: The semipermeable outer portion of the red corpuscle. It is known as a 'ghost' after hemolysis. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Erythromycin: A bacteriostatic antibiotic substance produced by Streptomyces erythreus. Erythromycin A is considered its major active component. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins. [NIH]
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Escalation: Progressive use of more harmful drugs. [NIH] Esophagitis: Inflammation, acute or chronic, of the esophagus caused by bacteria, chemicals, or trauma. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]
Essential Tremor: A rhythmic, involuntary, purposeless, oscillating movement resulting from the alternate contraction and relaxation of opposing groups of muscles. [NIH] Ethanol: A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. [NIH] Ether: One of a class of organic compounds in which any two organic radicals are attached directly to a single oxygen atom. [NIH] Ethylene Glycol: A colorless, odorless, viscous dihydroxy alcohol. It has a sweet taste, but is poisonous if ingested. Ethylene glycol is the most important glycol commercially available and is manufactured on a large scale in the United States. It is used as an antifreeze and coolant, in hydraulic fluids, and in the manufacture of low-freezing dynamites and resins. [NIH]
Etretinate: An oral retinoid used in the treatment of keratotic genodermatosis, lichen planus, and psoriasis. Beneficial effects have also been claimed in the prophylaxis of epithelial neoplasia. The compound may be teratogenic. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Evoke: The electric response recorded from the cerebral cortex after stimulation of a peripheral sense organ. [NIH] Evoked Potentials: The electric response evoked in the central nervous system by stimulation of sensory receptors or some point on the sensory pathway leading from the receptor to the cortex. The evoked stimulus can be auditory, somatosensory, or visual, although other modalities have been reported. Event-related potentials is sometimes used synonymously with evoked potentials but is often associated with the execution of a motor, cognitive, or psychophysiological task, as well as with the response to a stimulus. [NIH] Excimer laser: An ultraviolet laser used in refractive surgery to remove corneal tissue. [NIH] Excipient: Any more or less inert substance added to a prescription in order to confer a suitable consistency or form to the drug; a vehicle. [EU] Excisional: The surgical procedure of removing a tumor by cutting it out. The biopsy is then examined under a microscope. [NIH] Excitability: Property of a cardiac cell whereby, when the cell is depolarized to a critical level (called threshold), the membrane becomes permeable and a regenerative inward current causes an action potential. [NIH] Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] Excrete: To get rid of waste from the body. [NIH] Exfoliation: A falling off in scales or layers. [EU] Exocrine: Secreting outwardly, via a duct. [EU] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Exon: The part of the DNA that encodes the information for the actual amino acid sequence
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of the protein. In many eucaryotic genes, the coding sequences consist of a series of exons alternating with intron sequences. [NIH] Expectorant: 1. Promoting the ejection, by spitting, of mucus or other fluids from the lungs and trachea. 2. An agent that promotes the ejection of mucus or exudate from the lungs, bronchi, and trachea; sometimes extended to all remedies that quiet cough (antitussives). [EU]
Extender: Any of several colloidal substances of high molecular weight, used as a blood or plasma substitute in transfusion for increasing the volume of the circulating blood. [NIH] Extensor: A muscle whose contraction tends to straighten a limb; the antagonist of a flexor. [NIH]
External-beam radiation: Radiation therapy that uses a machine to aim high-energy rays at the cancer. Also called external radiation. [NIH] Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extracellular Matrix Proteins: Macromolecular organic compounds that contain carbon, hydrogen, oxygen, nitrogen, and usually, sulfur. These macromolecules (proteins) form an intricate meshwork in which cells are embedded to construct tissues. Variations in the relative types of macromolecules and their organization determine the type of extracellular matrix, each adapted to the functional requirements of the tissue. The two main classes of macromolecules that form the extracellular matrix are: glycosaminoglycans, usually linked to proteins (proteoglycans), and fibrous proteins (e.g., collagen, elastin, fibronectins and laminin). [NIH] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extravasation: A discharge or escape, as of blood, from a vessel into the tissues. [EU] Extravascular: Situated or occurring outside a vessel or the vessels. [EU] Extremity: A limb; an arm or leg (membrum); sometimes applied specifically to a hand or foot. [EU] Facial: Of or pertaining to the face. [EU] Fallopian tube: The oviduct, a muscular tube about 10 cm long, lying in the upper border of the broad ligament. [NIH] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fasciitis: Inflammation of the fascia. There are three major types: 1) Eosinophilic fasciitis, an inflammatory reaction with eosinophilia, producing hard thickened skin with an orangepeel configuration suggestive of scleroderma and considered by some a variant of scleroderma; 2) Necrotizing fasciitis, a serious fulminating infection (usually by a beta hemolytic Streptococcus) causing extensive necrosis of superficial fascia; 3) Nodular/Pseudosarcomatous/Proliferative fasciitis, characterized by a rapid growth of fibroblasts with mononuclear inflammatory cells and proliferating capillaries in soft tissue, often the forearm; it is not malignant but is sometimes mistaken for fibrosarcoma. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli.
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[NIH]
Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Femoral: Pertaining to the femur, or to the thigh. [EU] Femur: The longest and largest bone of the skeleton, it is situated between the hip and the knee. [NIH] Fertilizers: Substances or mixtures that are added to the soil to supply nutrients or to make available nutrients already present in the soil, in order to increase plant growth and productivity. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrin: A protein derived from fibrinogen in the presence of thrombin, which forms part of the blood clot. [NIH] Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three nonidentical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products. [NIH] Fibroblast Growth Factor: Peptide isolated from the pituitary gland and from the brain. It is a potent mitogen which stimulates growth of a variety of mesodermal cells including chondrocytes, granulosa, and endothelial cells. The peptide may be active in wound healing and animal limb regeneration. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibrosarcoma: A type of soft tissue sarcoma that begins in fibrous tissue, which holds bones, muscles, and other organs in place. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Fine-needle aspiration: The removal of tissue or fluid with a needle for examination under a microscope. Also called needle biopsy. [NIH] Fish Oils: Oils high in unsaturated fats extracted from the bodies of fish or fish parts, especially the livers. Those from the liver are usually high in vitamin A. The oils are used as dietary supplements, in soaps and detergents, as protective coatings, and as a base for other food products such as vegetable shortenings. [NIH] Fistula: Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body. [NIH] Fixation: 1. The act or operation of holding, suturing, or fastening in a fixed position. 2. The condition of being held in a fixed position. 3. In psychiatry, a term with two related but distinct meanings : (1) arrest of development at a particular stage, which like regression (return to an earlier stage), if temporary is a normal reaction to setbacks and difficulties but if protracted or frequent is a cause of developmental failures and emotional problems, and (2) a close and suffocating attachment to another person, especially a childhood figure, such as one's mother or father. Both meanings are derived from psychoanalytic theory and refer to 'fixation' of libidinal energy either in a specific erogenous zone, hence fixation at the oral, anal, or phallic stage, or in a specific object, hence mother or father fixation. 4. The use of a fixative (q.v.) to preserve histological or cytological specimens. 5. In chemistry, the process whereby a substance is removed from the gaseous or solution phase and localized, as in carbon dioxide fixation or nitrogen fixation. 6. In ophthalmology, direction of the gaze so
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that the visual image of the object falls on the fovea centralis. 7. In film processing, the chemical removal of all undeveloped salts of the film emulsion, leaving only the developed silver to form a permanent image. [EU] Flexor: Muscles which flex a joint. [NIH] Flow Cytometry: Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake. [NIH] Fludarabine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH]
Fluocinonide: A topical glucocorticoid used in the treatment of eczemas. [NIH] Fluorescence: The property of emitting radiation while being irradiated. The radiation emitted is usually of longer wavelength than that incident or absorbed, e.g., a substance can be irradiated with invisible radiation and emit visible light. X-ray fluorescence is used in diagnosis. [NIH] Fluorescent Dyes: Dyes that emit light when exposed to light. The wave length of the emitted light is usually longer than that of the incident light. Fluorochromes are substances that cause fluorescence in other substances, i.e., dyes used to mark or label other compounds with fluorescent tags. They are used as markers in biochemistry and immunology. [NIH] Fluorouracil: A pyrimidine analog that acts as an antineoplastic antimetabolite and also has immunosuppressant. It interferes with DNA synthesis by blocking the thymidylate synthetase conversion of deoxyuridylic acid to thymidylic acid. [NIH] Folate: A B-complex vitamin that is being studied as a cancer prevention agent. Also called folic acid. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Folic Acid: N-(4-(((2-Amino-1,4-dihydro-4-oxo-6-pteridinyl)methyl)amino)benzoyl)-Lglutamic acid. A member of the vitamin B family that stimulates the hematopoietic system. It is present in the liver and kidney and is found in mushrooms, spinach, yeast, green leaves, and grasses. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. [NIH] Folliculitis: Inflammation of follicles, primarily hair follicles. [NIH] Foramen: A natural hole of perforation, especially one in a bone. [NIH] Forearm: The part between the elbow and the wrist. [NIH] Fossa: A cavity, depression, or pit. [NIH] Fovea: The central part of the macula that provides the sharpest vision. [NIH] Fractionation: Dividing the total dose of radiation therapy into several smaller, equal doses delivered over a period of several days. [NIH] Frameshift: A type of mutation which causes out-of-phase transcription of the base sequence; such mutations arise from the addition or delection of nucleotide(s) in numbers other than 3 or multiples of 3. [NIH] Frameshift Mutation: A type of mutation in which a number of nucleotides not divisible by
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three is deleted from or inserted into a coding sequence, thereby causing an alteration in the reading frame of the entire sequence downstream of the mutation. These mutations may be induced by certain types of mutagens or may occur spontaneously. [NIH] Free Radicals: Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated. [NIH] Fucose: Deoxysugar. [NIH] Fucosyltransferases: Enzymes catalyzing the transfer of fucose from a nucleoside diphosphate fucose to an acceptor molecule which is frequently another carbohydrate, a glycoprotein, or a glycolipid molecule. Elevated activity of some fucosyltransferases in human serum may serve as an indicator of malignancy. The class includes EC 2.4.1.65; EC 2.4.1.68; EC 2.4.1.69; EC 2.4.1.89. [NIH] Fungi: A kingdom of eukaryotic, heterotrophic organisms that live as saprobes or parasites, including mushrooms, yeasts, smuts, molds, etc. They reproduce either sexually or asexually, and have life cycles that range from simple to complex. Filamentous fungi refer to those that grow as multicelluar colonies (mushrooms and molds). [NIH] Fungistatic: Inhibiting the growth of fungi. [EU] Fungus: A general term used to denote a group of eukaryotic protists, including mushrooms, yeasts, rusts, moulds, smuts, etc., which are characterized by the absence of chlorophyll and by the presence of a rigid cell wall composed of chitin, mannans, and sometimes cellulose. They are usually of simple morphological form or show some reversible cellular specialization, such as the formation of pseudoparenchymatous tissue in the fruiting body of a mushroom. The dimorphic fungi grow, according to environmental conditions, as moulds or yeasts. [EU] Gadolinium: An element of the rare earth family of metals. It has the atomic symbol Gd, atomic number 64, and atomic weight 157.25. Its oxide is used in the control rods of some nuclear reactors. [NIH] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gamma Rays: Very powerful and penetrating, high-energy electromagnetic radiation of shorter wavelength than that of x-rays. They are emitted by a decaying nucleus, usually between 0.01 and 10 MeV. They are also called nuclear x-rays. [NIH] Gamma-interferon: Interferon produced by T-lymphocytes in response to various mitogens and antigens. Gamma interferon appears to have potent antineoplastic, immunoregulatory and antiviral activity. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Ganglioside: Protein kinase C's inhibitor which reduces ischemia-related brain damage. [NIH]
Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gas exchange: Primary function of the lungs; transfer of oxygen from inhaled air into the blood and of carbon dioxide from the blood into the lungs. [NIH] Gastric: Having to do with the stomach. [NIH] Gastric Juices: Liquids produced in the stomach to help break down food and kill bacteria.
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[NIH]
Gastric Mucosa: Surface epithelium in the stomach that invaginates into the lamina propria, forming gastric pits. Tubular glands, characteristic of each region of the stomach (cardiac, gastric, and pyloric), empty into the gastric pits. The gastric mucosa is made up of several different kinds of cells. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]
Gastroduodenal: Pertaining to or communicating with the stomach and duodenum, as a gastroduodenal fistula. [EU] Gastroenteritis: An acute inflammation of the lining of the stomach and intestines, characterized by anorexia, nausea, diarrhoea, abdominal pain, and weakness, which has various causes, including food poisoning due to infection with such organisms as Escherichia coli, Staphylococcus aureus, and Salmonella species; consumption of irritating food or drink; or psychological factors such as anger, stress, and fear. Called also enterogastritis. [EU] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal Neoplasms: Tumors or cancer of the gastrointestinal system. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gelatin: A product formed from skin, white connective tissue, or bone collagen. It is used as a protein food adjuvant, plasma substitute, hemostatic, suspending agent in pharmaceutical preparations, and in the manufacturing of capsules and suppositories. [NIH] Gels: Colloids with a solid continuous phase and liquid as the dispersed phase; gels may be unstable when, due to temperature or other cause, the solid phase liquifies; the resulting colloid is called a sol. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]
Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Targeting: The integration of exogenous DNA into the genome of an organism at sites where its expression can be suitably controlled. This integration occurs as a result of homologous recombination. [NIH] Gene Therapy: The introduction of new genes into cells for the purpose of treating disease by restoring or adding gene expression. Techniques include insertion of retroviral vectors, transfection, homologous recombination, and injection of new genes into the nuclei of single cell embryos. The entire gene therapy process may consist of multiple steps. The new genes may be introduced into proliferating cells in vivo (e.g., bone marrow) or in vitro (e.g., fibroblast cultures) and the modified cells transferred to the site where the gene expression is required. Gene therapy may be particularly useful for treating enzyme deficiency diseases, hemoglobinopathies, and leukemias and may also prove useful in restoring drug sensitivity, particularly for leukemia. [NIH] Generator: Any system incorporating a fixed parent radionuclide from which is produced a daughter radionuclide which is to be removed by elution or by any other method and used in a radiopharmaceutical. [NIH] Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called
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codons (codon). [NIH] Genetic Engineering: Directed modification of the gene complement of a living organism by such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetic testing: Analyzing DNA to look for a genetic alteration that may indicate an increased risk for developing a specific disease or disorder. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genital: Pertaining to the genitalia. [EU] Genitourinary: Pertaining to the genital and urinary organs; urogenital; urinosexual. [EU] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Germ Cells: The reproductive cells in multicellular organisms. [NIH] Germ-Line Mutation: Any detectable and heritable alteration in the lineage of germ cells. Mutations in these cells (i.e., "generative" cells ancestral to the gametes) are transmitted to progeny while those in somatic cells are not. [NIH] Giardiasis: An infection of the small intestine caused by the flagellated protozoan Giardia lamblia. It is spread via contaminated food and water and by direct person-to-person contact. [NIH] Gingival Recession: The exposure of root surface by an apical shift in the position of the gingiva. [NIH] Gingivitis: Inflammation of the gingivae. Gingivitis associated with bony changes is referred to as periodontitis. Called also oulitis and ulitis. [EU] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Gliadin: Simple protein, one of the prolamines, derived from the gluten of wheat, rye, etc. May be separated into 4 discrete electrophoretic fractions. It is the toxic factor associated with celiac disease. [NIH] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]
Glossitis: Inflammation of the tongue. [NIH] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glucose Intolerance: A pathological state in which the fasting plasma glucose level is less than 140 mg per deciliter and the 30-, 60-, or 90-minute plasma glucose concentration following a glucose tolerance test exceeds 200 mg per deciliter. This condition is seen frequently in diabetes mellitus but also occurs with other diseases. [NIH] Glucuronic Acid: Derivatives of uronic acid found throughout the plant and animal kingdoms. They detoxify drugs and toxins by conjugating with them to form glucuronides in the liver which are more water-soluble metabolites that can be easily eliminated from the body. [NIH]
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Glucuronides: Glycosides of glucuronic acid formed by the reaction of uridine diphosphate glucuronic acid with certain endogenous and exogenous substances. Their formation is important for the detoxification of drugs, steroid excretion and bilirubin metabolism to a more water-soluble compound that can be eliminated in the urine and bile. [NIH] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH]
Glutathione Peroxidase: An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9. [NIH]
Gluten: The protein of wheat and other grains which gives to the dough its tough elastic character. [EU] Glycerol: A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent. [NIH]
Glycerophospholipids: Derivatives of phosphatidic acid in which the hydrophobic regions are composed of two fatty acids and a polar alcohol is joined to the C-3 position of glycerol through a phosphodiester bond. They are named according to their polar head groups, such as phosphatidylcholine and phosphatidylethanolamine. [NIH] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycogen: A sugar stored in the liver and muscles. It releases glucose into the blood when cells need it for energy. Glycogen is the chief source of stored fuel in the body. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Glycosaminoglycans: Heteropolysaccharides which contain an N-acetylated hexosamine in a characteristic repeating disaccharide unit. The repeating structure of each disaccharide involves alternate 1,4- and 1,3-linkages consisting of either N-acetylglucosamine or Nacetylgalactosamine. [NIH] Glycosidic: Formed by elimination of water between the anomeric hydroxyl of one sugar and a hydroxyl of another sugar molecule. [NIH] Gonadal: Pertaining to a gonad. [EU] Gout: Hereditary metabolic disorder characterized by recurrent acute arthritis, hyperuricemia and deposition of sodium urate in and around the joints, sometimes with formation of uric acid calculi. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Gp120: 120-kD HIV envelope glycoprotein which is involved in the binding of the virus to its membrane receptor, the CD4 molecule, found on the surface of certain cells in the body. [NIH]
Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Graft Rejection: An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient. [NIH] Graft Survival: The survival of a graft in a host, the factors responsible for the survival and the changes occurring within the graft during growth in the host. [NIH] Grafting: The operation of transfer of tissue from one site to another. [NIH]
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Graft-versus-host disease: GVHD. A reaction of donated bone marrow or peripheral stem cells against a person's tissue. [NIH] Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [NIH] Grasses: A large family, Gramineae, of narrow-leaved herbaceous monocots. Many grasses produce highly allergenic pollens and are hosts to cattle parasites and toxic fungi. [NIH] Gravis: Eruption of watery blisters on the skin among those handling animals and animal products. [NIH] Groin: The external junctural region between the lower part of the abdomen and the thigh. [NIH]
Growth: The progressive development of a living being or part of an organism from its earliest stage to maturity. [NIH] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Guanine: One of the four DNA bases. [NIH] Guanylate Cyclase: An enzyme that catalyzes the conversion of GTP to 3',5'-cyclic GMP and pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC 4.6.1.2. [NIH] Habitual: Of the nature of a habit; according to habit; established by or repeated by force of habit, customary. [EU] Hair follicles: Shafts or openings on the surface of the skin through which hair grows. [NIH] Hairy cell leukemia: A type of chronic leukemia in which the abnormal white blood cells appear to be covered with tiny hairs when viewed under a microscope. [NIH] Half-Life: The time it takes for a substance (drug, radioactive nuclide, or other) to lose half of its pharmacologic, physiologic, or radiologic activity. [NIH] Haploid: An organism with one basic chromosome set, symbolized by n; the normal condition of gametes in diploids. [NIH] Haplotypes: The genetic constitution of individuals with respect to one member of a pair of allelic genes, or sets of genes that are closely linked and tend to be inherited together such as those of the major histocompatibility complex. [NIH] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Hay Fever: A seasonal variety of allergic rhinitis, marked by acute conjunctivitis with lacrimation and itching, regarded as an allergic condition triggered by specific allergens. [NIH]
Headache: Pain in the cranial region that may occur as an isolated and benign symptom or as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; craniocerebral trauma; central nervous system infections; intracranial hypertension; and other disorders. In general, recurrent headaches that are not associated with a primary disease process are referred to as headache disorders (e.g., migraine). [NIH] Headache Disorders: Common conditions characterized by persistent or recurrent headaches. Headache syndrome classification systems may be based on etiology (e.g., vascular headache, post-traumatic headaches, etc.), temporal pattern (e.g., cluster headache, paroxysmal hemicrania, etc.), and precipitating factors (e.g., cough headache). [NIH]
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Health Care Costs: The actual costs of providing services related to the delivery of health care, including the costs of procedures, therapies, and medications. It is differentiated from health expenditures, which refers to the amount of money paid for the services, and from fees, which refers to the amount charged, regardless of cost. [NIH] Health Expenditures: The amounts spent by individuals, groups, nations, or private or public organizations for total health care and/or its various components. These amounts may or may not be equivalent to the actual costs (health care costs) and may or may not be shared among the patient, insurers, and/or employers. [NIH] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Heat-Shock Proteins: Proteins which are synthesized in eukaryotic organisms and bacteria in response to hyperthermia and other environmental stresses. They increase thermal tolerance and perform functions essential to cell survival under these conditions. [NIH] Heat-Shock Proteins 90: A class of molecular chaperones whose members act in the mechanism of signal transduction by steroid receptors. [NIH] Heliotherapy: Sunbathing as a therapeutic measure. [NIH] Helix-loop-helix: Regulatory protein of cell cycle. [NIH] Helminths: Commonly known as parasitic worms, this group includes the acanthocephala, nematoda, and platyhelminths. Some authors consider certain species of leeches that can become temporarily parasitic as helminths. [NIH] Heme: The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins. [NIH] Hemodialysis: The use of a machine to clean wastes from the blood after the kidneys have failed. The blood travels through tubes to a dialyzer, which removes wastes and extra fluid. The cleaned blood then flows through another set of tubes back into the body. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemoglobin M: A group of abnormal hemoglobins in which amino acid substitutions take place in either the alpha or beta chains but near the heme iron. This results in facilitated oxidation of the hemoglobin to yield excess methemoglobin which leads to cyanosis. [NIH] Hemoglobinopathies: A group of inherited disorders characterized by structural alterations within the hemoglobin molecule. [NIH] Hemoglobinuria: The presence of free hemoglobin in the urine. [NIH] Hemolysis: The destruction of erythrocytes by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity. [NIH] Hemolytic: A disease that affects the blood and blood vessels. It destroys red blood cells, cells that cause the blood to clot, and the lining of blood vessels. HUS is often caused by the Escherichia coli bacterium in contaminated food. People with HUS may develop acute renal
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failure. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hemostasis: The process which spontaneously arrests the flow of blood from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements, and the process of blood or plasma coagulation. [NIH]
Heparan Sulfate Proteoglycan: A substance released by astrocytes, which is critical in stopping nervous fibers in their tracks. [NIH] Heparin: Heparinic acid. A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts. [NIH] Heparin-binding: Protein that stimulates the proliferation of endothelial cells. [NIH] Hepatic: Refers to the liver. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatocellular: Pertaining to or affecting liver cells. [EU] Hepatocellular carcinoma: A type of adenocarcinoma, the most common type of liver tumor. [NIH] Hepatocyte: A liver cell. [NIH] Hepatocyte Growth Factor: Multifunctional growth factor which regulates both cell growth and cell motility. It exerts a strong mitogenic effect on hepatocytes and primary epithelial cells. Its receptor is proto-oncogene protein C-met. [NIH] Hepatotoxic: Toxic to liver cells. [EU] Hepatotoxicity: How much damage a medicine or other substance does to the liver. [NIH] Herbicides: Pesticides used to destroy unwanted vegetation, especially various types of weeds, grasses, and woody plants. [NIH] Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one generation to another. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Herpes: Any inflammatory skin disease caused by a herpesvirus and characterized by the formation of clusters of small vesicles. When used alone, the term may refer to herpes simplex or to herpes zoster. [EU] Herpes virus: A member of the herpes family of viruses. [NIH] Herpes Zoster: Acute vesicular inflammation. [NIH] Herpetiformis: Duhring's disease a recurring, inflammatory disease of the skin of unknown etiology characterized by erythematous, papular, pustular, or vesicular lesions which tend to group and are accompanied by itching and burning. [NIH] Heterodimers: Zippered pair of nonidentical proteins. [NIH] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]
Heterozygotes: Having unlike alleles at one or more corresponding loci on homologous
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chromosomes. [NIH] Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] Histamine Release: The secretion of histamine from mast cell and basophil granules by exocytosis. This can be initiated by a number of factors, all of which involve binding of IgE, cross-linked by antigen, to the mast cell or basophil's Fc receptors. Once released, histamine binds to a number of different target cell receptors and exerts a wide variety of effects. [NIH] Histidine: An essential amino acid important in a number of metabolic processes. It is required for the production of histamine. [NIH] Histocompatibility: The degree of antigenic similarity between the tissues of different individuals, which determines the acceptance or rejection of allografts. [NIH] Histocompatibility Antigens: A group of antigens that includes both the major and minor histocompatibility antigens. The former are genetically determined by the major histocompatibility complex. They determine tissue type for transplantation and cause allograft rejections. The latter are systems of allelic alloantigens that can cause weak transplant rejection. [NIH] Histology: The study of tissues and cells under a microscope. [NIH] Homeobox: Distinctive sequence of DNA bases. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homodimer: Protein-binding "activation domains" always combine with identical proteins. [NIH]
Homogeneous: Consisting of or composed of similar elements or ingredients; of a uniform quality throughout. [EU] Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Homotypic: Adhesion between neutrophils. [NIH] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Horny layer: The superficial layer of the epidermis containing keratinized cells. [NIH] Host: Any animal that receives a transplanted graft. [NIH] Human growth hormone: A protein hormone, secreted by the anterior lobe of the pituitary, which promotes growth of the whole body by stimulating protein synthesis. The human gene has already been cloned and successfully expressed in bacteria. [NIH] Human papillomavirus: HPV. A virus that causes abnormal tissue growth (warts) and is often associated with some types of cancer. [NIH] Humoral: Of, relating to, proceeding from, or involving a bodily humour - now often used of endocrine factors as opposed to neural or somatic. [EU] Humour: 1. A normal functioning fluid or semifluid of the body (as the blood, lymph or bile) especially of vertebrates. 2. A secretion that is itself an excitant of activity (as certain hormones). [EU] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see
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also crossing. [NIH] Hybridization: The genetic process of crossbreeding to produce a hybrid. Hybrid nucleic acids can be formed by nucleic acid hybridization of DNA and RNA molecules. Protein hybridization allows for hybrid proteins to be formed from polypeptide chains. [NIH] Hybridomas: Cells artificially created by fusion of activated lymphocytes with neoplastic cells. The resulting hybrid cells are cloned and produce pure or "monoclonal" antibodies or T-cell products, identical to those produced by the immunologically competent parent, and continually grow and divide as the neoplastic parent. [NIH] Hydration: Combining with water. [NIH] Hydrocortisone: The main glucocorticoid secreted by the adrenal cortex. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. [NIH] Hydrogel: A network of cross-linked hydrophilic macromolecules used in biomedical applications. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrophilic: Readily absorbing moisture; hygroscopic; having strongly polar groups that readily interact with water. [EU] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxylation: Hydroxylate, to introduce hydroxyl into (a compound or radical) usually by replacement of hydrogen. [EU] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hydroxyurea: An antineoplastic agent that inhibits DNA synthesis through the inhibition of ribonucleoside diphosphate reductase. [NIH] Hyperbilirubinemia: Pathologic process consisting of an abnormal increase in the amount of bilirubin in the circulating blood, which may result in jaundice. [NIH] Hypercalcemia: Abnormally high level of calcium in the blood. [NIH] Hypercalciuria: Abnormally large amounts of calcium in the urine. [NIH] Hyperkeratosis: 1. Hypertrophy of the corneous layer of the skin. 2a. Any of various conditions marked by hyperkeratosis. 2b. A disease of cattle marked by thickening and wringling of the hide and formation of papillary outgrowths on the buccal mucous membranes, often accompanied by watery discharge from eyes and nose, diarrhoea, loss of condition, and abortion of pregnant animals, and now believed to result from ingestion of
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the chlorinated naphthalene of various lubricating oils. [EU] Hyperostosis: Increase in the mass of bone per unit volume. [NIH] Hyperplasia: An increase in the number of cells in a tissue or organ, not due to tumor formation. It differs from hypertrophy, which is an increase in bulk without an increase in the number of cells. [NIH] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypersensitivity, Immediate: Hypersensitivity reactions which occur within minutes of exposure to challenging antigen due to the release of histamine which follows the antigenantibody reaction and causes smooth muscle contraction and increased vascular permeability. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hyperthermia: A type of treatment in which body tissue is exposed to high temperatures to damage and kill cancer cells or to make cancer cells more sensitive to the effects of radiation and certain anticancer drugs. [NIH] Hypertriglyceridemia: Condition of elevated triglyceride concentration in the blood; an inherited form occurs in familial hyperlipoproteinemia IIb and hyperlipoproteinemia type IV. It has been linked to higher risk of heart disease and arteriosclerosis. [NIH] Hypertrophy: General increase in bulk of a part or organ, not due to tumor formation, nor to an increase in the number of cells. [NIH] Hyperuricemia: A buildup of uric acid (a byproduct of metabolism) in the blood; a side effect of some anticancer drugs. [NIH] Hypnotic: A drug that acts to induce sleep. [EU] Hypoglycemic: An orally active drug that produces a fall in blood glucose concentration. [NIH]
Hypotension: Abnormally low blood pressure. [NIH] Hypotensive: Characterized by or causing diminished tension or pressure, as abnormally low blood pressure. [EU] Hypothalamus: Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle. [NIH] Hypoxia: Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood. [EU] Hypoxic: Having too little oxygen. [NIH] Ibuprofen: A nonsteroidal anti-inflammatory agent with analgesic properties used in the therapy of rheumatism and arthritis. [NIH] Ichthyosis: Any of several generalized skin disorders characterized by dryness, roughness, and scaliness, due to hypertrophy of the stratum corneum epidermis. Most are genetic, but some are acquired, developing in association with other systemic disease or genetic syndrome. [NIH] Ichthyosis Vulgaris: Most common form of ichthyosis characterized by prominent scaling especially on the exterior surfaces of the extremities. It is inherited as an autosomal dominant trait. [NIH] Id: The part of the personality structure which harbors the unconscious instinctive desires
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and strivings of the individual. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH] Idiotype: The unique antigenic determinant in the variable region. [NIH] Ileum: The lower end of the small intestine. [NIH] Imidazole: C3H4N2. The ring is present in polybenzimidazoles. [NIH] Immersion: The placing of a body or a part thereof into a liquid. [NIH] Immune function: Production and action of cells that fight disease or infection. [NIH] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]
Immune Sera: Serum that contains antibodies. It is obtained from an animal that has been immunized either by antigen injection or infection with microorganisms containing the antigen. [NIH] Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immunity: Nonsusceptibility to the invasive or pathogenic microorganisms or to the toxic effect of antigenic substances. [NIH]
effects
of
foreign
Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH] Immunoassay: Immunochemical assay or detection of a substance by serologic or immunologic methods. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance. [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunology: The study of the body's immune system. [NIH] Immunomodulator: New type of drugs mainly using biotechnological methods. Treatment of cancer. [NIH] Immunophilin: A drug for the treatment of Parkinson's disease. [NIH] Immunosuppressant: An agent capable of suppressing immune responses. [EU] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunosuppressive Agents: Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of suppressor T-cell populations or by inhibiting the activation of helper cells. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of interleukins and other cytokines are emerging. [NIH] Immunosuppressive therapy: Therapy used to decrease the body's immune response, such
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as drugs given to prevent transplant rejection. [NIH] Immunotherapy: Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection. [NIH] Immunotoxins: Semisynthetic conjugates of various toxic molecules, including radioactive isotopes and bacterial or plant toxins, with specific immune substances such as immunoglobulins, monoclonal antibodies, and antigens. The antitumor or antiviral immune substance carries the toxin to the tumor or infected cell where the toxin exerts its poisonous effect. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Impetigo: A common superficial bacterial infection caused by staphylococcus aureus or group A beta-hemolytic streptococci. Characteristics include pustular lesions that rupture and discharge a thin, amber-colored fluid that dries and forms a crust. This condition is commonly located on the face, especially about the mouth and nose. [NIH] Implant radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called [NIH] Implantation: The insertion or grafting into the body of biological, living, inert, or radioactive material. [EU] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In Situ Hybridization: A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes. [NIH] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incision: A cut made in the body during surgery. [NIH] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU] Individuality: Those psychological characteristics which differentiate individuals from one another. [NIH] Indomethacin: A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes. [NIH] Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Induration: 1. The quality of being hard; the process of hardening. 2. An abnormally hard spot or place. [EU] Infancy: The period of complete dependency prior to the acquisition of competence in walking, talking, and self-feeding. [NIH] Infant Mortality: Perinatal, neonatal, and infant deaths in a given population. [NIH] Infant, Newborn: An infant during the first month after birth. [NIH] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus,
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or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]
Infertility: The diminished or absent ability to conceive or produce an offspring while sterility is the complete inability to conceive or produce an offspring. [NIH] Infestation: Parasitic attack or subsistence on the skin and/or its appendages, as by insects, mites, or ticks; sometimes used to denote parasitic invasion of the organs and tissues, as by helminths. [NIH] Infiltration: The diffusion or accumulation in a tissue or cells of substances not normal to it or in amounts of the normal. Also, the material so accumulated. [EU] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Inflammatory bowel disease: A general term that refers to the inflammation of the colon and rectum. Inflammatory bowel disease includes ulcerative colitis and Crohn's disease. [NIH]
Influenza: An acute viral infection involving the respiratory tract. It is marked by inflammation of the nasal mucosa, the pharynx, and conjunctiva, and by headache and severe, often generalized, myalgia. [NIH] Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH] Ingestion: Taking into the body by mouth [NIH] Inhalation: The drawing of air or other substances into the lungs. [EU] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Initiator: A chemically reactive substance which may cause cell changes if ingested, inhaled or absorbed into the body; the substance may thus initiate a carcinogenic process. [NIH] Inlay: In dentistry, a filling first made to correspond with the form of a dental cavity and then cemented into the cavity. [NIH] Inner ear: The labyrinth, comprising the vestibule, cochlea, and semicircular canals. [NIH] Inorganic: Pertaining to substances not of organic origin. [EU] Inpatients: Persons admitted to health facilities which provide board and room, for the purpose of observation, care, diagnosis or treatment. [NIH] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insomnia: Difficulty in going to sleep or getting enough sleep. [NIH] Insulator: Material covering the metal conductor of the lead. It is usually polyurethane or silicone. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of
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glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Insulin-like: Muscular growth factor. [NIH] Integrins: A family of transmembrane glycoproteins consisting of noncovalent heterodimers. They interact with a wide variety of ligands including extracellular matrix glycoproteins, complement, and other cells, while their intracellular domains interact with the cytoskeleton. The integrins consist of at least three identified families: the cytoadhesin receptors, the leukocyte adhesion receptors, and the very-late-antigen receptors. Each family contains a common beta-subunit combined with one or more distinct alpha-subunits. These receptors participate in cell-matrix and cell-cell adhesion in many physiologically important processes, including embryological development, hemostasis, thrombosis, wound healing, immune and nonimmune defense mechanisms, and oncogenic transformation. [NIH] Intercellular Adhesion Molecule-1: A cell-surface ligand with a role in leukocyte adhesion and inflammation. Its production is induced by gamma-interferon and it is required for neutrophil migration into inflamed tissue. [NIH] Intercellular Junctions: Strictly, and so far as it can be distinguished, the amorphous isotropic layer between adjacent primary walls of cells. [NIH] Interferon: A biological response modifier (a substance that can improve the body's natural response to disease). Interferons interfere with the division of cancer cells and can slow tumor growth. There are several types of interferons, including interferon-alpha, -beta, and gamma. These substances are normally produced by the body. They are also made in the laboratory for use in treating cancer and other diseases. [NIH] Interferon-alpha: One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells when exposed to live or inactivated virus, double-stranded RNA, or bacterial products. It is the major interferon produced by virus-induced leukocyte cultures and, in addition to its pronounced antiviral activity, it causes activation of NK cells. [NIH] Interleukin-1: A soluble factor produced by monocytes, macrophages, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. IL-1 consists of two distinct forms, IL-1 alpha and IL-1 beta which perform the same functions but are distinct proteins. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. The factor is distinct from interleukin-2. [NIH] Interleukin-10: Factor that is a coregulator of mast cell growth. It is produced by T-cells and B-cells and shows extensive homology with the Epstein-Barr virus BCRFI gene. [NIH] Interleukin-18: Cytokine which resembles IL-1 structurally and IL-12 functionally. It enhances the cytotoxic activity of NK cells and CTLs, and appears to play a role both as neuroimmunomodulator and in the induction of mucosal immunity. [NIH] Interleukin-2: Chemical mediator produced by activated T lymphocytes and which regulates the proliferation of T cells, as well as playing a role in the regulation of NK cell activity. [NIH] Interleukin-6: Factor that stimulates the growth and differentiation of human B-cells and is also a growth factor for hybridomas and plasmacytomas. It is produced by many different cells including T-cells, monocytes, and fibroblasts. [NIH] Interleukin-8: A cytokine that activates neutrophils and attracts neutrophils and Tlymphocytes. It is released by several cell types including monocytes, macrophages, T-
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lymphocytes, fibroblasts, endothelial cells, and keratinocytes by an inflammatory stimulus. IL-8 is a member of the beta-thromboglobulin superfamily and structurally related to platelet factor 4. [NIH] Interleukins: Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli. [NIH] Intermediate Filaments: Cytoplasmic filaments intermediate in diameter (about 10 nanometers) between the microfilaments and the microtubules. They may be composed of any of a number of different proteins and form a ring around the cell nucleus. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Internal Medicine: A medical specialty concerned with the diagnosis and treatment of diseases of the internal organ systems of adults. [NIH] Internal radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called brachytherapy, implant radiation, or interstitial radiation therapy. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intervention Studies: Epidemiologic investigations designed to test a hypothesized causeeffect relation by modifying the supposed causal factor(s) in the study population. [NIH] Intervertebral: Situated between two contiguous vertebrae. [EU] Intervertebral Disk Displacement: An intervertebral disk in which the nucleus pulposus has protruded through surrounding fibrocartilage. This occurs most frequently in the lower lumbar region. [NIH] Intestinal: Having to do with the intestines. [NIH] Intestinal Mucosa: The surface lining of the intestines where the cells absorb nutrients. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH] Intracellular Membranes: Membranes of subcellular structures. [NIH] Intramuscular: IM. Within or into muscle. [NIH] Intramuscular injection: IM. Injection into a muscle. [NIH] Intravascular: Within a vessel or vessels. [EU] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Involuntary: Reaction occurring without intention or volition. [NIH] Iodine: A nonmetallic element of the halogen group that is represented by the atomic symbol I, atomic number 53, and atomic weight of 126.90. It is a nutritionally essential element, especially important in thyroid hormone synthesis. In solution, it has anti-infective properties and is used topically. [NIH] Ion Channels: Gated, ion-selective glycoproteins that traverse membranes. The stimulus for
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channel gating can be a membrane potential, drug, transmitter, cytoplasmic messenger, or a mechanical deformation. Ion channels which are integral parts of ionotropic neurotransmitter receptors are not included. [NIH] Ionizing: Radiation comprising charged particles, e. g. electrons, protons, alpha-particles, etc., having sufficient kinetic energy to produce ionization by collision. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Irradiation: The use of high-energy radiation from x-rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Irradiation is also called radiation therapy, radiotherapy, and x-ray therapy. [NIH] Irritants: Drugs that act locally on cutaneous or mucosal surfaces to produce inflammation; those that cause redness due to hyperemia are rubefacients; those that raise blisters are vesicants and those that penetrate sebaceous glands and cause abscesses are pustulants; tear gases and mustard gases are also irritants. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Islet: Cell producing insulin in pancreas. [NIH] Isopropyl: A gene mutation inducer. [NIH] Jaundice: A clinical manifestation of hyperbilirubinemia, consisting of deposition of bile pigments in the skin, resulting in a yellowish staining of the skin and mucous membranes. [NIH]
Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [NIH] Juniper: A slow growing coniferous evergreen tree or shrub, genus Juniperus. The Juniper is cultivated for its berries, which take up to three years to ripen. The resinous, sweetly flavored berries are borne only by the female juniper, and can be found in various stages of ripeness on the same plant. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Keratin: A class of fibrous proteins or scleroproteins important both as structural proteins and as keys to the study of protein conformation. The family represents the principal constituent of epidermis, hair, nails, horny tissues, and the organic matrix of tooth enamel. Two major conformational groups have been characterized, alpha-keratin, whose peptide backbone forms an alpha-helix, and beta-keratin, whose backbone forms a zigzag or pleated sheet structure. [NIH] Keratinocytes: Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell. [NIH] Keratitis: Inflammation of the cornea. [NIH] Keratolytic: An agent that promotes keratolysis. [EU]
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Keratolytic Agents: Agents that soften, separate, and cause desquamation of the cornified epithelium or horny layer of skin. They are used to expose mycelia of infecting fungi or to treat corns, warts, and certain other skin diseases. [NIH] Keratosis: Any horny growth such as a wart or callus. [NIH] Ketoconazole: Broad spectrum antifungal agent used for long periods at high doses, especially in immunosuppressed patients. [NIH] Kidney Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Kidney Failure: The inability of a kidney to excrete metabolites at normal plasma levels under conditions of normal loading, or the inability to retain electrolytes under conditions of normal intake. In the acute form (kidney failure, acute), it is marked by uremia and usually by oliguria or anuria, with hyperkalemia and pulmonary edema. The chronic form (kidney failure, chronic) is irreversible and requires hemodialysis. [NIH] Kidney Failure, Acute: A clinical syndrome characterized by a sudden decrease in glomerular filtration rate, often to values of less than 1 to 2 ml per minute. It is usually associated with oliguria (urine volumes of less than 400 ml per day) and is always associated with biochemical consequences of the reduction in glomerular filtration rate such as a rise in blood urea nitrogen (BUN) and serum creatinine concentrations. [NIH] Kidney Failure, Chronic: An irreversible and usually progressive reduction in renal function in which both kidneys have been damaged by a variety of diseases to the extent that they are unable to adequately remove the metabolic products from the blood and regulate the body's electrolyte composition and acid-base balance. Chronic kidney failure requires hemodialysis or surgery, usually kidney transplantation. [NIH] Killer Cells: Lymphocyte-like effector cells which mediate antibody-dependent cell cytotoxicity. They kill antibody-coated target cells which they bind with their Fc receptors. [NIH]
Kilobase: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Lacerations: Torn, ragged, mangled wounds. [NIH] Lanolin: A yellow fat obtained from sheep's wool. It is used as an emollient, cosmetic, and pharmaceutic aid. [NIH] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Lectin: A complex molecule that has both protein and sugars. Lectins are able to bind to the outside of a cell and cause biochemical changes in it. Lectins are made by both animals and plants. [NIH] Leflunomide: An anticancer drug that works by inhibiting a cancer cell growth factor. Also called SU101. [NIH]
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Leg Ulcer: Ulceration of the skin and underlying structures of the lower extremity. About 90% of the cases are due to venous insufficiency (varicose ulcer), 5% to arterial disease, and the remaining 5% to other causes. [NIH] Lens: The transparent, double convex (outward curve on both sides) structure suspended between the aqueous and vitreous; helps to focus light on the retina. [NIH] Lethal: Deadly, fatal. [EU] Leucocyte: All the white cells of the blood and their precursors (myeloid cell series, lymphoid cell series) but commonly used to indicate granulocytes exclusive of lymphocytes. [NIH]
Leukemia: Cancer of blood-forming tissue. [NIH] Leukocyte Count: A count of the number of white blood cells per unit volume in venous blood. A differential leukocyte count measures the relative numbers of the different types of white cells. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Leukoplakia: A white patch that may develop on mucous membranes such as the cheek, gums, or tongue and may become cancerous. [NIH] Leukotrienes: A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system. [NIH] Liarozole: An anticancer drug that promotes differentiation by increasing the levels of retinoic acid within the tumor. [NIH] Libraries, Hospital: Information centers primarily serving the needs of hospital medical staff and sometimes also providing patient education and other services. [NIH] Library Services: Services offered to the library user. They include reference and circulation. [NIH]
Lichenification: Hypertrophy of the epidermis, resulting in thickening of the skin with exaggeration of the normal skin markings, giving the skin a leathery barklike appearance, which is caused by prolonged rubbing or scratching. It may arise on seemingly normal skin, or it may develop at the site of another pruritic cutaneous disorder. [EU] Lidocaine: A local anesthetic and cardiac depressant used as an antiarrhythmia agent. Its actions are more intense and its effects more prolonged than those of procaine but its duration of action is shorter than that of bupivacaine or prilocaine. [NIH] Ligament: A band of fibrous tissue that connects bones or cartilages, serving to support and strengthen joints. [EU] Ligands: A RNA simulation method developed by the MIT. [NIH] Linkage: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Linkage Disequilibrium: Nonrandom association of linked genes. This is the tendency of the alleles of two separate but already linked loci to be found together more frequently than would be expected by chance alone. [NIH] Lip: Either of the two fleshy, full-blooded margins of the mouth. [NIH]
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Lipid: Fat. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lipophilic: Having an affinity for fat; pertaining to or characterized by lipophilia. [EU] Lipopolysaccharide: Substance consisting of polysaccaride and lipid. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] Liposomal: A drug preparation that contains the active drug in very tiny fat particles. This fat-encapsulated drug is absorbed better, and its distribution to the tumor site is improved. [NIH]
Lipoxygenase: An enzyme of the oxidoreductase class that catalyzes reactions between linoleate and other fatty acids and oxygen to form hydroperoxy-fatty acid derivatives. Related enzymes in this class include the arachidonate lipoxygenases, arachidonate 5lipoxygenase, arachidonate 12-lipoxygenase, and arachidonate 15-lipoxygenase. EC 1.13.11.12. [NIH] Lipoxygenase Inhibitors: Compounds or agents that combine with lipoxygenase and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of the eicosanoid products hydroxyeicosatetraenoic acid and various leukotrienes. [NIH] Liquor: 1. A liquid, especially an aqueous solution containing a medicinal substance. 2. A general term used in anatomical nomenclature for certain fluids of the body. [EU] Lithium: An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight 6.94. Salts of lithium are used in treating manic-depressive disorders. [NIH]
Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Liver cancer: A disease in which malignant (cancer) cells are found in the tissues of the liver. [NIH]
Lobe: A portion of an organ such as the liver, lung, breast, or brain. [NIH] Local therapy: Treatment that affects cells in the tumor and the area close to it. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Lod: The lowest analyte content which, if actually present, will be detected with reasonable statistical certainty and can be identified according to the identification criteria of the method. If both accuracy and precision are constant over a concentration range. [NIH] Long-Term Care: Care over an extended period, usually for a chronic condition or disability, requiring periodic, intermittent, or continuous care. [NIH] Loop: A wire usually of platinum bent at one end into a small loop (usually 4 mm inside diameter) and used in transferring microorganisms. [NIH] Low Back Pain: Acute or chronic pain in the lumbar or sacral regions, which may be
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associated with musculo-ligamentous sprains and strains; intervertebral disk displacement; and other conditions. [NIH] Low-density lipoprotein: Lipoprotein that contains most of the cholesterol in the blood. LDL carries cholesterol to the tissues of the body, including the arteries. A high level of LDL increases the risk of heart disease. LDL typically contains 60 to 70 percent of the total serum cholesterol and both are directly correlated with CHD risk. [NIH] Lubricants: Oily or slippery substances. [NIH] Luciferase: Any one of several enzymes that catalyze the bioluminescent reaction in certain marine crustaceans, fish, bacteria, and insects. The enzyme is a flavoprotein; it oxidizes luciferins to an electronically excited compound that emits energy in the form of light. The color of light emitted varies with the organism. The firefly enzyme is a valuable reagent for measurement of ATP concentration. (Dorland, 27th ed) EC 1.13.12.-. [NIH] Lumbar: Pertaining to the loins, the part of the back between the thorax and the pelvis. [EU] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [NIH] Lupus Nephritis: Glomerulonephritis associated with systemic lupus erythematosus. It is classified into four histologic types: mesangial, focal, diffuse, and membranous. [NIH] Lye: Generally speaking, it is the alkaline substance obtained from wood ashes by percolation. Preparations of lye can either be solutions of potassium or sodium hydroxide. The term lye, is also used to refer to the household product which is a mixture of sodium hydroxide and sodium carbonate. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH] Lymph node: A rounded mass of lymphatic tissue that is surrounded by a capsule of connective tissue. Also known as a lymph gland. Lymph nodes are spread out along lymphatic vessels and contain many lymphocytes, which filter the lymphatic fluid (lymph). [NIH]
Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphedema: Edema due to obstruction of lymph vessels or disorders of the lymph nodes. [NIH]
Lymphocyte: A white blood cell. Lymphocytes have a number of roles in the immune system, including the production of antibodies and other substances that fight infection and diseases. [NIH] Lymphocyte Count: A count of the number of lymphocytes in the blood. [NIH] Lymphocyte Subsets: A classification of lymphocytes based on structurally or functionally different populations of cells. [NIH] Lymphocytic: Referring to lymphocytes, a type of white blood cell. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lymphokines: Soluble protein factors generated by activated lymphocytes that affect other cells, primarily those involved in cellular immunity. [NIH]
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Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Lymphomatoid Papulosis: Clinically benign, histologically malignant, recurrent cutaneous eruption characterized by an infiltration of large atypical cells surrounded by inflammatory cells. The atypical cells resemble Reed-Sternberg cells of Hodgkin's disease or the malignant cells of cutaneous T-cell lymphoma. In some cases, lymphomatoid papulosis progresses to lymphomatous conditions including mycosis fungoides, Hodgkin's disease, cutaneous T-cell lymphoma, or Ki-1 lymphoma. [NIH] Lymphoproliferative: Disorders characterized by proliferation of lymphoid tissue, general or unspecified. [NIH] Lysine: An essential amino acid. It is often added to animal feed. [NIH] Lytic: 1. Pertaining to lysis or to a lysin. 2. Producing lysis. [EU] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH] Macula: A stain, spot, or thickening. Often used alone to refer to the macula retinae. [EU] Macula Lutea: An oval area in the retina, 3 to 5 mm in diameter, usually located temporal to the superior pole of the eye and slightly below the level of the optic disk. [NIH] Macular Degeneration: Degenerative changes in the macula lutea of the retina. [NIH] Maculopapular: Both macular and papular, as an eruption consisting of both macules and papules; sometimes erroneously used to designate a papule that is only slightly elevated. [EU]
Magnesium Chloride: Magnesium chloride. An inorganic compound consisting of one magnesium and two chloride ions. The compound is used in medicine as a source of magnesium ions, which are essential for many cellular activities. It has also been used as a cathartic and in alloys. [NIH] Maintenance therapy: Treatment that is given to help a primary (original) treatment keep working. Maintenance therapy is often given to help keep cancer in remission. [NIH] Major Histocompatibility Complex: The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) transplantation antigens, genes which control the structure of the immune responseassociated (Ia) antigens, the immune response (Ir) genes which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement. [NIH] Malabsorption: Impaired intestinal absorption of nutrients. [EU] Malignancy: A cancerous tumor that can invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]
Malondialdehyde: The dialdehyde of malonic acid. [NIH] Mandible: The largest and strongest bone of the face constituting the lower jaw. It supports the lower teeth. [NIH] Mange: Sarcoptic infestation of human skin, particularly a contagious skin disease caused by invasion of the epidermis with Sarcoptes scabiei. [NIH] Mania: Excitement of psychotic proportions manifested by mental and physical hyperactivity, disorganization of behaviour, and elevation of mood. [EU]
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Manic: Affected with mania. [EU] Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Mannans: Polysaccharides consisting of mannose units. [NIH] Matrix metalloproteinase: A member of a group of enzymes that can break down proteins, such as collagen, that are normally found in the spaces between cells in tissues (i.e., extracellular matrix proteins). Because these enzymes need zinc or calcium atoms to work properly, they are called metalloproteinases. Matrix metalloproteinases are involved in wound healing, angiogenesis, and tumor cell metastasis. [NIH] Mechlorethamine: A vesicant and necrotizing irritant destructive to mucous membranes. It was formerly used as a war gas. The hydrochloride is used as an antineoplastic in Hodgkin's disease and lymphomas. It causes severe gastrointestinal and bone marrow damage. [NIH] Medial: Lying near the midsaggital plane of the body; opposed to lateral. [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU] Medical Staff: Professional medical personnel who provide care to patients in an organized facility, institution or agency. [NIH] Medicament: A medicinal substance or agent. [EU] Medicine, Herbal: Use of plants or herbs to treat diseases or to alleviate pain. [NIH] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Megakaryocytes: Very large bone marrow cells which release mature blood platelets. [NIH] Megaloblastic: A large abnormal red blood cell appearing in the blood in pernicious anaemia. [EU] Meiosis: A special method of cell division, occurring in maturation of the germ cells, by means of which each daughter nucleus receives half the number of chromosomes characteristic of the somatic cells of the species. [NIH] Melanin: The substance that gives the skin its color. [NIH] Melanocytes: Epidermal dendritic pigment cells which control long-term morphological color changes by alteration in their number or in the amount of pigment they produce and store in the pigment containing organelles called melanosomes. Melanophores are larger cells which do not exist in mammals. [NIH] Melanoma: A form of skin cancer that arises in melanocytes, the cells that produce pigment. Melanoma usually begins in a mole. [NIH] Melanosomes: Melanin-containing organelles found in melanocytes and melanophores. [NIH]
Membrane: A very thin layer of tissue that covers a surface. [NIH] Membrane Fluidity: The motion of phospholipid molecules within the lipid bilayer, dependent on the classes of phospholipids present, their fatty acid composition and degree of unsaturation of the acyl chains, the cholesterol concentration, and temperature. [NIH] Membrane Lipids: Lipids, predominantly phospholipids, cholesterol and small amounts of
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glycolipids found in membranes including cellular and intracellular membranes. These lipids may be arranged in bilayers in the membranes with integral proteins between the layers and peripheral proteins attached to the outside. Membrane lipids are required for active transport, several enzymatic activities and membrane formation. [NIH] Membrane Proteins: Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Meningitis: Inflammation of the meninges. When it affects the dura mater, the disease is termed pachymeningitis; when the arachnoid and pia mater are involved, it is called leptomeningitis, or meningitis proper. [EU] Menopause: Permanent cessation of menstruation. [NIH] Menstrual Cycle: The period of the regularly recurring physiologic changes in the endometrium occurring during the reproductive period in human females and some primates and culminating in partial sloughing of the endometrium (menstruation). [NIH] Menstruation: The normal physiologic discharge through the vagina of blood and mucosal tissues from the nonpregnant uterus. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Disorders: Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function. [NIH] Menthol: An alcohol produced from mint oils or prepared synthetically. [NIH] Mepacrine: An antimalarial drug. [NIH] Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to mercury poisoning. Because of its toxicity, the clinical use of mercury and mercurials is diminishing. [NIH] Mesenchymal: Refers to cells that develop into connective tissue, blood vessels, and lymphatic tissue. [NIH] Mesentery: A layer of the peritoneum which attaches the abdominal viscera to the abdominal wall and conveys their blood vessels and nerves. [NIH] Mesoderm: The middle germ layer of the embryo. [NIH] Meta-Analysis: A quantitative method of combining the results of independent studies (usually drawn from the published literature) and synthesizing summaries and conclusions which may be used to evaluate therapeutic effectiveness, plan new studies, etc., with application chiefly in the areas of research and medicine. [NIH] Metabolic disorder: A condition in which normal metabolic processes are disrupted, usually because of a missing enzyme. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metaphase: The second phase of cell division, in which the chromosomes line up across the
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equatorial plane of the spindle prior to separation. [NIH] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH] Metastatic: Having to do with metastasis, which is the spread of cancer from one part of the body to another. [NIH] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [NIH] Methotrexate: An antineoplastic antimetabolite with immunosuppressant properties. It is an inhibitor of dihydrofolate reductase and prevents the formation of tetrahydrofolate, necessary for synthesis of thymidylate, an essential component of DNA. [NIH] Methoxsalen: A naturally occurring furocoumarin compound found in several species of plants, including Psoralea corylifolia. It is a photoactive substance that forms DNA adducts in the presence of ultraviolet A irradiation. [NIH] Methyl salicylate: Non-steroidal anti-inflammatory drugs. [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiological: Pertaining to microbiology : the science that deals with microorganisms, including algae, bacteria, fungi, protozoa and viruses. [EU] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microcirculation: The vascular network lying between the arterioles and venules; includes capillaries, metarterioles and arteriovenous anastomoses. Also, the flow of blood through this network. [NIH] Microfilaments: The smallest of the cytoskeletal filaments. They are composed chiefly of actin. [NIH] Microgram: A unit of mass (weight) of the metric system, being one-millionth of a gram (106 gm.) or one one-thousandth of a milligram (10-3 mg.). [EU] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living organisms, they are sometimes classified as microorganisms. [NIH] Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Microsomal: Of or pertaining to microsomes : vesicular fragments of endoplasmic reticulum formed after disruption and centrifugation of cells. [EU] Microtubules: Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein tubulin. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Milligram: A measure of weight. A milligram is approximately 450,000-times smaller than a pound and 28,000-times smaller than an ounce. [NIH] Milliliter: A measure of volume for a liquid. A milliliter is approximately 950-times smaller
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than a quart and 30-times smaller than a fluid ounce. A milliliter of liquid and a cubic centimeter (cc) of liquid are the same. [NIH] Millimeter: A measure of length. A millimeter is approximately 26-times smaller than an inch. [NIH] Mineralization: The action of mineralizing; the state of being mineralized. [EU] Mineralocorticoids: A group of corticosteroids primarily associated with the regulation of water and electrolyte balance. This is accomplished through the effect on ion transport in renal tubules, resulting in retention of sodium and loss of potassium. Mineralocorticoid secretion is itself regulated by plasma volume, serum potassium, and angiotensin II. [NIH] Minor Histocompatibility Antigens: Allelic alloantigens often responsible for weak graft rejection in cases when (major) histocompatibility has been established by standard tests. In the mouse they are coded by more than 500 genes at up to 30 minor histocompatibility loci. The most well-known minor histocompatibility antigen in mammals is the H-Y antigen. [NIH]
Mitochondria: Parts of a cell where aerobic production (also known as cell respiration) takes place. [NIH] Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Mitotic: Cell resulting from mitosis. [NIH] Mobility: Capability of movement, of being moved, or of flowing freely. [EU] Mobilization: The process of making a fixed part or stored substance mobile, as by separating a part from surrounding structures to make it accessible for an operative procedure or by causing release into the circulation for body use of a substance stored in the body. [EU] Mode of Transmission: Hepatitis A [NIH] Modeling: A treatment procedure whereby the therapist presents the target behavior which the learner is to imitate and make part of his repertoire. [NIH] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Modulator: A specific inductor that brings out characteristics peculiar to a definite region. [EU]
Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecular Chaperones: A family of cellular proteins that mediate the correct assembly or disassembly of other polypeptides, and in some cases their assembly into oligomeric structures, but which are not components of those final structures. It is believed that chaperone proteins assist polypeptides to self-assemble by inhibiting alternative assembly pathways that produce nonfunctional structures. Some classes of molecular chaperones are the nucleoplasmins, the chaperonins, the heat-shock proteins 70, and the heat-shock proteins 90. [NIH] Molecular Probes: A group of atoms or molecules attached to other molecules or cellular structures and used in studying the properties of these molecules and structures. Radioactive DNA or RNA sequences are used in molecular genetics to detect the presence of a complementary sequence by molecular hybridization. [NIH] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA,
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can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] Monoclonal antibodies: Laboratory-produced substances that can locate and bind to cancer cells wherever they are in the body. Many monoclonal antibodies are used in cancer detection or therapy; each one recognizes a different protein on certain cancer cells. Monoclonal antibodies can be used alone, or they can be used to deliver drugs, toxins, or radioactive material directly to a tumor. [NIH] Monocyte: A type of white blood cell. [NIH] Mononuclear: A cell with one nucleus. [NIH] Monotherapy: A therapy which uses only one drug. [EU] Mood Disorders: Those disorders that have a disturbance in mood as their predominant feature. [NIH] Morphogenesis: The development of the form of an organ, part of the body, or organism. [NIH]
Morphological: Relating to the configuration or the structure of live organs. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Motility: The ability to move spontaneously. [EU] Motion Sickness: Sickness caused by motion, as sea sickness, train sickness, car sickness, and air sickness. [NIH] Mucocutaneous: Pertaining to or affecting the mucous membrane and the skin. [EU] Mucolytic: Destroying or dissolving mucin; an agent that so acts : a mucopolysaccharide or glycoprotein, the chief constituent of mucus. [EU] Mucosa: A mucous membrane, or tunica mucosa. [EU] Mucositis: A complication of some cancer therapies in which the lining of the digestive system becomes inflamed. Often seen as sores in the mouth. [NIH] Mucus: The viscous secretion of mucous membranes. It contains mucin, white blood cells, water, inorganic salts, and exfoliated cells. [NIH] Multicenter study: A clinical trial that is carried out at more than one medical institution. [NIH]
Multiple sclerosis: A disorder of the central nervous system marked by weakness, numbness, a loss of muscle coordination, and problems with vision, speech, and bladder control. Multiple sclerosis is thought to be an autoimmune disease in which the body's immune system destroys myelin. Myelin is a substance that contains both protein and fat (lipid) and serves as a nerve insulator and helps in the transmission of nerve signals. [NIH] Multivalent: Pertaining to a group of 5 or more homologous or partly homologous chromosomes during the zygotene stage of prophase to first metaphasis in meiosis. [NIH] Muscle Fibers: Large single cells, either cylindrical or prismatic in shape, that form the basic unit of muscle tissue. They consist of a soft contractile substance enclosed in a tubular sheath. [NIH] Muscular Atrophy: Derangement in size and number of muscle fibers occurring with aging,
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reduction in blood supply, or following immobilization, prolonged weightlessness, malnutrition, and particularly in denervation. [NIH] Muscular Dystrophies: A general term for a group of inherited disorders which are characterized by progressive degeneration of skeletal muscles. [NIH] Mustard Gas: Severe irritant and vesicant of skin, eyes, and lungs. It may cause blindness and lethal lung edema and was formerly used as a war gas. The substance has been proposed as a cytostatic and for treatment of psoriasis. It has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP-85-002, 1985) (Merck, 11th ed). [NIH] Mutagenic: Inducing genetic mutation. [EU] Mutagens: Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes. [NIH] Myalgia: Pain in a muscle or muscles. [EU] Myasthenia: Muscular debility; any constitutional anomaly of muscle. [EU] Mycophenolate mofetil: A drug that is being studied for its effectiveness in preventing graft-versus-host disease and autoimmune disorders. [NIH] Mycosis: Any disease caused by a fungus. [EU] Mycosis Fungoides: A chronic malignant T-cell lymphoma of the skin. In the late stages the lymph nodes and viscera are affected. [NIH] Mycotoxins: Toxins derived from bacteria or fungi. [NIH] Mydriatic: 1. Dilating the pupil. 2. Any drug that dilates the pupil. [EU] Myelin: The fatty substance that covers and protects nerves. [NIH] Myelogenous: Produced by, or originating in, the bone marrow. [NIH] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Myocardial Reperfusion: Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing myocardial reperfusion injury. [NIH] Myocardial Reperfusion Injury: Functional, metabolic, or structural changes in ischemic heart muscle thought to result from reperfusion to the ischemic areas. Changes can be fatal to muscle cells and may include edema with explosive cell swelling and disintegration, sarcolemma disruption, fragmentation of mitochondria, contraction band necrosis, enzyme washout, and calcium overload. Other damage may include hemorrhage and ventricular arrhythmias. One possible mechanism of damage is thought to be oxygen free radicals. Treatment currently includes the introduction of scavengers of oxygen free radicals, and injury is thought to be prevented by warm blood cardioplegic infusion prior to reperfusion. [NIH]
Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myopathy: Any disease of a muscle. [EU]
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Myosin: Chief protein in muscle and the main constituent of the thick filaments of muscle fibers. In conjunction with actin, it is responsible for the contraction and relaxation of muscles. [NIH] Myositis: Inflammation of a voluntary muscle. [EU] Myotonic Dystrophy: A condition presenting muscle weakness and wasting which may be progressive. [NIH] Myristate: Pharmacological activator of protein kinase C. [NIH] Naive: Used to describe an individual who has never taken a certain drug or class of drugs (e. g., AZT-naive, antiretroviral-naive), or to refer to an undifferentiated immune system cell. [NIH] Nasal Mucosa: The mucous membrane lining the nasal cavity. [NIH] Nasal Polyps: Focal accumulations of edema fluid in the nasal mucosa accompanied by hyperplasia of the associated submucosal connective tissue. Polyps may be neoplasms, foci of inflammation, degenerative lesions, or malformations. [NIH] Natural killer cells: NK cells. A type of white blood cell that contains granules with enzymes that can kill tumor cells or microbial cells. Also called large granular lymphocytes (LGL). [NIH] Natural selection: A part of the evolutionary process resulting in the survival and reproduction of the best adapted individuals. [NIH] Nausea: An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses. [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH] Necrolysis: Separation or exfoliation of tissue due to necrosis. [EU] Need: A state of tension or dissatisfaction felt by an individual that impels him to action toward a goal he believes will satisfy the impulse. [NIH] Needle biopsy: The removal of tissue or fluid with a needle for examination under a microscope. Also called fine-needle aspiration. [NIH] Neomycin: Antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C. It acts by inhibiting translation during protein synthesis. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Neoplasia: Abnormal and uncontrolled cell growth. [NIH] Neoplasm: A new growth of benign or malignant tissue. [NIH] Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] Nephrolithiasis: Kidney stones. [NIH] Nephrology: A subspecialty of internal medicine concerned with the anatomy, physiology, and pathology of the kidney. [NIH] Nephropathy: Disease of the kidneys. [EU] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH]
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Nerve Fibers: Slender processes of neurons, especially the prolonged axons that conduct nerve impulses. [NIH] Nerve Growth Factor: Nerve growth factor is the first of a series of neurotrophic factors that were found to influence the growth and differentiation of sympathetic and sensory neurons. It is comprised of alpha, beta, and gamma subunits. The beta subunit is responsible for its growth stimulating activity. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neurodermatitis: An extremely variable eczematous skin disease that is presumed to be a response to prolonged vigorous scratching, rubbing, or pinching to relieve intense pruritus. It varies in intensity, severity, course, and morphologic expression in different individuals. Neurodermatitis is believed by some to be psychogenic. The circumscribed or localized form is often referred to as lichen simplex chronicus. [NIH] Neurogenic: Loss of bladder control caused by damage to the nerves controlling the bladder. [NIH] Neurogenic Inflammation: Inflammation caused by an injurious stimulus of peripheral neurons and resulting in release of neuropeptides which affect vascular permeability and help initiate proinflammatory and immune reactions at the site of injury. [NIH] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropathy: A problem in any part of the nervous system except the brain and spinal cord. Neuropathies can be caused by infection, toxic substances, or disease. [NIH] Neuropeptide: A member of a class of protein-like molecules made in the brain. Neuropeptides consist of short chains of amino acids, with some functioning as neurotransmitters and some functioning as hormones. [NIH] Neuropharmacology: The branch of pharmacology dealing especially with the action of drugs upon various parts of the nervous system. [NIH] Neurophysiology: The scientific discipline concerned with the physiology of the nervous system. [NIH] Neuroretinitis: Inflammation of the optic nerve head and adjacent retina. [NIH] Neurosecretory Systems: A system of neurons that has the specialized function to produce and secrete hormones, and that constitutes, in whole or in part, an endocrine organ or system. [NIH] Neurotensin: A biologically active tridecapeptide isolated from the hypothalamus. It has been shown to induce hypotension in the rat, to stimulate contraction of guinea pig ileum and rat uterus, and to cause relaxation of rat duodenum. There is also evidence that it acts as both a peripheral and a central nervous system neurotransmitter. [NIH] Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins,
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endorphins, and serotonin. [EU] Neurotrophins: A nerve growth factor. [NIH] Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH] Neutrophil: A type of white blood cell. [NIH] Neutrophil Infiltration: The diffusion or accumulation of neutrophils in tissues or cells in response to a wide variety of substances released at the sites of inflammatory reactions. [NIH] Nevus: A benign growth on the skin, such as a mole. A mole is a cluster of melanocytes and surrounding supportive tissue that usually appears as a tan, brown, or flesh-colored spot on the skin. The plural of nevus is nevi (NEE-vye). [NIH] Nickel: A trace element with the atomic symbol Ni, atomic number 28, and atomic weight 58.69. It is a cofactor of the enzyme urease. [NIH] Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells. It is synthesized from arginine by a complex reaction, catalyzed by nitric oxide synthase. Nitric oxide is endothelium-derived relaxing factor. It is released by the vascular endothelium and mediates the relaxation induced by some vasodilators such as acetylcholine and bradykinin. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic guanylate cyclase and thus elevates intracellular levels of cyclic GMP. [NIH]
Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Nonverbal Communication: Transmission of emotions, ideas, and attitudes between individuals in ways other than the spoken language. [NIH] Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclear Proteins: Proteins found in the nucleus of a cell. Do not confuse with nucleoproteins which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleoproteins: Proteins conjugated with nucleic acids. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the
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chromosomes. [NIH] Nummular: Coin-sized and coin-shaped. [EU] Nursing Care: Care given to patients by nursing service personnel. [NIH] Occupational Groups: Members of the various professions (e.g., physicians) or occupations (e.g., police). [NIH] Ocular: 1. Of, pertaining to, or affecting the eye. 2. Eyepiece. [EU] Odour: A volatile emanation that is perceived by the sense of smell. [EU] Ointments: Semisolid preparations used topically for protective emollient effects or as a vehicle for local administration of medications. Ointment bases are various mixtures of fats, waxes, animal and plant oils and solid and liquid hydrocarbons. [NIH] Oleanolic Acid: Occurs in leaves of Olea europaea, Viscum album L., and other higher plants. It is also the aglycone component of many saponins. [NIH] Oligosaccharides: Carbohydrates consisting of between two and ten monosaccharides connected by either an alpha- or beta-glycosidic link. They are found throughout nature in both the free and bound form. [NIH] Oliguria: Clinical manifestation of the urinary system consisting of a decrease in the amount of urine secreted. [NIH] Omega-3 fatty acid: A type of fat obtained in the diet and involved in immunity. [NIH] Omeprazole: A highly effective inhibitor of gastric acid secretion used in the therapy of gastric ulcers and Zollinger-Ellison syndrome. The drug inhibits the H(+)-K(+)-ATPase (H(+)-K(+)-exchanging ATPase) in a pH-dependent manner. This ATPase is considered the proton pump in the secretory membrane of the parietal cell. [NIH] Oncogene: A gene that normally directs cell growth. If altered, an oncogene can promote or allow the uncontrolled growth of cancer. Alterations can be inherited or caused by an environmental exposure to carcinogens. [NIH] Oncogenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH] Oncology: The study of cancer. [NIH] Onychomycosis: Mycosis of the nails, possibly due to some extent to humidity. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Opalescent: Showing a milky iridescence, like an opal. [EU] Operon: The genetic unit consisting of a feedback system under the control of an operator gene, in which a structural gene transcribes its message in the form of mRNA upon blockade of a repressor produced by a regulator gene. Included here is the attenuator site of bacterial operons where transcription termination is regulated. [NIH] Ophthalmic: Pertaining to the eye. [EU] Ophthalmology: A surgical specialty concerned with the structure and function of the eye and the medical and surgical treatment of its defects and diseases. [NIH] Opisthorchiasis: Infection with flukes of the genus Opisthorchis. [NIH] Opportunistic Infections: An infection caused by an organism which becomes pathogenic under certain conditions, e.g., during immunosuppression. [NIH] Opsin: A protein formed, together with retinene, by the chemical breakdown of metarhodopsin. [NIH] Optic Disk: The portion of the optic nerve seen in the fundus with the ophthalmoscope. It is formed by the meeting of all the retinal ganglion cell axons as they enter the optic nerve.
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[NIH]
Optic Nerve: The 2nd cranial nerve. The optic nerve conveys visual information from the retina to the brain. The nerve carries the axons of the retinal ganglion cells which sort at the optic chiasm and continue via the optic tracts to the brain. The largest projection is to the lateral geniculate nuclei; other important targets include the superior colliculi and the suprachiasmatic nuclei. Though known as the second cranial nerve, it is considered part of the central nervous system. [NIH] Oral Manifestations: Disorders of the mouth attendant upon non-oral disease or injury. [NIH]
Orbit: One of the two cavities in the skull which contains an eyeball. Each eye is located in a bony socket or orbit. [NIH] Orbital: Pertaining to the orbit (= the bony cavity that contains the eyeball). [EU] Orderly: A male hospital attendant. [NIH] Organ Culture: The growth in aseptic culture of plant organs such as roots or shoots, beginning with organ primordia or segments and maintaining the characteristics of the organ. [NIH] Organelles: Specific particles of membrane-bound organized living substances present in eukaryotic cells, such as the mitochondria; the golgi apparatus; endoplasmic reticulum; lysomomes; plastids; and vacuoles. [NIH] Osmolarity: The concentration of osmotically active particles expressed in terms of osmoles of solute per litre of solution. [EU] Osmoles: The standard unit of osmotic pressure. [NIH] Ossification: The formation of bone or of a bony substance; the conversion of fibrous tissue or of cartilage into bone or a bony substance. [EU] Osteoarthritis: A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans. [NIH] Osteoclasts: A large multinuclear cell associated with the absorption and removal of bone. An odontoclast, also called cementoclast, is cytomorphologically the same as an osteoclast and is involved in cementum resorption. [NIH] Osteomalacia: A condition marked by softening of the bones (due to impaired mineralization, with excess accumulation of osteoid), with pain, tenderness, muscular weakness, anorexia, and loss of weight, resulting from deficiency of vitamin D and calcium. [EU]
Osteoporosis: Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis and age-related (or senile) osteoporosis. [NIH] Outpatient: A patient who is not an inmate of a hospital but receives diagnosis or treatment in a clinic or dispensary connected with the hospital. [NIH] Ovaries: The pair of female reproductive glands in which the ova, or eggs, are formed. The ovaries are located in the pelvis, one on each side of the uterus. [NIH] Ovary: Either of the paired glands in the female that produce the female germ cells and secrete some of the female sex hormones. [NIH] Overexpress: An excess of a particular protein on the surface of a cell. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH]
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Oxazolidinones: Derivatives of oxazolidin-2-one. They represent an important class of synthetic antibiotic agents. [NIH] Oxidants: Oxidizing agents or electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (oxidation-reduction). In vivo, it appears that phagocyte-generated oxidants function as tumor promoters or cocarcinogens rather than as complete carcinogens perhaps because of the high levels of endogenous antioxidant defenses. It is also thought that oxidative damage in joints may trigger the autoimmune response that characterizes the persistence of the rheumatoid disease process. [NIH]
Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]
Oxidation-Reduction: A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471). [NIH] Oxidative metabolism: A chemical process in which oxygen is used to make energy from carbohydrates (sugars). Also known as aerobic respiration, cell respiration, or aerobic metabolism. [NIH] Oxidative Phosphorylation: Electron transfer through the cytochrome system liberating free energy which is transformed into high-energy phosphate bonds. [NIH] Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] Oxides: Binary compounds of oxygen containing the anion O(2-). The anion combines with metals to form alkaline oxides and non-metals to form acidic oxides. [NIH] Oxygenase: Enzyme which breaks down heme, the iron-containing oxygen-carrying constituent of the red blood cells. [NIH] Pachymeningitis: Inflammation of the dura mater of the brain, the spinal cord or the optic nerve. [NIH] Paclitaxel: Antineoplastic agent isolated from the bark of the Pacific yew tree, Taxus brevifolia. Paclitaxel stabilizes microtubules in their polymerized form and thus mimics the action of the proto-oncogene proteins c-mos. [NIH] Palladium: A chemical element having an atomic weight of 106.4, atomic number of 46, and the symbol Pd. It is a white, ductile metal resembling platinum, and following it in abundance and importance of applications. It is used in dentistry in the form of gold, silver, and copper alloys. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Palliative therapy: Treatment given to relieve symptoms caused by advanced cancer. Palliative therapy does not alter the course of a disease but improves the quality of life. [NIH] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar
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gland that secretes digestive enzymes. [NIH] Pancreatic: Having to do with the pancreas. [NIH] Pancreatic cancer: Cancer of the pancreas, a salivary gland of the abdomen. [NIH] Pancreatic Juice: The fluid containing digestive enzymes secreted by the pancreas in response to food in the duodenum. [NIH] Pancreatitis: Acute or chronic inflammation of the pancreas, which may be asymptomatic or symptomatic, and which is due to autodigestion of a pancreatic tissue by its own enzymes. It is caused most often by alcoholism or biliary tract disease; less commonly it may be associated with hyperlipaemia, hyperparathyroidism, abdominal trauma (accidental or operative injury), vasculitis, or uraemia. [EU] Papilla: A small nipple-shaped elevation. [NIH] Papillary: Pertaining to or resembling papilla, or nipple. [EU] Papillomavirus: A genus of Papovaviridae causing proliferation of the epithelium, which may lead to malignancy. A wide range of animals are infected including humans, chimpanzees, cattle, rabbits, dogs, and horses. [NIH] Papule: A small circumscribed, superficial, solid elevation of the skin. [EU] Par excellence: The petrous portion of the temporal bone, containing the inner ear and wedged in at the base of the skull between the sphenoid and occipital bones. [NIH] Parapsoriasis: The term applied to a group of relatively uncommon inflammatory, maculopapular, scaly eruptions of unknown etiology and resistant to conventional treatment. Eruptions are both psoriatic and lichenoid in appearance, but the diseases are distinct from psoriasis, lichen planus, or other recognized dermatoses. Proposed nomenclature divides parapsoriasis into two distinct subgroups, pityriasis lichenoides and parapsoriasis en plaques (small- and large-plaque parapsoriasis). [NIH] Parasitic: Having to do with or being a parasite. A parasite is an animal or a plant that lives on or in an organism of another species and gets at least some of its nutrients from it. [NIH] Parathyroid: 1. Situated beside the thyroid gland. 2. One of the parathyroid glands. 3. A sterile preparation of the water-soluble principle(s) of the parathyroid glands, ad-ministered parenterally as an antihypocalcaemic, especially in the treatment of acute hypoparathyroidism with tetany. [EU] Parathyroid Glands: Two small paired endocrine glands in the region of the thyroid gland. They secrete parathyroid hormone and are concerned with the metabolism of calcium and phosphorus. [NIH] Parathyroid hormone: A substance made by the parathyroid gland that helps the body store and use calcium. Also called parathormone, parathyrin, or PTH. [NIH] Parenteral: Not through the alimentary canal but rather by injection through some other route, as subcutaneous, intramuscular, intraorbital, intracapsular, intraspinal, intrasternal, intravenous, etc. [EU] Parietal: 1. Of or pertaining to the walls of a cavity. 2. Pertaining to or located near the parietal bone, as the parietal lobe. [EU] Paroxysmal: Recurring in paroxysms (= spasms or seizures). [EU] Partial remission: The shrinking, but not complete disappearance, of a tumor in response to therapy. Also called partial response. [NIH] Patch: A piece of material used to cover or protect a wound, an injured part, etc.: a patch over the eye. [NIH]
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Pathogen: Any disease-producing microorganism. [EU] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]
Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] Pathologies: The study of abnormality, especially the study of diseases. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Advocacy: Promotion and protection of the rights of patients, frequently through a legal process. [NIH] Patient Care Management: Generating, planning, organizing, and administering medical and nursing care and services for patients. [NIH] Patient Compliance: Voluntary cooperation of the patient in following a prescribed regimen. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]
Pelvic: Pertaining to the pelvis. [EU] Pemphigus: Group of chronic blistering diseases characterized histologically by acantholysis and blister formation within the epidermis. [NIH] Penis: The external reproductive organ of males. It is composed of a mass of erectile tissue enclosed in three cylindrical fibrous compartments. Two of the three compartments, the corpus cavernosa, are placed side-by-side along the upper part of the organ. The third compartment below, the corpus spongiosum, houses the urethra. [NIH] Pentoxifylline: A methylxanthine derivative that inhibits phosphodiesterase and affects blood rheology. It improves blood flow by increasing erythrocyte and leukocyte flexibility. It also inhibits platelet aggregation. Pentoxifylline modulates immunologic activity by stimulating cytokine production. [NIH] Pepsin: An enzyme made in the stomach that breaks down proteins. [NIH] Pepsin A: Formed from pig pepsinogen by cleavage of one peptide bond. The enzyme is a single polypeptide chain and is inhibited by methyl 2-diaazoacetamidohexanoate. It cleaves peptides preferentially at the carbonyl linkages of phenylalanine or leucine and acts as the principal digestive enzyme of gastric juice. [NIH] Peptic: Pertaining to pepsin or to digestion; related to the action of gastric juices. [EU] Peptic Ulcer: Ulcer that occurs in those portions of the alimentary tract which come into contact with gastric juice containing pepsin and acid. It occurs when the amount of acid and pepsin is sufficient to overcome the gastric mucosal barrier. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Peptide T: N-(N-(N(2)-(N-(N-(N-(N-D-Alanyl L-seryl)-L-threonyl)-L-threonyl) L-threonyl)L-asparaginyl)-L-tyrosyl) L-threonine. Octapeptide sharing sequence homology with HIV envelope protein gp120. It is potentially useful as antiviral agent in AIDS therapy. The core pentapeptide sequence, TTNYT, consisting of amino acids 4-8 in peptide T, is the HIV envelope sequence required for attachment to the CD4 receptor. [NIH] Perception: The ability quickly and accurately to recognize similarities and differences
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among presented objects, whether these be pairs of words, pairs of number series, or multiple sets of these or other symbols such as geometric figures. [NIH] Percutaneous: Performed through the skin, as injection of radiopacque material in radiological examination, or the removal of tissue for biopsy accomplished by a needle. [EU] Perfusion: Bathing an organ or tissue with a fluid. In regional perfusion, a specific area of the body (usually an arm or a leg) receives high doses of anticancer drugs through a blood vessel. Such a procedure is performed to treat cancer that has not spread. [NIH] Perianal: Located around the anus. [EU] Pericardium: The fibroserous sac surrounding the heart and the roots of the great vessels. [NIH]
Periodontitis: Inflammation of the periodontal membrane; also called periodontitis simplex. [NIH]
Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Peripheral stem cells: Immature cells found circulating in the bloodstream. New blood cells develop from peripheral stem cells. [NIH] Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] Peritonitis: Inflammation of the peritoneum; a condition marked by exudations in the peritoneum of serum, fibrin, cells, and pus. It is attended by abdominal pain and tenderness, constipation, vomiting, and moderate fever. [EU] Perivascular: Situated around a vessel. [EU] Pesticides: Chemicals used to destroy pests of any sort. The concept includes fungicides (industrial fungicides), insecticides, rodenticides, etc. [NIH] Petrolatum: A colloidal system of semisolid hydrocarbons obtained from petroleum. It is used as an ointment base, topical protectant, and lubricant. [NIH] Petroleum: Naturally occurring complex liquid hydrocarbons which, after distillation, yield combustible fuels, petrochemicals, and lubricants. [NIH] PH: The symbol relating the hydrogen ion (H+) concentration or activity of a solution to that of a given standard solution. Numerically the pH is approximately equal to the negative logarithm of H+ concentration expressed in molarity. pH 7 is neutral; above it alkalinity increases and below it acidity increases. [EU] Phagocyte: An immune system cell that can surround and kill microorganisms and remove dead cells. Phagocytes include macrophages. [NIH] Phallic: Pertaining to the phallus, or penis. [EU] Pharmaceutical Preparations: Drugs intended for human or veterinary use, presented in their finished dosage form. Included here are materials used in the preparation and/or formulation of the finished dosage form. [NIH] Pharmaceutical Solutions: Homogeneous liquid preparations that contain one or more chemical substances dissolved, i.e., molecularly dispersed, in a suitable solvent or mixture of
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mutually miscible solvents. For reasons of their ingredients, method of preparation, or use, they do not fall into another group of products. [NIH] Pharmacist: A person trained to prepare and distribute medicines and to give information about them. [NIH] Pharmacodynamics: The study of the biochemical and physiological effects of drugs and the mechanisms of their actions, including the correlation of actions and effects of drugs with their chemical structure; also, such effects on the actions of a particular drug or drugs. [EU] Pharmacokinetic: The mathematical analysis of the time courses of absorption, distribution, and elimination of drugs. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Pharmacotherapy: A regimen of using appetite suppressant medications to manage obesity by decreasing appetite or increasing the feeling of satiety. These medications decrease appetite by increasing serotonin or catecholamine—two brain chemicals that affect mood and appetite. [NIH] Pharynx: The hollow tube about 5 inches long that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes to the stomach). [NIH] Phenolphthalein: An acid-base indicator which is colorless in acid solution, but turns pink to red as the solution becomes alkaline. It is used medicinally as a cathartic. [NIH] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH] Phenyl: Ingredient used in cold and flu remedies. [NIH] Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phloroglucinol: 1,3,5-Benzenetriol. A trinitrobenzene derivative with antispasmodic properties that is used primarily as a laboratory reagent. [NIH] Phosphodiesterase: Effector enzyme that regulates the levels of a second messenger, the cyclic GMP. [NIH] Phosphoglycerate Kinase: An enzyme catalyzing the transfer of a phosphate group from 3phospho-D-glycerate in the presence of ATP to yield 3-phospho-D-glyceroyl phosphate and ADP. EC 2.7.2.3. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylase: An enzyme of the transferase class that catalyzes the phosphorylysis of a terminal alpha-1,4-glycosidic bond at the non-reducing end of a glycogen molecule, releasing a glucose 1-phosphate residue. Phosphorylase should be qualified by the natural substance acted upon. EC 2.4.1.1. [NIH] Phosphorylase a: The phosphorylated and more active form of phosphorylase that functions
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as a regulatory enzyme during glycogen breakdown. The phosphate groups are hydrolytically removed by phosphorylase phosphatase to form phosphorylase B and orthophosphate. EC 2.4.1.-. [NIH] Phosphorylase b: The relatively inactive form of phosphorylase that is reactivated to form phosphorylase A by phosphorylase kinase, which catalyzes the enzymatic phosphorylation of the serine residues at the expense of ATP. [NIH] Phosphorylase Kinase: An enzyme that catalyzes the conversion of ATP and phosphorylase b to ADP and phosphorylase a. EC 2.7.1.38. [NIH] Phosphorylase Phosphatase: An enzyme that deactivates glycogen phosphorylase a by releasing inorganic phosphate and phosphorylase b, the inactive form. EC 3.1.3.17. [NIH] Phosphorylate: Attached to a phosphate group. [NIH] Phosphorylated: Attached to a phosphate group. [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Photoallergy: Sensitization of the skin to light usually due to the action of certain substances or drugs, may occur shortly after exposure to a substance or after a latent period of from days to months. [NIH] Photochemotherapy: Therapy using oral or topical photosensitizing agents with subsequent exposure to light. [NIH] Photocoagulation: Using a special strong beam of light (laser) to seal off bleeding blood vessels such as in the eye. The laser can also burn away blood vessels that should not have grown in the eye. This is the main treatment for diabetic retinopathy. [NIH] Photodermatitis: Dermatitis caused or elicited by exposure to ultraviolet light, may be phototoxic or photoallergic. [NIH] Photodynamic therapy: Treatment with drugs that become active when exposed to light. These drugs kill cancer cells. [NIH] Photoreceptor: Receptor capable of being activated by light stimuli, as a rod or cone cell of the eye. [NIH] Photosensitivity: An abnormal cutaneous response involving the interaction between photosensitizing substances and sunlight or filtered or artificial light at wavelengths of 280400 mm. There are two main types : photoallergy and photoxicity. [EU] Photosensitizer: A drug used in photodynamic therapy. When absorbed by cancer cells and exposed to light, the drug becomes active and kills the cancer cells. [NIH] Photosensitizing Agents: Drugs that are pharmacologically inactive but when exposed to ultraviolet radiation or sunlight are converted to their active metabolite to produce a beneficial reaction affecting the diseased tissue. These compounds can be administered topically or systemically and have been used therapeutically to treat psoriasis and various types of neoplasms. [NIH] Phototherapy: Treatment of disease by exposure to light, especially by variously concentrated light rays or specific wavelengths. [NIH] Physical Examination: Systematic and thorough inspection of the patient for physical signs of disease or abnormality. [NIH] Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]
Physiology: The science that deals with the life processes and functions of organismus, their
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cells, tissues, and organs. [NIH] Pigmentation: Coloration or discoloration of a part by a pigment. [NIH] Pigments: Any normal or abnormal coloring matter in plants, animals, or micro-organisms. [NIH]
Pilot study: The initial study examining a new method or treatment. [NIH] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [NIH] Pityriasis: A name originally applied to a group of skin diseases characterized by the formation of fine, branny scales, but now used only with a modifier. [EU] Pityriasis Lichenoides: A subgroup of parapsoriasis itself divided into acute and chronic forms. The acute form is characterized by the abrupt onset of a generalized, reddish-brown, maculopapular eruption. Lesions may be vesicular, hemorrhagic, crusted, or necrotic. Histologically the disease is characterized by epidermal necrolysis. The chronic form shows milder skin changes with necrosis. An important variant of the chronic form is lymphomatoid papulosis. [NIH] Pityriasis Rosea: A mild exanthematous inflammation of unknown etiology. It is characterized by the presence of salmon-colored maculopapular lesions. The most striking feature is the arrangement of the lesions such that the long axis is parallel to the lines of cleavage. The eruptions are usually generalized, affecting chiefly the trunk, and the course is often self-limiting. [NIH] Placebo Effect: An effect usually, but not necessarily, beneficial that is attributable to an expectation that the regimen will have an effect, i.e., the effect is due to the power of suggestion. [NIH] Placenta: A highly vascular fetal organ through which the fetus absorbs oxygen and other nutrients and excretes carbon dioxide and other wastes. It begins to form about the eighth day of gestation when the blastocyst adheres to the decidua. [NIH] Plant Oils: Oils derived from plants or plant products. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasmin: A product of the lysis of plasminogen (profibrinolysin) by plasminogen activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH] Plasminogen: Precursor of fibrinolysin (plasmin). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent. [NIH]
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Plasminogen Activators: A heterogeneous group of proteolytic enzymes that convert plasminogen to plasmin. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation. EC 3.4.21.-. [NIH] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Platinum: Platinum. A heavy, soft, whitish metal, resembling tin, atomic number 78, atomic weight 195.09, symbol Pt. (From Dorland, 28th ed) It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as "alutiae". [NIH]
Pleated: Particular three-dimensional pattern of amyloidoses. [NIH] Pneumoconiosis: Condition characterized by permanent deposition of substantial amounts of particulate matter in the lungs, usually of occupational or environmental origin, and by the tissue reaction to its presence. [NIH] Pneumonia: Inflammation of the lungs. [NIH] Podophyllotoxin: The main active constituent of the resin from the roots of may apple or mandrake (Podophyllum peltatum and P. emodi). It is a potent spindle poison, toxic if taken internally, and has been used as a cathartic. It is very irritating to skin and mucous membranes, has keratolytic actions, has been used to treat warts and keratoses, and may have antineoplastic properties, as do some of its congeners and derivatives. [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Polyarthritis: An inflammation of several joints together. [EU] Polycystic: An inherited disorder characterized by many grape-like clusters of fluid-filled cysts that make both kidneys larger over time. These cysts take over and destroy working kidney tissue. PKD may cause chronic renal failure and end-stage renal disease. [NIH] Polyethylene: A vinyl polymer made from ethylene. It can be branched or linear. Branched or low-density polyethylene is tough and pliable but not to the same degree as linear polyethylene. Linear or high-density polyethylene has a greater hardness and tensile strength. Polyethylene is used in a variety of products, including implants and prostheses. [NIH]
Polymerase: An enzyme which catalyses the synthesis of DNA using a single DNA strand as a template. The polymerase copies the template in the 5'-3'direction provided that sufficient quantities of free nucleotides, dATP and dTTP are present. [NIH] Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation
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analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships. [NIH] Polymers: Compounds formed by the joining of smaller, usually repeating, units linked by covalent bonds. These compounds often form large macromolecules (e.g., polypeptides, proteins, plastics). [NIH] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH] Polyphosphates: Linear polymers in which orthophosphate residues are linked with energy-rich phosphoanhydride bonds. They are found in plants, animals, and microorganisms. [NIH] Polyposis: The development of numerous polyps (growths that protrude from a mucous membrane). [NIH] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Polyunsaturated fat: An unsaturated fat found in greatest amounts in foods derived from plants, including safflower, sunflower, corn, and soybean oils. [NIH] Polyvinyl Chloride: A polyvinyl resin used extensively in the manufacture of plastics, including medical devices, tubing, and other packaging. It is also used as a rubber substitute. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postmenopausal: Refers to the time after menopause. Menopause is the time in a woman's life when menstrual periods stop permanently; also called "change of life." [NIH] Postnatal: Occurring after birth, with reference to the newborn. [EU] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Post-traumatic: Occurring as a result of or after injury. [EU] Potassium: An element that is in the alkali group of metals. It has an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte and it plays a significant role in the regulation of fluid volume and maintenance of the water-electrolyte balance. [NIH] Potassium Chloride: Potassium chloride. A white crystal or crystalline powder used as an electrolyte replenisher, in the treatment of hypokalemia, in buffer solutions, and in fertilizers and explosives. [NIH] Potassium Citrate: A powder that dissolves in water, which is administered orally, and is used as a diuretic, expectorant, systemic alkalizer, and electrolyte replenisher. [NIH] Potentiates: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Precancerous: A term used to describe a condition that may (or is likely to) become cancer. Also called premalignant. [NIH]
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Preclinical: Before a disease becomes clinically recognizable. [EU] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Predisposition: A latent susceptibility to disease which may be activated under certain conditions, as by stress. [EU] Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [NIH] Prednisone: A synthetic anti-inflammatory glucocorticoid derived from cortisone. It is biologically inert and converted to prednisolone in the liver. [NIH] Preeclampsia: A toxaemia of late pregnancy characterized by hypertension, edema, and proteinuria, when convulsions and coma are associated, it is called eclampsia. [EU] Premalignant: A term used to describe a condition that may (or is likely to) become cancer. Also called precancerous. [NIH] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Prickle: Several layers of the epidermis where the individual cells are connected by cell bridges. [NIH] Probe: An instrument used in exploring cavities, or in the detection and dilatation of strictures, or in demonstrating the potency of channels; an elongated instrument for exploring or sounding body cavities. [NIH] Procaine: A local anesthetic of the ester type that has a slow onset and a short duration of action. It is mainly used for infiltration anesthesia, peripheral nerve block, and spinal block. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1016). [NIH] Prodrug: A substance that gives rise to a pharmacologically active metabolite, although not itself active (i. e. an inactive precursor). [NIH] Progeny: The offspring produced in any generation. [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Promotor: In an operon, a nucleotide sequence located at the operator end which contains all the signals for the correct initiation of genetic transcription by the RNA polymerase holoenzyme and determines the maximal rate of RNA synthesis. [NIH] Promyelocytic leukemia: A type of acute myeloid leukemia, a quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. [NIH]
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Prone: Having the front portion of the body downwards. [NIH] Prophase: The first phase of cell division, in which the chromosomes become visible, the nucleus starts to lose its identity, the spindle appears, and the centrioles migrate toward opposite poles. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Propolis: Resinous substance obtained from beehives; contains many different substances which may have antimicrobial or antimycotic activity topically; its extracts are called propolis resin or balsam. Synonyms: bee bread; hive dross; bee glue. [NIH] Proportional: Being in proportion : corresponding in size, degree, or intensity, having the same or a constant ratio; of, relating to, or used in determining proportions. [EU] Prospective Studies: Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group. [NIH] Prospective study: An epidemiologic study in which a group of individuals (a cohort), all free of a particular disease and varying in their exposure to a possible risk factor, is followed over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] Prostaglandin: Any of a group of components derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway that are extremely potent mediators of a diverse group of physiologic processes. The abbreviation for prostaglandin is PG; specific compounds are designated by adding one of the letters A through I to indicate the type of substituents found on the hydrocarbon skeleton and a subscript (1, 2 or 3) to indicate the number of double bonds in the hydrocarbon skeleton e.g., PGE2. The predominant naturally occurring prostaglandins all have two double bonds and are synthesized from arachidonic acid (5,8,11,14-eicosatetraenoic acid) by the pathway shown in the illustration. The 1 series and 3 series are produced by the same pathway with fatty acids having one fewer double bond (8,11,14-eicosatrienoic acid or one more double bond (5,8,11,14,17-eicosapentaenoic acid) than arachidonic acid. The subscript a or ß indicates the configuration at C-9 (a denotes a substituent below the plane of the ring, ß, above the plane). The naturally occurring PGF's have the a configuration, e.g., PGF2a. All of the prostaglandins act by binding to specific cell-surface receptors causing an increase in the level of the intracellular second messenger cyclic AMP (and in some cases cyclic GMP also). The effect produced by the cyclic AMP increase depends on the specific cell type. In some cases there is also a positive feedback effect. Increased cyclic AMP increases prostaglandin synthesis leading to further increases in cyclic AMP. [EU] Prostaglandins A: (13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE. PGA(1) and PGA(2) as well as their 19hydroxy derivatives are found in many organs and tissues. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protease Inhibitors: Compounds which inhibit or antagonize biosynthesis or actions of proteases (endopeptidases). [NIH]
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Protective Agents: Synthetic or natural substances which are given to prevent a disease or disorder or are used in the process of treating a disease or injury due to a poisonous agent. [NIH]
Protein Binding: The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific proteinbinding measures are often used as assays in diagnostic assessments. [NIH] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Isoforms: Different forms of a protein that may be produced from different genes, or from the same gene by alternative splicing. [NIH] Protein Kinases: A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein. EC 2.7.1.37. [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Protein-Tyrosine Kinase: An enzyme that catalyzes the phosphorylation of tyrosine residues in proteins with ATP or other nucleotides as phosphate donors. EC 2.7.1.112. [NIH] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Proteoglycan: A molecule that contains both protein and glycosaminoglycans, which are a type of polysaccharide. Proteoglycans are found in cartilage and other connective tissues. [NIH]
Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Proteome: The protein complement of an organism coded for by its genome. [NIH] Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] Proton Pump: Integral membrane proteins that transport protons across a membrane against a concentration gradient. This transport is driven by hydrolysis of ATP by H(+)transporting ATP synthase. [NIH] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Proto-Oncogene Proteins: Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity. [NIH] Proto-Oncogene Proteins c-mos: Cellular proteins encoded by the c-mos genes. They function in the cell cycle to maintain maturation promoting factor in the active state and have protein-serine/threonine kinase activity. Oncogenic transformation can take place when c-mos proteins are expressed at the wrong time. [NIH] Proto-Oncogenes: Normal cellular genes homologous to viral oncogenes. The products of proto-oncogenes are important regulators of biological processes and appear to be involved
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in the events that serve to maintain the ordered procession through the cell cycle. Protooncogenes have names of the form c-onc. [NIH] Protozoa: A subkingdom consisting of unicellular organisms that are the simplest in the animal kingdom. Most are free living. They range in size from submicroscopic to macroscopic. Protozoa are divided into seven phyla: Sarcomastigophora, Labyrinthomorpha, Apicomplexa, Microspora, Ascetospora, Myxozoa, and Ciliophora. [NIH] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Pruritic: Pertaining to or characterized by pruritus. [EU] Pruritus: An intense itching sensation that produces the urge to rub or scratch the skin to obtain relief. [NIH] Psoralen: A substance that binds to the DNA in cells and stops them from multiplying. It is being studied in the treatment of graft-versus-host disease and is used in the treatment of psoriasis and vitiligo. [NIH] Psoriasis: A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis. [NIH] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychoactive: Those drugs which alter sensation, mood, consciousness or other psychological or behavioral functions. [NIH] Psychogenic: Produced or caused by psychic or mental factors rather than organic factors. [EU]
Psychoneuroimmunology: The field concerned with the interrelationship between the brain, behavior and the immune system. Neuropsychologic, neuroanatomic and psychosocial studies have demonstrated their role in accentuating or diminishing immune/allergic responses. [NIH] Psychotherapy: A generic term for the treatment of mental illness or emotional disturbances primarily by verbal or nonverbal communication. [NIH] Puberty: The period during which the secondary sex characteristics begin to develop and the capability of sexual reproduction is attained. [EU] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Pulmonary: Relating to the lungs. [NIH] Pulmonary Edema: An accumulation of an excessive amount of watery fluid in the lungs, may be caused by acute exposure to dangerous concentrations of irritant gasses. [NIH] Pulmonary Emphysema: Condition of the lungs characterized by increase beyond normal in the size of air spaces distal to the terminal bronchioles, either from dilatation of the alveoli or from destruction of their walls. [NIH] Pulmonary Fibrosis: Chronic inflammation and progressive fibrosis of the pulmonary alveolar walls, with steadily progressive dyspnea, resulting finally in death from oxygen lack or right heart failure. [NIH]
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Pulmonary hypertension: Abnormally high blood pressure in the arteries of the lungs. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Pupil: The aperture in the iris through which light passes. [NIH] Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include adenine and guanine, constituents of nucleic acids, as well as many alkaloids such as caffeine and theophylline. Uric acid is the metabolic end product of purine metabolism. [NIH] Purulent: Consisting of or containing pus; associated with the formation of or caused by pus. [EU] Pustular: Pertaining to or of the nature of a pustule; consisting of pustules (= a visible collection of pus within or beneath the epidermis). [EU] Pyoderma: Any purulent skin disease (Dorland, 27th ed). [NIH] Pyoderma Gangrenosum: An idiopathic, rapidly evolving, and severely debilitating disease occurring most commonly in association with chronic ulcerative colitis. It is characterized by the presence of boggy, purplish ulcers with undermined borders, appearing mostly on the legs. The majority of cases are in people between 40 and 60 years old. Its etiology is unknown. [NIH] Pyrazinamide: A pyrazine that is used therapeutically as an antitubercular agent. [NIH] Pyrimidines: A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (cytosine, thymine, and uracil) and form the basic structure of the barbiturates. [NIH] Quality of Life: A generic concept reflecting concern with the modification and enhancement of life attributes, e.g., physical, political, moral and social environment. [NIH] Quaternary: 1. Fourth in order. 2. Containing four elements or groups. [EU] Quiescent: Marked by a state of inactivity or repose. [EU] Quinacrine: N(4)-(6-Chloro-2-methoxy-9-acridinyl)-N(1),N(1)-diethyl-1,4-pentanediamine. An acridine derivative formerly widely used as an antimalarial but superseded by chloroquine in recent years. It has also been used as an anthelmintic and in the treatment of giardiasis and malignant effusions. It is used in cell biological experiments as an inhibitor of phospholipase A2. [NIH] Quinidine: An optical isomer of quinine, extracted from the bark of the Cinchona tree and similar plant species. This alkaloid dampens the excitability of cardiac and skeletal muscles by blocking sodium and potassium currents across cellular membranes. It prolongs cellular action potential, and decreases automaticity. Quinidine also blocks muscarinic and alphaadrenergic neurotransmission. [NIH] Quinine: An alkaloid derived from the bark of the cinchona tree. It is used as an antimalarial drug, and is the active ingredient in extracts of the cinchona that have been used for that purpose since before 1633. Quinine is also a mild antipyretic and analgesic and has been used in common cold preparations for that purpose. It was used commonly and as a bitter and flavoring agent, and is still useful for the treatment of babesiosis. Quinine is also useful in some muscular disorders, especially nocturnal leg cramps and myotonia congenita, because of its direct effects on muscle membrane and sodium channels. The mechanisms of its antimalarial effects are not well understood. [NIH] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not
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sufficiently so as to achieve the status of a taxon. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radioactive: Giving off radiation. [NIH] Radioactivity: The quality of emitting or the emission of corpuscular or electromagnetic radiations consequent to nuclear disintegration, a natural property of all chemical elements of atomic number above 83, and possible of induction in all other known elements. [EU] Radiography: Examination of any part of the body for diagnostic purposes by means of roentgen rays, recording the image on a sensitized surface (such as photographic film). [NIH] Radioimmunotherapy: Radiotherapy where cytotoxic radionuclides are linked to antibodies in order to deliver toxins directly to tumor targets. Therapy with targeted radiation rather than antibody-targeted toxins (immunotoxins) has the advantage that adjacent tumor cells, which lack the appropriate antigenic determinants, can be destroyed by radiation cross-fire. Radioimmunotherapy is sometimes called targeted radiotherapy, but this latter term can also refer to radionuclides linked to non-immune molecules (radiotherapy). [NIH] Radiolabeled: Any compound that has been joined with a radioactive substance. [NIH] Radiological: Pertaining to radiodiagnostic and radiotherapeutic procedures, and interventional radiology or other planning and guiding medical radiology. [NIH] Radiotherapy: The use of ionizing radiation to treat malignant neoplasms and other benign conditions. The most common forms of ionizing radiation used as therapy are x-rays, gamma rays, and electrons. A special form of radiotherapy, targeted radiotherapy, links a cytotoxic radionuclide to a molecule that targets the tumor. When this molecule is an antibody or other immunologic molecule, the technique is called radioimmunotherapy. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Randomized clinical trial: A study in which the participants are assigned by chance to separate groups that compare different treatments; neither the researchers nor the participants can choose which group. Using chance to assign people to groups means that the groups will be similar and that the treatments they receive can be compared objectively. At the time of the trial, it is not known which treatment is best. It is the patient's choice to be in a randomized trial. [NIH] Randomized Controlled Trials: Clinical trials that involve at least one test treatment and one control treatment, concurrent enrollment and follow-up of the test- and control-treated groups, and in which the treatments to be administered are selected by a random process, such as the use of a random-numbers table. Treatment allocations using coin flips, odd-even numbers, patient social security numbers, days of the week, medical record numbers, or other such pseudo- or quasi-random processes, are not truly randomized and trials employing any of these techniques for patient assignment are designated simply controlled clinical trials. [NIH]
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Reactive Oxygen Species: Reactive intermediate oxygen species including both radicals and non-radicals. These substances are constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been implicated in a number of diseases. Scientific data exist that link the reactive oxygen species produced by inflammatory phagocytes to cancer development. [NIH] Reagent: A substance employed to produce a chemical reaction so as to detect, measure, produce, etc., other substances. [EU] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] Reconstitution: 1. A type of regeneration in which a new organ forms by the rearrangement of tissues rather than from new formation at an injured surface. 2. The restoration to original form of a substance previously altered for preservation and storage, as the restoration to a liquid state of blood serum or plasma that has been dried and stored. [EU] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Recur: To occur again. Recurrence is the return of cancer, at the same site as the original (primary) tumor or in another location, after the tumor had disappeared. [NIH] Recurrence: The return of a sign, symptom, or disease after a remission. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Red Nucleus: A pinkish-yellow portion of the midbrain situated in the rostral mesencephalic tegmentum. It receives a large projection from the contralateral half of the cerebellum via the superior cerebellar peduncle and a projection from the ipsilateral motor cortex. [NIH] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Refractory: Not readily yielding to treatment. [EU] Regeneration: The natural renewal of a structure, as of a lost tissue or part. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Relapse: The return of signs and symptoms of cancer after a period of improvement. [NIH] Reliability: Used technically, in a statistical sense, of consistency of a test with itself, i. e. the extent to which we can assume that it will yield the same result if repeated a second time. [NIH]
Remission: A decrease in or disappearance of signs and symptoms of cancer. In partial remission, some, but not all, signs and symptoms of cancer have disappeared. In complete remission, all signs and symptoms of cancer have disappeared, although there still may be cancer in the body. [NIH] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and
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progressive renal glomerular tubular or interstitial disease. [NIH] Renal Osteodystrophy: Decalcification of bone due to hyperparathyroidism secondary to chronic kidney disease. [NIH] Renin: An enzyme which is secreted by the kidney and is formed from prorenin in plasma and kidney. The enzyme cleaves the Leu-Leu bond in angiotensinogen to generate angiotensin I. EC 3.4.23.15. (Formerly EC 3.4.99.19). [NIH] Reperfusion: Restoration of blood supply to tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. It is primarily a procedure for treating infarction or other ischemia, by enabling viable ischemic tissue to recover, thus limiting further necrosis. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing reperfusion injury. [NIH] Reperfusion Injury: Functional, metabolic, or structural changes, including necrosis, in ischemic tissues thought to result from reperfusion to ischemic areas of the tissue. The most common instance is myocardial reperfusion injury. [NIH] Repressor: Any of the specific allosteric protein molecules, products of regulator genes, which bind to the operator of operons and prevent RNA polymerase from proceeding into the operon to transcribe messenger RNA. [NIH] Reproductive cells: Egg and sperm cells. Each mature reproductive cell carries a single set of 23 chromosomes. [NIH] Reproductive system: In women, this system includes the ovaries, the fallopian tubes, the uterus (womb), the cervix, and the vagina (birth canal). The reproductive system in men includes the prostate, the testes, and the penis. [NIH] Research Design: A plan for collecting and utilizing data so that desired information can be obtained with sufficient precision or so that an hypothesis can be tested properly. [NIH] Resolving: The ability of the eye or of a lens to make small objects that are close together, separately visible; thus revealing the structure of an object. [NIH] Resorption: The loss of substance through physiologic or pathologic means, such as loss of dentin and cementum of a tooth, or of the alveolar process of the mandible or maxilla. [EU] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Respiratory distress syndrome: A lung disease that occurs primarily in premature infants; the newborn must struggle for each breath and blueing of its skin reflects the baby's inability to get enough oxygen. [NIH] Response Elements: Nucleotide sequences, usually upstream, which are recognized by specific regulatory transcription factors, thereby causing gene response to various regulatory agents. These elements may be found in both promotor and enhancer regions. [NIH]
Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH]
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Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retinaldehyde: A carotenoid constituent of visual pigments. It is the oxidized form of retinol which functions as the active component of the visual cycle. It is bound to the protein opsin forming the complex rhodopsin. When stimulated by visible light, the retinal component of the rhodopsin complex undergoes isomerization at the 11-position of the double bond to the cis-form; this is reversed in "dark" reactions to return to the native transconfiguration. [NIH] Retinitis: Inflammation of the retina. It is rarely limited to the retina, but is commonly associated with diseases of the choroid (chorioretinitis) and of the optic nerve (neuroretinitis). The disease may be confined to one eye, but since it is generally dependent on a constitutional factor, it is almost always bilateral. It may be acute in course, but as a rule it lasts many weeks or even several months. [NIH] Retinoblastoma: An eye cancer that most often occurs in children younger than 5 years. It occurs in hereditary and nonhereditary (sporadic) forms. [NIH] Retinoid: Vitamin A or a vitamin A-like compound. [NIH] Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous membranes. Retinol is being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Retinopathy: 1. Retinitis (= inflammation of the retina). 2. Retinosis (= degenerative, noninflammatory condition of the retina). [EU] Retreatment: The therapy of the same disease in a patient, with the same agent or procedure repeated after initial treatment, or with an additional or alternate measure or follow-up. It does not include therapy which requires more than one administration of a therapeutic agent or regimen. Retreatment is often used with reference to a different modality when the original one was inadequate, harmful, or unsuccessful. [NIH] Retrospective: Looking back at events that have already taken place. [NIH] Retroviral vector: RNA from a virus that is used to insert genetic material into cells. [NIH] Retrovirus: A member of a group of RNA viruses, the RNA of which is copied during viral replication into DNA by reverse transcriptase. The viral DNA is then able to be integrated into the host chromosomal DNA. [NIH] Rheology: The study of the deformation and flow of matter, usually liquids or fluids, and of the plastic flow of solids. The concept covers consistency, dilatancy, liquefaction, resistance to flow, shearing, thixotrophy, and viscosity. [NIH] Rheumatic Diseases: Disorders of connective tissue, especially the joints and related structures, characterized by inflammation, degeneration, or metabolic derangement. [NIH] Rheumatism: A group of disorders marked by inflammation or pain in the connective tissue structures of the body. These structures include bone, cartilage, and fat. [NIH] Rheumatoid: Resembling rheumatism. [EU] Rheumatoid arthritis: A form of arthritis, the cause of which is unknown, although infection, hypersensitivity, hormone imbalance and psychologic stress have been suggested
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as possible causes. [NIH] Rhinitis: Inflammation of the mucous membrane of the nose. [NIH] Rhodopsin: A photoreceptor protein found in retinal rods. It is a complex formed by the binding of retinal, the oxidized form of retinol, to the protein opsin and undergoes a series of complex reactions in response to visible light resulting in the transmission of nerve impulses to the brain. [NIH] Ribonucleoside Diphosphate Reductase: An enzyme of the oxidoreductase class that catalyzes the formation of 2'-deoxyribonucleotides from the corresponding ribonucleotides using NADPH as the ultimate electron donor. The deoxyribonucleoside diphosphates are used in DNA synthesis. (From Dorland, 27th ed) EC 1.17.4.1. [NIH] Ribose: A pentose active in biological systems usually in its D-form. [NIH] Ribosome: A granule of protein and RNA, synthesized in the nucleolus and found in the cytoplasm of cells. Ribosomes are the main sites of protein synthesis. Messenger RNA attaches to them and there receives molecules of transfer RNA bearing amino acids. [NIH] Rickets: A condition caused by deficiency of vitamin D, especially in infancy and childhood, with disturbance of normal ossification. The disease is marked by bending and distortion of the bones under muscular action, by the formation of nodular enlargements on the ends and sides of the bones, by delayed closure of the fontanelles, pain in the muscles, and sweating of the head. Vitamin D and sunlight together with an adequate diet are curative, provided that the parathyroid glands are functioning properly. [EU] Rigidity: Stiffness or inflexibility, chiefly that which is abnormal or morbid; rigor. [EU] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Rod: A reception for vision, located in the retina. [NIH] Rod cells: One type of specialized light-sensitive cells (photoreceptors) in the retina that provide side vision and the ability to see objects in dim light (night vision). [NIH] Roxithromycin: Semisynthetic derivative of erythromycin. It is concentrated by human phagocytes and is bioactive intracellularly. While the drug is active against a wide spectrum of pathogens, it is particularly effective in the treatment of respiratory and genital tract infections. [NIH] Rubber: A high-molecular-weight polymeric elastomer derived from the milk juice (latex) of Hevea brasiliensis and other trees. It is a substance that can be stretched at room temperature to atleast twice its original length and after releasing the stress, retractrapidly, and recover its original dimensions fully. Synthetic rubber is made from many different chemicals, including styrene, acrylonitrile, ethylene, propylene, and isoprene. [NIH] Rye: A hardy grain crop, Secale cereale, grown in northern climates. It is the most frequent host to ergot (claviceps), the toxic fungus. Its hybrid with wheat is triticale, another grain. [NIH]
Salicylate: Non-steroidal anti-inflammatory drugs. [NIH] Salicylic: A tuberculosis drug. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics
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when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] Scabies: A contagious cutaneous inflammation caused by the bite of the mite Sarcoptes scabiei. It is characterized by pruritic papular eruptions and burrows and affects primarily the axillae, elbows, wrists, and genitalia, although it can spread to cover the entire body. [NIH]
Scatter: The extent to which relative success and failure are divergently manifested in qualitatively different tests. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to characterize schizophrenia. [NIH] Sciatica: A condition characterized by pain radiating from the back into the buttock and posterior/lateral aspects of the leg. Sciatica may be a manifestation of sciatic neuropathy; radiculopathy (involving the L4, L5, S1 or S2 spinal nerve roots; often associated with intervertebral disk displacement); or lesions of the cauda equina. [NIH] Sclera: The tough white outer coat of the eyeball, covering approximately the posterior fivesixths of its surface, and continuous anteriorly with the cornea and posteriorly with the external sheath of the optic nerve. [EU] Scleroderma: A chronic disorder marked by hardening and thickening of the skin. Scleroderma can be localized or it can affect the entire body (systemic). [NIH] Scleroderma, Systemic: A chronic, progressive dermatosis characterized by boardlike hardening and immobility of the affected skin, with visceral involvement, especially of lungs, esophagus, kidneys and heart. It may be accompanied by calcinosis, Raynaud's phenomenon, and telangiectasis (CREST syndrome). It includes acrosclerosis and sclerodactyly. [NIH] Scleroproteins: Simple proteins characterized by their insolubility and fibrous structure. Within the body, they perform a supportive or protective function. [NIH] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] Sebaceous: Gland that secretes sebum. [NIH] Sebaceous gland: Gland that secretes sebum. [NIH] Seborrhea: Hypersecretion of sebum with excessive oily secretion from the sweat glands. [NIH]
Sebum: The oily substance secreted by sebaceous glands. It is composed of keratin, fat, and cellular debris. [NIH] Second Messenger Systems: Systems in which an intracellular signal is generated in response to an intercellular primary messenger such as a hormone or neurotransmitter. They are intermediate signals in cellular processes such as metabolism, secretion, contraction, phototransduction, and cell growth. Examples of second messenger systems are the adenyl cyclase-cyclic AMP system, the phosphatidylinositol diphosphate-inositol
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triphosphate system, and the cyclic GMP system. [NIH] Secondary tumor: Cancer that has spread from the organ in which it first appeared to another organ. For example, breast cancer cells may spread (metastasize) to the lungs and cause the growth of a new tumor. When this happens, the disease is called metastatic breast cancer, and the tumor in the lungs is called a secondary tumor. Also called secondary cancer. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Secretory: Secreting; relating to or influencing secretion or the secretions. [NIH] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Selenium: An element with the atomic symbol Se, atomic number 34, and atomic weight 78.96. It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of glutathione peroxidase. [NIH] Semen: The thick, yellowish-white, viscid fluid secretion of male reproductive organs discharged upon ejaculation. In addition to reproductive organ secretions, it contains spermatozoa and their nutrient plasma. [NIH] Seminiferous tubule: Tube used to transport sperm made in the testes. [NIH] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Sensitization: 1. Administration of antigen to induce a primary immune response; priming; immunization. 2. Exposure to allergen that results in the development of hypersensitivity. 3. The coating of erythrocytes with antibody so that they are subject to lysis by complement in the presence of homologous antigen, the first stage of a complement fixation test. [EU] Sepsis: The presence of bacteria in the bloodstream. [NIH] Septic: Produced by or due to decomposition by microorganisms; putrefactive. [EU] Sequence Homology: The degree of similarity between sequences. Studies of amino acid and nucleotide sequences provide useful information about the genetic relatedness of certain species. [NIH] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [NIH] Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines, and other amino acids. [NIH] Serologic: Analysis of a person's serum, especially specific immune or lytic serums. [NIH] Serology: The study of serum, especially of antigen-antibody reactions in vitro. [NIH] Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-tryptophan. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (receptors, serotonin) explain the
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broad physiological actions and distribution of this biochemical mediator. [NIH] Serous: Having to do with serum, the clear liquid part of blood. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Serum Albumin: A major plasma protein that serves in maintaining the plasma colloidal osmotic pressure and transporting large organic anions. [NIH] Sex Characteristics: Those characteristics that distinguish one sex from the other. The primary sex characteristics are the ovaries and testes and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction. [NIH] Sex Determination: The biological characteristics which distinguish human beings as female or male. [NIH] Shedding: Release of infectious particles (e. g., bacteria, viruses) into the environment, for example by sneezing, by fecal excretion, or from an open lesion. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock. [NIH]
Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Signal Transduction: The intercellular or intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GABA-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptormediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. [NIH] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] Sirolimus: A macrolide compound obtained from Streptomyces hygroscopicus that acts by selectively blocking the transcriptional activation of cytokines thereby inhibiting cytokine production. It is bioactive only when bound to immunophilins. Sirolimus is a potent immunosuppressant and possesses both antifungal and antineoplastic properties. [NIH] Sister Chromatid Exchange: An exchange of segments between the sister chromatids of a chromosome, either between the sister chromatids of a meiotic tetrad or between the sister chromatids of a duplicated somatic chromosome. Its frequency is increased by ultraviolet and ionizing radiation and other mutagenic agents and is particularly high in Bloom syndrome. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects
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many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skin Aging: The process of aging due to changes in the structure and elasticity of the skin over time. It may be a part of physiological aging or it may be due to the effects of ultraviolet radiation, usually through exposure to sunlight. [NIH] Skin graft: Skin that is moved from one part of the body to another. [NIH] Skin Pigmentation: Coloration of the skin. [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smallpox: A generalized virus infection with a vesicular rash. [NIH] Smoking Cessation: Discontinuation of the habit of smoking, the inhaling and exhaling of tobacco smoke. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]
Sneezing: Sudden, forceful, involuntary expulsion of air from the nose and mouth caused by irritation to the mucous membranes of the upper respiratory tract. [NIH] Soaps: Sodium or potassium salts of long chain fatty acids. These detergent substances are obtained by boiling natural oils or fats with caustic alkali. Sodium soaps are harder and are used as topical anti-infectives and vehicles in pills and liniments; potassium soaps are soft, used as vehicles for ointments and also as topical antimicrobials. [NIH] Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Social Security: Government sponsored social insurance programs. [NIH] Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Sodium salicylate: A drug that belongs to the family of drugs called nonsteroidal antiinflammatory drugs. Sodium salicylate may be tolerated by people who are sensitive to aspirin. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Solid tumor: Cancer of body tissues other than blood, bone marrow, or the lymphatic system. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Somatic cells: All the body cells except the reproductive (germ) cells. [NIH] Somatostatin: A polypeptide hormone produced in the hypothalamus, and other tissues and organs. It inhibits the release of human growth hormone, and also modulates important
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physiological functions of the kidney, pancreas, and gastrointestinal tract. Somatostatin receptors are widely expressed throughout the body. Somatostatin also acts as a neurotransmitter in the central and peripheral nervous systems. [NIH] Soybean Oil: Oil from soybean or soybean plant. [NIH] Spasmogenic: Capable of producing convulsions. [NIH] Spatial disorientation: Loss of orientation in space where person does not know which way is up. [NIH] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectroscopic: The recognition of elements through their emission spectra. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Sperm: The fecundating fluid of the male. [NIH] Sphenoid: An unpaired cranial bone with a body containing the sphenoid sinus and forming the posterior part of the medial walls of the orbits. [NIH] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spinal Nerve Roots: The paired bundles of nerve fibers entering and leaving the spinal cord at each segment. The dorsal and ventral nerve roots join to form the mixed segmental spinal nerves. The dorsal roots are generally afferent, formed by the central projections of the spinal (dorsal root) ganglia sensory cells, and the ventral roots efferent, comprising the axons of spinal motor and autonomic preganglionic neurons. There are, however, some exceptions to this afferent/efferent rule. [NIH] Spinal Nerves: The 31 paired peripheral nerves formed by the union of the dorsal and ventral spinal roots from each spinal cord segment. The spinal nerve plexuses and the spinal roots are also included. [NIH] Spinous: Like a spine or thorn in shape; having spines. [NIH] Spirochete: Lyme disease. [NIH] Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Spondylitis: Inflammation of the vertebrae. [EU] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Sprains and Strains: A collective term for muscle and ligament injuries without dislocation or fracture. A sprain is a joint injury in which some of the fibers of a supporting ligament are ruptured but the continuity of the ligament remains intact. A strain is an overstretching or
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overexertion of some part of the musculature. [NIH] Squamous: Scaly, or platelike. [EU] Squamous cell carcinoma: Cancer that begins in squamous cells, which are thin, flat cells resembling fish scales. Squamous cells are found in the tissue that forms the surface of the skin, the lining of the hollow organs of the body, and the passages of the respiratory and digestive tracts. Also called epidermoid carcinoma. [NIH] Squamous cell carcinoma: Cancer that begins in squamous cells, which are thin, flat cells resembling fish scales. Squamous cells are found in the tissue that forms the surface of the skin, the lining of the hollow organs of the body, and the passages of the respiratory and digestive tracts. Also called epidermoid carcinoma. [NIH] Squamous cells: Flat cells that look like fish scales under a microscope. These cells cover internal and external surfaces of the body. [NIH] Stabilizer: A device for maintaining constant X-ray tube voltage or current. [NIH] Staphylococcus: A genus of gram-positive, facultatively anaerobic, coccoid bacteria. Its organisms occur singly, in pairs, and in tetrads and characteristically divide in more than one plane to form irregular clusters. Natural populations of Staphylococcus are membranes of warm-blooded animals. Some species are opportunistic pathogens of humans and animals. [NIH] Staphylococcus aureus: Potentially pathogenic bacteria found in nasal membranes, skin, hair follicles, and perineum of warm-blooded animals. They may cause a wide range of infections and intoxications. [NIH] Steel: A tough, malleable, iron-based alloy containing up to, but no more than, two percent carbon and often other metals. It is used in medicine and dentistry in implants and instrumentation. [NIH] Stem cell transplantation: A method of replacing immature blood-forming cells that were destroyed by cancer treatment. The stem cells are given to the person after treatment to help the bone marrow recover and continue producing healthy blood cells. [NIH] Stem Cells: Relatively undifferentiated cells of the same lineage (family type) that retain the ability to divide and cycle throughout postnatal life to provide cells that can become specialized and take the place of those that die or are lost. [NIH] Sterile: Unable to produce children. [NIH] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Steroid therapy: Treatment with corticosteroid drugs to reduce swelling, pain, and other symptoms of inflammation. [NIH] Stilbenes: Organic compounds that contain 1,2-diphenylethylene as a functional group. [NIH]
Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU]
Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH]
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Stippling: A dotted appearance in cells on staining. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [NIH] Streptococcal: Caused by infection due to any species of streptococcus. [NIH] Streptococcal Infections: Infections with bacteria of the genus Streptococcus. [NIH] Streptococci: A genus of spherical Gram-positive bacteria occurring in chains or pairs. They are widely distributed in nature, being important pathogens but often found as normal commensals in the mouth, skin, and intestine of humans and other animals. [NIH] Streptococcus: A genus of gram-positive, coccoid bacteria whose organisms occur in pairs or chains. No endospores are produced. Many species exist as commensals or parasites on man or animals with some being highly pathogenic. A few species are saprophytes and occur in the natural environment. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stria: 1. A streak, or line. 2. A narrow bandlike structure; a general term for such longitudinal collections of nerve fibres in the brain. [EU] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Stroma: The middle, thickest layer of tissue in the cornea. [NIH] Stromal: Large, veil-like cell in the bone marrow. [NIH] Stromal Cells: Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the hematopoietic system and elsewhere. [NIH] Strontium: An element of the alkaline earth family of metals. It has the atomic symbol Sr, atomic number 38, and atomic weight 87.62. [NIH] Styrene: A colorless, toxic liquid with a strong aromatic odor. It is used to make rubbers, polymers and copolymers, and polystyrene plastics. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU] Subarachnoid: Situated or occurring between the arachnoid and the pia mater. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Sublingual: Located beneath the tongue. [EU] Submaxillary: Four to six lymph glands, located between the lower jaw and the submandibular salivary gland. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and
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peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]
Substrate: A substance upon which an enzyme acts. [EU] Sulfates: Inorganic salts of sulfuric acid. [NIH] Sulfur: An element that is a member of the chalcogen family. It has an atomic symbol S, atomic number 16, and atomic weight 32.066. It is found in the amino acids cysteine and methionine. [NIH] Sulfuric acid: A strong acid that, when concentrated is extemely corrosive to the skin and mucous membranes. It is used in making fertilizers, dyes, electroplating, and industrial explosives. [NIH] Sunburn: An injury to the skin causing erythema, tenderness, and sometimes blistering and resulting from excessive exposure to the sun. The reaction is produced by the ultraviolet radiation in sunlight. [NIH] Superantigens: Microbial antigens that have in common an extremely potent activating effect on T-cells that bear a specific variable region. Superantigens cross-link the variable region with class II MHC proteins regardless of the peptide binding in the T-cell receptor's pocket. The result is a transient expansion and subsequent death and anergy of the T-cells with the appropriate variable regions. [NIH] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Superoxide Dismutase: An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC 1.15.1.1. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Support group: A group of people with similar disease who meet to discuss how better to cope with their cancer and treatment. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Suppressive: Tending to suppress : effecting suppression; specifically : serving to suppress activity, function, symptoms. [EU] Surfactant: A fat-containing protein in the respiratory passages which reduces the surface tension of pulmonary fluids and contributes to the elastic properties of pulmonary tissue. [NIH]
Sweat: The fluid excreted by the sweat glands. It consists of water containing sodium chloride, phosphate, urea, ammonia, and other waste products. [NIH] Sweat Glands: Sweat-producing structures that are embedded in the dermis. Each gland consists of a single tube, a coiled body, and a superficial duct. [NIH] Symphysis: A secondary cartilaginous joint. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Synapse: The region where the processes of two neurons come into close contiguity, and the nervous impulse passes from one to the other; the fibers of the two are intermeshed, but, according to the general view, there is no direct contiguity. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of
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meiosis). [EU] Synchrotron: An accelerator in which the particles are guided by an increasing magnetic field while they are accelerated several times in an approximately circular path by electric fields produced by a high-frequency generator. [NIH] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Synovial: Of pertaining to, or secreting synovia. [EU] Synovial Fluid: The clear, viscous fluid secreted by the synovial membrane. It contains mucin, albumin, fat, and mineral salts and serves to lubricate joints. [NIH] Synovial Membrane: The inner membrane of a joint capsule surrounding a freely movable joint. It is loosely attached to the external fibrous capsule and secretes synovial fluid. [NIH] Synthetic retinoid: A substance related to vitamin A that is produced in a laboratory. [NIH] Syphilis: A contagious venereal disease caused by the spirochete Treponema pallidum. [NIH]
Systemic: Affecting the entire body. [NIH] Systemic disease: Disease that affects the whole body. [NIH] Systemic lupus erythematosus: SLE. A chronic inflammatory connective tissue disease marked by skin rashes, joint pain and swelling, inflammation of the kidneys, inflammation of the fibrous tissue surrounding the heart (i.e., the pericardium), as well as other problems. Not all affected individuals display all of these problems. May be referred to as lupus. [NIH] Systemic therapy: Treatment that uses substances that travel through the bloodstream, reaching and affecting cells all over the body. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Tachyphylaxis: 1. Rapid immunization against the effect of toxic doses of an extract or serum by previous injection of small doses. 2. Rapidly decreasing response to a drug or physiologically active agent after administration of a few doses. [EU] Tacrolimus: A macrolide isolated from the culture broth of a strain of Streptomyces tsukubaensis that has strong immunosuppressive activity in vivo and prevents the activation of T-lymphocytes in response to antigenic or mitogenic stimulation in vitro. [NIH] Tear Gases: Gases that irritate the eyes, throat, or skin. Severe lacrimation develops upon irritation of the eyes. [NIH] Telangiectasia: The permanent enlargement of blood vessels, causing redness in the skin or mucous membranes. [NIH] Tellurium: Tellurium. An element that is a member of the chalcogen family. It has the atomic symbol Te, atomic number 52, and atomic weight 127.60. It has been used as a coloring agent and in the manufacture of electrical equipment. Exposure may cause nausea, vomiting, and CNS depression. [NIH] Telomerase: Essential ribonucleoprotein reverse transcriptase that adds telomeric DNA to the ends of eukaryotic chromosomes. Telomerase appears to be repressed in normal human somatic tissues but reactivated in cancer, and thus may be necessary for malignant transformation. EC 2.7.7.-. [NIH] Temporal: One of the two irregular bones forming part of the lateral surfaces and base of the skull, and containing the organs of hearing. [NIH] Tendon: A discrete band of connective tissue mainly composed of parallel bundles of collagenous fibers by which muscles are attached, or two muscles bellies joined. [NIH]
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Tenosynovitis: Inflammation of a tendon sheath. [EU] Teratogen: A substance which, through immediate, prolonged or repeated contact with the skin may involve a risk of subsequent non-hereditable birth defects in offspring. [NIH] Teratogenic: Tending to produce anomalies of formation, or teratism (= anomaly of formation or development : condition of a monster). [EU] Teratogenicity: The power to cause abnormal development. [NIH] Testis: Either of the paired male reproductive glands that produce the male germ cells and the male hormones. [NIH] Testosterone: A hormone that promotes the development and maintenance of male sex characteristics. [NIH] Tetany: 1. Hyperexcitability of nerves and muscles due to decrease in concentration of extracellular ionized calcium, which may be associated with such conditions as parathyroid hypofunction, vitamin D deficiency, and alkalosis or result from ingestion of alkaline salts; it is characterized by carpopedal spasm, muscular twitching and cramps, laryngospasm with inspiratory stridor, hyperreflexia and choreiform movements. 2. Tetanus. [EU] Tetracaine: A potent local anesthetic of the ester type used for surface and spinal anesthesia. [NIH]
Tetracycline: An antibiotic originally produced by Streptomyces viridifaciens, but used mostly in synthetic form. It is an inhibitor of aminoacyl-tRNA binding during protein synthesis. [NIH] Thalamic: Cell that reaches the lateral nucleus of amygdala. [NIH] Thalamic Diseases: Disorders of the centrally located thalamus, which integrates a wide range of cortical and subcortical information. Manifestations include sensory loss, movement disorders; ataxia, pain syndromes, visual disorders, a variety of neuropsychological conditions, and coma. Relatively common etiologies include cerebrovascular disorders; craniocerebral trauma; brain neoplasms; brain hypoxia; intracranial hemorrhages; and infectious processes. [NIH] Thalidomide: A pharmaceutical agent originally introduced as a non-barbiturate hypnotic, but withdrawn from the market because of its known tetratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppresive and anti-angiogenic activity. It inhibits release of tumor necrosis factor alpha from monocytes, and modulates other cytokine action. [NIH] Theophylline: Alkaloid obtained from Thea sinensis (tea) and others. It stimulates the heart and central nervous system, dilates bronchi and blood vessels, and causes diuresis. The drug is used mainly in bronchial asthma and for myocardial stimulation. Among its more prominent cellular effects are inhibition of cyclic nucleotide phosphodiesterases and antagonism of adenosine receptors. [NIH] Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thermal: Pertaining to or characterized by heat. [EU] Thigh: A leg; in anatomy, any elongated process or part of a structure more or less comparable to a leg. [NIH] Thimerosal: A topical antiseptic used on skin and mucous membranes. It is also used as a preservative in pharmaceuticals. [NIH] Thioguanine: An antineoplastic compound which also has antimetabolite action. The drug is used in the therapy of acute leukemia. [NIH]
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Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. [NIH] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] Thrombocytes: Blood cells that help prevent bleeding by causing blood clots to form. Also called platelets. [NIH] Thrombocytopenia: A decrease in the number of blood platelets. [NIH] Thrombolytic: 1. Dissolving or splitting up a thrombus. 2. A thrombolytic agent. [EU] Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation. [NIH]
Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thromboxanes: Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase. [NIH] Thrombus: An aggregation of blood factors, primarily platelets and fibrin with entrapment of cellular elements, frequently causing vascular obstruction at the point of its formation. Some authorities thus differentiate thrombus formation from simple coagulation or clot formation. [EU] Thymus: An organ that is part of the lymphatic system, in which T lymphocytes grow and multiply. The thymus is in the chest behind the breastbone. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Thyroid Gland: A highly vascular endocrine gland consisting of two lobes, one on either side of the trachea, joined by a narrow isthmus; it produces the thyroid hormones which are concerned in regulating the metabolic rate of the body. [NIH] Thyroiditis: Inflammation of the thyroid gland. [NIH] Ticks: Blood-sucking arachnids of the order Acarina. [NIH] Tin: A trace element that is required in bone formation. It has the atomic symbol Sn, atomic number 50, and atomic weight 118.71. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Banks: Centers for acquiring, characterizing, and storing organs or tissue for future use. [NIH] Tissue Culture: Maintaining or growing of tissue, organ primordia, or the whole or part of an organ in vitro so as to preserve its architecture and/or function (Dorland, 28th ed). Tissue culture includes both organ culture and cell culture. [NIH] Tissue Distribution: Accumulation of a drug or chemical substance in various organs (including those not relevant to its pharmacologic or therapeutic action). This distribution depends on the blood flow or perfusion rate of the organ, the ability of the drug to penetrate organ membranes, tissue specificity, protein binding. The distribution is usually expressed as tissue to plasma ratios. [NIH]
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Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] Tone: 1. The normal degree of vigour and tension; in muscle, the resistance to passive elongation or stretch; tonus. 2. A particular quality of sound or of voice. 3. To make permanent, or to change, the colour of silver stain by chemical treatment, usually with a heavy metal. [EU] Tonus: A state of slight tension usually present in muscles even when they are not undergoing active contraction. [NIH] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Topical: On the surface of the body. [NIH] Torsion: A twisting or rotation of a bodily part or member on its axis. [NIH] Toxaemia: 1. The condition resulting from the spread of bacterial products (toxins) by the bloodstream. 2. A condition resulting from metabolic disturbances, e.g. toxaemia of pregnancy. [EU] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicodendron: A genus (formerly Rhus) of shrubs, vines, or trees that yields a highly allergenic oleoresin which causes a severe contact dermatitis. The most toxic species are Toxicodendron vernix (poison sumac), T. diversilobum (poison oak), and T. radicans (poison ivy). T. vernicifera yields a useful varnish from which certain enzymes (laccases) are obtained. [NIH] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] Toxin: A poison; frequently used to refer specifically to a protein produced by some higher plants, certain animals, and pathogenic bacteria, which is highly toxic for other living organisms. Such substances are differentiated from the simple chemical poisons and the vegetable alkaloids by their high molecular weight and antigenicity. [EU] Trace element: Substance or element essential to plant or animal life, but present in extremely small amounts. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Traction: The act of pulling. [NIH] Transcriptase: An enzyme which catalyses the synthesis of a complementary mRNA molecule from a DNA template in the presence of a mixture of the four ribonucleotides (ATP, UTP, GTP and CTP). [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transdermal: Entering through the dermis, or skin, as in administration of a drug applied to the skin in ointment or patch form. [EU]
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Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transfer Factor: Factor derived from leukocyte lysates of immune donors which can transfer both local and systemic cellular immunity to nonimmune recipients. [NIH] Transforming Growth Factor alpha: Factor isolated in a variety of tissues including epithelium, and maternal decidua. It is closely related to epidermal growth factor and binds to the EGF receptor. TGF-alpha acts synergistically with TGF-beta in inducing phenotypic transformation, but its physiological role is unknown. [NIH] Transforming Growth Factor beta: A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGFbeta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins. [NIH]
Transfusion: The infusion of components of blood or whole blood into the bloodstream. The blood may be donated from another person, or it may have been taken from the person earlier and stored until needed. [NIH] Transgenes: Genes that are introduced into an organism using gene transfer techniques. [NIH]
Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Translocating: The attachment of a fragment of one chromosome to a non-homologous chromosome. [NIH] Translocation: The movement of material in solution inside the body of the plant. [NIH] Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH] Transplantation: Transference of a tissue or organ, alive or dead, within an individual, between individuals of the same species, or between individuals of different species. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Trees: Woody, usually tall, perennial higher plants (Angiosperms, Gymnosperms, and some Pterophyta) having usually a main stem and numerous branches. [NIH] Tretinoin: An important regulator of gene expression, particularly during growth and development and in neoplasms. Retinoic acid derived from maternal vitamin A is essential for normal gene expression during embryonic development and either a deficiency or an excess can be teratogenic. It is also a topical dermatologic agent which is used in the treatment of psoriasis, acne vulgaris, and several other skin diseases. It has also been approved for use in promyelocytic leukemia. [NIH] Triamcinolone Acetonide: An esterified form of triamcinolone. It is an anti-inflammatory
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glucocorticoid used topically in the treatment of various skin disorders. Intralesional, intramuscular, and intra-articular injections are also administered under certain conditions. [NIH]
Triazolam: A short-acting benzodiazepine used in the treatment of insomnia. Some countries temporarily withdrew triazolam from the market because of concerns about adverse reactions, mostly psychological, associated with higher dose ranges. Its use at lower doses with appropriate care and labeling has been reaffirmed by the FDA and most other countries. [NIH] Tricuspid Atresia: Absence of the orifice between the right atrium and ventricle, with the presence of an atrial defect through which all the systemic venous return reaches the left heart. As a result, there is left ventricular hypertrophy because the right ventricle is absent or not functional. [NIH] Triglyceride: A lipid carried through the blood stream to tissues. Most of the body's fat tissue is in the form of triglycerides, stored for use as energy. Triglycerides are obtained primarily from fat in foods. [NIH] Trioxsalen: Pigmenting photosensitizing agent obtained from several plants, mainly Psoralea corylifolia. It is administered either topically or orally in conjunction with ultraviolet light in the treatment of vitiligo. [NIH] Tropism: Directed movements and orientations found in plants, such as the turning of the sunflower to face the sun. [NIH] Trypsin: A serine endopeptidase that is formed from trypsinogen in the pancreas. It is converted into its active form by enteropeptidase in the small intestine. It catalyzes hydrolysis of the carboxyl group of either arginine or lysine. EC 3.4.21.4. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tuberous Sclerosis: A rare congenital disease in which the essential pathology is the appearance of multiple tumors in the cerebrum and in other organs, such as the heart or kidneys. [NIH] Tumor model: A type of animal model which can be used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Tumor Necrosis Factor: Serum glycoprotein produced by activated macrophages and other mammalian mononuclear leukocytes which has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. It mimics the action of endotoxin but differs from it. It has a molecular weight of less than 70,000 kDa. [NIH] Tumour: 1. Swelling, one of the cardinal signs of inflammations; morbid enlargement. 2. A new growth of tissue in which the multiplication of cells is uncontrolled and progressive; called also neoplasm. [EU] Tunica: A rather vague term to denote the lining coat of hollow organs, tubes, or cavities. [NIH]
Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Ubiquinone: A lipid-soluble benzoquinone which is involved in electron transport in mitochondrial preparations. The compound occurs in the majority of aerobic organisms, from bacteria to higher plants and animals. [NIH] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH] Ulcerative colitis: Chronic inflammation of the colon that produces ulcers in its lining. This
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condition is marked by abdominal pain, cramps, and loose discharges of pus, blood, and mucus from the bowel. [NIH] Ultraviolet radiation: Invisible rays that are part of the energy that comes from the sun. UV radiation can damage the skin and cause melanoma and other types of skin cancer. UV radiation that reaches the earth's surface is made up of two types of rays, called UVA and UVB rays. UVB rays are more likely than UVA rays to cause sunburn, but UVA rays pass deeper into the skin. Scientists have long thought that UVB radiation can cause melanoma and other types of skin cancer. They now think that UVA radiation also may add to skin damage that can lead to skin cancer and cause premature aging. For this reason, skin specialists recommend that people use sunscreens that reflect, absorb, or scatter both kinds of UV radiation. [NIH] Ultraviolet Therapy: The use of ultraviolet electromagnetic radiation in the treatment of disease, usually of the skin. This is the part of the sun's spectrum that causes sunburn and tanning. Ultraviolet A, used in PUVA, is closer to visible light and less damaging than Ultraviolet B, which is ionizing. [NIH] Umbilical Arteries: Either of a pair of arteries originating from the internal iliac artery and passing through the umbilical cord to carry blood from the fetus to the placenta. [NIH] Umbilical Cord: The flexible structure, giving passage to the umbilical arteries and vein, which connects the embryo or fetus to the placenta. [NIH] Umbilicus: The pit in the center of the abdominal wall marking the point where the umbilical cord entered in the fetus. [NIH] Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [NIH] Unsaturated Fats: A type of fat. [NIH] Uracil: An anticancer drug that belongs to the family of drugs called alkylating agents. [NIH] Uraemia: 1. An excess in the blood of urea, creatinine, and other nitrogenous end products of protein and amino acids metabolism; more correctly referred to as azotemia. 2. In current usage the entire constellation of signs and symptoms of chronic renal failure, including nausea, vomiting anorexia, a metallic taste in the mouth, a uraemic odour of the breath, pruritus, uraemic frost on the skin, neuromuscular disorders, pain and twitching in the muscles, hypertension, edema, mental confusion, and acid-base and electrolyte imbalances. [EU]
Urban Health: The status of health in urban populations. [NIH] Urban Population: The inhabitants of a city or town, including metropolitan areas and suburban areas. [NIH] Urea: A compound (CO(NH2)2), formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids. [NIH] Urease: An enzyme that catalyzes the conversion of urea and water to carbon dioxide and ammonia. EC 3.5.1.5. [NIH] Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]
Uric: A kidney stone that may result from a diet high in animal protein. When the body breaks down this protein, uric acid levels rise and can form stones. [NIH]
Dictionary 531
Uridine Diphosphate: A uracil nucleotide containing a pyrophosphate group esterified to C5 of the sugar moiety. [NIH] Uridine Diphosphate Glucuronic Acid: A nucleoside diphosphate sugar which serves as a source of glucuronic acid for polysaccharide biosynthesis. It may also be epimerized to UDP iduronic acid, which donates iduronic acid to polysaccharides. In animals, UDP glucuronic acid is used for formation of many glucosiduronides with various aglycones. [NIH] Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Urocanic Acid: 4-Imidazoleacrylic acid. [NIH] Urogenital: Pertaining to the urinary and genital apparatus; genitourinary. [EU] Urokinase: A drug that dissolves blood clots or prevents them from forming. [NIH] Urticaria: A vascular reaction of the skin characterized by erythema and wheal formation due to localized increase of vascular permeability. The causative mechanism may be allergy, infection, or stress. [NIH] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH] Uvea: The middle coat of the eyeball, consisting of the choroid in the back of the eye and the ciliary body and iris in the front of the eye. [NIH] Uveitis: An inflammation of part or all of the uvea, the middle (vascular) tunic of the eye, and commonly involving the other tunics (the sclera and cornea, and the retina). [EU] Vaccination: Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vaccinia: The cutaneous and occasional systemic reactions associated with vaccination using smallpox (variola) vaccine. [NIH] Vaccinia Virus: The type species of Orthopoxvirus, related to cowpox virus, but whose true origin is unknown. It has been used as a live vaccine against smallpox. It is also used as a vector for inserting foreign DNA into animals. Rabbitpox virus is a subspecies of vaccinia virus. [NIH] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Varicose: The common ulcer in the lower third of the leg or near the ankle. [NIH] Varicose Ulcer: Ulcer due to varicose veins. Chronic venous insufficiency in the deep veins of the legs leads to shunting the venous return into the superficial veins, in which pressure and flow rate, as well as oxygen content, are increased. [NIH] Variola: A generalized virus infection with a vesicular rash. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vascular endothelial growth factor: VEGF. A substance made by cells that stimulates new blood vessel formation. [NIH] Vasculitis: Inflammation of a blood vessel. [NIH] Vasoactive: Exerting an effect upon the calibre of blood vessels. [EU]
532 Psoriasis
Vasoconstriction: Narrowing of the blood vessels without anatomic change, for which constriction, pathologic is used. [NIH] Vasodilator: An agent that widens blood vessels. [NIH] VE: The total volume of gas either inspired or expired in one minute. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venereal: Pertaining or related to or transmitted by sexual contact. [EU] Venous: Of or pertaining to the veins. [EU] Venous blood: Blood that has given up its oxygen to the tissues and carries carbon dioxide back for gas exchange. [NIH] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Vertebrae: A bony unit of the segmented spinal column. [NIH] Vesicular: 1. Composed of or relating to small, saclike bodies. 2. Pertaining to or made up of vesicles on the skin. [EU] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Viral vector: A type of virus used in cancer therapy. The virus is changed in the laboratory and cannot cause disease. Viral vectors produce tumor antigens (proteins found on a tumor cell) and can stimulate an antitumor immune response in the body. Viral vectors may also be used to carry genes that can change cancer cells back to normal cells. [NIH] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Viscosity: A physical property of fluids that determines the internal resistance to shear forces. [EU] Vitamin A: A substance used in cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Vitelline Membrane: The plasma membrane of the egg. [NIH] Vitiligo: A disorder consisting of areas of macular depigmentation, commonly on extensor aspects of extremities, on the face or neck, and in skin folds. Age of onset is often in young adulthood and the condition tends to progress gradually with lesions enlarging and extending until a quiescent state is reached. [NIH]
Dictionary 533
Vitreous: Glasslike or hyaline; often used alone to designate the vitreous body of the eye (corpus vitreum). [EU] Vitreous Hemorrhage: Hemorrhage into the vitreous body. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] Vulgaris: An affection of the skin, especially of the face, the back and the chest, due to chronic inflammation of the sebaceous glands and the hair follicles. [NIH] War: Hostile conflict between organized groups of people. [NIH] Wart: A raised growth on the surface of the skin or other organ. [NIH] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]
Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH] Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] Womb: A hollow, thick-walled, muscular organ in which the impregnated ovum is developed into a child. [NIH] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xanthine: An urinary calculus. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] X-ray therapy: The use of high-energy radiation from x-rays to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. X-ray therapy is also called radiation therapy, radiotherapy, and irradiation. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] Yolk Sac: An embryonic membrane formed from endoderm and mesoderm. In reptiles and birds it incorporates the yolk into the digestive tract for nourishing the embryo. In placental mammals its nutritional function is vestigial; however, it is the source of most of the intestinal mucosa and the site of formation of the germ cells. It is sometimes called the vitelline sac, which should not be confused with the vitelline membrane of the egg. [NIH] Yttrium: An element of the rare earth family of metals. It has the atomic symbol Y, atomic number 39, and atomic weight 88.91. In conjunction with other rare earths, yttrium is used as a phosphor in television receivers and is a component of the yttrium-aluminum garnet
534 Psoriasis
(YAG) lasers. [NIH] Zygote: The fertilized ovum. [NIH] Zymogen: Inactive form of an enzyme which can then be converted to the active form, usually by excision of a polypeptide, e. g. trypsinogen is the zymogen of trypsin. [NIH]
535
INDEX 6 6-Aminonicotinamide, 331, 333, 337, 425 A Abdomen, 425, 438, 460, 469, 479, 483, 498, 520, 522 Abdominal, 425, 466, 487, 497, 498, 500, 530 Abdominal Pain, 425, 466, 500, 530 Aberrant, 14, 45, 85, 303, 425, 447 Abortion, 425, 473 Acantholysis, 425, 499 Acatalasia, 425, 442 Acceptor, 22, 32, 425, 465, 483, 497 Acetic Acids, 287, 425 Acetohexamide, 279, 425 Acetylcholine, 425, 493, 494 Acetylcysteine, 244, 425 Acetylgalactosamine, 425, 468 Acetylglucosamine, 425, 468 Acidity, 425, 500 Acitretin, 7, 103, 111, 201, 223, 256, 257, 378, 399, 404, 425 Acne Vulgaris, 189, 205, 261, 310, 316, 426, 528 Acquired Immunodeficiency Syndrome, 272, 341, 426 Acrodermatitis, 151, 399, 426 Acrylonitrile, 426, 515 Actin, 53, 426, 488, 492 Actinic keratosis, 327, 426 Acute Disease, 56, 426 Acute leukemia, 426, 525 Acute renal, 40, 426, 470 Acyl, 310, 338, 426, 486 Adaptability, 426, 443 Adaptation, 155, 426 Adenine, 426, 510 Adenocarcinoma, 426, 471 Adenosine, 82, 110, 174, 194, 200, 426, 439, 501, 525 Adenosine Deaminase, 110, 174, 426 Adenosine Monophosphate, 82, 200, 426 Adenylate Cyclase, 130, 279, 426 Adhesions, 267, 339, 342, 427 Adipose Tissue, 204, 427 Adjunctive Therapy, 8, 427 Adjustment, 426, 427 Adjuvant, 55, 301, 427, 466
Adolescence, 398, 427, 444 Adrenal Cortex, 427, 428, 451, 473, 506 Adrenergic, 42, 427, 456, 460, 510 Adverse Effect, 6, 27, 85, 147, 194, 378, 427, 518 Aerobic, 427, 489, 497, 529 Aerosol, 340, 427 Aetiology, 349, 427 Affinity, 14, 15, 19, 22, 30, 45, 76, 179, 427, 428, 434, 483, 519 Affinity Chromatography, 19, 427 Agar, 427, 451, 503 Age Groups, 263, 345, 346, 352, 427 Age of Onset, 127, 427 Aged, 80 and Over, 427, 428 Agonist, 66, 428, 456 Agranulocytosis, 167, 428 Agrochemicals, 320, 428 Airway, 340, 428 Albumin, 428, 454, 524 Aldosterone, 314, 428 Algorithms, 48, 428, 437 Alimentary, 355, 428, 498, 499 Alkaline, 317, 428, 430, 440, 484, 497, 501, 522, 525 Alkaloid, 428, 436, 441, 447, 510, 525 Alleles, 31, 43, 304, 428, 471, 482 Allergen, 428, 454, 517 Allergic Rhinitis, 428, 469 Allogeneic, 37, 124, 169, 428, 468 Allogeneic bone marrow transplantation, 169, 428 Allograft, 428, 472 Alloys, 428, 485, 497 Allylamine, 428, 429 Alopecia, 8, 67, 88, 119, 192, 301, 362, 377, 429 Alpha Particles, 429, 511 Alpha-1, 429, 501 Alpha-helix, 429, 480 Alternative medicine, 236, 374, 429 Alternative Splicing, 174, 429, 508 Aluminum, 317, 322, 429, 533 Alveolar Process, 429, 513 Alveoli, 429, 509 Amber, 429, 476 Ameliorating, 49, 269, 429 Amine, 277, 279, 292, 429, 472
536 Psoriasis
Amino Acid Sequence, 429, 431, 461, 466 Aminolevulinic Acid, 377, 429 Aminopterin, 315, 325, 430 Ammonia, 426, 429, 430, 523, 530 Anabolic, 16, 430, 455 Anaesthesia, 430, 476 Anal, 355, 430, 463 Analgesic, 278, 430, 474, 510 Analog, 5, 6, 56, 73, 78, 252, 430, 464 Analogous, 39, 53, 57, 261, 335, 430, 456, 528 Anaphase, 28, 430 Anaphylatoxins, 23, 430, 448 Anaplasia, 430 Anatomical, 430, 434, 445, 449, 458, 476, 483, 516 Androgens, 427, 430, 451 Anemia, 389, 430, 464 Anergy, 77, 430, 523 Anesthesia, 428, 430, 506, 525 Angina, 34, 430 Angiogenesis, 11, 20, 25, 32, 43, 46, 58, 64, 69, 70, 79, 89, 141, 227, 304, 430, 459, 486 Angiogenesis Factor, 70, 141, 430 Angiogenesis inhibitor, 430, 459 Angiotensinogen, 430, 513 Anhydrous, 274, 296, 302, 431 Animal model, 28, 36, 38, 50, 56, 67, 69, 72, 74, 175, 262, 303, 313, 345, 346, 431, 529 Anionic, 269, 431 Anions, 73, 317, 428, 431, 480, 518, 523 Ankle, 6, 431, 531 Annealing, 431, 504 Anode, 79, 431 Anogenital, 319, 431 Anomalies, 29, 431, 525 Anorexia, 431, 466, 496, 530 Antagonism, 431, 439, 455, 525 Anthelmintic, 431, 510 Antibacterial, 163, 431, 520 Antibiotic, 68, 190, 255, 299, 326, 329, 339, 431, 439, 460, 492, 497, 520, 525 Antibody Affinity, 299, 347, 431 Anticoagulant, 431, 508 Anticonvulsant, 376, 431 Antidepressant, 432, 439 Antidote, 432, 440 Antifungal, 432, 481, 518 Antigen-Antibody Complex, 432, 448 Antigen-presenting cell, 76, 97, 102, 432, 453 Anti-infective, 432, 441, 473, 479, 519
Anti-inflammatory, 4, 12, 27, 28, 53, 71, 76, 157, 264, 265, 271, 273, 278, 293, 296, 324, 336, 339, 350, 355, 373, 431, 432, 434, 451, 467, 474, 476, 488, 506, 515, 519, 528 Anti-Inflammatory Agents, 271, 432, 434, 451 Antimetabolite, 7, 315, 325, 432, 464, 488, 525 Antimicrobial, 400, 432, 454, 456, 507 Antimycotic, 432, 507 Antineoplastic, 432, 451, 464, 465, 473, 486, 488, 497, 504, 518, 525 Antioxidant, 73, 90, 115, 263, 270, 271, 324, 350, 355, 432, 497 Antiproliferative, 4, 192, 205, 305, 432 Antipruritic, 273, 432, 441, 447 Antiseptic, 432, 525 Antiserum, 63, 432, 435 Antispasmodic, 432, 501 Antitumour, 191, 432 Antiviral, 252, 327, 425, 432, 465, 476, 478, 499 Anuria, 432, 481 Anus, 398, 430, 431, 432, 438, 447, 500 Apolipoproteins, 175, 432, 483 Apoptosis, 17, 33, 39, 44, 59, 77, 134, 181, 188, 197, 433, 443, 452 Approximate, 12, 13, 311, 433 Aqueous, 118, 314, 315, 433, 436, 452, 458, 473, 482, 483 Arachidonate 15-Lipoxygenase, 433, 483 Arachidonate Lipoxygenases, 433, 483 Arachidonic Acid, 265, 278, 320, 433, 457, 482, 483, 507 Arginine, 72, 430, 433, 494, 529 Aromatic, 227, 265, 433, 446, 501, 522 Arsenates, 322, 433 Arterial, 46, 428, 433, 445, 450, 474, 482, 508, 524 Arteries, 355, 433, 438, 450, 484, 488, 491, 510, 526, 530 Arteriolar, 23, 433, 439 Arterioles, 24, 433, 438, 441, 488 Arteriolosclerosis, 433 Arteriosclerosis, 355, 433, 474 Arteriovenous, 130, 433, 488 Arteriovenous Fistula, 130, 433 Artery, 433, 438, 450, 458, 491, 510, 513, 530, 532 Arthropathy, 154, 160, 163, 171, 409, 433 Articular, 321, 434, 496, 529
Index 537
Artifacts, 143, 434 Asbestos, 267, 339, 342, 434 Asbestosis, 434 Aseptic, 434, 496, 521 Aspiration, 251, 434 Aspirin, 271, 320, 434, 519 Assay, 16, 19, 30, 52, 434, 475 Astringents, 434, 487 Astrocytes, 434, 471 Asymptomatic, 425, 434, 498 Ataxia, 389, 434, 525 Atopic Eczema, 166, 434 Atrial, 434, 450, 529 Atrioventricular, 434, 450 Atrium, 434, 450, 529, 532 Atrophy, 4, 196, 389, 425, 434 Attenuation, 53, 435 Atypical, 91, 379, 435, 485 Auditory, 435, 461 Autacoids, 435, 476 Autoantibodies, 40, 52, 435 Autoantigens, 40, 52, 435 Autodigestion, 435, 498 Autoimmunity, 14, 23, 35, 38, 74, 75, 97, 124, 358, 407, 435 Autologous, 38, 435 Autonomic, 180, 425, 435, 494, 500, 520 Autonomic Nervous System, 180, 435, 500 Avidity, 68, 431, 435 Axonal, 78, 435 Axons, 78, 435, 493, 495, 496, 520 B Bacterial Physiology, 426, 435 Bacterial toxin, 68, 435 Bactericidal, 435, 461 Bacteriophage, 435, 503, 528 Bacterium, 435, 449, 470 Barbiturate, 435, 525 Basal cell carcinoma, 80, 132, 143, 193, 256, 301, 327, 403, 436 Basal cells, 295, 436 Basal Ganglia, 434, 436 Basal Ganglia Diseases, 434, 436 Base Sequence, 436, 464, 466 Basement Membrane, 436, 462 Basophils, 428, 436, 469, 482 Baths, 9, 212, 215, 399, 436 Bed Rest, 399, 436 Benign, 19, 63, 274, 284, 305, 354, 364, 433, 436, 469, 485, 492, 494, 511 Benzoic Acid, 325, 436 Berberine, 324, 350, 436
Beta 2-Microglobulin, 177, 436 Beta-Thromboglobulin, 436, 479 Bilateral, 92, 180, 437, 514 Bile, 437, 445, 465, 468, 472, 480, 483, 521 Bile duct, 437, 445 Bile Pigments, 437, 480 Biliary, 437, 441, 498 Biliary Tract, 437, 441, 498 Bilirubin, 428, 437, 468, 473 Binding Sites, 16, 62, 298, 437 Bioavailability, 266, 437 Biogenesis, 12, 46, 437 Biological response modifier, 437, 478 Biological therapy, 437, 469 Biopsy, 4, 10, 251, 254, 255, 404, 421, 437, 461, 500 Biotechnology, 79, 80, 119, 170, 362, 374, 385, 387, 388, 389, 390, 437 Biotransformation, 27, 320, 437 Bismuth, 270, 437 Bladder, 437, 490, 493, 507, 530, 531 Blastocyst, 437, 449, 503 Blister, 438, 499 Blood Coagulation, 438, 440, 526 Blood Coagulation Factors, 438 Blood Glucose, 438, 470, 474, 478 Blood Platelets, 438, 486, 517, 526 Blood pressure, 438, 441, 474, 490, 510, 519 Blood Proteins, 250, 438 Blood Stains, 375, 438 Blot, 38, 438 Body Fluids, 438, 456, 519 Bone Density, 34, 438 Bone Marrow Cells, 54, 438, 486 Bone Marrow Transplantation, 169, 285, 305, 438 Bone Resorption, 49, 289, 438, 440 Boron, 438, 451 Bowel, 147, 430, 438, 455, 477, 479, 500, 522, 530 Bowel Movement, 438, 455, 522 Brachytherapy, 438, 479, 480, 511, 533 Bradykinin, 439, 494 Brain Stem, 439, 444 Branch, 417, 439, 484, 493, 499, 520, 525 Breakdown, 439, 455, 465, 495, 502 Broadband, 78, 439 Broad-spectrum, 439, 454 Bromine, 231, 439 Bronchi, 439, 460, 462, 525, 527 Bronchial, 439, 472, 525 Bronchioles, 429, 439, 509
538 Psoriasis
Bronchitis, 43, 439, 446 Bronchoconstriction, 52, 439 Bronchus, 439 Buccal, 10, 439, 473, 484 Buccal mucosa, 10, 439 Bullous, 23, 52, 94, 100, 439 Bupivacaine, 439, 482 Bupropion, 121, 190, 439 Burns, 6, 9, 118, 353, 422, 439 Burns, Electric, 439 C Caffeine, 439, 510 Calcifediol, 439, 440 Calcification, 433, 440 Calcineurin, 142, 440 Calcinosis, 440, 516 Calcitonin, 28, 42, 65, 78, 440 Calcitonin Gene-Related Peptide, 42, 78, 440 Calcitriol, 95, 96, 99, 111, 137, 256, 440 Calcium channel blocker, 96, 290, 376, 440 Calcium Channel Blockers, 376, 440 Calcium Chloride, 317, 440 Calculi, 441, 468 Calendula, 241, 322, 335, 336, 441 Callus, 441, 458, 481 Calmodulin, 290, 291, 440, 441 Camphor, 325, 441 Capillary, 43, 70, 181, 439, 441, 532 Capsaicin, 63, 241, 441 Capsules, 441, 456, 466 Carbohydrate, 32, 71, 278, 441, 451, 465, 468, 505 Carbon Dioxide, 441, 453, 463, 465, 503, 513, 530, 532 Carboxy, 337, 441 Carcinogen, 70, 403, 441, 491 Carcinogenesis, 57, 70, 143, 273, 355, 441 Carcinogenic, 264, 374, 441, 447, 477, 495, 506, 521 Carcinoma, 45, 55, 57, 70, 256, 274, 291, 328, 441, 454 Cardiac, 428, 439, 441, 450, 457, 460, 461, 466, 482, 491, 510, 521 Cardiovascular, 32, 34, 107, 355, 441, 482, 517 Cardiovascular Abnormalities, 32, 441 Cardiovascular disease, 107, 441 Cardiovascular System, 355, 441 Carotene, 241, 441, 514 Carotenoids, 441, 442
Case report, 7, 10, 92, 100, 118, 169, 173, 182, 202, 203, 213, 214, 442, 446 Case series, 442, 446 Case-Control Studies, 59, 442 Catabolism, 294, 344, 442 Catalase, 85, 271, 425, 442 Catecholamine, 442, 455, 501 Cathode, 431, 442 Cations, 317, 442, 480 Cauda Equina, 442, 516 Causal, 17, 38, 195, 290, 442, 470, 479 Cause of Death, 287, 302, 442 Caustic, 442, 519 Caveolae, 46, 442 Caveolins, 442 Celiac Disease, 442, 467 Cell Adhesion, 31, 33, 304, 442, 478 Cell Aging, 355, 442 Cell Communication, 31, 443 Cell Death, 74, 282, 312, 350, 433, 443 Cell Differentiation, 4, 19, 30, 80, 335, 443, 518 Cell membrane, 298, 334, 336, 343, 440, 442, 443, 453, 501 Cell Membrane Structures, 442, 443 Cell motility, 21, 53, 443, 471 Cell Movement, 53, 443 Cell Respiration, 443, 489, 497, 513 Cell Size, 443, 464 Cell Survival, 44, 443, 469, 470 Cell Transplantation, 443 Cellular adhesion, 56, 443 Cellulose, 443, 465, 503 Central Nervous System Infections, 443, 469 Centrifugation, 443, 488 Centromere, 272, 444 Cerebellar, 21, 434, 444, 512 Cerebellum, 21, 444, 512 Cerebral, 299, 355, 434, 436, 439, 444, 450, 460, 461 Cerebral Cortex, 434, 444, 461 Cerebrospinal, 126, 444, 451 Cerebrospinal fluid, 126, 444, 451 Cerebrovascular, 359, 436, 440, 441, 444, 525 Cerebrum, 444, 529 Cerium, 334, 444 Cervix, 128, 425, 444, 513 Chaperonins, 444, 489 Character, 322, 444, 453, 468 Chemokines, 20, 40, 64, 66, 68, 255, 444
Index 539
Chemotactic Factors, 444, 448 Chemotaxis, 30, 51, 64, 444 Chemotherapeutic agent, 60, 295, 444 Chemotherapy, 56, 62, 298, 338, 357, 361, 422, 444 Child Development, 34, 444 Chimera, 70, 444 Chin, 200, 214, 218, 227, 232, 355, 379, 445, 487 Chlorine, 398, 445 Chlorophyll, 325, 445, 465 Chloroquine, 284, 289, 325, 376, 445, 510 Cholangitis, 168, 445 Cholesterol, 59, 355, 437, 442, 445, 446, 450, 483, 484, 486, 521 Cholesterol Esters, 445, 483 Chondrocytes, 445, 463 Chorioallantoic membrane, 69, 445 Chorioretinitis, 445, 514 Choroid, 445, 513, 514, 531 Chromaffin System, 445, 458 Chromatin, 16, 433, 445 Chromosomal, 35, 174, 291, 445, 514 Chromosome Segregation, 28, 445 Chronic Disease, 38, 61, 90, 324, 332, 337, 350, 407, 445, 447 Chronic granulocytic leukemia, 445, 446 Chronic leukemia, 445, 469 Chronic myelogenous leukemia, 124, 169, 445 Chronic Obstructive Pulmonary Disease, 268, 340, 342, 446 Chronic renal, 119, 446, 504, 530 Chylomicrons, 446, 483 Chymotrypsin, 270, 446 Circulatory system, 287, 302, 446, 458 Cirrhosis, 378, 446 CIS, 17, 45, 58, 79, 319, 330, 331, 333, 334, 336, 446, 514 Clamp, 19, 24, 446 Clinical Medicine, 5, 446, 506 Clinical Protocols, 56, 446 Clinical study, 81, 108, 227, 257, 446, 450 Clobetasol, 84, 95, 100, 109, 119, 148, 168, 177, 187, 201, 314, 446 Clone, 16, 18, 37, 66, 446 Cloning, 15, 20, 44, 74, 291, 437, 446 Clot Retraction, 446, 503 Coagulation, 124, 438, 446, 471, 526 Coal Tar, 4, 5, 8, 102, 104, 152, 184, 202, 264, 273, 274, 276, 280, 309, 312, 314,
315, 316, 317, 324, 325, 338, 350, 353, 375, 377, 397, 401, 404, 447 Cod Liver Oil, 447, 458 Cofactor, 447, 494, 508, 526 Cognition, 447 Cognitive Therapy, 402, 447 Colchicine, 294, 314, 447 Colitis, 264, 447 Collagen, 54, 263, 264, 300, 429, 436, 447, 462, 463, 466, 473, 486, 504, 506 Collagen disease, 447, 473 Collapse, 55, 439, 447 Colloidal, 428, 447, 457, 462, 500, 518 Colon, 78, 147, 388, 447, 477, 481, 529 Colorectal, 143, 447 Colorectal Cancer, 143, 447 Combination Therapy, 95, 114, 448 Communicable disease, 315, 325, 448 Community Health Centers, 34, 448 Complement, 23, 57, 87, 149, 219, 279, 430, 448, 467, 478, 485, 517 Complement Activation, 23, 430, 448 Complementary and alternative medicine, 211, 245, 448 Complementary medicine, 59, 211, 448 Complete remission, 102, 326, 331, 332, 333, 448, 512 Complete response, 448 Computational Biology, 385, 387, 448 Conception, 379, 401, 425, 449, 450, 463, 521 Concomitant, 160, 268, 449 Cone, 449, 502 Congestion, 449, 460 Conjugated, 27, 72, 436, 449, 452, 494 Conjugation, 27, 266, 437, 449 Conjunctiva, 449, 477 Conjunctivitis, 299, 400, 449, 469 Connective Tissue, 63, 438, 447, 449, 454, 463, 465, 466, 484, 487, 492, 508, 514, 522, 524 Connective Tissue Cells, 449 Consciousness, 430, 449, 453, 455, 509 Constipation, 449, 500 Constitutional, 449, 491, 514 Constriction, 24, 449, 480, 532 Constriction, Pathologic, 449, 532 Consultation, 4, 449 Consumption, 7, 222, 422, 449, 466, 513 Contact dermatitis, 27, 72, 81, 213, 214, 219, 284, 285, 301, 329, 348, 449, 453, 454, 527
540 Psoriasis
Contraception, 7, 449 Contraindications, ii, 7, 450 Contrast Media, 113, 450 Controlled clinical trial, 39, 101, 111, 450, 511 Controlled study, 84, 89, 120, 153, 182, 252, 450 Conventional therapy, 450 Conventional treatment, 267, 277, 450, 498 Convulsions, 431, 436, 450, 457, 506, 520 Coordination, 28, 444, 450, 490 Cor, 63, 450 Coreceptors, 64, 450 Cornea, 450, 480, 516, 522, 531 Corneum, 72, 151, 178, 303, 312, 450, 460, 474 Coronary, 226, 441, 450, 488, 491 Coronary heart disease, 226, 441, 450 Coronary Thrombosis, 450, 488, 491 Corpus, 451, 499, 506, 533 Corpus Luteum, 451, 506 Corpuscle, 451, 460 Cortex, 451, 461, 512 Cortical, 48, 451, 517, 525 Cortisone, 309, 451, 506 Cowpox, 451, 531 Cowpox Virus, 451, 531 Cranial, 444, 451, 469, 496, 500, 520 Craniocerebral Trauma, 436, 451, 469, 525 Criterion, 3, 451 Crossing-over, 451, 512 CSF, 436, 444, 451 Culture Media, 47, 427, 451 Cultured cells, 18, 33, 451 Curative, 264, 273, 311, 322, 451, 515, 525 Curcumin, 290, 451 Curettage, 328, 452 Curette, 452 Cyclic, 69, 82, 200, 279, 291, 426, 439, 441, 443, 452, 469, 494, 501, 507, 516, 525 Cyclin, 28, 452 Cyst, 137, 452 Cysteinyl, 15, 24, 452 Cytochrome, 50, 104, 452, 497 Cytokinesis, 28, 452 Cytomegalovirus, 138, 452 Cytoplasm, 67, 433, 436, 443, 452, 459, 469, 515 Cytosine, 287, 302, 452, 510 Cytoskeleton, 53, 55, 452, 478, 488 Cytostatic, 286, 336, 452, 491
Cytotoxic, 7, 81, 260, 261, 292, 441, 452, 475, 478, 511, 518 D Daclizumab, 191, 251, 452 Day Care, 357, 452 Deamination, 453, 530 Decarboxylation, 453, 472 Decidua, 453, 503, 528 Defense Mechanisms, 453, 478 Degenerative, 453, 471, 485, 492, 496, 514 Deletion, 12, 163, 433, 453 Delivery of Health Care, 448, 453, 470 Dementia, 426, 453 Denaturation, 453, 504 Dendrites, 453, 493 Dendritic, 20, 36, 37, 66, 76, 152, 162, 453, 486 Dendritic cell, 20, 36, 37, 77, 152, 162, 453 Denileukin diftitox, 82, 453 Density, 13, 42, 94, 230, 355, 438, 443, 453, 464, 483, 495, 504 Deoxyguanosine, 194, 260, 453 Depigmentation, 453, 532 Depolarization, 24, 453, 518 Depressive Disorder, 453, 483 Dermal, 25, 41, 70, 71, 72, 138, 151, 174, 272, 273, 294, 304, 314, 316, 317, 341, 344, 453 Dermatitis, Allergic Contact, 301, 453 Dermatitis, Contact, 265, 453 Dermatitis, Irritant, 28, 454 Dermatologist, 4, 5, 249, 253, 278, 398, 454 Dermatosis, 24, 171, 262, 265, 272, 276, 289, 292, 297, 310, 316, 318, 330, 341, 454, 516 DES, 430, 454 Desensitization, 20, 454 Desiccation, 315, 325, 454 Desquamation, 322, 454, 481 Detergents, 454, 463 Detoxification, 454, 468 Deuterium, 60, 454, 473 Diabetes Mellitus, 285, 454, 467, 470 Diabetic Retinopathy, 11, 58, 79, 454, 502 Diagnostic procedure, 259, 374, 454 Diarrhoea, 454, 466, 473 Diastolic, 454, 474 Dideoxynucleosides, 305, 454 Diflucortolone, 108, 454 Digestion, 428, 437, 438, 455, 479, 483, 499, 522 Digestive system, 258, 455, 490
Index 541
Digestive tract, 455, 519, 521, 533 Digital photography, 253, 455 Dihydrotestosterone, 455, 512 Dihydroxy, 274, 335, 428, 455, 461 Dilatation, 425, 455, 506, 509 Dilation, 304, 439, 455 Diltiazem, 290, 455 Diploid, 455, 503 Discoid, 31, 52, 330, 455 Discrete, 7, 276, 314, 324, 351, 455, 467, 524 Disinfectant, 455, 461 Disposition, 31, 320, 455 Dissection, 29, 66, 455 Dissociation, 427, 455 Distal, 35, 272, 290, 297, 435, 455, 457, 509 Dizziness, 397, 455 Domesticated, 282, 283, 284, 288, 455 Dominance, 455, 460 Dopamine, 439, 455, 493, 501 Dorsal, 64, 77, 456, 505, 520 Dosage Forms, 351, 456 Double-blind, 83, 84, 88, 99, 108, 111, 145, 153, 182, 212, 224, 226, 227, 252, 254, 456 Double-blinded, 252, 456 Doxycycline, 17, 456 Drive, ii, vi, 18, 199, 357, 456 Dross, 456, 507 Drug Approval, 372, 456 Drug Design, 21, 28, 66, 456 Drug Eruptions, 194, 456 Drug Tolerance, 456, 527 Duct, 456, 461, 497, 515, 523 Duodenum, 437, 446, 456, 466, 493, 498, 522 Dura mater, 457, 487, 497 Dysplasia, 389, 457 Dyspnea, 457, 509 Dyspnoea, 322, 457 Dystrophy, 389, 457 E Eclampsia, 436, 457, 506 Ectopic, 10, 457 Edema, 25, 449, 454, 457, 484, 491, 492, 506, 530 Effector, 36, 39, 40, 76, 120, 190, 425, 448, 457, 481, 501 Effector cell, 457, 481 Eicosanoids, 15, 355, 457 Elastic, 457, 468, 523 Elasticity, 433, 457, 519 Elastin, 263, 264, 447, 457, 462 Elective, 174, 457
Electrocardiogram, 251, 253, 457 Electrocoagulation, 447, 457 Electrode, 431, 442, 457 Electrodesiccation, 328, 457 Electrolysis, 431, 442, 457 Electrolyte, 17, 428, 451, 457, 481, 489, 505, 519, 530 Electrophoresis, 16, 26, 46, 457 Emaciation, 426, 458 Embolus, 458, 476 Embryo, 425, 437, 443, 458, 476, 487, 530, 533 Embryogenesis, 32, 458 Emollient, 324, 325, 350, 397, 458, 468, 481, 495 Emphysema, 446, 458 Empiric, 332, 337, 458 Emulsion, 94, 311, 338, 378, 458, 464 Enamel, 458, 480 Encapsulated, 458, 483 Encephalitis, 458 Encephalomyelitis, 46, 74, 458 Endemic, 458, 520 Endocrine Glands, 458, 498 Endocrine System, 65, 458 Endocytosis, 442, 458 Endoderm, 458, 533 Endometrial, 58, 459 Endometrium, 453, 459, 487 Endopeptidases, 459, 507 Endostatin, 58, 459 Endothelial cell, 20, 25, 29, 32, 38, 43, 47, 58, 68, 70, 141, 281, 304, 459, 463, 471, 479, 526 Endothelium, 25, 29, 32, 46, 68, 88, 459, 494, 504 Endothelium, Lymphatic, 459 Endothelium, Vascular, 459 Endothelium-derived, 459, 494 Endotoxin, 459, 529 End-stage renal, 446, 459, 504 Enhancer, 17, 45, 272, 459, 513 Enteropeptidase, 459, 529 Environmental Exposure, 459, 495 Environmental Health, 384, 386, 459 Enzymatic, 24, 263, 335, 354, 429, 440, 442, 448, 459, 472, 487, 502, 504, 514 Eosinophil, 15, 459 Eosinophilia, 15, 459, 462 Eosinophilic, 24, 459, 462 Epidemic, 460, 520
542 Psoriasis
Epidermal Growth Factor, 13, 323, 460, 528 Epidermal growth factor receptor, 13, 19, 323, 460 Epidermoid carcinoma, 45, 460, 521 Epigastric, 460, 497 Epinephrine, 427, 456, 460, 493, 494, 529 Epistasis, 129, 460 Epithelial, 17, 20, 52, 57, 66, 131, 300, 322, 323, 426, 453, 454, 460, 461, 471 Epithelial Cells, 20, 52, 57, 66, 460, 471 Epithelium, 66, 266, 304, 328, 436, 459, 460, 466, 481, 498, 528 Epitope, 97, 138, 460 Erythema, 5, 9, 34, 113, 262, 275, 281, 295, 319, 331, 338, 419, 449, 460, 523, 531 Erythrocyte Membrane, 82, 108, 200, 460 Erythrocytes, 274, 430, 438, 460, 470, 512, 517 Erythromycin, 460, 515 Escalation, 37, 82, 461 Esophagitis, 299, 461 Esophagus, 455, 461, 501, 516, 522 Essential Tremor, 389, 461 Ethanol, 327, 378, 461 Ether, 284, 286, 461 Ethylene Glycol, 284, 461 Etretinate, 7, 201, 202, 203, 212, 215, 218, 223, 236, 257, 290, 358, 378, 404, 425, 461 Eukaryotic Cells, 461, 476, 496 Evoke, 461, 521 Evoked Potentials, 195, 461 Excimer laser, 84, 112, 126, 146, 168, 169, 190, 461 Excipient, 267, 306, 309, 325, 338, 461 Excisional, 53, 461 Excitability, 461, 510 Excitation, 48, 461, 464, 493 Excrete, 432, 461, 481 Exfoliation, 286, 297, 454, 461, 492 Exocrine, 461, 497 Exogenous, 38, 267, 339, 342, 437, 457, 458, 461, 466, 468, 508 Exon, 52, 429, 461 Expectorant, 462, 505 Extender, 295, 462 Extensor, 6, 276, 292, 293, 319, 324, 462, 509, 532 External-beam radiation, 462, 480, 511, 533 Extracellular, 12, 41, 44, 63, 64, 70, 79, 434, 449, 458, 462, 463, 478, 486, 519, 525
Extracellular Matrix, 12, 41, 44, 63, 70, 449, 462, 463, 478, 486 Extracellular Matrix Proteins, 462, 486 Extracellular Space, 462 Extravasation, 51, 63, 462 Extravascular, 24, 462 Extremity, 462, 482 F Facial, 8, 137, 189, 294, 379, 400, 462 Fallopian tube, 462, 513 Family Planning, 385, 462 Fasciitis, 119, 462 Fatigue, 397, 420, 462, 470 Fatty acids, 50, 209, 220, 221, 226, 334, 336, 428, 457, 463, 468, 483, 507, 519 Femoral, 92, 463 Femur, 463 Fertilizers, 428, 463, 505, 523 Fetus, 425, 463, 503, 530, 531 Fibrin, 438, 446, 463, 500, 503, 526 Fibrinogen, 463, 503, 526 Fibroblast Growth Factor, 79, 463 Fibroblasts, 25, 47, 133, 138, 281, 291, 295, 300, 449, 462, 463, 478, 479 Fibrosarcoma, 462, 463 Fibrosis, 43, 46, 54, 389, 428, 463, 509, 516 Fine-needle aspiration, 463, 492 Fish Oils, 220, 463 Fistula, 463, 466 Fixation, 328, 463, 517 Flexor, 462, 464 Flow Cytometry, 75, 77, 97, 464 Fludarabine, 252, 464 Fluocinonide, 6, 446, 464 Fluorescence, 13, 29, 464 Fluorescent Dyes, 464 Fluorouracil, 266, 292, 294, 314, 315, 464 Folate, 62, 208, 464 Fold, 35, 60, 162, 295, 300, 464 Folic Acid, 207, 234, 430, 464 Folliculitis, 431, 464 Foramen, 445, 464 Forearm, 73, 438, 462, 464 Fossa, 444, 464 Fovea, 464 Fractionation, 46, 464 Frameshift, 140, 464 Frameshift Mutation, 140, 464 Free Radicals, 232, 271, 355, 432, 455, 465, 491 Fucose, 31, 465 Fucosyltransferases, 31, 465
Index 543
Fungi, 432, 449, 465, 469, 481, 488, 491, 533 Fungistatic, 436, 465 Fungus, 187, 297, 376, 465, 491, 515 G Gadolinium, 49, 465 Gallbladder, 425, 437, 455, 465 Gamma Rays, 465, 511 Gamma-interferon, 465, 478 Ganglia, 64, 77, 425, 436, 465, 493, 500, 520 Ganglioside, 33, 299, 347, 465 Gas, 430, 441, 445, 465, 473, 486, 491, 494, 532 Gas exchange, 465, 532 Gastric, 102, 193, 336, 435, 456, 460, 465, 466, 472, 495, 499 Gastric Juices, 465, 499 Gastric Mucosa, 466, 499 Gastrin, 466, 472 Gastroduodenal, 160, 466 Gastroenteritis, 439, 466 Gastrointestinal, 68, 132, 328, 379, 434, 439, 460, 461, 466, 482, 486, 517, 520, 523 Gastrointestinal Neoplasms, 434, 466 Gastrointestinal tract, 328, 461, 466, 482, 517, 520 Gelatin, 451, 466, 468, 526 Gels, 28, 466 Gene Expression, 16, 17, 47, 59, 61, 66, 75, 135, 291, 312, 390, 466, 528 Gene Targeting, 46, 57, 466 Gene Therapy, 308, 466 Generator, 466, 524 Genetic Code, 466, 494 Genetic Engineering, 437, 446, 467 Genetic testing, 254, 467, 505 Genital, 186, 287, 301, 302, 398, 420, 467, 515, 531 Genitourinary, 201, 215, 467, 531 Genotype, 38, 42, 123, 467, 501 Germ Cells, 15, 467, 486, 496, 525, 533 Germ-Line Mutation, 44, 467 Giardiasis, 467, 510 Gingival Recession, 10, 467 Gingivitis, 299, 467 Gland, 311, 427, 445, 451, 467, 484, 497, 498, 503, 507, 516, 517, 521, 522, 523, 526 Gliadin, 139, 467 Glomerular, 467, 481, 513 Glossitis, 123, 467 Glucocorticoid, 27, 68, 284, 310, 454, 464, 467, 473, 506, 529
Glucose, 278, 282, 389, 438, 443, 454, 467, 468, 470, 477, 501, 515 Glucose Intolerance, 454, 467 Glucuronic Acid, 467, 468, 471, 531 Glucuronides, 278, 467, 468 Glutamic Acid, 430, 464, 468, 493, 506 Glutathione Peroxidase, 224, 468, 517 Gluten, 123, 209, 442, 467, 468 Glycerol, 468, 501 Glycerophospholipids, 468, 501 Glycine, 255, 429, 436, 468, 493, 517 Glycogen, 288, 468, 501, 502 Glycoprotein, 463, 465, 468, 490, 526, 529 Glycosaminoglycans, 206, 282, 462, 468, 508 Glycosidic, 336, 468, 495, 501 Gonadal, 254, 468, 521 Gout, 98, 260, 261, 447, 468 Governing Board, 468, 505 Gp120, 468, 499 Graft, 10, 13, 17, 67, 78, 102, 124, 285, 339, 468, 469, 472, 476, 489, 491, 509 Graft Rejection, 78, 285, 339, 468, 476, 489 Graft Survival, 13, 468 Grafting, 16, 468, 476 Graft-versus-host disease, 102, 469, 491, 509 Granulocytes, 281, 428, 469, 482, 518, 533 Grasses, 464, 469, 471 Gravis, 35, 100, 162, 261, 469 Groin, 6, 398, 399, 469 Growth, 4, 11, 13, 17, 19, 20, 28, 37, 38, 43, 45, 47, 50, 54, 58, 60, 62, 63, 64, 65, 66, 69, 70, 79, 122, 131, 135, 138, 149, 170, 253, 263, 274, 281, 282, 283, 287, 291, 292, 293, 295, 301, 302, 304, 326, 330, 335, 345, 346, 350, 389, 408, 427, 430, 431, 432, 433, 443, 444, 451, 452, 459, 460, 462, 463, 465, 468, 469, 471, 472, 478, 479, 481, 485, 492, 493, 494, 495, 496, 503, 508, 516, 517, 526, 528, 529, 533 Growth factors, 13, 47, 62, 69, 469 Guanine, 261, 453, 469, 510 Guanylate Cyclase, 469, 494 H Habitual, 444, 469 Hair follicles, 454, 464, 469, 521, 533 Hairy cell leukemia, 168, 469 Half-Life, 5, 257, 321, 425, 469 Haploid, 469, 503 Haplotypes, 43, 103, 141, 469 Haptens, 40, 427, 469
544 Psoriasis
Hay Fever, 348, 428, 469 Headache, 260, 397, 439, 469, 477 Headache Disorders, 469 Health Care Costs, 77, 470 Health Expenditures, 470 Heart attack, 441, 470 Heart failure, 470, 509 Heat-Shock Proteins, 470, 489 Heat-Shock Proteins 90, 470, 489 Heliotherapy, 221, 233, 470 Helix-loop-helix, 43, 470 Helminths, 470, 477 Heme, 429, 437, 452, 470, 497 Hemodialysis, 470, 481 Hemoglobin, 40, 430, 460, 470 Hemoglobin M, 470 Hemoglobinopathies, 34, 466, 470 Hemoglobinuria, 389, 470 Hemolysis, 460, 470 Hemolytic, 186, 462, 470, 476 Hemorrhage, 451, 457, 469, 471, 491, 522, 533 Hemostasis, 471, 478, 517 Heparan Sulfate Proteoglycan, 13, 471 Heparin, 13, 79, 471 Heparin-binding, 13, 471 Hepatic, 190, 202, 428, 471 Hepatitis, 115, 118, 126, 154, 193, 213, 471, 489 Hepatocellular, 160, 471 Hepatocellular carcinoma, 160, 471 Hepatocyte, 12, 471 Hepatocyte Growth Factor, 12, 471 Hepatotoxic, 59, 471 Hepatotoxicity, 59, 285, 471 Herbicides, 320, 471 Hereditary, 292, 309, 326, 363, 426, 468, 471, 514 Heredity, 185, 426, 466, 467, 471 Herpes, 138, 167, 327, 471 Herpes virus, 138, 471 Herpes Zoster, 327, 471 Herpetiformis, 121, 471 Heterodimers, 45, 59, 65, 471, 478, 528 Heterogeneity, 14, 427, 471 Heterozygotes, 162, 455, 471 Histamine, 64, 112, 296, 430, 472, 474 Histamine Release, 430, 472 Histidine, 472 Histocompatibility, 159, 262, 309, 326, 345, 346, 472, 489
Histocompatibility Antigens, 262, 345, 346, 472 Histology, 11, 472 Homeobox, 45, 472 Homeostasis, 65, 96, 343, 472 Homodimer, 18, 472, 528 Homogeneous, 286, 433, 472, 500 Homologous, 13, 20, 32, 54, 57, 97, 118, 428, 451, 466, 471, 472, 490, 508, 517, 523, 528 Homotypic, 13, 472 Hormonal, 16, 269, 434, 451, 472 Horny layer, 330, 460, 472, 481 Human growth hormone, 293, 472, 519 Human papillomavirus, 105, 108, 128, 177, 472 Humoral, 35, 468, 472 Humour, 472 Hybrid, 52, 446, 472, 473, 515 Hybridization, 473, 489 Hybridomas, 473, 478 Hydration, 114, 377, 473 Hydrocortisone, 83, 271, 473 Hydrogel, 265, 473 Hydrogen Peroxide, 442, 468, 473, 483, 523 Hydrolysis, 426, 437, 473, 501, 508, 529 Hydrophilic, 145, 226, 276, 454, 473 Hydrophobic, 276, 431, 454, 468, 473, 483 Hydroxylation, 335, 440, 473 Hydroxylysine, 447, 473 Hydroxyproline, 429, 447, 473 Hydroxyurea, 106, 128, 147, 168, 194, 401, 473 Hyperbilirubinemia, 324, 473, 480 Hypercalcemia, 6, 66, 306, 365, 473 Hypercalciuria, 6, 128, 473 Hyperkeratosis, 4, 262, 284, 287, 302, 305, 316, 473 Hyperostosis, 172, 177, 474 Hyperplasia, 7, 123, 276, 285, 291, 305, 323, 324, 350, 421, 474, 492 Hypersensitivity, 28, 40, 47, 64, 220, 267, 339, 342, 428, 453, 454, 459, 474, 482, 514, 517 Hypersensitivity, Immediate, 474 Hypertension, 24, 34, 46, 217, 323, 433, 440, 441, 469, 474, 506, 530 Hyperthermia, 45, 55, 218, 317, 470, 474 Hypertriglyceridemia, 215, 223, 474 Hypertrophy, 450, 473, 474, 482, 529 Hyperuricemia, 468, 474
Index 545
Hypnotic, 435, 474, 525 Hypoglycemic, 425, 474 Hypotension, 450, 474, 493 Hypotensive, 320, 474 Hypothalamus, 435, 474, 493, 503, 519 Hypoxia, 70, 474, 525 Hypoxic, 430, 474 I Ibuprofen, 27, 474 Ichthyosis, 55, 129, 220, 262, 271, 284, 287, 300, 302, 316, 474 Ichthyosis Vulgaris, 55, 262, 316, 474 Id, 207, 237, 395, 405, 407, 416, 418, 474 Idiopathic, 106, 158, 185, 328, 426, 475, 510 Idiotype, 299, 347, 475 Ileum, 475, 493 Imidazole, 326, 329, 472, 475 Immersion, 318, 436, 475 Immune function, 38, 42, 475, 528 Immune Sera, 475 Immunity, 23, 37, 39, 42, 69, 279, 323, 426, 475, 478, 484, 495, 528 Immunization, 255, 475, 476, 517, 524 Immunoassay, 52, 475 Immunodeficiency, 175, 298, 388, 426, 475 Immunoglobulin, 152, 164, 431, 475, 490 Immunohistochemistry, 24, 25, 64, 68, 475 Immunologic, 42, 68, 90, 99, 185, 217, 254, 273, 304, 377, 444, 475, 499, 511 Immunomodulator, 261, 475 Immunophilin, 440, 475 Immunosuppressant, 285, 330, 464, 475, 488, 518 Immunosuppressive, 4, 8, 9, 12, 24, 40, 60, 62, 285, 304, 330, 440, 467, 475, 476, 524 Immunosuppressive Agents, 8, 40, 285, 304, 475 Immunosuppressive therapy, 475, 476 Immunotherapy, 54, 74, 131, 301, 437, 454, 476 Immunotoxins, 34, 476, 511 Impairment, 119, 147, 332, 337, 434, 476, 487 Impetigo, 121, 476 Implant radiation, 476, 479, 480, 511, 533 Implantation, 449, 476 In situ, 41, 47, 63, 310, 476 In Situ Hybridization, 47, 476 In vitro, 13, 17, 20, 22, 24, 25, 29, 30, 32, 43, 45, 48, 50, 54, 57, 64, 67, 68, 70, 72, 78, 107, 108, 176, 295, 334, 335, 355, 466, 476, 504, 517, 524, 526
Incision, 271, 476, 479 Indicative, 63, 358, 476, 499, 531 Individuality, 104, 476 Indomethacin, 27, 376, 476 Induction, 17, 31, 33, 36, 41, 42, 74, 77, 171, 203, 430, 476, 478, 511 Induration, 34, 281, 476 Infancy, 161, 348, 398, 476, 515 Infant Mortality, 409, 476 Infant, Newborn, 427, 476 Infarction, 299, 476, 513 Infertility, 299, 366, 477 Infestation, 313, 477, 485 Infiltration, 15, 40, 63, 263, 272, 285, 312, 322, 341, 344, 345, 346, 477, 485, 506 Inflammatory bowel disease, 13, 15, 24, 29, 51, 67, 77, 261, 339, 477 Influenza, 37, 477 Infusion, 37, 72, 212, 227, 253, 477, 491, 528 Ingestion, 6, 352, 456, 473, 477, 504, 525 Inhalation, 427, 434, 477, 504 Initiation, 8, 14, 52, 355, 477, 506, 527 Initiator, 193, 477 Inlay, 477, 513 Inner ear, 477, 498 Inorganic, 282, 283, 311, 433, 477, 485, 490, 502, 523 Inpatients, 310, 477 Insight, 13, 20, 28, 36, 52, 58, 78, 398, 477 Insomnia, 477, 529 Insulator, 477, 490 Insulin, 40, 135, 138, 142, 170, 477, 478, 480 Insulin-dependent diabetes mellitus, 478 Insulin-like, 135, 138, 170, 478 Integrins, 14, 35, 68, 84, 478 Intercellular Adhesion Molecule-1, 303, 478 Intercellular Junctions, 25, 46, 478 Interferon, 24, 107, 108, 112, 115, 118, 135, 168, 176, 182, 202, 304, 327, 345, 465, 478 Interferon-alpha, 115, 478 Interleukin-1, 12, 21, 76, 131, 136, 159, 170, 175, 254, 291, 304, 372, 403, 478 Interleukin-10, 12, 21, 131, 136, 170, 254, 372, 478 Interleukin-18, 175, 478 Interleukin-2, 24, 37, 179, 181, 273, 478 Interleukin-6, 135, 478 Interleukin-8, 137, 170, 351, 478 Interleukins, 475, 479 Intermediate Filaments, 57, 479 Intermittent, 137, 142, 165, 252, 479, 483
546 Psoriasis
Internal Medicine, 11, 75, 203, 295, 305, 306, 479, 492 Internal radiation, 479, 480, 511, 533 Interstitial, 46, 438, 462, 479, 480, 513, 533 Intervention Studies, 40, 479 Intervertebral, 479, 484, 516 Intervertebral Disk Displacement, 479, 484, 516 Intestinal, 17, 66, 68, 225, 233, 336, 365, 440, 442, 459, 479, 485, 533 Intestinal Mucosa, 442, 479, 533 Intestine, 438, 447, 479, 481, 522 Intoxication, 85, 479, 533 Intracellular Membranes, 479, 487 Intramuscular, 88, 263, 345, 346, 479, 498, 529 Intramuscular injection, 263, 345, 346, 479 Intravascular, 124, 479 Intravenous, 28, 164, 169, 191, 253, 296, 422, 477, 479, 498 Intrinsic, 427, 436, 479 Invasive, 46, 56, 73, 475, 479 Involuntary, 436, 461, 479, 491, 519 Iodine, 325, 479 Ion Channels, 24, 434, 479 Ionizing, 429, 459, 480, 511, 518, 530 Ions, 425, 436, 441, 455, 457, 473, 480, 485 Irradiation, 77, 100, 224, 260, 295, 321, 331, 480, 488, 533 Irritants, 8, 254, 454, 480 Ischemia, 56, 355, 434, 465, 480, 491, 513 Islet, 39, 480 Isopropyl, 267, 278, 480 J Jaundice, 168, 169, 473, 480 Joint, 10, 49, 69, 133, 221, 251, 263, 345, 346, 352, 420, 433, 434, 464, 480, 496, 520, 523, 524 Juniper, 223, 243, 480 K Kb, 17, 142, 384, 480, 481 Keratin, 12, 55, 57, 97, 130, 138, 262, 303, 316, 480, 516 Keratinocytes, 12, 13, 15, 17, 18, 19, 20, 33, 34, 37, 38, 40, 41, 44, 47, 48, 50, 52, 53, 55, 61, 66, 68, 76, 84, 135, 140, 141, 142, 145, 149, 151, 154, 194, 228, 248, 263, 272, 274, 281, 285, 291, 295, 300, 301, 304, 306, 312, 323, 324, 330, 340, 341, 343, 345, 346, 350, 354, 361, 479, 480 Keratitis, 167, 480
Keratolytic, 4, 8, 277, 297, 310, 324, 350, 480, 481, 504 Keratolytic Agents, 8, 277, 481 Keratosis, 201, 215, 256, 262, 284, 316, 425, 426, 481 Ketoconazole, 8, 481 Kidney Disease, 78, 256, 258, 365, 384, 389, 481, 513 Kidney Failure, 366, 459, 481 Kidney Failure, Acute, 481 Kidney Failure, Chronic, 481 Killer Cells, 481 Kilobase, 57, 481 Kinetic, 60, 97, 480, 481 L Labile, 27, 448, 481 Lacerations, 6, 481 Lanolin, 286, 294, 295, 481 Large Intestine, 447, 455, 479, 481, 512, 519 Latent, 12, 481, 502, 506 Lectin, 481, 487 Leflunomide, 191, 481 Leg Ulcer, 106, 482 Lens, 482, 513 Lethal, 69, 435, 482, 491 Leucocyte, 328, 429, 459, 482 Leukemia, 21, 23, 34, 66, 78, 126, 388, 445, 446, 452, 466, 482, 506 Leukocyte Count, 47, 482 Leukocytes, 20, 29, 31, 54, 71, 117, 279, 330, 341, 436, 438, 444, 469, 476, 478, 479, 482, 529 Leukoplakia, 327, 482 Leukotrienes, 15, 24, 50, 234, 433, 457, 482, 483 Liarozole, 153, 482 Libraries, Hospital, 408, 482 Library Services, 416, 482 Lichenification, 293, 482 Lidocaine, 284, 482 Ligament, 462, 482, 507, 520 Ligands, 13, 15, 60, 66, 68, 71, 478, 482 Linkage, 27, 35, 42, 47, 101, 122, 129, 141, 185, 272, 304, 482 Linkage Disequilibrium, 43, 129, 482 Lip, 10, 170, 482 Lipid Peroxidation, 85, 483, 497 Lipophilic, 16, 276, 338, 483 Lipopolysaccharide, 53, 483 Lipoprotein, 115, 278, 483, 484 Liposomal, 29, 483
Index 547
Lipoxygenase, 50, 52, 62, 265, 278, 320, 433, 482, 483 Lipoxygenase Inhibitors, 50, 483 Liquor, 377, 483 Lithium, 225, 291, 317, 376, 483 Liver cancer, 274, 483 Lobe, 472, 483, 498 Local therapy, 276, 483 Localization, 14, 18, 29, 35, 41, 50, 52, 67, 97, 131, 142, 172, 174, 290, 475, 483 Localized, 4, 8, 19, 129, 137, 142, 276, 295, 317, 324, 351, 397, 399, 458, 463, 477, 483, 493, 503, 516, 529, 531 Locomotion, 43, 483, 503 Lod, 42, 483 Long-Term Care, 57, 483 Loop, 171, 483 Low Back Pain, 126, 483 Low-density lipoprotein, 483, 484 Lubricants, 5, 297, 484, 500 Luciferase, 17, 484 Lumbar, 442, 479, 483, 484 Lupus, 31, 35, 52, 75, 352, 484, 524 Lupus Nephritis, 31, 484 Lye, 280, 484 Lymph, 74, 446, 451, 459, 472, 484, 491, 522 Lymph node, 74, 484, 491 Lymphatic, 459, 477, 484, 487, 519, 520, 526 Lymphatic system, 484, 519, 520, 526 Lymphedema, 160, 484 Lymphocyte, 6, 31, 36, 38, 39, 68, 76, 87, 102, 112, 168, 183, 203, 285, 289, 290, 304, 362, 426, 432, 481, 484, 485, 486 Lymphocyte Count, 87, 426, 484 Lymphocyte Subsets, 68, 77, 484 Lymphocytic, 285, 484 Lymphoid, 14, 68, 364, 431, 482, 484, 485 Lymphokines, 41, 291, 484 Lymphoma, 91, 96, 102, 249, 250, 388, 453, 485, 491 Lymphomatoid Papulosis, 485, 503 Lymphoproliferative, 71, 364, 485 Lysine, 473, 485, 529 Lytic, 485, 517 M Macrophage, 54, 126, 127, 194, 478, 485 Macula, 464, 485 Macula Lutea, 485 Macular Degeneration, 29, 58, 485 Maculopapular, 485, 498, 503
Magnesium Chloride, 317, 485 Maintenance therapy, 377, 485 Major Histocompatibility Complex, 14, 125, 173, 290, 303, 469, 472, 485 Malabsorption, 389, 442, 485 Malignancy, 33, 171, 186, 379, 465, 485, 498 Malnutrition, 428, 434, 485, 491 Malondialdehyde, 94, 221, 485 Mandible, 429, 445, 485, 513 Mange, 284, 485 Mania, 485, 486 Manic, 376, 483, 486 Manifest, 287, 301, 435, 486 Mannans, 465, 486 Matrix metalloproteinase, 123, 145, 353, 354, 486 Mechlorethamine, 296, 332, 333, 486 Medial, 433, 486, 520 Mediate, 5, 12, 13, 23, 31, 37, 40, 44, 49, 51, 56, 59, 62, 304, 456, 481, 486, 489 Mediator, 15, 32, 478, 486, 518 Medical Staff, 456, 482, 486 Medicament, 278, 325, 486 Medicine, Herbal, 399, 486 MEDLINE, 385, 387, 389, 486 Megakaryocytes, 438, 486 Megaloblastic, 464, 486 Meiosis, 445, 486, 490, 524 Melanin, 453, 486, 501, 529 Melanocytes, 20, 47, 486, 494 Melanoma, 6, 20, 26, 40, 54, 55, 144, 171, 301, 318, 388, 406, 486, 530 Melanosomes, 486 Membrane Fluidity, 33, 113, 486 Membrane Lipids, 486, 501 Membrane Proteins, 176, 442, 487, 508 Memory, 68, 77, 120, 190, 431, 453, 487 Meninges, 443, 451, 457, 487 Meningitis, 51, 104, 487 Menopause, 487, 505 Menstrual Cycle, 58, 487, 506 Menstruation, 453, 487 Mental Disorders, 258, 298, 487, 509 Menthol, 280, 487 Mepacrine, 284, 487 Mercury, 278, 279, 315, 325, 464, 487 Mesenchymal, 460, 487 Mesentery, 487, 500 Mesoderm, 32, 487, 533 Meta-Analysis, 35, 105, 128, 487 Metabolic disorder, 468, 487
548 Psoriasis
Metabolite, 5, 15, 22, 50, 78, 257, 319, 334, 365, 425, 437, 439, 487, 502, 506 Metaphase, 314, 316, 487 Metastasis, 12, 31, 70, 79, 287, 302, 486, 488 Metastatic, 132, 488, 517 Methionine, 488, 523 Methoxsalen, 9, 219, 273, 294, 314, 488 Methyl salicylate, 200, 214, 488 MI, 21, 23, 42, 75, 161, 228, 260, 284, 288, 294, 298, 299, 302, 379, 423, 488 Microbe, 488, 527 Microbiological, 318, 488 Microbiology, 115, 147, 339, 426, 435, 488 Microcirculation, 24, 488, 504 Microfilaments, 479, 488 Microgram, 73, 488 Microorganism, 447, 488, 499, 533 Microscopy, 24, 29, 46, 47, 173, 436, 488 Microsomal, 202, 488 Microtubules, 479, 488, 497 Migration, 12, 20, 21, 25, 29, 31, 33, 42, 43, 53, 63, 70, 71, 126, 127, 397, 478, 488 Milligram, 296, 488 Milliliter, 438, 488 Millimeter, 317, 489 Mineralization, 489, 496 Mineralocorticoids, 427, 451, 489 Minor Histocompatibility Antigens, 472, 489 Mitochondria, 29, 444, 489, 491, 496 Mitosis, 28, 433, 445, 489 Mitotic, 16, 28, 273, 337, 489 Mobility, 16, 30, 489 Mobilization, 15, 20, 489 Mode of Transmission, 354, 489 Modeling, 456, 489 Modification, 18, 67, 250, 429, 467, 489, 510 Modulator, 319, 489 Molecular Chaperones, 22, 444, 470, 489 Molecular Probes, 272, 489 Monitor, 73, 85, 490, 494 Monoclonal antibodies, 37, 69, 452, 476, 490 Monocyte, 51, 54, 154, 162, 490 Mononuclear, 107, 151, 187, 202, 272, 341, 462, 490, 529 Monotherapy, 5, 81, 83, 108, 111, 112, 134, 175, 188, 490 Mood Disorders, 376, 490 Morphogenesis, 41, 490 Morphological, 46, 458, 465, 486, 490
Morphology, 33, 63, 363, 490 Motility, 33, 53, 476, 490, 517 Motion Sickness, 490, 492 Mucocutaneous, 31, 147, 490 Mucolytic, 425, 490 Mucosa, 10, 57, 160, 180, 193, 466, 484, 490, 522 Mucositis, 10, 490 Mucus, 462, 490, 530 Multicenter study, 112, 205, 490 Multiple sclerosis, 32, 74, 77, 261, 267, 299, 339, 341, 342, 397, 490 Multivalent, 13, 435, 490 Muscle Fibers, 490, 492 Muscular Atrophy, 389, 490 Muscular Dystrophies, 457, 491 Mustard Gas, 480, 491 Mutagenic, 491, 518 Mutagens, 465, 491 Myalgia, 194, 477, 491 Myasthenia, 35, 100, 261, 491 Mycophenolate mofetil, 39, 101, 188, 197, 206, 491 Mycosis, 250, 300, 362, 364, 485, 491, 495 Mycosis Fungoides, 250, 300, 362, 364, 485, 491 Mycotoxins, 428, 491 Mydriatic, 455, 491 Myelin, 490, 491 Myelogenous, 491 Myocardial infarction, 299, 436, 450, 488, 491 Myocardial Reperfusion, 491, 513 Myocardial Reperfusion Injury, 491, 513 Myocardium, 488, 491 Myopathy, 26, 491 Myosin, 53, 440, 492 Myositis, 163, 492 Myotonic Dystrophy, 389, 492 Myristate, 267, 278, 351, 352, 492 N Naive, 68, 492 Nasal Mucosa, 477, 492 Nasal Polyps, 268, 340, 342, 492 Natural killer cells, 98, 328, 492 Natural selection, 437, 492 Nausea, 260, 397, 456, 466, 492, 524, 530 NCI, 1, 249, 250, 252, 253, 254, 255, 256, 258, 383, 446, 492 Necrolysis, 492, 503 Needle biopsy, 251, 463, 492 Neomycin, 270, 492
Index 549
Neonatal, 30, 45, 476, 492 Neoplasia, 33, 388, 461, 492 Neoplasm, 492, 529 Neoplastic, 14, 33, 70, 341, 342, 430, 473, 485, 492 Nephrolithiasis, 6, 492 Nephrology, 130, 492 Nephropathy, 481, 492 Nerve Fibers, 63, 77, 493, 520 Nerve Growth Factor, 493, 494 Nervous System, 21, 42, 285, 328, 389, 425, 435, 439, 440, 443, 461, 465, 468, 482, 486, 490, 492, 493, 496, 500, 517, 525 Neural, 42, 283, 440, 472, 493 Neurodermatitis, 222, 493 Neurogenic, 27, 493 Neurogenic Inflammation, 28, 493 Neuronal, 70, 78, 493 Neurons, 42, 453, 465, 493, 520, 523 Neuropathy, 493, 516 Neuropeptide, 440, 493 Neuropharmacology, 61, 227, 493 Neurophysiology, 453, 493 Neuroretinitis, 493, 514 Neurosecretory Systems, 458, 493 Neurotensin, 63, 493 Neurotransmitter, 425, 426, 429, 439, 440, 443, 455, 468, 472, 480, 493, 494, 516, 518, 520, 522 Neurotrophins, 42, 494 Neutrons, 429, 480, 494, 511 Neutrophil, 15, 40, 44, 64, 171, 212, 478, 494 Neutrophil Infiltration, 40, 494 Nevus, 133, 253, 494 Nickel, 282, 283, 494 Nitric Oxide, 90, 141, 145, 494 Nitrogen, 261, 303, 308, 428, 429, 430, 462, 463, 481, 494, 529 Nonverbal Communication, 494, 509 Norepinephrine, 353, 427, 456, 493, 494 Nuclear, 17, 43, 45, 48, 52, 59, 62, 64, 65, 67, 78, 291, 305, 436, 449, 461, 465, 494, 511 Nuclear Proteins, 65, 494 Nuclei, 15, 303, 429, 449, 466, 467, 489, 494, 496, 508 Nucleic acid, 266, 307, 327, 341, 436, 452, 466, 473, 476, 491, 494, 510 Nucleoproteins, 494 Nummular, 330, 348, 495 Nursing Care, 495, 499
O Occupational Groups, 363, 495 Ocular, 43, 269, 495 Odour, 433, 495, 530 Ointments, 6, 9, 279, 280, 317, 319, 321, 322, 354, 399, 400, 404, 456, 495, 519 Oleanolic Acid, 286, 495 Oligosaccharides, 31, 495 Oliguria, 481, 495 Omega-3 fatty acid, 209, 225, 227, 495 Omeprazole, 294, 495 Oncogene, 60, 291, 307, 388, 471, 495 Oncogenic, 28, 44, 478, 495, 508 Oncology, 29, 55, 131, 218, 495 Onychomycosis, 8, 106, 495 Opacity, 453, 495 Opalescent, 319, 323, 495 Operon, 495, 506, 513 Ophthalmic, 379, 400, 495 Ophthalmology, 118, 144, 195, 463, 495 Opisthorchiasis, 160, 495 Opportunistic Infections, 426, 495 Opsin, 495, 514, 515 Optic Disk, 454, 485, 495 Optic Nerve, 493, 495, 496, 497, 513, 514, 516 Oral Manifestations, 10, 11, 496 Orbit, 496 Orbital, 163, 496 Orderly, 17, 445, 496 Organ Culture, 47, 49, 130, 223, 496, 526 Organelles, 443, 452, 486, 496 Osmolarity, 55, 496 Osmoles, 496 Ossification, 496, 515 Osteoarthritis, 75, 299, 496 Osteoclasts, 49, 440, 496 Osteomalacia, 289, 366, 440, 496 Osteoporosis, 17, 23, 65, 66, 78, 289, 299, 365, 496 Outpatient, 4, 34, 353, 366, 496 Ovaries, 496, 513, 518 Ovary, 451, 496, 522 Overexpress, 41, 496 Ovum, 451, 453, 496, 506, 533, 534 Oxazolidinones, 298, 497 Oxidants, 186, 350, 497 Oxidation, 266, 277, 425, 432, 433, 437, 452, 468, 470, 483, 497 Oxidation-Reduction, 437, 497 Oxidative metabolism, 482, 497 Oxidative Phosphorylation, 29, 497
550 Psoriasis
Oxidative Stress, 107, 271, 355, 497 Oxides, 292, 497 Oxygenase, 124, 497 P Pachymeningitis, 487, 497 Paclitaxel, 253, 267, 497 Palladium, 307, 497 Palliative, 27, 273, 283, 497, 525 Palliative therapy, 27, 497 Pancreas, 74, 425, 446, 455, 477, 480, 497, 498, 520, 529 Pancreatic, 74, 388, 446, 498 Pancreatic cancer, 388, 498 Pancreatic Juice, 446, 498 Pancreatitis, 299, 498 Papilla, 113, 330, 498 Papillary, 291, 300, 473, 498 Papillomavirus, 498 Papule, 292, 328, 420, 485, 498 Par excellence, 27, 498 Parapsoriasis, 159, 364, 498, 503 Parasitic, 436, 470, 477, 498 Parathyroid, 65, 257, 289, 365, 440, 498, 515, 525 Parathyroid Glands, 498, 515 Parathyroid hormone, 65, 257, 289, 365, 440, 498 Parenteral, 24, 456, 498 Parietal, 495, 498, 500 Paroxysmal, 389, 469, 498 Partial remission, 498, 512 Patch, 19, 24, 120, 121, 270, 282, 283, 348, 482, 498, 527 Pathogen, 20, 31, 499 Pathogenesis, 7, 11, 23, 27, 31, 36, 43, 47, 56, 58, 59, 67, 74, 75, 77, 84, 105, 134, 139, 158, 167, 188, 234, 281, 309, 323, 326, 343, 352, 363, 499 Pathologic, 43, 50, 433, 437, 440, 450, 473, 474, 499, 509, 513 Pathologic Processes, 433, 499 Pathologies, 25, 71, 73, 355, 499 Pathophysiology, 9, 38, 46, 50, 64, 155, 163, 186, 304, 329, 499 Patient Advocacy, 409, 499 Patient Care Management, 6, 499 Patient Compliance, 92, 201, 499 Patient Education, 4, 7, 8, 158, 396, 414, 416, 423, 482, 499 Pelvic, 499, 507 Pemphigus, 52, 425, 499 Penis, 499, 500, 513
Pentoxifylline, 86, 268, 499 Pepsin, 499 Pepsin A, 499 Peptic, 299, 499 Peptic Ulcer, 299, 499 Peptide, 13, 14, 28, 33, 39, 97, 297, 308, 429, 440, 459, 463, 480, 499, 507, 508, 523 Peptide T, 13, 40, 499 Perception, 3, 106, 449, 499, 516 Percutaneous, 85, 292, 500 Perfusion, 474, 500, 526 Perianal, 124, 500 Pericardium, 500, 524 Periodontitis, 467, 500 Peripheral blood, 23, 25, 39, 49, 68, 96, 97, 107, 129, 151, 158, 178, 187, 202, 254, 478, 500 Peripheral Nervous System, 77, 493, 500, 520, 523 Peripheral stem cells, 469, 500 Peritoneum, 23, 487, 500 Peritonitis, 23, 47, 500 Perivascular, 440, 500 Pesticides, 428, 471, 500 Petrolatum, 73, 294, 295, 375, 458, 500 Petroleum, 239, 286, 500 PH, 29, 92, 99, 100, 269, 344, 438, 500 Phagocyte, 497, 500 Phallic, 463, 500 Pharmaceutical Preparations, 338, 443, 461, 466, 500 Pharmaceutical Solutions, 456, 500 Pharmacist, 34, 501 Pharmacodynamics, 156, 501 Pharmacokinetic, 34, 73, 156, 501 Pharmacologic, 6, 54, 60, 430, 435, 469, 501, 526, 527 Pharmacotherapy, 61, 501 Pharynx, 477, 501 Phenolphthalein, 458, 501 Phenotype, 14, 19, 35, 38, 39, 43, 47, 58, 130, 291, 301, 501 Phenyl, 298, 337, 501 Phenylalanine, 499, 501, 529 Phloroglucinol, 260, 501 Phosphodiesterase, 499, 501 Phosphoglycerate Kinase, 291, 501 Phospholipases, 51, 501, 518 Phospholipids, 50, 462, 483, 486, 501 Phosphorus, 440, 498, 501, 502 Phosphorylase, 109, 134, 260, 290, 501, 502 Phosphorylase a, 134, 501, 502
Index 551
Phosphorylase b, 502 Phosphorylase Kinase, 109, 290, 502 Phosphorylase Phosphatase, 502 Phosphorylate, 44, 502 Phosphorylated, 43, 54, 55, 454, 501, 502 Phosphorylation, 20, 33, 41, 43, 53, 291, 502, 508 Photoallergy, 502 Photochemotherapy, 5, 7, 125, 149, 165, 213, 222, 224, 225, 273, 275, 295, 338, 401, 502 Photocoagulation, 447, 502 Photodermatitis, 28, 238, 260, 502 Photodynamic therapy, 131, 180, 377, 502 Photoreceptor, 19, 502, 515 Photosensitivity, 353, 502 Photosensitizer, 377, 502 Photosensitizing Agents, 502 Phototherapy, 5, 9, 84, 95, 98, 100, 101, 102, 103, 148, 149, 150, 156, 157, 167, 195, 203, 215, 222, 223, 224, 226, 228, 231, 268, 273, 313, 338, 353, 357, 360, 364, 366, 373, 376, 377, 378, 396, 401, 403, 404, 502 Physical Examination, 250, 253, 502 Physiologic, 33, 43, 69, 340, 428, 469, 487, 502, 507, 512, 513 Physiology, 18, 23, 24, 84, 88, 95, 108, 119, 150, 184, 186, 492, 493, 502 Pigmentation, 201, 215, 270, 275, 503 Pigments, 437, 441, 503, 514 Pilot study, 38, 73, 99, 100, 102, 110, 167, 189, 190, 202, 212, 222, 250, 503 Pituitary Gland, 451, 463, 503 Pityriasis, 91, 271, 364, 498, 503 Pityriasis Lichenoides, 364, 498, 503 Pityriasis Rosea, 91, 503 Placebo Effect, 60, 250, 503 Placenta, 503, 506, 530 Plant Oils, 495, 503 Plasma cells, 431, 503 Plasmin, 12, 43, 503, 504 Plasminogen, 12, 43, 112, 300, 503, 504 Plasminogen Activators, 503, 504 Platelet Activation, 504, 518 Platelet Aggregation, 355, 430, 494, 499, 504, 526 Platelets, 15, 355, 436, 494, 504, 526 Platinum, 483, 497, 504 Pleated, 480, 504 Pneumoconiosis, 268, 340, 342, 504 Pneumonia, 47, 450, 504
Podophyllotoxin, 235, 504 Poisoning, 440, 466, 479, 487, 492, 504 Polyarthritis, 124, 504 Polycystic, 389, 504 Polyethylene, 9, 236, 276, 504 Polymerase, 125, 166, 180, 504, 506, 513 Polymerase Chain Reaction, 125, 166, 180, 504 Polymers, 72, 310, 505, 508, 522 Polymorphism, 107, 119, 123, 129, 136, 157, 159, 172, 195, 204, 272, 309, 326, 505 Polyphosphates, 305, 505 Polyposis, 448, 505 Polysaccharide, 432, 443, 505, 508, 531 Polyunsaturated fat, 224, 505, 526 Polyvinyl Chloride, 276, 505 Posterior, 430, 434, 444, 445, 456, 497, 505, 516, 520 Postmenopausal, 366, 496, 505 Postnatal, 505, 521 Postsynaptic, 505, 518 Post-traumatic, 153, 469, 505 Potassium, 277, 283, 310, 311, 317, 428, 484, 489, 505, 510, 519 Potassium Chloride, 311, 317, 505 Potassium Citrate, 311, 505 Potentiates, 478, 505 Potentiation, 505, 518 Practice Guidelines, 386, 405, 505 Precancerous, 60, 403, 426, 505, 506 Preclinical, 71, 506 Precursor, 49, 285, 431, 433, 456, 457, 459, 494, 501, 503, 506, 528, 529 Predisposition, 6, 128, 295, 299, 347, 506 Prednisolone, 27, 270, 506 Prednisone, 7, 271, 506 Preeclampsia, 299, 506 Premalignant, 284, 505, 506 Prevalence, 7, 68, 126, 133, 158, 165, 186, 290, 349, 351, 363, 379, 506 Prickle, 425, 480, 506 Probe, 26, 60, 307, 506 Procaine, 284, 482, 506 Prodrug, 5, 27, 287, 506 Progeny, 449, 467, 506 Progesterone, 33, 506, 521 Progression, 7, 14, 17, 41, 71, 355, 431, 506, 529 Progressive, 433, 443, 446, 453, 456, 461, 469, 481, 491, 492, 496, 504, 506, 509, 512, 516, 529 Proline, 447, 473, 506
552 Psoriasis
Promoter, 17, 31, 45, 70, 107, 122, 136, 159, 319, 327, 506 Promotor, 506, 513 Promyelocytic leukemia, 506, 528 Prone, 51, 507 Prophase, 490, 507, 523 Prophylaxis, 264, 329, 336, 351, 461, 507, 531 Propolis, 219, 228, 507 Proportional, 260, 507 Prospective Studies, 59, 507 Prospective study, 147, 182, 507 Prostaglandin, 187, 222, 233, 284, 293, 507, 526 Prostaglandins A, 476, 507 Prostate, 23, 65, 78, 388, 507, 513 Protease, 60, 64, 174, 312, 448, 507 Protease Inhibitors, 312, 507 Protective Agents, 440, 508 Protein Binding, 79, 508, 526 Protein C, 23, 32, 64, 67, 79, 255, 371, 428, 429, 432, 435, 480, 483, 508, 530 Protein Isoforms, 17, 429, 508 Protein Kinases, 44, 291, 508 Protein S, 18, 43, 65, 75, 172, 362, 389, 390, 437, 460, 466, 472, 492, 508, 515, 525 Protein-Tyrosine Kinase, 355, 508 Proteinuria, 506, 508 Proteoglycan, 14, 508 Proteolytic, 12, 43, 55, 429, 448, 459, 463, 503, 504, 508 Proteome, 52, 508 Protocol, 30, 78, 220, 249, 254, 508 Proton Pump, 495, 508 Protons, 429, 473, 480, 508, 511 Proto-Oncogene Proteins, 497, 508 Proto-Oncogene Proteins c-mos, 497, 508 Proto-Oncogenes, 291, 508 Protozoa, 449, 488, 509 Proximal, 8, 19, 57, 143, 455, 509 Pruritic, 457, 482, 509, 516 Pruritus, 106, 203, 420, 493, 509, 530 Psoralen, 5, 9, 81, 126, 132, 141, 148, 171, 186, 193, 213, 236, 260, 268, 275, 295, 312, 314, 317, 353, 357, 364, 376, 379, 400, 401, 403, 404, 509 Psychiatric, 164, 376, 487, 509 Psychiatry, 60, 155, 225, 463, 509 Psychic, 487, 509, 517 Psychoactive, 509, 533 Psychogenic, 493, 509 Psychoneuroimmunology, 234, 509
Psychotherapy, 213, 217, 247, 447, 509 Puberty, 269, 509 Public Policy, 385, 509 Pulmonary, 23, 43, 46, 268, 340, 342, 379, 438, 445, 449, 450, 459, 481, 482, 509, 510, 523, 532 Pulmonary Edema, 445, 481, 509 Pulmonary Emphysema, 43, 509 Pulmonary Fibrosis, 268, 340, 342, 509 Pulmonary hypertension, 450, 510 Pulse, 48, 280, 292, 317, 490, 510 Pupil, 450, 455, 491, 510 Purines, 62, 436, 510, 517 Purulent, 510 Pyoderma, 90, 132, 510 Pyoderma Gangrenosum, 90, 510 Pyrazinamide, 337, 510 Pyrimidines, 62, 260, 436, 510, 517 Q Quaternary, 60, 510 Quiescent, 32, 43, 443, 510, 532 Quinacrine, 376, 510 Quinidine, 376, 510 Quinine, 510 R Race, 281, 311, 350, 354, 488, 510 Radiation therapy, 321, 462, 464, 479, 480, 511, 533 Radioactive, 469, 473, 476, 479, 480, 489, 490, 494, 495, 511, 533 Radioactivity, 321, 511 Radiography, 450, 511 Radioimmunotherapy, 511 Radiolabeled, 480, 511, 533 Radiological, 500, 511 Radiotherapy, 160, 438, 480, 511, 533 Randomized clinical trial, 56, 166, 511 Randomized Controlled Trials, 116, 511 Reactive Oxygen Species, 44, 512 Reagent, 445, 484, 501, 512 Recombinant, 12, 14, 20, 33, 99, 254, 512, 532 Recombination, 57, 449, 466, 512 Reconstitution, 37, 43, 512 Rectum, 432, 438, 447, 455, 465, 477, 481, 507, 512 Recur, 305, 512 Recurrence, 45, 55, 130, 266, 273, 319, 379, 512 Red blood cells, 460, 470, 497, 512, 516 Red Nucleus, 434, 512 Reductase, 15, 62, 307, 488, 512
Index 553
Refer, 1, 306, 348, 439, 448, 455, 463, 465, 471, 483, 484, 485, 492, 494, 511, 512, 527 Refraction, 512, 520 Refractory, 4, 54, 126, 188, 342, 457, 512 Regeneration, 47, 463, 512 Regimen, 60, 94, 95, 104, 231, 292, 318, 399, 400, 446, 457, 499, 501, 503, 512, 514 Relapse, 8, 119, 131, 168, 196, 251, 274, 512 Reliability, 146, 512 Remission, 5, 87, 109, 168, 178, 181, 229, 252, 261, 262, 273, 282, 283, 285, 288, 295, 301, 312, 313, 316, 319, 343, 371, 377, 485, 512 Renal failure, 169, 289, 436, 512 Renal Osteodystrophy, 78, 513 Renin, 314, 431, 513 Reperfusion, 56, 299, 491, 513 Reperfusion Injury, 56, 299, 513 Repressor, 307, 495, 513 Reproductive cells, 467, 513 Reproductive system, 70, 513 Research Design, 19, 22, 513 Resolving, 113, 513 Resorption, 49, 496, 513 Respiration, 441, 490, 497, 513 Respiratory distress syndrome, 23, 56, 513 Response Elements, 319, 513 Restoration, 293, 326, 343, 491, 512, 513, 533 Retina, 430, 445, 454, 482, 485, 493, 496, 513, 514, 515, 531 Retinal, 300, 449, 454, 495, 496, 514, 515 Retinaldehyde, 331, 514 Retinitis, 299, 514 Retinoblastoma, 388, 514 Retinoid, 5, 6, 7, 8, 23, 59, 117, 170, 204, 215, 236, 256, 257, 267, 319, 369, 371, 425, 461, 514 Retinol, 208, 319, 514, 515 Retinopathy, 46, 454, 514 Retreatment, 158, 514 Retrospective, 213, 514 Retroviral vector, 54, 466, 514 Retrovirus, 54, 514 Rheology, 499, 514 Rheumatic Diseases, 64, 75, 107, 363, 514 Rheumatism, 130, 158, 162, 172, 321, 322, 358, 474, 514 Rhinitis, 299, 515 Rhodopsin, 331, 495, 514, 515 Ribonucleoside Diphosphate Reductase, 473, 515
Ribose, 426, 515 Ribosome, 515, 528 Rickets, 289, 366, 440, 515 Rigidity, 503, 515 Risk factor, 88, 119, 132, 143, 232, 507, 515 Rod, 19, 435, 446, 502, 515 Rod cells, 19, 515 Roxithromycin, 97, 515 Rubber, 168, 426, 505, 515 Rye, 209, 279, 467, 515 S Salicylate, 85, 277, 320, 515, 519 Salivary, 452, 455, 498, 515, 522 Salivary glands, 452, 455, 515 Saponins, 441, 495, 515, 521 Scabies, 104, 516 Scatter, 516, 530 Schizoid, 516, 533 Schizophrenia, 173, 516, 533 Schizotypal Personality Disorder, 516, 533 Sciatica, 126, 516 Sclera, 445, 449, 516, 531 Scleroderma, 35, 54, 352, 433, 462, 516 Scleroderma, Systemic, 352, 516 Scleroproteins, 480, 516 Sclerosis, 43, 74, 180, 267, 299, 339, 342, 389, 433, 447, 490, 516 Screening, 13, 28, 46, 52, 84, 254, 262, 272, 303, 345, 346, 446, 516 Sebaceous, 454, 480, 516, 533 Sebaceous gland, 454, 480, 516, 533 Seborrhea, 283, 310, 311, 349, 359, 516 Sebum, 261, 316, 426, 516 Second Messenger Systems, 516 Secondary tumor, 488, 517 Secretory, 495, 517 Segregation, 29, 43, 101, 445, 512, 517 Seizures, 498, 517 Selenium, 8, 208, 218, 224, 233, 517 Semen, 507, 517 Seminiferous tubule, 15, 517 Senile, 262, 316, 426, 496, 517 Sensitization, 37, 453, 502, 517 Sepsis, 20, 517 Septic, 13, 23, 56, 434, 517 Sequence Homology, 499, 517 Sequencing, 59, 75, 505, 517 Serine, 20, 44, 174, 312, 446, 459, 502, 508, 517, 529 Serologic, 40, 128, 475, 517 Serology, 35, 409, 517 Serotonin, 494, 501, 517, 529
554 Psoriasis
Serous, 459, 518 Serum Albumin, 438, 518 Sex Characteristics, 427, 430, 509, 518, 525 Sex Determination, 389, 518 Shedding, 282, 283, 293, 301, 326, 375, 454, 518 Shock, 13, 23, 56, 119, 444, 473, 518, 528 Signal Transduction, 13, 18, 20, 44, 51, 60, 61, 65, 323, 343, 440, 442, 470, 518 Signs and Symptoms, 263, 264, 266, 286, 512, 518, 530 Sirolimus, 112, 181, 518 Sister Chromatid Exchange, 183, 518 Skeletal, 177, 430, 446, 491, 510, 518 Skeleton, 426, 463, 480, 507, 518, 519 Skin Aging, 73, 271, 519 Skin graft, 39, 519 Skin Pigmentation, 275, 519 Skull, 451, 496, 498, 519, 524 Small intestine, 289, 446, 456, 467, 472, 475, 479, 519, 529 Smallpox, 519, 531 Smoking Cessation, 439, 519 Smooth muscle, 428, 430, 435, 439, 440, 449, 472, 474, 519, 523 Sneezing, 518, 519 Soaps, 8, 400, 463, 519 Social Environment, 510, 519 Social Security, 299, 347, 511, 519 Sodium, 271, 296, 312, 317, 428, 468, 484, 489, 510, 519, 523 Sodium salicylate, 271, 519 Soft tissue, 263, 345, 346, 352, 438, 462, 463, 518, 519 Solid tumor, 32, 69, 430, 459, 519 Solvent, 60, 289, 292, 336, 461, 468, 500, 519 Somatic, 359, 427, 458, 467, 472, 486, 489, 500, 518, 519, 524 Somatic cells, 467, 486, 489, 519 Somatostatin, 177, 314, 519 Soybean Oil, 505, 520 Spasmogenic, 430, 520 Spatial disorientation, 455, 520 Specialist, 410, 455, 520 Specificity, 16, 32, 43, 45, 67, 427, 433, 459, 520, 526 Spectroscopic, 78, 331, 520 Spectrum, 24, 34, 45, 52, 59, 164, 204, 280, 284, 319, 334, 408, 452, 481, 515, 520, 530 Sperm, 430, 445, 513, 517, 520 Sphenoid, 498, 520
Spinal cord, 64, 434, 439, 442, 443, 444, 445, 451, 457, 458, 487, 493, 497, 500, 520 Spinal Nerve Roots, 516, 520 Spinal Nerves, 500, 520 Spinous, 460, 480, 520 Spirochete, 520, 524 Spleen, 192, 452, 484, 520 Spondylitis, 128, 520 Sporadic, 35, 514, 520 Sprains and Strains, 484, 520 Squamous, 6, 19, 20, 51, 70, 126, 128, 132, 177, 301, 327, 330, 403, 460, 521 Squamous cell carcinoma, 6, 19, 20, 70, 126, 128, 132, 177, 301, 327, 403, 460, 521 Squamous cells, 521 Stabilizer, 63, 521 Staphylococcus, 67, 318, 466, 476, 521 Staphylococcus aureus, 67, 318, 466, 476, 521 Steel, 446, 521 Stem cell transplantation, 124, 521 Stem Cells, 30, 38, 55, 428, 500, 521 Sterile, 163, 434, 498, 521 Sterility, 477, 521 Steroid therapy, 104, 521 Stilbenes, 339, 521 Stimulant, 439, 472, 521 Stimulus, 16, 51, 77, 250, 263, 282, 283, 345, 346, 456, 457, 461, 479, 493, 521, 526 Stippling, 297, 522 Stomach, 425, 435, 455, 461, 465, 466, 472, 492, 499, 501, 519, 520, 522 Stool, 447, 481, 522 Strand, 504, 522 Streptococcal, 6, 97, 103, 113, 119, 124, 129, 151, 174, 176, 178, 203, 522 Streptococcal Infections, 6, 522 Streptococci, 151, 176, 186, 476, 522 Streptococcus, 129, 462, 522 Stria, 106, 421, 522 Stroke, 258, 384, 441, 522 Stroma, 43, 70, 522 Stromal, 40, 132, 438, 522 Stromal Cells, 40, 438, 522 Strontium, 317, 522 Styrene, 515, 522 Subacute, 477, 522 Subarachnoid, 469, 522 Subclinical, 147, 179, 477, 517, 522 Subcutaneous, 254, 296, 457, 498, 522 Sublingual, 298, 522 Submaxillary, 460, 522
Index 555
Subspecies, 520, 522, 531 Substance P, 460, 487, 512, 517, 522 Substrate, 12, 18, 22, 483, 523 Sulfates, 14, 523 Sulfur, 314, 462, 488, 523 Sulfuric acid, 523 Sunburn, 6, 73, 77, 238, 289, 421, 523, 530 Superantigens, 37, 68, 93, 115, 129, 290, 523 Superoxide, 85, 523 Superoxide Dismutase, 85, 523 Supplementation, 213, 215, 220, 221, 222, 223, 233, 234, 523 Support group, 409, 422, 423, 523 Suppression, 4, 36, 45, 48, 54, 106, 109, 170, 202, 265, 286, 311, 322, 379, 446, 451, 454, 523 Suppressive, 27, 274, 523 Surfactant, 269, 327, 338, 523 Sweat, 454, 516, 523 Sweat Glands, 454, 516, 523 Symphysis, 445, 507, 523 Symptomatic, 11, 180, 283, 286, 322, 498, 523 Synapse, 427, 523, 528 Synaptic, 493, 518, 523 Synchrotron, 79, 524 Synergistic, 27, 74, 108, 263, 329, 524 Synovial, 49, 251, 524 Synovial Fluid, 251, 524 Synovial Membrane, 524 Synthetic retinoid, 312, 357, 524 Syphilis, 267, 339, 342, 524 Systemic disease, 474, 524 Systemic lupus erythematosus, 31, 35, 261, 267, 339, 341, 342, 445, 447, 484, 524 Systemic therapy, 4, 86, 143, 181, 273, 276, 400, 445, 524 Systolic, 474, 524 T Tachyphylaxis, 4, 118, 524 Tacrolimus, 181, 189, 524 Tear Gases, 480, 524 Telangiectasia, 389, 524 Tellurium, 297, 524 Telomerase, 106, 202, 524 Temporal, 73, 469, 485, 498, 524 Tendon, 177, 524, 525 Tenosynovitis, 139, 525 Teratogen, 7, 525 Teratogenic, 5, 21, 425, 430, 455, 461, 525, 528
Teratogenicity, 21, 378, 525 Testis, 15, 525 Testosterone, 512, 525 Tetany, 498, 525 Tetracaine, 284, 525 Tetracycline, 270, 354, 456, 525 Thalamic, 434, 525 Thalamic Diseases, 434, 525 Thalidomide, 115, 525 Theophylline, 314, 316, 510, 525 Therapeutics, 22, 56, 63, 75, 77, 213, 268, 525 Thermal, 55, 214, 216, 229, 434, 455, 470, 494, 504, 525 Thigh, 398, 463, 469, 525 Thimerosal, 255, 525 Thioguanine, 188, 190, 315, 325, 525 Threonine, 499, 508, 517, 526 Threshold, 29, 338, 461, 474, 526 Thrombin, 463, 504, 508, 526 Thrombocytes, 504, 526 Thrombocytopenia, 46, 526 Thrombolytic, 503, 526 Thrombomodulin, 508, 526 Thrombosis, 355, 436, 478, 508, 522, 526 Thromboxanes, 433, 457, 526 Thrombus, 450, 476, 491, 504, 526 Thymus, 14, 301, 475, 484, 526 Thyroid, 16, 65, 110, 291, 440, 479, 498, 526, 529 Thyroid Gland, 498, 526 Thyroiditis, 77, 526 Ticks, 477, 526 Tin, 323, 324, 504, 526 Tissue Banks, 59, 526 Tissue Culture, 354, 526 Tissue Distribution, 18, 52, 526 Tolerance, 36, 56, 74, 111, 254, 296, 426, 467, 470, 527 Tomography, 438, 527 Tone, 23, 359, 527 Tonus, 527 Tooth Preparation, 426, 527 Torsion, 477, 527 Toxaemia, 506, 527 Toxicodendron, 239, 527 Toxicology, 101, 143, 171, 386, 527 Toxin, 9, 21, 59, 68, 76, 304, 459, 476, 527 Trace element, 438, 494, 526, 527 Trachea, 439, 462, 501, 526, 527 Traction, 446, 527 Transcriptase, 180, 514, 524, 527
556 Psoriasis
Transcription Factors, 17, 45, 58, 65, 513, 527 Transdermal, 270, 527 Transduction, 13, 20, 44, 62, 66, 518, 528 Transfection, 33, 45, 62, 437, 466, 528 Transfer Factor, 475, 528 Transforming Growth Factor alpha, 19, 528 Transforming Growth Factor beta, 90, 528 Transfusion, 462, 528 Transgenes, 17, 528 Translation, 52, 363, 429, 460, 492, 528 Translational, 21, 528 Translocating, 67, 528 Translocation, 43, 67, 291, 460, 528 Transmitter, 425, 434, 456, 480, 486, 494, 528 Transplantation, 33, 36, 37, 38, 75, 89, 93, 130, 260, 261, 281, 330, 446, 472, 475, 481, 485, 528 Trauma, 6, 7, 44, 58, 140, 255, 289, 293, 295, 328, 354, 461, 498, 528 Trees, 429, 515, 527, 528 Tretinoin, 319, 331, 528 Triamcinolone Acetonide, 8, 153, 350, 528 Triazolam, 328, 529 Tricuspid Atresia, 450, 529 Triglyceride, 474, 529 Trioxsalen, 219, 225, 236, 529 Tropism, 71, 298, 529 Trypsin, 270, 446, 459, 529 Tryptophan, 447, 517, 529 Tuberous Sclerosis, 389, 529 Tumor model, 70, 529 Tumor Necrosis Factor, 90, 93, 132, 156, 159, 183, 191, 290, 304, 309, 397, 525, 529 Tumour, 120, 132, 191, 432, 529 Tunica, 490, 529 Tyrosine, 20, 79, 94, 134, 135, 455, 508, 529 U Ubiquinone, 270, 529 Ulcer, 271, 299, 499, 529, 531 Ulcerative colitis, 27, 477, 510, 529 Ultraviolet radiation, 128, 166, 215, 277, 318, 334, 502, 519, 523, 530 Ultraviolet Therapy, 358, 530 Umbilical Arteries, 530 Umbilical Cord, 64, 530 Umbilicus, 319, 530 Unconscious, 453, 474, 530 Unsaturated Fats, 463, 530 Uracil, 510, 530, 531
Uraemia, 498, 530 Urban Health, 34, 530 Urban Population, 530 Urea, 276, 293, 310, 338, 481, 523, 530 Urease, 494, 530 Uremia, 481, 512, 530 Urethra, 499, 507, 530, 531 Uric, 468, 474, 510, 530 Uridine Diphosphate, 468, 531 Uridine Diphosphate Glucuronic Acid, 468, 531 Urinary, 194, 206, 441, 467, 495, 530, 531, 533 Urine, 253, 432, 436, 437, 460, 468, 470, 473, 481, 495, 508, 530, 531 Urocanic Acid, 221, 531 Urogenital, 467, 531 Urokinase, 12, 312, 531 Urticaria, 106, 299, 531 Uterus, 425, 444, 451, 453, 459, 487, 493, 496, 506, 513, 531 Uvea, 531 Uveitis, 299, 531 V Vaccination, 301, 531 Vaccine, 312, 363, 427, 508, 531 Vaccinia, 298, 531 Vaccinia Virus, 298, 531 Vagina, 444, 454, 487, 513, 531 Varicose, 482, 531 Varicose Ulcer, 482, 531 Variola, 531 Vascular endothelial growth factor, 70, 112, 141, 146, 304, 531 Vasculitis, 85, 498, 531 Vasoactive, 63, 531 Vasoconstriction, 24, 460, 532 Vasodilator, 439, 440, 456, 472, 491, 532 VE, 29, 361, 532 Vector, 54, 75, 528, 531, 532 Vein, 251, 253, 255, 433, 479, 494, 530, 532 Venereal, 524, 532 Venous, 232, 433, 436, 482, 508, 529, 531, 532 Venous blood, 232, 482, 532 Ventricle, 434, 450, 474, 510, 524, 529, 532 Ventricular, 450, 491, 529, 532 Venules, 68, 438, 441, 459, 488, 532 Vertebrae, 479, 520, 532 Vesicular, 434, 471, 488, 503, 519, 531, 532 Veterinary Medicine, 385, 532
Index 557
Viral, 13, 21, 37, 51, 261, 298, 425, 454, 458, 477, 495, 508, 514, 528, 532 Viral vector, 21, 532 Virulence, 527, 532 Visceral, 32, 435, 500, 516, 532 Viscosity, 425, 514, 532 Vitamin A, 207, 208, 271, 406, 425, 514, 532 Vitelline Membrane, 532, 533 Vitiligo, 100, 164, 180, 195, 275, 394, 395, 509, 529, 532 Vitreous, 445, 454, 482, 513, 533 Vitreous Hemorrhage, 454, 533 Vivo, 17, 18, 20, 21, 22, 23, 26, 28, 30, 33, 36, 39, 41, 42, 44, 45, 46, 50, 54, 55, 56, 57, 63, 68, 71, 72, 76, 78, 132, 179, 265, 278, 335, 355, 466, 471, 476, 497, 524, 526, 533 W War, 139, 486, 491, 533
Wart, 481, 533 White blood cell, 37, 251, 255, 283, 403, 431, 445, 446, 469, 482, 484, 485, 490, 492, 494, 503, 533 Windpipe, 439, 501, 526, 533 Withdrawal, 120, 121, 266, 289, 533 Womb, 513, 531, 533 X Xanthine, 268, 533 Xenograft, 431, 529, 533 X-ray therapy, 278, 328, 480, 533 Y Yeasts, 465, 501, 533 Yolk Sac, 32, 533 Yttrium, 334, 533 Z Zygote, 449, 534 Zymogen, 446, 508, 534
558 Psoriasis
Index 559
560 Psoriasis
