Dermatitis - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References

DERMATITIS 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., 1960Dermatitis: 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: 0-597-83881-X 1. Dermatitis-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.

Copyright Notice If a physician wishes to copy limited passages from this book for patient use, this right is automatically granted without written permission from ICON Group International, Inc. (ICON Group). However, all of ICON Group publications have copyrights. With exception to the above, copying our publications in whole or in part, for whatever reason, is a violation of copyright laws and can lead to penalties and fines. Should you want to copy tables, graphs, or other materials, please contact us to request permission (E-mail: [email protected]). ICON Group often grants permission for very limited reproduction of our publications for internal use, press releases, and academic research. Such reproduction requires confirmed permission from ICON Group International Inc. The disclaimer above must accompany all reproductions, in whole or in part, of this book.

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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 dermatitis. 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 DERMATITIS .............................................................................................. 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Dermatitis ..................................................................................... 8 E-Journals: PubMed Central ....................................................................................................... 66 The National Library of Medicine: PubMed ................................................................................ 68 CHAPTER 2. NUTRITION AND DERMATITIS .................................................................................. 113 Overview.................................................................................................................................... 113 Finding Nutrition Studies on Dermatitis.................................................................................. 113 Federal Resources on Nutrition ................................................................................................. 117 Additional Web Resources ......................................................................................................... 118 CHAPTER 3. ALTERNATIVE MEDICINE AND DERMATITIS ............................................................ 121 Overview.................................................................................................................................... 121 National Center for Complementary and Alternative Medicine................................................ 121 Additional Web Resources ......................................................................................................... 140 General References ..................................................................................................................... 153 CHAPTER 4. DISSERTATIONS ON DERMATITIS .............................................................................. 155 Overview.................................................................................................................................... 155 Dissertations on Dermatitis....................................................................................................... 155 Keeping Current ........................................................................................................................ 156 CHAPTER 5. CLINICAL TRIALS AND DERMATITIS ......................................................................... 157 Overview.................................................................................................................................... 157 Recent Trials on Dermatitis....................................................................................................... 157 Keeping Current on Clinical Trials ........................................................................................... 159 CHAPTER 6. PATENTS ON DERMATITIS ......................................................................................... 161 Overview.................................................................................................................................... 161 Patents on Dermatitis ................................................................................................................ 161 Patent Applications on Dermatitis ............................................................................................ 185 Keeping Current ........................................................................................................................ 218 CHAPTER 7. BOOKS ON DERMATITIS ............................................................................................ 219 Overview.................................................................................................................................... 219 Book Summaries: Federal Agencies............................................................................................ 219 Book Summaries: Online Booksellers......................................................................................... 220 The National Library of Medicine Book Index ........................................................................... 223 Chapters on Dermatitis.............................................................................................................. 224 CHAPTER 8. MULTIMEDIA ON DERMATITIS .................................................................................. 227 Overview.................................................................................................................................... 227 Video Recordings ....................................................................................................................... 227 Bibliography: Multimedia on Dermatitis................................................................................... 228 CHAPTER 9. PERIODICALS AND NEWS ON DERMATITIS ............................................................... 231 Overview.................................................................................................................................... 231 News Services and Press Releases.............................................................................................. 231 Newsletters on Dermatitis ......................................................................................................... 235 Newsletter Articles .................................................................................................................... 236 Academic Periodicals covering Dermatitis ................................................................................ 237 CHAPTER 10. RESEARCHING MEDICATIONS................................................................................. 239 Overview.................................................................................................................................... 239 U.S. Pharmacopeia..................................................................................................................... 239 Commercial Databases ............................................................................................................... 241 Researching Orphan Drugs ....................................................................................................... 242

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APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 245 Overview.................................................................................................................................... 245 NIH Guidelines.......................................................................................................................... 245 NIH Databases........................................................................................................................... 247 Other Commercial Databases..................................................................................................... 250 The Genome Project and Dermatitis.......................................................................................... 250 APPENDIX B. PATIENT RESOURCES ............................................................................................... 255 Overview.................................................................................................................................... 255 Patient Guideline Sources.......................................................................................................... 255 Finding Associations.................................................................................................................. 267 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 269 Overview.................................................................................................................................... 269 Preparation................................................................................................................................. 269 Finding a Local Medical Library................................................................................................ 269 Medical Libraries in the U.S. and Canada ................................................................................. 269 ONLINE GLOSSARIES................................................................................................................ 275 Online Dictionary Directories ................................................................................................... 275 DERMATITIS DICTIONARY..................................................................................................... 277 INDEX .............................................................................................................................................. 381

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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 dermatitis 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 dermatitis, 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 dermatitis, 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 dermatitis. 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 dermatitis, 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 dermatitis. 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 DERMATITIS Overview In this chapter, we will show you how to locate peer-reviewed references and studies on dermatitis.

The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and dermatitis, 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 “dermatitis” (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: •

Allergic Contact Dermatitis in Dental Professionals: Effective Diagnosis and Treatment Source: JADA. Journal of the American Dental Association. 134(2): 185-194. February 2003. Contact: Available from American Dental Association. ADA Publishing Co, Inc., 211 East Chicago Avenue, Chicago, IL 60611. (312) 440-2867. Website: www.ada.org. Summary: Dental professionals are at risk of developing allergic contact dermatitis (ACD) after exposure to allergenic chemicals. Common allergens include antimicrobials, preservatives, rubber additives, and methacrylates. In this article, the authors describe an orthodontic assistant with severe skin disease, whose symptoms included redness, cracking and bleeding that persisted for 10 years. The patient had previously received

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an incomplete diagnosis. After performing patch testing, assessing symptoms, and evaluating the patient's medical history, the authors diagnosed ACD resulting from exposure to several dental allergens. The patient received appropriate treatment and counseling to better manage her allergies; this resulted in resolution of all symptoms and averted permanent occupational disability. The authors conclude that not all skin reactions are related to gloves or natural rubber latex. Dental professionals should be aware of common chemical allergens, symptoms of ACD, and the appropriate treatment of occupational skin disease. 3 figures. 3 tables. 26 references. •

Incidence of Familial Dermatitis Herpetiformis Source: British Journal of Dermatology. 134(3): 394-398. March 1996. Contact: Available from Blackwell Science, Ltd. Journal Subscriptions, P.O. Box 88, Oxford, England OX2 0NE. Phone (44) 1865 206180. Fax (44) 1865 206219. Summary: Dermatitis herpetiformis (DH) and celiac disease (CD) are gluten sensitive diseases which have a common immunogenetic background, with the histocompatibility locus antigen (HLA) alleles DQA1-0501 and B1-0201 in the short arm of chromosome 6. CD is well known to cluster in families whereas DH has not been generally regarded as a familial disease. This article reports on a study undertaken to evaluate the familial incidence of DH. The prospective study was started in 1969 at the Department of Dermatology of Helsinki University Hospital and in 1976 at the Department of Dermatology of Tampere University Hospital. A total of 1018 patients with DH were diagnosed and questioned for positive family histories. Of the 999 unrelated DH patients, 105 (10.5 percent) had one or several affected first-degree relatives. The disease in the relatives was either DH (4.4 percent) or CD (6.1 percent). Analysis of the 105 families showed that 13.6 percent of parents, 18.7 percent of siblings, and 14.0 percent of children were affected, a segregation pattern which fits well to a dominant mode of Mendelian inheritance. Gender may also be important because the first-degree relatives affected with DH were more often females and those affected with CD twice as often females as males. In contrast, there were more males among the 105 participants with DH and also among the 894 DH patients with no affected relatives. The author concludes that this study clearly shows that DH is a familial disease. Parents, siblings, and children were almost equally affected in the study group. The frequent occurrence of CD among the first-degree relatives of DH patients comports with the hypothesis that a genetically determined gluten-sensitive enteropathy, i.e. CD, is a prerequisite for the development of DH. 5 tables. 33 references. (AA-M).

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Protective Effect of Gluten-Free Diet Against Development of Lymphoma in Dermatitis Herpetiformis Source: British Journal of Dermatology. 134(3): 363-367. September 1996. Contact: Available from Blackwell Science, Ltd. Journal Subscriptions, P.O. Box 88, Oxford, England OX2 0NE. Phone (44) 1865 206180. Fax (44) 1865 206219. Summary: This article reports on a retrospective study of 487 patients with dermatitis herpetiformis (DH). The study showed that lymphoma developed in eight patients (the expected incidence being 0.21). All lymphomas occurred in patients whose dermatitis herpetiformis had been controlled without a gluten-free diet (GFD) or in those who had been treated with a GFD for less than 5 years. The results suggest that GFD plays a protective role against lymphoma in DH and give further support for advising patients to adhere to a strict GFD for life. 2 tables. 22 references. (AA-M).

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Diseases Associated with Dermatitis Herpetiformis Source: British Journal of Dermatology. 136(3): 315-318. March 1997. Contact: Available from Blackwell Science, Ltd. Journal Subscriptions, P.O. Box 88, Oxford, England OX2 0NE. Phone (44) 1865 206180. Fax (44) 1865 206219. Summary: This article reports on a study of the occurrence of associated diseases in a cohort of 305 patients with dermatitis herpetiformis (DH) followed up for a mean of 10 years. The results were compared with those from 383 patients with celiac disease (CD). Twenty-nine (9.5 percent) patients with DH and 73 (19.1 percent) with CD had concomitant endocrine or connective tissue disorders. The following associations were found: autoimmune thyroid disease (4.3 percent of DH patients and 6.0 percent of CD patients), type 1 diabetes (1.0 percent DH and 5.5 percent CD), lupus erythematosus (1.3 percent DH and 0.3 percent CD), Sjogren's syndrome (1.0 percent DH and 2.9 percent CD), sarcoidosis (1.3 percent DH and 1.8 percent CD), and vitiligo or alopecia areata (1.6 percent DH and 0 percent CD). The authors have shown that patients with DH are similar to those with CD in that many have associated endocrine or connective tissue disorders. Most of these diseases began before DH had been diagnosed, suggesting that those on a gluten-free diet are not at special risk of contracting them. 1 table. 26 references. (AA-M).

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Malignancy and Survival in Dermatitis Herpetiformis: A Comparison with Coeliac Disease Source: Gut. Journal of the British Society of Gastroenterology. 38(4): 528-530. April 1996. Contact: Available from British Medical Journal. P.O. Box 408, Franklin, MA 02038. Summary: This article reports on a study that investigated the occurrence of malignancy and the survival of patients with dermatitis herpetiformis (DH); the results were compared with those seen in patients with celiac disease (CD), and the general population. A total of 305 adult patients with DH diagnosed at the University Hospital of Tampere from 1970 to 1992 were studied. Most patients started a gluten free diet and at the end of the study, 93 percent of the patients were adhering to the diet. A control group comprised 383 adult patients with celiac disease; 81 percent of them adhered to a gluten free diet, 6 percent had a normal diet, and in 13 percent the diet history remained unknown. The occurrence of malignant diseases and survival of the patients was assessed up to the end of 1993. The survival of the patients was compared with that of the general population. Thirteen (4.3 percent) patients with DH developed 14 malignant disorders during the followup. A non-Hodgkin's lymphoma occurred in four patients with dermatitis herpetiformis, significantly more than expected. Thirteen (4.3 percent) patients with DH died during followup, but there was no increased general mortality. In celiac disease, 13 (3.4 percent) patients developed malignancy, 31 (8.1 percent) patients died, but the survival rate did not differ from that in the general population. The authors conclude that the incidence of non-Hodgkin's lymphoma was significantly increased in patients with dermatitis herpetiformis. The results also confirm that the patients with DH treated mainly with a gluten free diet have no increased general mortality. 4 tables. 13 references. (AA-M).

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Topical Tacrolimus: A New Therapy for Atopic Dermatitis Source: American Family Physician. 66(10): 1899-1902. November 15, 2002.

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Summary: This journal article discusses the use of the drug tacrolimus, a medication derived from macrolides that suppresses the immune system, in treating atopic dermatitis. Used topically it has been found to be effective in treating moderate to severe atopic dermatitis without causing the atrophy that might occur with prolonged use of topical corticosteroids. Tacrolimus works equally well in children and adults, with more than two-thirds of both groups having an improvement of greater than 50 percent. Despite its potency, very little of the medication is systemically absorbed, and absorption decreases as the atopic dermatitis resolves. The main side effects are burning and itching, but these also decrease with improvement of the atopic dermatitis. 20 references. (AAM). •

Eczematous Dermatitis: A Practical Review Source: American Family Physician. 54(4):1243-1250. September 5, 1996. 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 for dermatologists discusses various types eczematous dermatitis and their treatment. Eczematous dermatitis can interfere with social function, sleep, and employment, and that its persistence and accompanying pruritus may be stressful and frustrating for patients. The most common and best characterized type of eczema, atopic dermatitis, appears to be increasing in incidence. The authors suggest that other common eczematous dermatoses, particularly allergic dermatitis and irritant contact dermatitis, must be accurately diagnosed, since improvement and resolution rely on appropriate diagnosis and avoidance of pertinent triggering factors. Principles of treatment include general skin care, patient education about avoidance of irritants, skin hydration and the use of topical corticosteroids when necessary. Use of systemic corticosteroids is not generally recommended for the treatment of chronic eczematous dermatitis. (AA-M).

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Irritant Contact Dermatitis: Clues to Causes, Clinical Characteristics, and Control Source: Postgraduate Medicine. 103(5): 199-200, 207-208, 212-213. May 1998. Summary: This journal article for health professionals discusses the causes, clinical characteristics, and management of irritant contact dermatitis. This condition is reportedly more common in women than in men, and heredity may be a factor in susceptibility. Typically, hands are most often involved. In adults, irritant contact dermatitis is often occupation-related, and it is seen most frequently in workers in the food, agriculture, construction, and rubber and plastics industries, and in workers whose jobs involve wet work or extensive exposure to oil or petroleum products. The concentration of an irritant, its volume, and the length of time it is actually in contact with the skin are important variables. Reactions may be acute, chronic, delayed, cumulative, traumatic, and pustular or acneiform. Nonerythematous and subjective irritation also occur. Diagnosis of irritant contact dermatitis is based on clinical appearance, history, and, when needed, diagnostic patch testing. Avoiding exposure to the irritant is important, but if the dermatitis does not heal once the offending irritant is removed, topical corticosteroids may be used. 7 figures, 3 tables, and 27 references.

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Eyelid Dermatitis: A Common, Often Confounding Rash Source: Postgraduate Medicine. 100(2):231-240; August 1996.

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Summary: This journal article for physicians examines what causes eyelid dermatitis, including rare causes; diagnostic steps and types of physical examination techniques that should be used; and the inteation of diagnosis and treatment to clear the rash. A study is provided to illustrate the importance of inteating diagnosis and treatment and the value of perseverance. The author indicates that because eyelid rashes, regardless of cause, look very much alike, they are often difficult to diagnose and treat. Successful diagnosis depends on four factors: familiarity with certain common skin diseases, a selective and probing history, a careful skin examination, and properly administered and interpreted patch tests. Effective therapy requires a asp of treatment options and perseverance on the part of both physician and patient. Tables include a list of factors to address in selective history taking in eyelid dermatitis, precautions for patients allergic to cosmetics and toiletries, environmental precautions for patients with atopic dermatitis, and factors implicated in recurrent contact dermatitis of the eyelids. 12 references, and 4 tables. (AA-M). •

Atopic Dermatitis: How To Incorporate Advances in Management Source: Postgraduate Medicine. 109(6): 119-121,123-127. June 2001. Summary: This journal article provides health professionals with information on the etiology, symptoms, diagnosis, and treatment of atopic dermatitis. This genetically determined, distinctive eczematous condition usually occurs in people who have a personal or family history of asthma or seasonal or perennial allergic rhinitis. The condition is becoming increasingly common in northern, industrialized, temperate countries. Factors implicated in the increased prevalence of the disorder include environmental pollutants, food additives, a decrease in breast feeding, and lifestyles involving primarily indoor living. The rash of atopic dermatitis consists of red, elevated, scaly, and often excoriated and oozing plaques. Scratching and rubbing act as triggers that cause flare, spread the skin disease, and account for papular eruptions. The pattern of the rash can be helpful in making the diagnosis, and age of onset is a key factor when evaluating a patient who may have atopic dermatitis. Diagnostic criteria for atopic dermatitis published by the United Kingdom Working Party in 1994 require a pruritic skin condition and three additional criteria, including a history of flexural dermatitis or dermatitis on the cheeks of children under 10 years old, a personal history of asthma or hay fever or atopy in a first degree relative if the patient is less than 4 years old, generalized xerosis in the last year, and visible flexural eczema or eczema on the cheek or forehead, or both, and on the extensor extremities if the patient is less than 4 years old. The final criterion is onset before 2 years of age. Although positive radioallergosorbent or prick tests to various foodstuffs can be documented for the majority of patients with atopic dermatitis, very few of these reactions appear to be relevant. Treatment of atopic dermatitis consists of using proper bathing techniques and applying topical corticosteroids. Antihistamines may be useful in promoting sleep in some patients. Patients who have a widespread or severe rash may need systemic corticosteroids. A new drug, tacrolimus ointment, was recently approved for treatment of atopic eczema. Other alternatives for severe cases of the disease include ultraviolet B, psoralen plus ultraviolet A, cyclosporine, azathioprine, and methotrexate. 2 figures, 2 tables, and 12 references.

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Managing Atopic Dermatitis in Children and Adults Source: Nurse Practitioner. 25(4): 58-59,63-64,69-70,73,76,79-81. April 2000. Summary: This journal article provides nurse practitioners with information on the epidemiology, pathogenesis, clinical features, diagnosis, complications, and treatment of

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atopic dermatitis. This common skin inflammation, which is characterized by intense pruritus, is most common in children. The prevalence of atopic dermatitis has tripled in the past 30 years, and the condition affects about 10 percent of the U.S. population at some point in their lifetime. Although the etiology of atopic dermatitis is not well understood, it appears to be linked to a combination of genetic and environmental factors, and it is usually associated with other atopic diseases such as asthma and hay fever. The initial clinical feature of atopic dermatitis is skin dryness and roughness. Erythema, papules, and pruritus may develop after additional irritation. The pattern of atopic dermatitis lesions varies by age. A definitive diagnosis in children and adults depends on identifying the nature and distribution of the lesions and on eliciting a personal or family history of the disease. Although no cure exists, atopic dermatitis often resolves spontaneously and can be controlled through proper management. Avoiding factors that precipitate or exacerbate inflammation, including aeroallergens, food allergens, and irritants, is key to preventing disease flares. In children and adults, hydration and topical corticosteroids are the mainstays of therapy. Recalcitrant disease may be treated with ultraviolet light therapy or psoralen phototherapy and cyclosporin. Current advances in understanding the immunologic basis of the disease have led to the development of highly effective new treatments. Using patient education and support, the clinician can help adults and children successfully manage their disease. The article includes a continuing education test. 2 figures, 4 tables, and 42 references. (AA-M). •

Living with Dermatitis Herpetiformis: The Ultimate Itch Source: Gluten-Free Living. 5(1): 3. January-February 2000. Contact: Available from Gluten-Free Living. P.O. Box 105, Hastings-on-Hudson, NY 10706. E-mail: [email protected]. Summary: This newsletter article offers suggestions and support for patients with celiac disease who are living with the complication called dermatitis herpetiformis (DH). DH, a hereditary, autoimmune response to dietary gluten, is the skin manifestation of celiac disease (gluten intolerance). It is characterized by an extremely itchy, watery blister or rash found on the limbs, trunk, face and scalp. Scratching further irritates the blisters and can cause scarring. The eruptions are often misdiagnosed and treated as other skin conditions. The author cautions that DH is a chronic, permanent condition and that if it is not treated with a gluten free diet, it may cause gastrointestinal symptoms at a later date whether or not the intestine shows damage initially. The condition is diagnosed by a small skin biopsy at the edge of an eruption. Current treatment for DH is twofold: strict adherence to a gluten free diet and use of medications to relieve the itching and burning of the blisters. The author reviews triggers for DH, including ingested gluten (the obvious trigger), and other substances or triggers such as stress, iodine, some antiinflammatory agents, and other foods. The article concludes by encouraging readers to share their experiences with DH with the newsletter (mail and email addresses are provided).

Federally Funded Research on Dermatitis The U.S. Government supports a variety of research studies relating to dermatitis. These studies are tracked by the Office of Extramural Research at the National Institutes of

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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 dermatitis. 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 dermatitis. The following is typical of the type of information found when searching the CRISP database for dermatitis: •

Project Title: A TWIN STUDY OF CHRONIC FATIGUE SYNDROME IN SWEDEN Principal Investigator & Institution: Pedersen, Nancy L.; Karolinska Institute Tomtebodavagen 11F Stockholm, Timing: Fiscal Year 2001; Project Start 15-AUG-2001; Project End 31-JUL-2004 Summary: Despite considerable research, fundamental questions about CFS remain at best partially answered. These questions include its definition, validity, the degree to which it results from genetic versus environmental factors, the nature of the substantial comorbidity observed with other conditions, and the basis of the female preponderance. The overarching aim of this project is to shed light on a number of basic questions about CFS via a large, population-based classical twin study. First, we will collect data on approximately 32,000 adults aged 42-65 years (13,000 complete twin pairs) who are members of the population- based Swedish Twin Registry for persistent fatigue, several overlapping conditions (fibromyalgia, irritable bowel syndrome, tension headache, allergy/eczema, generalized anxiety disorder, and major depression), and a detailed medical history. Second, the medical records of all twins who appear to have CFS-like illness and a subset of those with "CFS-explained" will be requested via an efficient national retrieval system. Following expert review, these individuals will be classified in regard to the CDC CFS criteria. Obtaining these unique data will allow us to address a set of critical questions regarding CFS. First, we will estimate the prevalence of CFS and its common comorbidities (fibromyalgia, irritable bowel syndrome, tension headache, allergy/eczema, generalized anxiety disorder, and major depression) in one of the largest samples yet studied. Second, we will use a variety of multivariate techniques to derive an empirical typology of prolonged fatigue and to assess how this typology compares to the CFS definition. Third, we will quantify the genetic and environmental sources of variation for CFS and its comorbid conditions. Fourth, critically, we will examine the influence of gender on these sources of variation. Finally, we will analyze the patterns of comorbidity between CFS and fibromyalgia, irritable bowel syndrome, tension headache, allergy/eczema, generalized anxiety disorder, and major depression using multivariate twin analyses and thereby to estimate the extent of overlap between the shared and unique genetic and environmental sources of variation. In concert with other twin studies being conducted by the investigators and their collaborators, we hope to hasten progress in understanding the etiology of CFS by parallel studies in multiple populations. The current proposal has several unique aims and represents a cost-

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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).

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effective means to extend this work in an epidemiological sample that is arguably the best twin registry in the world. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ACTIVATION OF SKIN CELLS AND TRANSCRIPTION FACTORS BY S* Principal Investigator & Institution: Swerlick, Robert A.; Associate Professor; Dermatology; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2001; Project Start 30-SEP-2000; Project End 29-SEP-2002 Summary: Irritant dermatitis is a major cause of workplace injury. It affects individuals in a variety of work environments and is a source of significant morbidity and lost work time. The pathophysiology of irritant dermatitis is only poorly defined. Exposure of the skin to irritant chemicals results in the rapid appearance of the cardinal features of inflammation associated with cytokine activation and leukocyte infiltration. How irritants activate inflammation is not known. We believe that irritants may activate signaling pathways common to innate immune mechanisms. Centered in these pathways are transcription factors that are linked to pro-inflammatory cytokine genes, cell adhesion molecules, and proteins that trigger capillary leak. One key family of transcription factors linked to the activation of these diverse gene sets is the nuclear factor kappa B (NF-kB) family of transcription factors. Our hypothesis is that irritant exposure results in NF-kB activation in skin cells. This activation results in the triggering of a pro-inflammatory cascade and the clinical appearance of dermatitis. In order to test this hypothesis, we propose the following specific aims: 1) To examine whether irritants can activate NF-kB in cultured skin cells in vitro using epithelial and endothelial cells as targets. We will examine whether irritant treatment of cultured skin cells results in translocation of active NF-kB complexes from the cytoplasm to the nucleus; examine whether irritant treatment of HDMEC, HK, or HDF induces the phosphorylation and ubiquitination of IkBa, necessary steps for proteosome mediated degradation; examine whether translocated NF-kB complexes are capable of binding to relevant response elements of cytokine and cell adhesion molecule gene protomers. 2) To examine whether irritants can activate specific genes in cultured skin cells in vitro using epithelial and endothelial cells as targets. We will examine whether irritants induce or upregulate the expression of adhesion molecules ICAM-1 and E-selectin, and proinflammatory cytokines IL-8 and VEGF-C; examine whether irritants increase steady state mRNA expression of ICAM-1, E-selectin, IL-8, or VEGF-C; examine whether irritant treatment of cultured skin cells results in increase transcription of adhesion molecule or cytokine genes dependent upon NF-kB responsive elements. These studies will provide a framework to define the mechanisms by which irritants cause inflammation in the skin and provide a rational and mechanistic targets for prevention and treatment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ADVANCES IN ALLERGY, ASTHMA AND IMMUNOLOGY Principal Investigator & Institution: Bielory, Leonard; Medicine; Univ of Med/Dent Nj Newark Newark, Nj 07103 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2003 Summary: (provided by applicant): Allergy is one of the most common reasons that individuals use alternative and complementary medicine (CAM). There is a plethora of reports regarding CAM in the treatment of allergy, asthma and immunology, but there is a dirth of scientific studies, plenary sessions, workshops presented in the nationally

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recognized forums. Objective: This application plans to explore "state of the art" CAM practices and "integrate" them into the annual meetings of the 2 major Allergy and Immunology organizations (American College of Allergy, Asthma and Immunology (ACAAI) and the American Academy of Allergy, Asthma and immunology (AAAAI) by: 1) providing the initial infrastructure for the submission of rigorous original scientific information related to allergic, asthmatic and immunologic disorders; 2) developing an ongoing scientific forum within the framework of the national organizations; 3) generating new research ideas and facilitating collaboration; and 4) publishing the proceedings and providing an ongoing internet resource site related to this application. This will be coordinated by the CAM Oversight Committee (CAMOC) consisting of respected allergy and immunology researchers in conjunction with the UMDNJ - Asthma & Allergy Research Center and the Center for the Study of Alternative and Complementary Medicine. The CAM Advisory Board (CAMAB) will be constituted with leaders from professional national organizations to provide multidisciplinary panel discussions and to generate CAM research priorities for these disciplines as they relate to allergy, asthma and immunology. Preliminary Work: Single workshops have been instituted at each of the upcoming annual meetings (ACAAI 11/01 and AAAAI 03/02). Commitments for a whole day CAM symposium at the ACAAI (11/14/02) and the publication of the proceedings have been obtained. The tentative schedule provides for the Overview of CAM; Overview of Herbal Medicine in Asthma; Overview of Homeopathy in Allergies; Overview of Probiotics in Atopic Dermatitis; Medico-Legal Aspects and Adverse Reactions. Summary: This application will provide the catalyst for establishing an ongoing forum for the review and promotion of scientifically based research assessing the impact of CAM in allergy, asthma and immunology. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: AIDS AND OPIATES--A MONKEY MODEL Principal Investigator & Institution: Donahoe, Robert M.; Associate Professor; Psychiatry and Behavioral Scis; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2001; Project Start 10-FEB-1997; Project End 31-MAR-2002 Summary: (Applicant's Abstract) Since exogenous and endogenous opioids are known to modulate immune function and opiate abuse is a major etiologic factor in human AIDS, there is reason to suspect that opiates themselves affect progression of AIDS. Evidence defining the role of opiates in progression of AIDS is less than clear, however, since there are various reasonable data to support any of three possible outcomes relative to opiate effects on AIDS progression. That is, no effects, exacerbatory effects, and protective effects. Data from our laboratory, using the best model of human AIDS, a monkey model, have, in fact, shown the potential of opiates to protect as well as exacerbate progression of AIDS. The most provocative aspect of these data was that none (0/6) of our SIV-infected opiate-dependent monkeys died over a 2-yr course of study, even though the expected death rate from AIDS was near to 1 in 2. Countering these seeming protective effects, however, was evidence that withdrawal of opiates, precipitated by naloxone, caused apparent SIV induction and prominent immune disturbance, that could be regarded as exacerbatory forces in the progression of AIDS. We also found that 2/6 monkeys developed iatrogenically induced opportunistic bacterial dermatitis near the end of this study, at the site of repeated opiate injections. These findings led us to hypothesize that the effects of opiates on progression of AIDS are conditionally dependent on the stability of opiate dependency, virulence of the AIDS virus, and the nature of secondary opportunistic infections. Unfortunately, the fact that

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this monkey study was only a pilot study meant that firm conclusions from these findings are unwarranted. The present proposal, therefore, is aimed at validating the main findings of our previous pilot study: protection against AIDS progression, induction of SIV upon opiate withdrawal; and, potential depression of anti-bacterial phagocytic capacity. This task is to be done in a statistically meaningful way that will not compromise animal welfare. These studies should improve understanding of the role of opiates in AIDS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ELICITATION

ALLERGIC

CONTACT

DERMATITIS--MECHANISMS

OF

Principal Investigator & Institution: Xu, Hui; Research Assistant Professor; Dermatology; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2001; Project Start 01-AUG-1999; Project End 31-JUL-2003 Summary: The skin is the primary barrier protecting other organs and internal tissues from the external environment. Epicutaneous application of some environmental chemicals results in a T cell- mediated inflammatory response termed allergic contact dermatitis or contact hypersensitivity (CHS). Most studies examining the immmunpathogenesis of allergic contact dermatitis have focused on the induction phase of the response. Much less is known about the cellular and molecular requirements for elicitation of allergic contact dermatitis once sensitization has occurred. In this proposal, we hypothesize that: the requirement of antigen presenting cells and the costimulatory molecules that they express for induction and elicitation of CHS reactions are different. We will examine this issue in mice by assessing the types of cells that can serve as antigen presenting cells for elicitation of the response. MHC class I and class II antigens that are known to be important for induction of allergic contact dermatitis will be examined for their role during the elicitation phase of the response. Based on our preliminary data indicating that transfer of hapten primed T cells to ICAM-1 deficient mice elicited a reduced CHS response and the development of hapten primed T cells in the mice was impaired, the role of ICAM-1 in the elicitation of CHS will be determined. We will also evaluate whether those antigen-presenting cells that are unable to elicit CHS have the capacity to desensitize animals that have already been sensitized to hapten. Because our current results indicate that CHS is significantly increased in gammadeltaT cell deficient mice, the potential regulatory effects of gammadeltaT cells will also be evaluated. On a basic level, the results will provide new information concerning the pathogenesis of allergic contact dermatitis and interactions between the skin and the immune system. On a clinical level, the information should be useful for the development of new specific strategies for the prevention and treatment of this common skin disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ALLERGY PEPTIDE(ECP)VACCINE

PREVENTION

BY

LGE

CYTOTOXIC

Principal Investigator & Institution: Chen, Swey-Shen A.; Ige Therapeutics, Inc. 6827 Nancy Ridge Dr San Diego, Ca 92121 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 31-AUG-2003 Summary: (Provided by the applicant): IgE-mediated allergic asthma, rhinitis, food allergy, atopic dermatitis, anaphylaxis cost annual 18 billions in medical costs and loss of productivity in this country. Regulation of IgE production by B cells is orchestrated

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by Th2 cytokines. This paradigm dictates a treatment modality of IgE-mediated hypersensitive diseases that diminishes endogenous levels of IL-4, thereby IgE production by IgE-committed B cells. Alternatively, studies initiated by PI indicated that following IgE immunization, CD8 T cells play an important role in inhibiting IgE production by IgE-committed B cells, and profound IgE deficiency ensued and is maintained in IgE-immunized mice. This observation leads to the current passive antiIgE therapeutic product concept. However, this treatment modality suffers drawbacks in failing to inhibit IgE synthesis as well as to remove circulating IgE-anti-IgE complexes, which accumulates to levels 10 fold higher, compared to the levels prior to treatment. And it is yet to be determined whether patients may be given a second heavy dose without eliciting neutralizing antibodies, including internal image-type of antibodies that potentially can cause mast cell degranulation. It is imperative to design alternative therapeutic modality based on active IgE immunization with higher safety standards. Herein, we provide a long-term strategy of reducing IgE levels by active immunization with IgE cytotoxic peptides (ECP) that are independent of requirement of conformation. Since B cells and plasma cells of the IgE lineage exhibiting natural ECP onto the binding site pocket of MHC class I, these targets are Iysed by ECP-specific CTL due to active vaccination. The advantages of this commercial vaccine are: (i) ECP is sequence-dependent, and does not elicit anti-IgE; (ii) ECP is economic and its effect long-lasting. To achieve this immediate goal, our two Aims are: Aim I: To Determine the Structure of Natural Human IgE (huIgE) CTL Epitopes Restricted To HLA-A2.1 and Ascertain Their Efficacies with huIgE-Producing Cells. Aim II: To Determine Whether ECP-specific CTL Elicited By Active Immunization Inhibit Human IgE Production In A Pre-clinical Model of huIgE/HLA-A2.1 Transgenic Mice. PROPOSED COMMERCIAL APPLICATION: IgE cytotoxic peptide (ECP) vaccine aims at an open market of active allergy immunization. Unlike the conventional allergen-desensitization, ECP technology based on targeting the universal IgE epitope can desensitize allergic syndromes caused by a myriad of allergens with a booser dose. Furthernore, unlike the current passive anti-IgE therapy, ECP is economic for one or two injections; risk-free since it is directed to linear sequence not recognize by anti-IgE, as compared to the current anti-IgE therapy that may actually cause mast cell degranulation due to induction of anti-idiotype. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ANTIGEN IMMUNOSUPPRESSION BY KILLER LANGERHANS CELLS Principal Investigator & Institution: Matsue, Hiroyuki; Dermatology; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2001; Project Start 01-JUN-2000; Project End 31-MAY-2005 Summary: Langerhans cells (LC) ordinarily deliver activation signals to T cells. We hypothesized that LC genetically modified to over-express CD95L (Fas ligand) termed "killer" LC, would deliver apoptotic signals to T cells upon antigen-specific interaction. To test this, we introduced CD95L cDNA into our LC line XS106 (derived from A/J mice) and selected a stable clone (XS 10-6-CD95L) that expressed abundant surface CD95L. This killer LC clone, when pulsed with ovalbumin (OVA), triggered apoptosis of OVA-reactive CD4+ T cells in vitro by an antigen-specific and CD95L-dependent mechanism. OVA-pulsed killer LC, when injected into A/J mice before or after sensitization, suppressed ear swelling responses to DNFB. Importantly, OVA-pulsed killer LC suppressed OVA responses, but not responses to the irrelevant antigen HEL, whereas HEL- pulsed killer LC inhibited only the HEL responses, establishing antigenspecificity. We will define mechanisms, under the new hypothesis that killer LC

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suppress diverse immunological responses by triggering apoptosis of putative effector T cells that recognize respective antigens. Specifically, we will study the impact of killer LC using five-established animal models: 1) Delayed type hypersensitivity: We will inject OVA- pulsed killer LC before or after sensitization to study the impact of CD4+ effect T cells and memory T cells, the fate of effector cells (adoptive transfer of OVAreactive, naive CD4+ T cells from the D011.10 transgenic mice), and the critical timing for cytotoxic interaction of killer LC with T cells (drug-inducible suicide system). 2) Contact hypersensitivity. We will inject DNFB-pulsed killer LC before or after sensitization to study the impact of CD8+ effector T cells and on Th2-like regulatory T cells, killer LC interaction with CD8+ T cells and antigen- specificity. 3) Th2-biased immune responses. Mice will be sensitized epicutaneously with an OVA-absorbed "patch" to produce OVA-specific IgE and IgG1 antibodies and atopic dermatitis-like skin lesions. We will inject OVA-pulsed killer LC to study the impact on Th2-biased effector and helper T cells and "therapeutic" efficacy for skin lesions. 4) Experimental autoimmune myocarditis. Mice will be sensitized with cardiac myosin (CM) to produce autoimmune myocarditis. We will inject CM-pulsed killer LC to study the impact on CD4+ pathogenic T cells that recognize tissue-specific autoantigen, the fate of pathogenic T cells, and therapeutic efficacy and safety. 5) Skin graft rejection. We will study the impact of killer LC and "killer LC hybrids" on allo-reactive CD4+ and CD8+ T cells, which are ordinary activated via "direct" and "indirect" pathways. These studies will form the framework for establishing an entirely new immunosuppressive therapy for inflammatory skin diseases, the therapy designed to eliminate selectively the effector T cells that recognize pathogenic antigens (e.g., haptens, allergens, autoantigens, and alloantigens). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ASSESSMENT OF IMMUNITY TO VACCINIA AND MVA Principal Investigator & Institution: Dolin, Raphael C.; Dana-Farber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-AUG-2008 Summary: Despite its extraordinary effectiveness against smallpox infection, the parameters of protective immunity generated by vaccinia remain incompletely understood. Large numbers of individuals are at high risk for serious toxicities if vaccinated with or exposed to vaccinia, and the need to develop safer vaccines against smallpox underscores the importance of understanding the immunologic basis for such protection. This project will undertake a detailed examination of T and B cell responses to immunization with vaccinia and MVA under carefully controlled conditions in normal subjects, and to MVA in patients with atopic dermatitis or patients with hematologic malignancies and immune deficiency after hematopoietic stem cell transplantation. The studies will measure neutralizing and other binding antibodies, lymphoproliferative responses by 3H Thymidine incorporation, cytotoxic T-cell activity by a 51Cr release assay, and T-cell gamma interferon responses by ELISPOT. Normal subjects who were vaccinated with either vaccinia or MVA, will be challenged with vaccinia to determine whether protection against challenge was conferred. Measurements of immune responses will be conducted sequentially at multiple time points, including those before and after challenge. Rates and patterns of responses wilt be compared between vaccinia and MVA recipients, and between normals and the patient cohorts. The specificity of the B and T cell responses will be examined employing bioinformatics approaches and molecular techniques of the Research Resource Technical Development Component of the Center. These studies will measure antibody responses

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to a panel of recombinant vaccinia-encoded proteins identified by bioinformatics as potentially important in neutralization, including the EGF-like domain of DIL (SPGF). Since all subjects in our initial studies will be HLA-A*0201 positive, we will be able to utilize peptides from the recombinant vaccinia proteins to characterize class I allele specific T-cell responses by ELISPOT, cytokine flow cytometry, and peptide-MHC tetramers. Non-class I allele specific T-cell responses will be examined using whole recombinant proteins. Spectratype analysis will also be used to identify predominant Tcell epitopes. These studies wilt provide a comprehensive picture of the immune responses to vaccination with vaccinia and MVA, and identify epitopes against which important responses are directed. These studies will also demonstrate whether 2 groups of high-risk patients respond to MVA in a similar fashion to normals. The proposed studies in years 1 and 2 focus on MVA, but similar approaches would be utilized to study other candidate vaccines against smallpox, as well as vaccines against other agents important in biodefense. 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 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

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Project Title: CHEMICAL RELEASE & IMMUNE SENSITIZATION BY DENTAL RESINS Principal Investigator & Institution: Hume, Wyatt R.; Dental Research Institute; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2001; Project Start 01-SEP-1993; Project End 30-APR-2003 Summary: (Adapted from investigator's Abstract): This is a competing continuation application whose overall goal is to ensure that resin-based materials which are placed onto teeth as part of dental care can continue to be used safely. Resin based materials which polymerize in the mouth are now used by dentists in many ways to help prevent tooth decay and for tooth repair and replacement. Bonding technologies, which are all based on this class of materials, are used for fissure sealing to help prevent decay, for bonding orthodontic brackets to teeth, and as part of many different types of tooth repair to improve appearance and function. It is very likely that new and modified materials of the same general type will continue to be developed and that the use of this type of material in dentistry will continue to increase in the coming years. The materials are very helpful to patients and have remarkably few negative side effects. However, severe allergic dermatitis in some dentists and other dental workers is linked to the use of the materials, and the incidence of such allergy appears to be increasing. Fortunately, allergic responses are less common in patients, but we do not know why this is so or whether it will continue to be so. Some patients experience pain in the dental pulp after resins are used in deep fillings, for reasons that may be related to direct chemical damage caused by released chemicals, by allergy to them, or to both. It has previously been shown in laboratory studies that two chemicals are released from these materials during the first days after they are placed on teeth. The first aim will be to confirm this release in experimental animals (guinea pigs), and study what happens to the chemicals in the body (their uptake, distribution, time of storage, breakdown and excretion). The second aim will be to study mechanisms of allergic responses to these chemicals at the cellular and molecular level using guinea pigs and mice. The third aim will be to determine whether there are differences between the risk of allergy with skin contact (as can occur in dental workers) relative to contact with the inside of the mouth and through tooth structure to the tooth pulp (as can occur in patients) in the same animals. The fourth aim will be to study allergic responses at the cellular and molecular level using blood and other tissues donated by volunteer dentists and other dental workers, to ensure that the experimental studies of the phenomenon using animal models and animal tissues in culture are valid. The studies described will help to prevent and treat adverse effects of this class of dental materials. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CHILDHOOD ASTHMA PREVENTION STUDY (CAPS) FOR PACRN Principal Investigator & Institution: Zeiger, Robert S.; Clinical Professor of Pediatrics; Pediatrics; University of California San Diego 9500 Gilman Dr, Dept. 0934 La Jolla, Ca 92093 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-AUG-2004 Summary: Asthma is the most common chronic respiratory disease of childhood with prevalence, morbidity and mortality increasing in epidemic proportions throughout the world despite better diagnosis and improved anti-inflammatory treatment. Recombinant humanized monoclonal anti-IgE is the most promising immunomodulatory agent available today to non-specifically modulate IgE, the major

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effector molecule in allergic asthma. Anti-IgE reduces free IgE and IgE receptors more than 95 percent, improves asthma symptoms, lung function, and reduces prn bronchodilator use and corticosteroid use in moderate to severe persistent allergic asthma in adolescents and adults. Proposed here are two projects, each prospective, randomized, masked, and placebo-controlled, to evaluate the effectiveness and safety of anti-IgE in primary and secondary asthma prevention in children. Proposal number 1 or primary asthma prevention will determine whether anti-IgE can prevent the development of asthma in 232 high-risk infants 1 to 2 years of age with atopic dermatitis, food allergy, or allergic rhinitis and specific IgE and a parental history of atopy. Patients will be randomized into anti-IgE or placebo groups, given bimonthly subcutaneous injections of anti-IgE or placebo, and followed for the development of asthma for 3 years. Secondary objectives include determination if anti-IgE compared to placebo differ with respect to (1) the onset of at least mild persistent asthma, (2) lung impedance and bronchial responsiveness determined by impulse oscillation, (3) skin test reactivity and markers of inflammation, (4) effect on atopic disorders, and (5) long-term safety and growth. Proposal number 2 or secondary asthma prevention will determine the effectiveness of anti-IgE compared to placebo to reduce inhaled corticosteroid (ICS) requirements (steroid sparing) in 140 children 5-12 years of age with moderate to severe persistent allergic asthma requiring ICS. Subjects will be randomized into anti-IgE or placebo groups, given bimonthly subcutaneous injections of anti-IgE or placebo for 1 year, and followed in two phases. During Phase I or the 12-week adjunctive phase, patients will maintain their stable dose of ICS, and during Phase II or the 40-week ICS withdrawal phase, subjects will have their ICS reduced according to protocol. The efficacy and safety of anti- IgE therapy versus placebo will be compared in terms of (1) the reduction in ICS dose measured by real time monitoring of ICS use electronically (primary aim), (2) asthma symptom scores, medication use, and peak expiratory flow levels monitored electronically, (3) levels of lung function and bronchial responsiveness, (4) humanistic and pharmacoeconomic measures, (6) skin test reactivity and markers of inflammation, (7) somatic growth, and (8) adverse events. 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

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Dermatitis

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: CONFOCAL HISTOPATHOLOGY OF CONTACT DERMATITIS IN VIVO Principal Investigator & Institution: Gonzalez, Salvador; Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2001; Project Start 30-SEP-2000; Project End 29-SEP-2003 Summary: The overall goal of this work is to establish new criteria to differentiate acute Irritant Contact Dermatitis (ICD) from Allergic Contact Dermatitis (ACD) by using a video rate (real-time), near-infrared confocal reflectance microscope (CM). The specific aims are (I) to optimize a video-rate CM for imaging, characterizing and distinguishing acute allergic and irritant contact dermatitis in vivo; (ii) to investigate the kinetic changes of both forms of CD using this non-invasive imaging technique in order to determine their characteristic features versus time to better understand their pathogenesis; and (iii) to measure the sensitivity of patch testing enhanced by noninvasive CM evaluation. Contact Dermatitis affects approximately 20 percent of the population in the US, and is the most common form of occupational dermatosis. It is divided mechanistically into ICD and ACD. The ICD is produced by the toxic effect of certain chemicals on the skin while ACD is induced by a delayed hypersensitivity response of the host to an antigenic chemical. The latter form is characterized by a cascade of immunologic events that occurs mostly in the superficial layers of the skin. Morphologic features of both forms of CD, however, are very similar on gross and microscopic examination and it is difficult to differentiate one from the other. Our realtime CM has been used effectively to non-invasively image normal and diseased skin in vivo. Using near-infrared laser and water immersion objective lenses (NA=0.7-1.2), images can be obtained at high lateral (<1.0 micron) and transverse (virtual section thickness) resolutions down to a depth of 300-400 microns. The use of a non-invasive CM for evaluating the stages of allergic and irritant skin reactions in vivo, as well as to enhance patch testing, may help physicians to improve their diagnostic skills in this area, and may help to have a better understanding of the pathogenesis of these inflammatory skin conditions. The lack of artifacts from conventional histology gives a more realistic picture of pathophysiology. We also expect that our results may ultimately translate into more rational and effective care for patients with this common and frequently disabling problem. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CORE--ANIMAL EXPERIMENTATION Principal Investigator & Institution: Mccormick, Thomas S.; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106

Studies

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Timing: Fiscal Year 2002; Project Start 01-MAY-2002; Project End 30-APR-2006 Summary: Rodents, in particular mice, are extensively used by research projects of several SDRC investigators. An animal core is thus an important component of the SDRC that has been providing expertise and training in the successful completion of animal experiments in a cost effective and highly predictable manner. There is considerable emphasis on skin cancer in the SDRC. There is evident by the fact that 1) five nationally funded projects of this faculty either conduct murine skin tumorigenicity experiments or utilize cutaneous tumors developed on murine skin for biochemical morphological , and molecular biological studies, 2) one of the pilot and feasibility proposed in this renewal application will conduct murine skin tumorigenesis experiments, 3) in the NIH funded training program in Investigative and Molecular Dermatology there are four training tracks, one of which emphasizes skin carcinogenesis. Out of the two current trainees supported by this training grant, one utilizes murine skin tumors and the other conducts animal experiments. The developing emphasis is to utilize chemically mutagenized mice which have clinical phenotypes for dermatitis, susceptibility to UV, cancer and blistering diseases. The additional areas of research in SDRC are a) structural biology and genetics of the skin, and b) immunodermatology. Several investigators conducting research in these areas do animal experimentation. This core has enabled SDRC investigators to conduct animal experimentation more efficiently. The core has four specific functions. The first function is to provide SDRC faculty with a) tissue, in particular tumors, from cutaneous tumorbearing and age- and sex- matched normal mice, and b) homogenate, RNA, DNA, and single cell suspensions, from defined tumors of variously treated mice. The second function is to provide expertise in planning, procurement, and handling of specialized animals for experiments to be conducted by SDRC faculty. Within this objective, the core serves as a resource center in a) providing technical expertise and advise in producing transgenic and knockout mice, and b) conducting experiments on nude mice, e.g. tumor development and their histological verification. The third, which is a newly added function, relates to screening, maintaining and breeding chemically mutagenized mice with clinical phenotypes of skin disease of interest to SDRC investigators. These mice should prove valuable in dissecting complex multi-gene phenotypes. The fourth function of the core is to provide SDRC faculty with biostatistical expertise. For all, experiments involving animal work being conducted and planned for the near future, expertise in murine skin carcinogenesis, biochemistry, genetics, biostatisticians, histopathology and veterinary husbandry and care is needed. Together Core Director, Co-Directors and Consultants represent a team capable of providing expertise in all aspects of animal experimentation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CUTANEOUS BIOLOGY OF KIT LIGAND Principal Investigator & Institution: Longley, Jack B.; Dermatology; Columbia University Health Sciences New York, Ny 10032 Timing: Fiscal Year 2001; Project Start 01-JAN-1997; Project End 31-JAN-2002 Summary: (provided by applicant): Stem Cell Factor (SCF, also known as mast cell growth factor), is the ligand for KIT, a receptor tyrosine kinase. The goal of this proposal is to determine the role of the SCF-KIT signaling pathway in mastocytosis and cutaneous inflammation. Mastocytosis occurring sporadically in adults is caused by somatic mutations affecting the primary sequence of KIT and causing constitutive activation of KIT and its downstream transducing molecule PI3-K, which causes phosphorylation of AKT. Familial and most pediatric cases of mastocytosis cases show

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normal KIT protein coding sequence but have phosphorylated AKT in lesional mast cells. Our first hypothesis is that familial and sporadic pediatric mastocytosis are caused by mutations affecting the SCF-KIT signaling pathway, or pathways convergent with it at or above AKT. Human epidermal keratincytes produce SCF, and dermal injection of SCF causes inflammation. Trangenic mice which express epidermal SCF, like humans, show an exaggerated ear swelling response to allergic and irritant contactants. Our second hypothesis is that SCF-KIT signaling plays an active role in the cutaneous inflammatory response. Our specific aims are: 1. To determine the mechanism(s) of oncogenesis in c-KIT mutation negative pediatric mastocytosis, mRNA from lesional mast cells will be RT-PCR amplified and sequenced to detect mutations in genes encoding molecules which may affect AKT phosphorylation including AKT, PTEN, Lyn and PI3-K. Since loss of PTEN could result in increased PI3-K signaling, lesional mast cell DNAk will also be tested for loss of heterozygosity in region 10q23 by microsatellite analysis. The functional effects of mutations or gene loss will be determined in cultured bone marrow derived mast cells an mast cell lines by retroviral expression of mutant activating or dominant negative proteins, or by anti-sense suppression. 2. To determine the genetic basis of familial mastocytosis, two separate kindreds with dominantly inherited mastocytosis will be tested for linkage to genes known to affect the KIT-P13-K signaling pathway using microsatellite analysis. If necessary, a genome-wide screen of affected and genetically relevant unaffected individuals will be performed using loci at 10 cM intervals followed by positional cloning and gene identification. 3. To test the hypothesis that SCF-KIT signaling is actively involved in the afferent, efferent, or both arms of the cutaneous immune response, we will use adoptive transfer of immune lymphocytes, KIT blocking antibodies, and small molecule inhibitors of KIT in a series of DNFGB sensitivity studies in normal mice, and in a proven transgenic model of SCFKIT mediated cutaneous inflammation. These studies will determine specific contributions of SCF-KIT signaling to contact dermatitis, an provide support for the hypothesis that inhibitors of KIT may be novel therapeutic agents for human cutaneous inflammation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CYTOKINE DYSREGULATION, VIRUSES, AND CHILDHOOD ASTHMA Principal Investigator & Institution: Lemanske, Robert F.; Professor of Medicine and Pediatrics; Pediatrics; University of Wisconsin Madison 750 University Ave Madison, Wi 53706 Timing: Fiscal Year 2001; Project Start 30-SEP-1998; Project End 31-AUG-2002 Summary: For many asthmatic patients, the syndrome or disease has its roots in infancy. From preliminary observations in humans, and from experiments performed in a rodent model of virus-induced airway dysfunction in our laboratory, two factors appear to influence the development of persistent wheezing or the asthmatic phenotype. First, a hereditary component, which is clinically manifested by the development of allergic diseases, and immunologically mediated by the presence of increased levels of IgE antibody and/or a dysregulation in cytokine production [most likely a decreased production of interferon gamma (IFN-gamma)]. Second, an environmental component, which appears biologically related to the development of a significant viral lower respiratory tract illness (most likely respiratory syncytial virus), and temporarily related tot a critical stage in the physiological development of the lower airway. However, the relative contribution of either of these factors, either alone or in combination, has yet to be clearly established during infancy and/or early childhood. To establish and advance

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our knowledge about these very important relationships, this grant application proposed to conduct experiments designed to answer the following questions: Is IFNgamma dysregulated in persistent wheezers or asthmatic children? If so, how early in life can these abnormalities be demonstrated? At birth? Following infection? As the child encounters his/her environment for various periods of time? Is IFN-gamma the only cytokine that can be linked with such outcomes, or can other cytokines be involved as well? If IFN-gamma dysregulation can be shown to be casually linked with various outcomes, what is the mechanisms of the defect? How closely do any demonstratable abnormalities in cytokine responses or regulation track with the development of clinically apparent allergic diseases such as atopic dermatitis, allergic rhinitis, and or asthma? To answer these questions, a prospective longitudinal study has not been designed that will evaluate the interaction and time dependencies of relevant immunological, microbiological, and clinical parameters. The results of these studies will provide information that will be a major step forward in our understanding of the relative influence that genetic and environmental risk factors on the development of childhood asthma. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DERMAL ABSORPTION OF CUTTING FLUID MIXTURES Principal Investigator & Institution: Baynes, Ronald E.; Assistant Professor of Pharmacology; Anatomy/Physiological Scis Rad; North Carolina State University Raleigh 2230 Stinson Drive Raleigh, Nc 27695 Timing: Fiscal Year 2001; Project Start 01-AUG-2000; Project End 31-JUL-2004 Summary: The long-term goal is to understand chemical and biological interactions in a chemical mixture that modulate dermal disposition of irritants or chemicals and to be able to predict chemical and biological interactions in a chemically-defined mixture in the workplace. As it is very difficult to experimentally test all commercial cutting fluids or oils, the primary objective of this research project is to investigate the influence of chemical mixtures on the dermal disposition and cutaneous toxicity of several cutting fluid additives and contaminants using a novel experimental paradigm. Complete or partial factorial experiments can be designed to determine the various levels of interactions using appropriate skin models with various levels of biological complexity. The central hypothesis to be tested is that chemical-chemical and chemical- biological interactions can occur on or in the skin which eventually determine the fate of the irritant(s) and thus its potential to cause irritant dermatitis. The rationale for this proposed approach is that many of the chemical additives or components in a cutting fluid formulation behave as solvents, co-solvents, or surfactants, which can modulate percutaneous absorption by altering the normal anatomy and physiology of the skin by discrete mechanisms. The following three specific aims will be pursued to accomplish the stated objectives: 1) Determine statistically significant chemical-chemical and chemical-biological interactions for five component mixtures using three skin model systems possessing increasing levels of biological complexity. Silastic membranes, porcine skin sections, and isolated perfused porcine skin flaps (IPPSFs) will be used to probe for various levels of interactions. (2) Determine interactions with common cutting fluid contaminants, nickel and nitrosodiethanolamine, and a cleansing solvent, trichloroethylene. IPPSFs will be used in these reduced factorial experiments. (3) Using biomarkers of irritation, determine significant changes in epidermal barrier structure and function in skin flaps exposed to mixtures that significantly alter component(s) disposition within skin. These latter experiments will primarily focus on subclinical effects, such as prostaglandin and cytokine release. At the completion of this project, we

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expect to identify significant interactions between functional components of the mixture that will contribute to a better understanding of additive deposition and irritancy of related cutting fluid products. This experimental approach allows interaction models to be built which can be used to assess other workplace mixtures. 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: DERMATITIS HERPETIFORMIS AND THE MUCOSAL IMMUNE RESPONSE Principal Investigator & Institution: Hall, Russell P.; Professor and Chair; Medicine; Duke University Durham, Nc 27706 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2006 Summary: (Verbatim) Dermatitis herpetiformis (DH) is a blistering skin disease characterized by the presence of cutaneous IgA deposits and an associated, almost always asymptomatic, gluten sensitive enteropathy (GSE). The critical role of the mucosal immune response (MIR) in DH has been demonstrated by the observation that, despite the lack of clinical symptoms of GSE in the majority of DH patients, the cutaneous manifestations of DH can be controlled by a gluten free diet. The mechanisms

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that allow for the development of cutaneous IgA deposits and skin disease yet that prevent the development of symptoms of GSE are not known. The purpose of this project is to characterize the MIR in patients with DH in order to determine the factors that prevent the development of clinical signs of gastrointestinal disease yet result in cutaneous deposits of IgA and the development of the cutaneous manifestations of DH. In addition, this project will provide new information regarding factors that may modify and regulate the mucosal immune response to dietary proteins in man and how mucosal inflammation results in inflammatory disease in the skin, joints and other organs. The specific aims of this project are: 1. Determine the antigenic patients with DH and isolated GSE and control subjects using organ culture of specificity and dose response of the T cells in small bowel biopsies from isolated GSE. 2. Characterization of the circulating neutrophils in patient with small bowel biopsies and gliadin peptides, some of which induce disease in DH on gluten containing diets and of the level of cytokine(IL1/TNFa)/chemokine(IL-8) expression in the skin. Skin biopsies from patients with DH from areas predisposed to develop skin lesions (extensor, surfaces) and those areas which normally do not develop skin lesions (upper inner arm) will be analyzed for IL1a, TNF-a, IL-8, and other cyto/chemokine expression during periods of control of the skin disease and no skin lesions and during disease activity. Neutrophils will be analyzed during periods when skin lesions are present and not present to assess the level of activation and expression of cell surface molecules which play a role in neutrophil migration 3. Characterization of the CDR3 region of the T cell Vb families expressed in the small bowel biopsies of patients with DH and of patients with isolated symptomatic and asymptomatic GSE. cDNA from the small bowel of patients with DH, patients with isolated symptomatic GSE and patients with isolated, asymptomatic (treated) GSE and patients with non-gluten sensitive intestinal disease will be analyzed by RT-PCR for the evidence of clonality of the T cells in the gut using CDR3 spectrotype analysis and single strand conformational polymorphisms. These studies will provide insights into the pathogenesis of DH and isolated GSE, the relationship between the MIR and the skin and factors important in controlling the mucosal immune response in man. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

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 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.

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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 MECHANISMS OF EARLY LIFE ECZEMA Principal Investigator & Institution: Halonen, Marilyn J.; Professor; University of Arizona P O Box 3308 Tucson, Az 857223308 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 31-AUG-2006 Summary: (Applicant's Abstract) The long term goal of this project is to characterize the immune status of infants at birth and to determine directly in human infants the susceptibility factors and antecedent pathway(s) that lead to eczema in the first two years of life. Early life eczema is a major risk factor for asthma. We will focus on clarifying the relative roles and identifying the participants of the innate and the adaptive immune system in the development of eczema. Preliminary data lead us to discard the current concept that infants at birth have a Th2 "default" status in favor of a more general state of limited cytokine production in cord blood cells. The hypothetical scenario proposed and tested here is that the immune system at birth has a limited capacity for producing many immune cytokines compared to the adult. This limited capacity may be a result of T cell naivete, immune cell immaturity or active suppression possibly via IL-10 (or some combination of these events). Eczema (we hypothesize) develops in children via complex gene by environment interactions, with an important role for a delayed capacity to produce IFN-gamma that provides a window of opportunity for allergen sensitization. We predict that with full maturation of the response, new sensitization will be reduced but sensitization that has occurred during this window will then be facilitated by LPS. The nature of the fully matured response will be influenced by gene variants in CD14, IL-10 and IL-13. Three specific aims are proposed. 1. Establish the main cellular mechanisms for the limited capacity of cytokine production of the immune cells of human infants at birth and assess the role of IL-10 in inducing and/or maintaining that status. 2. Test the hypothesis that the development of the response to pattern recognition molecules like LPS is delayed in infants who develop eczema and the delay permits enhanced allergen sensitization. 3. Determine the influence of IL-10, IL-13 and CD14 gene polymorphisms on the mechanism of overcoming the decreased capacity to produce IFN-gamma and on allergic sensitization. This project is a cell biology oriented project that focuses on dissecting immune

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development in early life in both normal infants and infants at risk for asthma and in doing so interfaces with each of the other projects mainly through providing a biologic context for testing in vivo the impact of genetic polymorphisms and the molecular mechanisms identified. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DIET, IMMUNE MODULATION, AND ASTHMA IN EARLY LIFE Principal Investigator & Institution: Weiss, Scott T.; Professor; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 30-SEP-1998; Project End 31-AUG-2003 Summary: Asthma is the most common chronic disease of childhood in the developed world, affecting about 10 million U.S. children under the age of sixteen. Asthma prevalence in Western industrialized countries is increasing at an alarming rate, and this increase is coincident with an increase in type I hypersensitivity (allergy). Eighty percent of childhood asthmatics exhibit hypersensitivity to indoor aeroallergens. Maternal diet represents an important exposure that has significant potential to modify immune function and, hence, the development of allergy. To study the evolution of the asthmatic immune response, focusing on the cellular response to allergens and foods, this application proposes a collaborative study involving pulmonary and dietary epidemiologists (Drs. Weiss, Colditz, and Gold), experts in lipid biochemistry (Dr. Sacks) and immunologists specializing in the role of T- and B-cells in the asthmatic response (Drs. Finn and Perkins). The application proposes to utilize a prospective longitudinal cohort study of children of asthmatic mothers to examine the role of maternal dietary fat intake (N-3 polyunsaturated fat) in the development of (1) nonspecific and specific cellular immune responses by age 2-3; (2) asthma/wheeze, atopic dermatitis, food allergy, and allergic rhinitis by age 3. In a subset of 50 five year old children with asthmatic mothers, 25 with high and 25 with low N-3 fatty acid intake during pregnancy, studies will assess lymphocyte proliferation and cytokine production (IL-4, IL-5, and interferon-gamma [IFN-gamma]) to nonspecific (PHA) and representative specific antigenic stimulation: beta-lactoglobin (food), cockroach (Bla g2) and dust mite (Der fI) (indoor allergen). Additional potentially influential host and environmental factors to be examined include: parental asthma history, maternal age, perinatal history, acute lower respiratory illness history, day care, environmental tobacco smoke, birthweight, head circumference, sex, and race. The application proposes to test the following hypotheses: 1. At birth, maternal dietary N-3 fatty acid levels assessed in the second and third trimester of pregnancy with a semiquantitative food frequency questionnaire will be correlated with N-3 fatty acid levels in cord blood. 2. At birth, infants with high cord blood levels of N-3 fatty acids will have reduced lymphocyte proliferative responses to cockroach, dust mite (indoor allergen), and betalactoglobin and reduced levels of inflammatory cytokines (IL-4, IL-5) and increased levels of interferon-gamma. 3. High cord blood levels of N-3 fatty acids and reduced lymphoproliferative responses to cockroach, dust mite and beta-lactoglobin will independently predict decreased development of allergic disease (asthma/wheeze, atopic dermatitis, food allergy, and allergic rhinitis) at age 3. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ENHANCED LOCAL LYMPH NODE ASSAY USING FLOW CYTOMETRY Principal Investigator & Institution: Degeorge, George L.; Mb Research Laboratories, Inc. Box 178, 1756 Wentz Rd Spinnerstown, Pa 18968

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Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 30-SEP-2004 Summary: (Applicant?s abstract): Although the murine Local Lymph Node Assay (LLNA) is effective at detecting potential irritants/sensitizers, this assay, in its current standard form: 1) cannot readily differentiate some types of irritants from respiratory and contact sensitizers; 2) utilizes moderate amounts of radioactive material and; 3) requires increased numbers of animals to determine the different endpoints (i.e., proliferation, immunophenotype) to fully characterize the response of an animal to a topically-applied chemical. To enhance and improve this important test, our company has implemented several innovative modifications to the standard LLNA. We have applied flow cytometric techniques to this assay to increase the sensitivity/specificity of the assay, eliminate the use of radioactive material and decrease the number of animals used for screening. It has been determined by the results of SBIR Phase I studies that the proposed enhanced flow cytometry-based LLNA is technically and commercially feasible. However, to develop this assay to its full commercial potential, which our company would provide to the chemical, pharmaceutical and consumer products industries, our group must: 1) validate the enhanced version of the LLNA; 2) establish the cytometry-based LLNA as a GLP compliant assay at our company and; 3) develop and provide various versions of the enhanced LLNA for our clients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EPIDEMIOLOGY OF CELIAC DISEASE--A POPULATION BASED STUDY Principal Investigator & Institution: Murray, Joseph A.; Associate Professor of Medicine; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2001; Project Start 15-JUL-2000; Project End 30-JUN-2005 Summary: In parts of Europe celiac disease is considered one of the most common chronic autoimmune diseases. It has been identified as a cause of significant morbidity and an increased risk of malignancies. Celiac disease is thought to be quite rare in the United States. Because it is thought to be rare, it is rarely considered in the differential diagnosis of many common conditions. As general population screening requires a great expenditure of resources it would make sense to study the prevalence of the disease in those groups of people most likely to have it. If it is present in these groups at the same level as has been seen in countries where celiac disease is common then this would justify consideration of more widespread screening. This study aims to examine the prevalence of celiac disease in those thought most at risk: Type one diabetes, family history of celiac disease or dermatitis herpetiformis; osteoporosis, chronic diarrhea with abdominal pain, and iron deficiency anemia (Specific aim number 1). We will use standardized validated gastrointestinal questionnaires to identify any clinical predictors of the who may have celiac disease (Specific aim number 2). We aim to study whether the HLA associations seen in European populations are unaltered by the more heterogenous population of the US and screen for other predictive HLA genotypes for disease risk in American celiacs (Specific aim number 3). If celiac disease is a common condition, that is undiagnosed, it is important to know what benefit (or detriment) may accrue to the individual when the diagnosis has been made. To study how making the diagnosis of CD as the result of a screening project affects both gastrointestinal and nongastrointestinal symptoms, the patient's quality of life, and the utilization of health care resources (Specific aim number 4). If this proposal demonstrates that celiac disease is more common than believed, it will provide important insights into who it affects, how to detect the condition or predict risk, while demonstrating a substantial benefit in both relief of suffering, improved functioning and reduced utilization of health care. This will

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be possible, because the subjects who will be diagnosed with CD will actually live in Olmsted County, and their medical histories and ongoing medical care will be recorded in community medical records accumulated by the Rochester Epidemiology Project. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EVALUATION OF BASOPHIL INVOLVEMENT IN HUMAN DISEASE Principal Investigator & Institution: Schwartz, Lawrence B.; Professor; Internal Medicine; Virginia Commonwealth University Richmond, Va 232980568 Timing: Fiscal Year 2001; Project Start 01-SEP-1998; Project End 31-AUG-2002 Summary: (Adapted from Investigator's abstract): Basophils and mast cells are major effector cells of immediate hypersensitivity reactions. In humans, mast cell involvement can be precisely identified by the presence of tryptase. For basophils, no such direct marker has been identified. The investigator hypothesizes that human basophil secretory granule proteins can be used as sensitive and specific markers of basophil involvement and that understanding the functions of such proteins will further our understanding of this cell type. The 2D7 mAb prepared by the investigator appears to recognize a basophil-specific component of the secretory granule. In skin during the late phase of an immediate hypersensitivity response, 2D7 immunohistochemistry reveals marked basophil involvement. Four specific aims are proposed. First, the 2D7 antigen will be purified by immunoaffinity chromatography and characterized. Second, basophils and deposits of activated basophils will be examined in human tissues using the 2D7 mAb, including skin in atopic dermatitis, chronic urticaria, and urticaria pigmentosa, nasal mucosa in allergic rhinitis and lung in asthma. Third, new mAbs against 2D7 antigen will be generated and used to develop a sandwich immunoassay. Fourth, basophil activation in various clinical situations will be assessed by measuring 2D7 antigen levels in biologic fluids. For example, the investigator hypothesizes that basophil-dependent anaphylaxis occurs in certain food-allergic reactions, and predict that 2D7 antigen, but not mast cell tryptase, will be elevated in the blood during such reactions. This research will provide novel and precise measures of basophil involvement in human diseases. This may enable more precise diagnostic criteria for flares of inflammation associated with atopic disease, facilitate selection of appropriate treatment, provide new prognostic information, and permit monitoring of inflammatory disease activity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: MEETINGS

EXPERIMENTAL

AND

CLINICAL

CONTACT

DERMATITIS

Principal Investigator & Institution: Cooper, Kevin D.; Professor; University Hospitals of Cleveland 11100 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2002; Project Start 20-SEP-2002; Project End 31-DEC-2002 Summary: (provided by applicant): This proposal requests support for the third meeting of the Experimental Contact Dermatitis Research Group (ECDRG). The ECDRG was founded in 1997 to provide a forum for North American scientists and physicians to discuss issues concerning irritant and allergic contact dermatitis. The first meeting was held in Cincinnati in May 1999 and the second in Dallas in Nov. 2000. The first two meetings have been useful in bringing together parties from academic medicine, university and research institute labs, industry, and government. This will be the second meeting held in conjunction with the American Contact Dermatitis Society (ACDS). The inclusion of the ACDS at the Dallas meeting brought together for the first time on a

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large scale a coalition of basic scientists and clinicians who have special expertise in contact dermatitis, which helped provide a translational research element in each segment of the meeting. This format was popular with the attendees and the meeting in Cleveland will follow the same combined format. In addition, a satellite meeting will be held on Skin Equivalents immediately prior to the ECDRG, which will help bring in scientists who use such technology to predict contact dermatitis, further enriching the meeting interactions. Three goals of the meeting are to provide an interdisciplinary forum: 1) To discuss: a) predictive methods that identify irritants and sensitizers before human exposure, b) methods to distinguish irritants from allergic responses with current tests, c) pathogenic mechanisms of dermatitis and possible interventions, d) factors that modify expression of dermatitis e) variables in sensitization that affect tolerance and disease expression, and translating these concepts into interventions that reduce or modify sensitization and elicitation and to induce tolerance. 2) To update attendees regarding: a) allergens that are newly recognized or increasingly recognized in clinical practice b) new technology as it applies to data analysis and epidemiology of dermatitis and c) opportunities arising from patient--centered interactions between clinicians, industry and government colleagues. 3) To enable participants to plan collaborative research projects and to introduce young scientists to the field. The proposed meeting will allow exchange not only among researchers in the various lab and clinical research settings, and clinicians but also between researchers interested in this field who see the practical outcomes in patients with diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: FOXP3: FUNCTIONAL ANALYSIS OF THE GENE MUTATED IN MICE Principal Investigator & Institution: Ziegler, Steven F.; Benaroya Research Inst at Virginia Mason 1201 9Th Ave Seattle, Wa 98101 Timing: Fiscal Year 2002; Project Start 01-MAY-2002; Project End 30-APR-2007 Summary: (provided by the applicant): Considerable progress has been made in the understanding of human immune-system diseases through the study of animal model systems. The availability of spontaneous inherited mutations in inbred mouse strains have proven to be an invaluable resource in the development of these models. For example, the beige mutation in mice and Chediak-Higashi syndrome in humans arise from mutations in the same gene. Induced mutations have also been used to successfully model human diseases. Among the immunologically relevant mouse models is the X-linked mutation scurfy (sf). Males hemizygous for the sf mutation develop a severe autoimmune lymphoproliferative disease that is fatal by 20-24 days of age. The mice exhibit several gross morphological abnormalities including runting and exfoliate dermatitis. They also develop lymphocytic infiltrates at several sites, including lymph nodes, spleen, liver, lungs and skin. Initial experiments have shown that these symptoms are the result of chronic in vivo T cell activation, with subsequent overproduction of a wide variety of cytokines. While available data point to a T cell defect in sf mice, the underlying mechanism remains to be elucidated. There are two possible explanations for the T cell defect seen in these mice. First, the sf gene product is involved directly in TCR signal transduction, and the sf mutation results in dysregulated TCR activation. Second, the sf product is involved in a pathway, such as the CTLA-4 pathway, that regulates TCR activation. The gene that is mutated in these mice has been cloned and shown to be a member of the forkhead/winged-helix family of transcriptional regulators. T cells from mice that overexpress this gene are nonresponsive to activating stimuli, supporting the notion that this gene regulates T cell

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function. Mutations in this gene result in the human IPEX syndrome, where affected males die in their first year of an autoimmune disease. It is not immediately apparent how mutations in this gene have such a dramatic affect on T cell activation. The experiments in this application will determine where in the T cell activation pathway Scurfin (the name given to the protein) acts. We will also determine its role in regulating cytokine gene expression and in regulating peripheral T cell activation. These analyses will shed light on the regulatory pathways involved in the development of autoimmune disease, and will serve as a model for human immune-system abnormalities. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: FUNCTION OF FCERI ON EPIDERMAL LANGERHANS CELLS Principal Investigator & Institution: Borkowski, Teresa A.; Professor; Pediatrics; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2001; Project Start 01-SEP-1997; Project End 31-AUG-2002 Summary: (provided by applicant): The candidate is an assistant professor of dermatology at Johns Hopkins and has commenced the fourth year of this KO8 research program. This application constitutes a request for the fifth year of funding. Langerhans cells (LC) are the principal antigen presenting cells in the skin and part of the network of professional antigen presenting cells. They are responsible for primary and secondary immune T cell responses. Recently the high affinity receptor of IgE (FcERI) has been identified on LC. FcERI complex plays a central role in allergic inflammation. While the function of FcERI in the degranulation of mast cells and basophils is well documented, little is known about the function of this receptor on antigen presenting cells. The aims of this proposal are: 1) To create a model system to study the role of FcERI on Langerhans cells and dendritic cells. 2) To determine the phenotype and changes induced in epidermal Langerhans cells following the ligation of FcERI, and 3) To determine in vivo and in vitro the functional changes induced in epidermal Langerhans cells following the ligation of FcERI. Related studies will determine if FcERI on LC plays a role in the polarization of T cells towards a Th2 phenotype. The studies proposed will be conducted in vitro, and in vivo using a unique transgenic murine model. Unlike human epidermal LC, FcERI is not expressed on murine epidermal LC. However, the mouse that is transgenic for human FcERI alpha (developed by the sponsor) expresses FcERI on epidermal LC. Thus, this mouse is uniquely suited for the study of FcERI on epidermal Langerhans cells in a murine system. Since LC occur in small numbers in human epidermis, a murine model may be the only meaningful way to study this receptor. This tansgenic mouse is exclusively available in the Laboratory of Jean-Pierre Kinet M.D., the candidate's sponsor. For this reason, the performance site of this grant is The Laboratory of Allergy and Immunology, Beth Israel Deaconess Medical Center, Boston MA. Preliminary studies of phenotype have determined that IgE regulates the expression of FcEl on Langerhans cells and that up-regulation is independent of transcriptional regulation or signaling. The studies proposed here will further explore the mechanisms of upregulation. Preliminary functional studies indicated a need to cross the human alpha transgenic mouse onto a murine alpha knock-out background. Mice are now backcrossed 9 generations, and studies of function may proceed. A fifth year is requested to complete the specific aims indicated above. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: GENE-ENVIRONMENT INTERACTIONS AND THE ORIGINS OF ASTHMA Principal Investigator & Institution: Ober, Carole; Professor; University of Wisconsin Madison 750 University Ave Madison, Wi 53706 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2007 Summary: Asthma is the most common chronic disease in industrialized nations, affecting >10 million people in the U.S. alone. Familial aggregation and concordance rates in monozygotic twins have suggested a genetic component to asthma, but elucidating the role of specific genes using traditional approaches has been challenging. We hypothesize that immunologic programming in the fetus results from the interplay between fetal genotype and the environmental challenges of pregnancy, which is influenced by both maternal genotype and her environmental exposures, and that such programming influences subsequent response to viral infections and risk for asthma and atopic disease. Our investigations will be conducted in families participating in the prospective COAST (Childhood Onset of Asthma) Study. We will genotype the COAST child and both parents for variation in 1) 16 genes that encode cytokines, chemokines, and their receptors, that have been implicated in asthma pathogenesis; 2) genes identified through positional cloning studies of asthma or atopy genes; and 3) two HLA class II genes that likely influence the overall immunologic milieu during pregnancy. Main effects of and interactions between genotypes and haplotypes at each locus on the following phenotypes will be assessed during the first 6 years of life: 1) cytokine responses in cord blood and in peripheral blood collected at yearly intervals; 2) cytokine levels in nasopharyngeal mucus specimens collected during RSV infection; 3) persistent wheezing after RSV infection and late-onset wheezing; 4) allergic sensitization; 5) development of atopic dermatitis, allergic rhinitis, and asthma; and 6) airway physiology. In addition, we will evaluate associations between maternal-fetal HLA compatibility and exacerbation of asthma symptoms during pregnancy in mothers with asthma. These studies have the potential to identify novel interactions that influence asthma pathogenesis. Thereby allowing for the development of new therapies and intervention strategies for these common diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: GENETIC ANALYSIS OF HEPARAN SULFATE IN VASCULAR BIOLOGY Principal Investigator & Institution: Esko, Jeffrey D.; Professor; University of California San Diego 9500 Gilman Dr, Dept. 0934 La Jolla, Ca 92093 Timing: Fiscal Year 2003; Project Start 01-FEB-2003; Project End 31-JAN-2008 Summary: Endothelial cells express heparan sulfate proteoglycans that bind to plasma and extracellular matrix proteins through carbohydrate-protein interactions. These interactions have led to the hypothesis that endothelial cell proteoglycans play important roles in vascular biology and hemostasis. The objective of this project is to test this idea by genetically altering endothelial HS in mice. The specific genes that will be studied include two N-deacetylase/N-sulfotransferase isozymes (NDST1 and NDST2) that initiate the modification reactions, the uronosyl 2-O-sulfotransferase (HS2OST) and glucosaminyl 6-O-sulfotransferase-1 (HS6OST1), which generate the binding sites for ligands on the chains. Systemic inactivation of NDST1 and HS2OST in mice have shown that they are essential for early development, making it difficult to assess their role in physiology in adult animals. Therefore, our plan consists of examining mutant mice with selective endothelial-cell null mutations in these genes, using the Cre-loxP

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recombination system. Mutant alleles of NDST1 have already been made, and targeting of HS2OST and HS6OST1 are in different stages of development. Targeted deletion of these genes in endothelial cells and leukocytes will be accomplished by breeding to Tie2Cre mice. For each mutant, the degree of penetrance of the mutations will be assessed in isolated cells, and the proteoglycan and glycosaminoglycan composition will be analyzed. Bone marrow transplantation and adoptive transfer experiments will allow us to study heparan sulfate in both the endothelium and in leukocytes. To examine the role of heparan sulfate in hemostasis, blood coagulation, thrombus formation and fibrinolysis will be examined, with particular emphasis on heparin-binding proteinases (Protein C and tissue plasminogen activator) and serpins (antithrombin, tissue factor pathway inhibitor, and plasminogen activator inhibitor-I). Initial experiments indicate that the bleeding time is altered in NDST1 deficient mice, which may reflect alterations in one or more of these factors. Inflammatory responses appear to be depressed in the mutant as well, in models of thioglycollate-induced peritonitis, oxazolone-induced allergic contact dermatitis, and excisional wound healing. To study these systems further, the effect of altering heparan sulfate on P- and Lselectin and neutrophil chemokines KC and MIP-2 will be examined. The long range goal of these studies is to determine the role of heparan sulfate in vascular biology, with the purpose of defining potential targets for pharmaceutical intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GORDON CONFERENCE--BIOLOGY OF THE SPIROCHETES Principal Investigator & Institution: Weis, Janis J.; Professor; Gordon Research Conferences Box 984, 512 Liberty Ln West Kingston, Ri 02892 Timing: Fiscal Year 2002; Project Start 01-JAN-2002; Project End 31-DEC-2002 Summary: The fifth Gordon Research Conference on the Biology of Spirochetes will be held in January 2002 in Ventura, California. The Biology of Spirochetes Conference is unique. This is the only ongoing international meeting devoted to discussions on basic research of all medically important and biologically relevant spirochetes, a unique group of Eubacteria. Many spirochetes are pathogens and cause a variety of diseases, including syphilis, Lyme disease, relapsing fever, leptospirosis, periodontal disease, digital dermatitis of cattle, and swine and human dysentery. Historically, spirochetes have been difficult to study. These bacteria often have fastidious nutritional requirements and some have yet to be successfully cultured in vitro. Methods for genetic manipulation and mutational analysis of several spirochete species do not exist. The opportunity for exchange of ideas among groups working on different spirochetes has been one of the greatest benefits of past conferences, particularly in the area of new techniques for genetic manipulation. The application of genetic advancements and the availability of genomic sequences of Borrelia burgdorferi, Treponema pallidum, T. denticola, and new sequencing projects in Leptospira spp, are proving a wealth of new information. Combined, these data are being integrated into ongoing studies on the physiology, structure, pathogenesis, and immunobiology of these bacteria. Each of the previous Biology of Spirochetes conferences have been highly successful, receiving high praise by attendees, forging new collaborations, providing a forum for presenting stateof-the-art research on these bacteria, and helping to set new research directions. As in previous conferences, we expect attendance at the 2002 conference to reach the maximum of 150 faculty, graduate students, postdoctoral fellows, and industrial scientists. A broad spectrum of scientists representing different research interests, geographic locations, and seniority will be invited to attend. Special efforts will be made to insure strong attendance of young investigators (graduate students, post-docs and

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junior faculty), and achieve a balance in gender and ethnicity of attendees. The oral and poster-presentations are organized to provide many opportunities for discussion, the exchange of ideas, and development of collaborations. Funding from the National Institutes of Health is requested to partially offset the travel and registration expenses of the participating graduate students, fellows, and junior faculty members. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: HEMOSTATIC FACTORS AND THE INFLAMMATORY RESPONSE Principal Investigator & Institution: Degen, Jay L.; Professor; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, Oh 45229 Timing: Fiscal Year 2001; Project Start 01-JUN-1999; Project End 31-MAY-2003 Summary: The long-term goal of this research program is to understand of the roles of coagulation and fibrinolytic factors in hemostasis, wound repair, inflammatory response, and disease pathobiology. The recent generation of viable mouse lines with selected deficits in key hemostatic factors has provided a unique opportunity to rigorously define the roles of specific factors in both physiological and disease processes. The primary objective of this research proposal is to exploit this opportunity to directly establish the importance and mechanistic role of hemostatic factors in bacterial virulence and host inflammatory response. The focus of these studies will be the bacterial pathogens, Y. pestis and S. aureus, two microorganisms that express welldescribed bacterial plasminogen activators, procoagulants, and fibrin(ogen) binding proteins. The project aims center on the following specific hypotheses: i) host coagulation and fibrinolytic factors are critical in bacterial virulence and pathogenesis, ii) fibrin(ogen) and plasmin(ogen) have a fundamental role in mediating host inflammatory response at sites of infection, iii) fibrin(ogen) alters inflammatory cell activity at sites of infection through the engagement of the integrin, CD11b/CD18, and iv) hemostatic factors play an important role in the inflammatory response, regardless of the challenge or tissue. These hypotheses will be tested though detailed studies of Y. pestis and S. aureus infection and host inflammatory response in mice with specific deficits in plasminogen activator, plasminogen, and fibrinogen (Specific Aims 1 and 2). The mechanistic role of fibrin(ogen)-integrin interaction in the inflammatory response will be explored by comparative studies of infection and inflammation in mice expressing mutant forms of fibrinogen lacking the motifs recognized by the platelet integrin, alphaIIbbeta3, and the leukocyte integrin, CD11b/CD18 (Specific Aims 2 and 3). Finally, the role of fibrin(ogen) in inflammatory processes unrelated to bacterial infection will be explored by studying the impact of fibrinogen deficiency on leukocyte emigration, adhesion, and function, using peritonitis and dermatitis model systems (Specific Aim 4). The proposed studies will provide a more detailed understanding of the role of coagulation/fibrinolytic factors in bacterial pathogenesis and the inflammatory response, and could ultimately lead to the development of new therapeutic strategies for the treatment of both bacterial infection and inflammatory diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: IL-3 AND IL-4R IN MAST CELL GROWTH AND HYPERSENSITIVITY Principal Investigator & Institution: Lantz, Chris S.; Biology; James Madison University Harrisonburg, Va 22801 Timing: Fiscal Year 2001; Project Start 01-SEP-2001; Project End 31-AUG-2004

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Summary: (provided by the applicant): Mast cells are of hematopoietic origin but complete their differentiation in peripheral connective tissues where they are thought to function as important effector cells in IgE-associated immune responses. Indeed, a large body of evidence indicates that mast cell mediator secretion significantly contributes to both allergic disorders, such as anaphylaxis and asthma, and to host resistance to certain parasites. The long-term objectives of this project are to understand to what extent the production of interleukin (IL)-3, and interactions between IL-3 and IL-4 receptor a chain (IL-4R alpha) signaling pathways, regulate the development and function of mast cells, and hypersensitivity responses in vivo. Studies using IL-3-deficient mice indicate that IL-3 contributes to increased numbers of tissue mast cells and immunity in mice infected with certain parasites. However, the ability of IL-3 to influence IgE- and mast cellassociated immune responses has not yet been examined in these mice. Therefore, we wish to employ IL-3-deficient mice to test the hypotheses that IL-3 is required for the full expression of local and systemic anaphylactic responses in vivo. Because mast cellderived chemokines represent potentially important mediators in allergic inflammation, we also wish to test the hypothesis that exogenous IL-3 can regulate mast cell chemokine production either in the absence or presence of IgE and specific antigen. Numerous in vitro studies have suggested that IL-4 may act in concert with IL-3 to control mast cell development and function in vivo, and recent evidence suggests that IL-3 and IL-4, and perhaps IL-l3, are involved in regulating contact hypersensitivity. It would be advantageous to study mouse lines in which the expression of all of these cytokines is disrupted. Unfortunately, the close linkage of these genes precludes the generation by simple interbreeding of mouse lines that simultaneously lack these cytokines. To circumvent this difficulty we will take advantage of an exciting new opportunity to develop and analyze mice with a combined deficiency of IL-3 and IL-4Ra (IL-4Ra is also a component of IL-13R), thereby allowing us to investigate the potential compensatory roles of these cytokines in vivo. Specifically, we will use mice deficient in both IL-3 and IL-4Ra to analyze the requirement of IL-3, IL-4, and IL-13 for: 1) generating physiological levels of tissue mast cells, 2) gastrointestinal parasite-induced mast cell hyperplasia, and 3) regulating the expression of contact hypersensitivity reactions to haptens. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: IMMUNE MEDIATORS IN INTERSTITIAL CYSTITIS Principal Investigator & Institution: Peters, Kenneth M.; Director of Clinical Research; William Beaumont Hospital 3601 W Thirteen Mile Rd Royal Oak, Mi 480736769 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-AUG-2002 Summary: Interstitial cystitis (IC) is a severe debilitating bladder disease of unknown etiology and no cure. A recent double-blind trial using intravesical Bacillus Calmette Guerin (BCG) to treat IC demonstrated a 60% clinical response rate to a single six week course of BCG. When subjects who responded to BCG were followed for a minimum of two years, 89% continued to have an excellent response, despite no additional treatment of their IC. The durability of this treatment leads one to speculate on the mechanism in which intravesical BCG may treat interstitial cystitis. There is evidence that interstitial cystitis may be mediated by a T-Helper Cell type-2 (Th-2) response within the bladder. Cytokine analysis from the urine of IC subjects showed elevated levels of Interleukin-6 and inhibitors of interleukin-2, suggesting a Th-2 response. In addition, similar autoantibodies have been identified in both atopic dermatitis, a Th-2 mediated disease, and interstitial cystitis. However, the role of the immune system in the etiology of IC remains controversial. We hypothesize that interstitial cystitis is a Th-2 mediated disease

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leading to chronic inflammation and that intravesical BCG is effective by converting the cytokine milieu to a Th-1 profile, leading to reparative conditions and long-term clinical response. Specifically, this study will: 1) determine the urine cytokine profiles in subjects meeting the NIDDK criteria for interstitial cystitis and in health control subjects; 2) determine in a blinded fashion the changes in urinary cytokines during six weekly instillations of either bacillus Calmette-Guerin (BCG) or placebo and at regular intervals during a 6 month follow-up; 3) correlate changes in cytokines with clinical response; and 4) determine whether a certain cytokine profile cytokine profile can predict clinical response to intravesical BCG therapy. This study will involve subjects enrolled in our present clinical trial of intravesical BCG therapy for IC. Cytokine levels will be determined in triplicate by enzyme-linked immunosorbant assays and normalized against urine creatine. Study results will be analyzed by non-parametric methods. In addition, a receiving operating characteristic analysis will be completed to determine the critical cytokines levels for predicting clinical response to treatment. In summary, this study will determine the cytokine profile in IC subjects and healthy subjects. By correlating the changes in cytokine levels before, during and following intravesical BCG therapy, we will establish the role of these cytokines in IC and use the pattern of change as a means to predict subject response to therapy. Additionally, this study will open a new avenue of research with specific long-term potential for the development of more effective, less toxic treatments of IC. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: IMMUNOBIOLOGY OF WALNUT FOOD ALLERGY Principal Investigator & Institution: Teuber, Suzanne S.; Internal Medicine; University of California Davis Sponsored Programs, 118 Everson Hall Davis, Ca 95616 Timing: Fiscal Year 2001; Project Start 01-MAY-1999; Project End 30-APR-2003 Summary: Over the last ten years, genes encoding food allergens have been cloned and sequenced but no consensus sequences or motifs associated with allergy have been determined. Indeed, my lab has cloned genes encoding 2 of the major English walnut kernel allergens, the 2S albumin and a vicilin-like seed storage protein, Jug r 1 and Jug r 2, respectively. Plant seed allergy is often life-threatening and permanent. Individuals with walnut allergy, for instance, can have high levels of specific IgE against several different, non-cross-reactive proteins in their sera into their seventh decade. Most patients who have life-threatening walnut allergy have a childhood history of atopic dermatitis (AD), in which it has been demonstrated that there is more of a tendency to develop IgE against multiple environmental and food allergens. Even in the face of this however, most children with AD are tolerant of most foods. The major thesis of this proposal is that plant seed proteins, because of the way they are packaged as whole proteins in the plant protein body storage organelle with associated lectins, enzymes, and polyphenolic compounds, are able to stimulate the APC in atopic persons to modulate the cytokine milieu towards increased IL-4 and IL-13, inducing an IgE response. As a prototype seed to study, the walnut (Juglans regia) will be used based on the availability of human subjects, recombinant allergens, multiple protein preparations, fractionated polyphenolics and its importance as a tree nut allergen. To characterize the APC-T cell interaction, T cell lines will be established from individuals with walnut food allergy and individuals with atopic dermatitis without food allergy. The proliferative response and Th2 related cytokine mRNA transcription will be assessed in response to different antigen packages delivered to the APC: recombinant Jug r 1 and Jug r 2, peptide fragments, whole purified proteins (albumins and large globulins), purified protein bodies (lectins and enzymes present), total walnut extract (pellicle polyphenolics

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and oil body lipids present), and the above protein sources with a quantified walnut total polyphenolic fraction added (rich in quercetin and ellagic acid). The above data will significantly advance our knowledge of the immunobiology of plant seed allergy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: IMMUNOLOGIC MECHANISMS OF ATOPIC DERMATITIS Principal Investigator & Institution: Geha, Raif S.; Professor; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2001; Project Start 20-MAR-2001; Project End 28-FEB-2006 Summary: (Adapted from the Investigator's abstract): Atopic dermatitis (AD) and asthma are common allergic inflammatory diseases that affect the airways and the skin. Although much information has been gained on the mechanism of allergic asthma, little is known about allergen-induced dermatitis, in part because of the lack of an animal model. We recently developed a mouse model of allergic dermatitis using repeated epicutaneous (EC) sensitization with ovalbumin (OVA). This model is unique because it elicits a predominantly Th2 response and generates skin lesions characterized by infiltration of CD4+ T cells and eosinophils and by expression of mRNA for the Th2 cytokines IL-4 and IL-5, and, to a lesser extent, for IFN-gamma. EC sensitized mice exhibit bronchial hyper-responsiveness to inhalation of a single dose of OVA. Thus, our model has histologic, immunologic and clinical features of human AD. EC sensitization requires tape stripping which results in skin injury. We found that tape stripping induces rapid expression of mRNA for IL-10, cyclooxygenase-2 (COX-2) and for the Th2 selective chemokine TARC in the skin. Moreover, IL-10 deficient mice have a severe reduction in IL-4 and IL-5 mRNA expression and decreased eosinophil influx in sensitized skin. We propose to apply state of the art knowledge and techniques to our unique model of allergen induced skin inflammation to gain better insight into the pathogenesis of AD. We plan to address three important questions: 1. What is the role of T cell subsets and Thl and Th2 cytokines in skin infiltration by CD4+ cells and eosinophils? We will characterize in detail the T cells that infiltrate the skin and we will assess the role of T cell subsets and T cell cytokines in our model, using genetically manipulated mice, B.M. chimeras and adoptive transfer experiments. 2. What is the mechanism(s) by which EC sensitization skews the response of Th-cells to Th2? We will examine the role of skin injury, IL-10, prostaglandin E2 and histamine in skewing the Th-cell response towards Th2 and investigate. In addition, dendritic cells from lymph nodes that drain EC sensitized skin of wild type and genetically manipulated mice will be examined for their capacity to skew the Th response. 3. What is the role of chemokines in the recruitment of Th2 cells to the skin? We will examine chemokine and chemokine receptor expression in injured and inflamed skin and assess their role in our model using neutralizing antibodies and chemokine receptor deficient mice. We will determine whether Th2 cells induced by immunization at other anatomical sites are recruited to the skin. Finally, we will examine the effects of inducible expression of chemokines in keratinocytes on Th2 cell recruitment to skin. The proposed studies should provide a better understanding of AD and help devise novel therapies for this disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: IMPLANTABLE ELECTRICAL CABLING AND INTERCONNECTS Principal Investigator & Institution: Ketterl, Joe R.; Microconnex Corporation 34935 Se Douglas St, Ste 200 Snoqualmie, Wa 98065

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Timing: Fiscal Year 2002; Project Start 15-JUN-2002; Project End 30-JUN-2004 Summary: In this Phase II SBIR effort, MicroSound Systems proposes to develop flexible implantable electrode and interconnect structures based on flexible printed wiring technology and Liquid Crystal Polymer dielectric materials. Implants for biological monitoring and neurological stimulation could potentially benefit millions of people suffering from a wide range of physiological conditions, including impaired hearing or vision, diabetes, and epilepsy. Additional applications include intracranial pressure and cerebral blood gas monitoring, and patient monitoring, for tracking parameters such as heart rate. This new technology utilizes leading-edge multi-layer flexible printed wiring fabrication techniques, including laser micromachining, thin films, plasma processing, and advanced photolithography techniques. In the Phase I effort, Liquid Crystal Polymer multi-layer high density interconnect flexible circuits with fine-scale features were fabricated. And MicroSound is now closer to demonstrating that the technology is capable of producing an "implant ready" circuit. In the Phase II effort, MicroSound will continue to aggressively push the development of this technology. Development of a fabrication process for making a prototype electrode array for a cochlear implant will continue, and our efforts will be expanded to include a retinal implant, patient monitoring, and some non-implant medical applications such as ultrasound imaging. PROPOSED COMMERCIAL APPLICATION: MicroSound's enabling implant cabling technology is seen as being essential for cochlear and retinal implants and similar devices, which together represent a market exceeding $200 million annually. This technology is also important for implantable and non-implanted patient monitoring products (for tracking pressure, gases, or fluids), and other medical non-implant applications such as ultrasound imaging, for which the total of the aggregate markets is in the billions of dollars. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: IMPROVED METHODS FOR DERMAL EXPOSURE ESTIMATION Principal Investigator & Institution: Kasting, Gerlad B.; Pharmaceutical Sciences; University of Cincinnati 2624 Clifton Ave Cincinnati, Oh 45221 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-AUG-2006 Summary: (provided by applicant): The investigators propose to develop a sophisticated, yet accessible mathematical model that closely mimics percutaneous penetration, tissue concentrations and clearance in human skin in vivo. This development will significantly advance the mechanistic understanding of allergic and irritant dermatitis and the mechanics of dermal exposure assessment. This objective will be accomplished through the construction and experimental verification of physiological and physical properties-based models for percutaneous absorption incorporating features not found in the mathematical models presently used to estimate dermal exposure. Successful completion of the specific aims of the proposal will lead to the following: (1) an experimentally verified, microscopic model of transport in human stratum corneum and skin appendages (hair follicles, sweat glands); (2) a dermal vascular model that allows accurate predictions of permeant concentrations and clearance in the viable skin layers; (3) a transient diffusion model for calculating dermal absorption subsequent to low-to-moderate exposures to potentially volatile compounds; (4) a skin hydration model for linking the above with steady-state permeability models presently in use; and (5) an easy-to-use spreadsheet for dermal exposure calculations incorporating the most important features from the investigation. The research methods include: Sophisticated numerical techniques for modeling transport in heterogeneous structures and advanced graphical representation of these results. Detailed examination

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of stratum corneum ultra structure and microtransport properties using laser scanning confocal microscopy, fluorescence photobleaching,and other light microscopic techniques. Determination of diffusivities and partition coefficients of selected permeants in stratum corneum, epidermis, dermis, and hypodermis and the role of protein binding on these values. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: INTERNATIONAL SYMPOSIUM ON ATOPIC DERMATITIS Principal Investigator & Institution: Hanifin, Jon M.; Professor; National Eczema Assn for Science & Educ for Science and Education Portland, or 97205 Timing: Fiscal Year 2001; Project Start 01-MAY-2001; Project End 30-APR-2002 Summary: This conference is being convened to bring together an international group of investigators in the field of atopic dermatitis. The objectives of the Symposium are to: 1) Provide a forum for presenting and discussing important research on atopic dermatitis (AD); 2) Assemble a cadre of recognized international experts from the fields of dermatology, allergy, molecular genetics, epidemiology and immunobiology to develop a comprehensive overview of the condition at the molecular, cellular, tissue, and population levels; 3) Encourage agreement on definitions and criteria for future genetic, epidemiologic and clinical investigations; 4) Identify a list of key research topics that deserve priority consideration by NIH Institutes, investigators. and public/ private sector funders; 5) Examine the impact of atopic disease on the prevalence, incidence, and costs of occupational dermatoses, specifically allergic contact dermatitis/hand eczema; 6) Improve the public awareness regarding the scope and prevalence of AD and the range of therapeutic options that are currently available to treat the condition in all of its clinical manifestations. Provide particular emphasis on the special problems faced by non-Caucasian populations with eczema/atopic dermatitis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: IRRITANTS EFFECTS ON EPIDERMAL ANTIGEN PRESENTATION Principal Investigator & Institution: Gaspari, Anthony A.; Professor; Dermatology; University of Maryland Balt Prof School Baltimore, Md 21201 Timing: Fiscal Year 2001; Project Start 30-SEP-1998; Project End 31-AUG-2003 Summary: (Adapted from the Investigator's Abstract) Irritant contact dermatitis (ICD) is a common and clinically important type of inflammatory skin disorder, and is thought to be the result of non-immunologic inflammation resulting from chemical injury to the skin. This is in contrast to allergic contact dermatitis (ACD), in which hapten specific CD4+ T-lymphocytes are thought to be critical in the immunopathogenesis of this type of dermatitis. However, previous clinical, histologic and immunologic research studies comparing irritant to allergic contact dermatitis indicated that in most assays, these two types of dermatitis are similar, if not identical. We hypothesize that irritant and allergic contact dermatitis share common pathways of immune-mediated skin damage, resulting in the common phenotype of the two kinds of contact dermatitis. Irritants and allergens damage the epidermis, resulting in the release of self-antigens. We hypothesize that these self-antigens are presented to auto-reactive T-lymphocytes by epidermal antigen presenting cells (APC), which are central to the pathogenesis of both irritant and allergic contact dermatitis. To test our hypothesis, we will study the direct effects of irritants on human keratinocytes (KC) and Langerhans cell (LC)-like dendritic cells (DC) in their expression of adhesion molecules and cytokines that are known to be critical for regulating APC-functions or T-lymphocyte growth. Antigen presentation by normal or

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irritant-treated epidermal KC or LC-like DC cells to skin homing T-lymphocyte populations will be studied. The autologous mixed lymphocyte reaction will be used a model for presentation of self-antigens to autoreactive T-lymphocytes by irritantstressed epidermal APC. The following T-lymphocyte populations will be studied for autoreactivity against irritant-treated APC: Skin homing T-cell populations (Cutaneous leukocyte antigen+) (CLA) derived from the peripheral blood; T-lymphocytes that infiltrate into irritant skin challenge sites; or non-classical T-lymphocytes (CD4-CD8-, Tcell receptor y/8 bearing) derived from normal human epidermis. These studies will define novel immunologic mechanisms of ICD, and will lead to a better understanding of the effects of irritants on the regulation of APC function and the subsequent interactions with skin homing T-lymphocytes. Some of these assays may be useful as an in vitro to identify individuals at risk for irritancy. Since ICD can be a debilitating skin problem that potentially affects millions of Americans, the identification of individuals at risk for irritancy using in vitro tests would be of utility in preventing this common and potentially disabling condition. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: LYMPHOTOXIN ALPHA IN SYSTEMIC IMMUNE RESPONSE Principal Investigator & Institution: Fu, Yang-Xin; Assistant Professor; Pathology; University of Chicago 5801 S Ellis Ave Chicago, Il 60637 Timing: Fiscal Year 2001; Project Start 01-APR-1997; Project End 31-MAR-2002 Summary: a. Candidate: Dr. Yang-Xin Fu received his M.D. degree in 1983 from the Shanghai Medical University in China and his Ph.D. degree in immunology from the University of Miami in 1990. From 1991-93 he was a Research Associate in the Division of Infectious Diseases at the National Jewish Center for Immunology and Respiratory Medicine in Denver. Since 1994 he has been a Resident in the Division of Laboratory Medicine, Department of Pathology, Washington University School of Medicine in St. Louis. b. Sponsor: David Chaplin, M.D., Ph.D., is Professor of Medicine, Genetics and Molecular Microbiology at Washington University in St. Louis. He has been Associate Investigator at the Howard Hughes Medical Institute in St. Louis since 1984 and is currently the Chief, Division of Allergy and Immunology, the Washington University School of Medicine. c. Career Development Plan: The candidate desires to gain experience in developing, analyzing and maintaining transgenic and knock-out mice. The career development plan also includes training in immunochemistry, flow cytometry, preparation of bone marrow chimeras, and in analysis of the maturation of the B-lymphocyte response. For the last one to three years of the award Dr. Fu will be appointed as an Instructor in Pathology so that he may direct an increasingly independent program. No formal course work is proposed. However, the candidate will take an English writing skills course so that his writing abilities can match his oral communication skills. He will devote 90 percent effort to the research project. d. Research Plan: The overall goal of the project is to define the role of peripheral lymphoid structures in the maturation of the host immune response and to identify essential actions of lymphotoxin (LT) in the regulation of these responses. The candidate states that the functions of lymphotoxin alpha (LT-alpha) need to be reevaluated in light of the discovery of a receptor for the heteromer of LT-alpha and lymphotoxin beta (LT-beta), called TNFRrp, and in light of the observation that LT-alpha deficient mice (LT-alpha-/) do not develop lymph nodes or Peyer's patches. The project is based on the hypothesis that LT plays an important role in the induction of contact sensitivity responses and that it may play a role either directly or indirectly in regulating Ig class switching after immunization with different antigens. Dr. Fu's preliminary research shows that LT-

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alpha deficient mice exhibit an impaired contact sensitivity response but mount a good cutaneous hypersensitivity response. In addition, these mice demonstrate impaired Ig class switching following sheep red blood cells (SRBC) challenge but normal Ig class switching following OVA immunization. These results suggest that the type of antigen and the structure of the antigen might determine the necessity for LT-alpha lymph nodes or Peyer's patches in generating normal immunoglobin responses. Dr. Fu's group has also demonstrated an impairment in IgA production in the LT-alpha-/- mouse. Bone marrow cell transfer from normal mice does not restore the development of Peyer's patches but does increase IgA production, suggesting there may be a dichotomy between the need for Peyer's patches and IgA production. The aims of the project are to: 1) investigate the role of LT-alpha in contact sensitivity, 2) test the role of LT-alpha and its receptors in Ig class switching, and 3) define the role of Peyer's patches and lymphotoxin in the immune response to orally administered antigens using normal and LT-alpha knock-out mice. e. Environment: The candidate will carry out his research at the Howard Hughes Medical Institute, Washington University School of Medicine, in the laboratories of the Clinical Sciences Research Building. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MAPPING OF NON-HLA LOCI FOR GLUTEN SENSITIVE ENTEROPATHY Principal Investigator & Institution: Neuhausen, Susan L.; Professor; Medical Informatics; University of Utah 200 S University St Salt Lake City, Ut 84112 Timing: Fiscal Year 2001; Project Start 16-SEP-1996; Project End 31-AUG-2002 Summary: (Adapted from the Investigator's Abstract): This is the first resubmission of a proposal for four years of support to map non-HLA-linked loci for gluten sensitive enteropathy (GSE) using affected sibling pair families. GSE is a histological abnormality of the jejunum which improves on withdrawal of gluten from the diet, and includes both patients with the malabsorption disorder celiac disease (CD) and those with the gluten sensitive skin disorder dermatitis herpetiformis (DH). Patients with CD have symptoms including growth failure, abdominal pain, and diarrhea. The risk to first degree relatives of an individual with GSE is 8-12% and the risk for MZ twins is 70%. GSE has a strong association with HLA DQ genotypes. However, HLA alone is not sufficient to explain the hereditary nature of GSE. The applicants propose to: (1) ascertain 100 kindreds with at least two affected siblings; (2) collect blood samples from the affected siblings, their parents, additional affected family members, and connecting family members; (3) confirm diagnoses through biopsy reports; (4) perform DNA-based HLA typing of DQA, DQB, and DQCAR (in between DQA and DQB) loci and assess the degree of association with individual loci and haplotypes at these loci; (5) test for linkage with a dozen candidate genes and regions suggested by the clinical correlations of GSE with various diseases and by tentative immunopathogenesis; and (6) perform a genome search with 250 primarily tri- and tetranucleotide repeat markers (intermarker distances 76%) on up to 400 individuals if none of the candidate genes show linkage to GSE. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: MECHANISMS OF BLISTER FORMATION BY STAPHYLOCOCCAL TOXINS Principal Investigator & Institution: Stanley, John R.; Milton B. Hartzell Professor; Dermatology; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104

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Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2007 Summary: Exfoliative toxin A (ETA), produced by Staphylococcus aureus, causes staphylococcal scalded skin syndrome (SSSS) and its more localized form, bullous impetigo. The crystal structure of ETA suggests that it is a serine protease with an inactive catalytic site which becomes activated when ETA binds a specific receptor. In pemphigus foliaceus autoantibodies that cause dysfunction of Dsg 1 cause blisters identical to those caused by ETA in the superficial epidermis of mouse and man. Therefore, we hypothesize that Dsg 1 specifically binds and activates ETA, which in turn cleaves the bound Dsg 1, resulting in blister formation. We propose that another staphylococcal toxin, exfoliative toxin B (ETB), that also causes bullous impetigo and SSSS, is also activated by, and cleaves, Dsg 1. Finally, we hypothesize that binding of ETA to Dsg 1 and/or cleavage of Dsg 1 by ETA might elicit an autoimmune response against Dsg 1, thus suggesting a mechanism for autoantibody production in PF patients. We have shown that ETA cleaves Dsg 1. Specific aim 1 will characterize this cleavage by determining if cleavage is dependent on Dsg 1 conformation, and by defining the site of cleavage and the domains of Dsg 1 needed for cleavage. Aim 2 will characterize binding of ETA to Dsg 1, and define the domains of each necessary. Aim 3 will determine, using Dsg 3 knockout and involucrin-Dsg 3 transgenic mice, if compensation by Dsg 3 can compensate for ETA-induced loss of function of Dsg 1, thereby explaining the sites of blister localization. Aim 4 contains studies designed to define the kinetics of Dsg 1 cleavage by ETA. Aim 5 will extend the results of the previous aims to include the mechanisms of action of ETB. The final aim will determine if patients with bullous impetigo and SSSS develop an antibody response against Dsg 1, if patients with pemphigus foliaceus have an enhanced immune response against ETA and ETB, and if mice injected with ETA develop an immune response against Dsg 1. These studies will provide insight regarding the molecular pathophysiology of a very common disease, bullous impetigo, and, for the first time, identify a potential trigger or exacerbating factor in a tissue-specific autoimmune disease, pemphigus. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MECHANISMS OF CUTANEOUS DRUG REACTIONS Principal Investigator & Institution: Svensson, Craig K.; Professor and Division Head; Pharmaceutical Sciences; Wayne State University 656 W. Kirby Detroit, Mi 48202 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2005 Summary: (provided by applicant): Cutaneous drug reactions (CDR) are among the most frequent adverse medical events. Recent studies suggest that between 30 and 45 percent of all adverse drug reactions involve the skin. Of particular interest are the delayed-type hypersensitivity reactions that occur with sulfonamides and sulfones. While most investigators have focused on the role of differences in hepatic bioactivation and detoxification in determining predisposition to these reactions, it is uncertain and perhaps unlikely that liver-generated reactive metabolites would survive transit to the skin. We have developed a novel hypothesis wherein metabolic activation of drugs in keratinocytes provokes the release of signals that result in the activation of cutaneous dendritic cells, thereby initiating the cascade of events resulting in the manifestations of a CDR. The long term-goal of our project is to elucidate the mechanism of CDR and develop means to predict and/or prevent their occurence. The objective of the present proposal is to test the validity of our hypothesis using sulfamethoxazole (SMX) and dapsone, which are among the most frequent CDR-inducing drugs, as model compounds. The Specific Aims of this project are to determine: 1) If cyclooxygenase is the enzyme that bioactivates SMX and dapsone in normal human epidermal

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keratinocytes (NHEK). Preliminary studies have indicated that these compounds can be bioactivated by cyclooxygenase-2. We will identify the enzyme responsible for this bioactivation in NHEK using selective inhibitors and inducers, as well as recombinant enzyme. 2) If cytokines alter the bioactivation or detoxification of SMX and dapsone in NHEK. An inflammatory response has been shown to alter enzymes important in drug bioactivation, an event that appears to be mediated by cytokines. Cytokines may also alter the glutathione content of cells, an alteration that may alter the susceptibility of cells to these hydroxylamine metabolites. We will assess the effects of proinflammatory cytokines on the bioactivation/detoxication of SMX and dapsone in NHEK. 3) If NHEK incubated with hydroxylamine metabolites of SMX and dapsone release signals resulting in the activation of dendritic cells. After determining the mechanism of cell death induced by these metabolites, we will test the hypthothesis that they activate dendritic cells, either directly or indirectly (i.e., via signals released from NHEK). We anticipate that the results of the proposed studies will identify key points of intervention that will permit the prevention or management of these reactions. Moreover, they should enable us to develop in vitro screening tests that will permit the pre-clinical identification of drugs likely to pose a significant risk for the development of such reactions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MODEL SURVEILLANE/INTERVENTIONS

OCCUPATIONAL

DERMATITIS

Principal Investigator & Institution: Huemann, Michael A.; Oregon Service Division 800 Ne Oregon St, Ste 722 Portland, or 97232 Timing: Fiscal Year 2001; Project Start 30-SEP-2000; Project End 29-SEP-2003 Summary: This proposal addresses the NORA priority area of enhancing state-based capacity to do surveillance and intervention for targeted occupational injuries, illnesses, and hazards. Specifically, the Oregon Health Division (OHD) is proposing to expand on an innovative model for surveillance and intervention for occupational dermatitis (OD) - a priority condition for both the Healthy People 2010 objectives and for NIOSH. This proposal is based on collaborations between the OHD, the Oregon Workers' Compensation Information System (OWCIS) and two major private workers' compensation (WC) insurance companies in Oregon. This project addresses important gaps in data available in the OWCIS, using additional information contained in the proprietary databases of the WC insurance companies. In addition, this proposal will assess the feasibility and utility of using the detailed medical encounter file of OWCIS for identifying and tracking OD claims from self-insured employers and other nonparticipating WC insurers in Oregon. Narrative data from the WC insurers databases will also be examined to look for antecedent events that cause the condition. Finally, comparisons will be made between the profiles of OD in the various databases. The information from this surveillance system can be used to recommend achievable and practical interventions to prevent OD and to evaluate the impact of these interventions. Because the component databases of this system are available in many other states, the lessons learned from this system should be applicable to other states, and to surveillance for other targeted occupational injuries, illnesses and hazards. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: MOLECULAR ANALYSIS OF STAPHYLOCOCCAL EXFOLIATIVE TOXIN A Principal Investigator & Institution: Plano, Lisa R.; Pediatrics; University of Miami Box 248293 Coral Gables, Fl 33124 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2008 Summary: (provided by applicant): Staphylococcal scalded skin syndrome, SSSS, is a disease primarily of the young and immunocompromised that is rarely seen in healthy adults. SSSS is characterized by specific exfoliation of the upper epidermis in the stratum granulosum of the skin at a site distal to a focus of infection with exfoliative toxin (ET) producing Staphylococcus aureus. The exact mechanism of the relative protection of adults or susceptibility of newborns is not known. In an animal model these skin manifestations result from the injection of one of two species-specific exfoliative toxins, ETA or ETB. The mechanism by which these toxins result in exfoliation is now assumed to involve cleavage of desmoglein 1 (Dsgl), a desmosomal protein member of the cadherin family of cell adhesion molecules, by a unique serine protease activity of the exfoliative toxins. Cleavage of this protein fits the clinical picture of SSSS as it is primarily expressed at this layer of this skin. Our hypothesis is that characteristics of the interaction between the exfoliative toxins of S. aureus and their target desmoglein 1 explain the species, target and age specificity of these toxins as well as contribute to the pathogenicity of these bacteria. We propose in this study to use molecular techniques to characterize the interaction between the toxin, ETA and the target, Dsgl of humans and mice. The goal is to determine the domains or amino acids of Dsgl needed for recognition and cleavage by ETA and the domains or amino acids of ETA responsible for target binding and localization to the skin. Results from these analyses will provide insight into the mechanism for the age and species specificity of this unique serine protease. We further propose to develop an animal model of staphylococcal impetigo to address the role of the exfoliative toxins in pathogenesis of these bacteria. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: MOLECULAR HISTOPLASMOSIS

PATHOGENESIS

OF

PULMONARY

Principal Investigator & Institution: Woods, Jon P.; Associate Professor; Medical Microbiol & Immunology; University of Wisconsin Madison 750 University Ave Madison, Wi 53706 Timing: Fiscal Year 2001; Project Start 30-SEP-1995; Project End 31-AUG-2005 Summary: Description (Adapted from applicant's abstract): The targets of this proposal are the functions and regulatory mechanisms of two Histoplasma capsulatum (Hc) genes that are up-regulated early in macrophage infection and may be important for pathogenic success in the hostile host environment. Histoplasmosis is the most common endemic mycoses in the world and is particularly dangerous for immunocompromised patients. Disease manifestations may be pulmonary or systemic, resulting from the respiratory route of infection and dissemination through the mononuclear phagocytic system. From host inhalation of mold elements through conversion to a budding yeast, entry in macrophages, and survival within a harsh intracellular compartment, this dimorphic fungus successfully faces a wide range of environmental stimuli and threats from host defense mechanisms. The ability for adaption to the host by a soil microorganisms is intriguing from an evolutionary standpoint and clinically significant. Examining genes that are specifically up regulated during infection can elucidate

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pathogenic mechanisms and the nature of the host micro-environmental niche in which the fungus persists. Such studies may also reveal new vaccine candidates or therapeutic drug targets. Differential display (dddRT-PCR) and in vivo expression technology (IVET) was used to identify a number of Hc early response genes including yps-3 and a gene encoding a small transcript in antisense orientation to a homology of an immunogenic protein found in the cell wall and culture supernatant. Its predicted homology with mammalian EGF-like proteins and a domain of the Blastomyces dermatitis WI-1 antigen is consistent with potential roles in attachment or intracellular signaling. DdRT-PCR was used identify yps-3 up regulation during infection and moreover revealed 3' untranslated region processing and alternate polyadenylation associated with novel sequence motifs. The first aim is to determine the function, pathogenic role and in vivo regulatory mechanisms for yps-3. IVET was used to identify up regulation during infection of the other gene targeted in this proposal. Our second aim is to determine the function of this gene, including its role in potential antisense down regulation of the protein kinase homolog as part of the fungus's adaption to the host intracellular environment. Both yps-3 and IVET-identified gene are up regulated within four hours after intracellular infection. The third aim is to determine the environmental stimuli regulating expression, using specific conditions relevant to Hc pathogenesis as well as macrophage cell culture and mouse infection models. These studies are designed to characterize unique biological aspects of each gene as well as potentially shared features of fungal adaptive responsiveness in a pathogenically relevant setting. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NAIL SALON HAZARDS AND HEALTH EFFECTS Principal Investigator & Institution: Roelofs, Cora R.; Work Environment; University of Massachusetts Lowell 1 University Ave Lowell, Ma 01854 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-AUG-2006 Summary: (provided by applicant): Nail salon employees are potentially exposed to dozens of recognized chemical hazards including acrylates, solvents, and biocides in dust and vapor form, yet little is known of salon workers' total exposure or work environment conditions. Even less is known about prevalence of health effects in this population of mostly Asian immigrant women workers. We do know that exposure to the chemicals with which they work have been linked to asthma, dermatitis, cognitive dysfunction and reproductive health hazards. Special barriers confront investigators in studying the nail work environment, including the smallness of nail salons businesses and potential language and cultural differences between investigators and salon owners and workers. The proposed study, by a new investigator, aims to develop methods for a community-based, comprehensive investigation of both the technical and social issues related to the nail salon work environment and health hazard prevalence in salon workers. Through consultation with a Research Advisory Group, site visits to salons, and in-depth and relationship-building interviews with stakeholders, the investigator will 1) design an exposure assessment strategy appropriate to the evaluation of nail salon work environments; 2) design a survey to assess occupationally-related health effects in nail salon workers; 3) pilot the exposure assessment strategy and health effects survey to evaluate feasibility and validity; 4) assess the social context of occupational health issues as they relate to nail salon work; 5) determine access strategies and build relationships to facilitate this project and a larger-scale study. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: NK T CELL DERIVED IL-4 ACTIVATES B-1 CELLS IN CONTACT SENSITIVITY Principal Investigator & Institution: Askenase, Philip W.; Professor of Medicine and Pathology; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2001; Project Start 30-SEP-1992; Project End 31-MAR-2004 Summary: Contact sensitivity (CS) responses are very common allergic disorders of the skin. Elicitation of the late T cell 24 hr phase of CS in immunized mice requires an early antigen-specific initiating phase. This peaks 2 hr after challenge and depends on local complement activation to elaborate C5a due to antigen binding IgM antibodies produced by B- I cells, leading to vascular activation for local T cell recruitment. We hypothesize that NK T cell derived IL-4 activates the B-1 cells to mediate this CSinitiation. Aim #1: Determine the role of IL-4 in the early CS response. CS responses in IL- 4-/- vs. wild type mice will be investigated. If IL-4-/- mice show an impaired early response, the deficient mice will be injected with different doses of IL-4. Activated immune B-1 cells from contact sensitized wild type mice will be transferred into sensitized IL-4 deficient mice and test for elicitation of CS. Mice with defective IL-4 signaling (Stat-6-/-) will also be evaluated similarly. Aim #2: Evaluate contact sensitivity in NK T cell- deficient mice. If IL-4 is found involved in CS-initiation, NK T cell deficient mice will be evaluated. Two strains of NK T cell deficient mice will be employed: CDld-/- and Jalpha281-/-. If there is deficient CS, then adoptive cell transfers of FACS purified NK T cells (using CD1d fluorescent tetramers) and B-1 cells (CD 19+ CD5+) will be performed, as well as treatment with different doses of IL-4. Aim #3: Analysis of the effects of IL-4 on activation of B-1 cells. The phenotype of the B-1 cells will be analyzed for evidence of activation induced by IL-4. The surface marker Thy-1, expressed in vitro on B cells after IL-4 treatment, and on activated CS-initiating cells, will be analyzed on B-1 cells in CS of wild type mice, as well as in CDld-/- and J281-/mice. CD23 expression, generally associated with IL-4 activation will be investigated similarly. Further the effect of the NK T cell non-specific activator alpha-GalCer, on activation of B-1 cells also will be evaluated. Summary: The current proposal will investigate the role of IL-4 produced by NK T cells in initiating CS responses. We hypothesize that NK T cellderived IL-4 activates B-1 cells to secrete specific IgM, lading to subsequent Ag- dependent elaboration of C5a to initiate CS. Recognized only a few years ago, NK T cells have not been associated with contact dermatitis, nor with the initiating phase of in vivo T cell mediated immunity, nor with allergies. Furthermore, our studies may have the important result of identifying a physiological ligand for the semi-invariant alpha/beta-TCR on regulatory NK T cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: NOVEL ANGIOGENIC CYTOKINE INDUCED ENDOTHELIAL ANTIGEN Principal Investigator & Institution: Koch, Alisa E.; Gallagher Research Professor; Medicine; Northwestern University 633 Clark St Evanston, Il 60208 Timing: Fiscal Year 2001; Project Start 01-SEP-1999; Project End 31-AUG-2003 Summary: Angiogenesis, or new blood vessel growth, is an important process in conditions such as atherosclerosis, tumor growth, and rheumatoid arthritis (RA). We have shown previously that interleukin-8 is a potent macrophage-derived mediator of angiogenesis (Koch, et al, Science 258: 1798, 1992). We have also shown that soluble endothelial cell adhesion molecules soluble E-selectin (sE-selectin), and soluble vascular cell adhesion molecule-1 can function in a manner similar to cytokines in inducing

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angiogenesis (Koch, et al, Nature 376:517, 1995). We demonstrated that the mechanism by which sE-selectin mediates angiogenesis is via its endothelial ligand sialyl-Lewis (sialyl-Lex). Currently, we focus on a novel endothelial (EC) molecule, 4A11, detected by monoclonal antibody (mAb) 4A11 produced in our laboratory. This antigen is virtually endothelial-specific, as well as endothelial selective, being expressed mainly on EC in normal synovium, lymphoid tissues, thymus, and skin, suggesting a possible role in cell homing to these areas. The 4A11 antigen is cytokine-inducible in vitro and is upregulated in human RA synovial tissue lining affected joints and in a human poison ivy model of contact dermatitis. Moreover, the antigen detected by monoclonal antibody 4A11 is contained in both Lewisy-6 (Ley) and H-5-2 (H-2). Ley is within the new family of carbohydrates which includes sialyl-Lex, the sE-selectin ligand through which the sE- selectin mediates angiogenesis. We have recently found that the soluble 4A11 antigen mediates angiogenesis. The aim of this proposal is to determine the mechanism by which the 4A11 antigen mediates angiogenesis and participates in cell adhesion, and the role of the 4A11 antigen in disease. We propose to confirm the angiogenic activity of the 4A11 antigen using in vitro and in vivo angiogenesis assays. We will determine whether the 4A11 antigen mediates upregulation of EC adhesion molecules and EC or leukocyte adhesion. We will characterize the role of this antigen in disease. Since the synthesis of the 4A11 antigen is regulated by fucosyltransferases, we will examine whether a defect in angiogenesis occurs in "knockout" mice deficient in fucosyltransferase. We will determine whether these mice have decreased corneal angiogenesis, wound repair, expression of other angiogenic mediators, or angiogenic arthritic responses compared to parental controls. These studies should broaden our understanding of the mode of action of this novel angiogenic mediator which may increase our ability to curb angiogenesis in conditions characterized by persistent neovascularization. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NOVEL MICROARRAY SYSTEM FOR IN VITRO ALLERGEN TESTING Principal Investigator & Institution: Olejnik, Jerzy; Director of Research; Ambergen, Inc. 1106 Commonwealth Ave Boston, Ma 02215 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 30-JUN-2005 Summary: (provided by applicant): Fifty million Americans suffer from allergic diseases including asthma, rhinitis, sinusitis, dermatitis and food allergy. Allergies constitute the 6th leading cause of chronic disease and involve at least $20 billion in annual health care costs. For type I allergy, which manifests itself by elevated levels of IgE in the serum, there is a growing need for in vitro immunoassays capable of rapidly quantifying allergen-specific IgEs for the over 300 most common allergens using a single drop of blood. Such a testing modality could significantly improve the efficiency of allergy diagnosis by providing the clinician with data to design a patient-specific, cost effective program of symptom management and therapy. One promising candidate is an allergen microarray system. However, current microarray technology is not sufficiently developed to meet the rigorous demands of clinical diagnostics in terms of low cost, reliability and automation. During Phase I, AmberGen in collaboration with Clinical MicroArrays (CMA), a subcontractor on this project, plans to develop and evaluate an integrated microarray system for simultaneous in vitro measurements of hundreds of allergen-specific IgEs. This integrated system will be based on innovations in several areas of microarray technology including array substrates, method for allergen immobilization, array immunoassays and fluorescent readout. Ultra-low fluorescence

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array substrates will be produced and evaluated which will be based on polystyrene and nitrocellulose thin films. Novel methods of allergen attachment through covalent bonding to surfaces and by directed binding using biotin-streptavidin bridges will be evaluated. A microarray reader which features high sensitivity evanescent wave detection technology will be evaluated. The integrated system including cassette processing of disposable microarrays will be low-cost and highly automated. Dr. Lynda Schneider, an expert in the field of pediatric in vitro allergy diagnostics and Director of the Allergy/Clinical immunology Program at Boston Children's Hospital and Dr. Helen Hollingsworth, an expert in adult allergies and Director of the allergy unit at Boston University Medical Center will serve as consultants. During Phase II, a complete integrated system including a scanner and array processor, along with a prototype microarray containing several hundred antigens will be developed and evaluated in a clinical setting. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: OCCUPATIONAL PROCESSING

ASTHMA

ASOCIATED

WITH

SEAFOOD

Principal Investigator & Institution: Robins, Thomas G.; Associate Professor; Environmental Health Sciences; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 29-SEP-2003 Summary: This study proposes to explore the associations between occupational exposure to lobster and saltwater bony fish (pilchard, Cape anchovy, mackerel, light fish, redeye, Cape horse mackerel, lantern fish) and health outcomes expected to be mediated through an immunologic IgE mechanism. The research proposes to investigate occupational asthma and other allergic conditions associated with rock lobster and saltwater bony fish processing in South Africa. Ingestion related seafood allergy is a common problem in the general population. Allergic reactions most often related to inhalation of antigens have been increasingly recognized as a serious problem among seafood workers. The predictors of occupational sensitization and health outcomes associated with lobster and bony fish processing are not well understood.Exposureresponse relationships for occupational seafood allergy have been best characterized for exposure to a few crustaceans notably crab species. No published studies have examined this problem among workers exposed to crustaceans and bony fish common in the South Atlantic. A cross-sectional study is proposed to characterize the occupational environmental exposure of workers in a factory on the West Coast of South Africa, involved in the processing of rock lobster and saltwater bony fish (pilchard, Cape anchovy, mackerel, light fish, redeye, Cape horse mackerel, lantern fish) through measurement of total protein and specific allergen collected by air sampling. A second aim is to determine the prevalence of allergic sensitization and health outcomes (rhinoconjunctivitis, urticaria/dermatitis and asthma) due to processing of rock lobster and saltwater bony fish through subject interviews, physical examination (skin), spirometry and methacholine challenge tests, skin prick tests (for common aeroallergens and specific seafood allergens) and skin patch testing. The third major aim is to characterize the relationship between exposure (measured as ambient concentrations of total protein and specific RAST inhibition), allergic responses to lobster and bony-fish allergens, and lung function changes. Statistical modeling will be used to identify the risk factors associated with the development of seafood allergy among seafood processing workers. Another aim is to isolate and characterize the seafood antigens present in aerosols generated during the processing of West Coast rock lobster and saltwater bony fish. The

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final aim is to investigate the extent to which any exposure response relationships are attenuated by the transfer of symptomatic workers from high to low exposure jobs. The development and application of state of the art techniques to address the specific aims is proposed. Potential public health benefits of this study would be the development of appropriate industrial hygiene monitoring techniques and medical surveillance protocols for monitoring the health of workers exposed to seafood allergens. By characterizing the occupational exposures among these high risk working populations. This study will also contribute towards a better understanding of the antigenic mechanisms causing seafood allergy among symptomatic individuals in the general population of the Western Cape province of South Africa and internationally. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: OPIOID-INDUCED IMMUNE ALTERATIONS: SEX DIFFERENCES Principal Investigator & Institution: Lysle, Donald T.; Professor; Psychology; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2003; Project Start 01-FEB-2003; Project End 31-DEC-2006 Summary: (provided by applicant): Recent research has produced a wealth of information on the immunomodulatory effects of opioids, but little is known about how the sex of the individual impacts opioid-induced immunomodulation. Given the widespread clinical use of opioids and their high abuse potential, an understanding of the interaction of sex with opioid-induced immune alterations is critical. Specific Aim I provides a pharmacological analysis of the effects of morphine on the contact hypersensitivity (CHS) response in males and females, with an emphasis on clinical outcome measures (i.e., swelling), as well as the immunological and receptor mechanisms that mediate these effects. Our initial findings indicate that morphine enhances CHS in both males and females, but in females, morphine is more than twice as potent, has a greater maximal effect, and the effects persist for a longer period of time. The proposed studies will determine the specific immune mechanisms that account for these dramatic sex differences by evaluating the role of immunologic mediators at the site of CHS, including IL-1-beta, TNF-alpha, IFN-gamma, IL-4, IL-6, IL-10, and nitric oxide expression. Studies will also test hypotheses that morphine activates different central and peripheral opioid receptor types in males and females. Specific Aim II will determine if the gonadal (or sex) hormones mediate sex differences in morphineinduced alterations of contact hypersensitivity (CHS). Given the ample evidence that gonadal hormones contribute to observed sex differences in both immune function and opioid sensitivity, depleting these hormones represents a logical and critical first step in the analysis of the hormonal mechanisms underlying the profound sex differences in opioid-induced immunomodulation. The proposed studies test if gonadal hormone depletion in males and females impacts morphine-induced alterations of CHS and the specific immunologic mediators of this sexually differentiated response. Specific Aim III determines the generality of sex differences across clinically relevant opioids, and whether the magnitude of the sex differences is related to the relative efficacy (i.e., ability to stimulate the mu opioid receptor) of the opioid. Our plan is to evaluate sex differences in opioid-immunomodulation with a series of clinically important opioids that differ along a continuum of efficacy. Our hypothesis is that the sex differences will be apparent with opioids other than morphine, and that the magnitude of the sexrelated differences will be inversely related to their ability to stimulate the mu opioid receptor. Given that virtually nothing is known about how the sex of the individual interacts with the immunomodulatory actions of opioids, the proposed studies are the first to advance our understanding of the regulatory role of sex in opioid-induced

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immunomodulation. These studies have clinical importance and will influence the selection of opioids for patient care, as well as enhance our understanding of potential sex differences in the adverse consequences of opioid use and abuse. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ORAL PATHOGENS AND DENDRITIC CELL SUBSETS Principal Investigator & Institution: Cutler, Christopher W.; Associate Professor; Periodontics; State University New York Stony Brook Stony Brook, Ny 11794 Timing: Fiscal Year 2001; Project Start 01-FEB-2001; Project End 30-NOV-2005 Summary: (Adapted from the Investigator's Abstract): The Principal Investigator has proposed a novel overall hypothesis and approach to understanding the pathophysiology of adult periodontitis (AP), one of the most common of diseases that afflict the US population. While mortality of the dentition is the most familiar outcome of AP, its links with other more severe diseases, including coronary artery disease, respiratory diseases and pre-term labor cannot be ignored. These investigators have called attention to the many intriguing parallels between AP and contact hypersensitivity (CHS). CHS is among the most common of dermatoses that afflicts mankind and one of the most intensively studied of in vivo immune responses. Both AP and CHS target the host integument (gingiva or skin) and appear to involve the activation and sensitization of similar subsets of antigen capture and presenting cells, the dendritic cells. Dendritic cells have been termed "Nature's adjuvant," being more efficient at antigen-presentation than macrophages or B cells and the only antigenpresenting cells (APCs) than can stimulate naive T cells to proliferate. This immunostimulatory capacity can also have detrimental effects for the host, as typified by contact hypersensitivity (CHS) responses. Both AP and CHS involve a predominantly destructive T cell response mediated by both regulatory and effector T cells. These investigators have shown that Porphyromonas gingivalis is a unique pathogen in this regard, able to infect, sensitize, and activate dendritic cells in vitro and likely, in situ. Many questions about the role of P. gingivalis-sensitized dendritic cells in AP, however, remain unanswered. The present proposal will definitively establish, using in situ, ex vivo and in vitro approaches, the role of dendritic cells in adult periodontitis, particularly that induced by P. gingivalis. Moreover, these studies will characterize the interactions of P. gingivalis with dendritic cells and will further our knowledge of the pathophysiology of AP as it relates to CHS. Future studies, outside the purview of this proposal, will involve understanding the T cell response to P. gingivalis-activated dendritic cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ORTHOPOX IMMUNIZATION IN PATIENTS WITH CANCER OR ECZEMA Principal Investigator & Institution: Reinherz, Ellis L.; Chief; Dana-Farber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-MAR-2008 Summary: (provided by applicant): While worldwide eradication of smallpox represents a major accomplishment of medicine in the 20th century, use of this virus as a bioterrorism agent against our largely disease-susceptible civilian population could result in unprecedented mortality. Individuals at risk for live-virus vaccine complications, including those with cancer and eczema, comprise a large percentage of the US population, mandating against massive large-scale vaccination. Recent

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developments in immunology, both with regard to mechanistic understanding of adaptive and innate immune responses now allow for evaluation of the cellular and humoral bases of protective immunity against orthopox and other classes of viruses. These advances include details of immune recognition at a structural level, antigen presentation, cell migration and T cell memory. Here, four groups of investigators will utilize their considerable talents in vaccinology, virology, immunology, cutaneous biology, structure and bioinformatics to identify critical orthopox epitopes affording protective human immunity. Project 1 will examine protective immunity to vaccinia virus in normal and high-risk patients elicited during virus vaccination trials based on parameters identified in Project 2. Project 2 will identify T cell epitopes shared by vaccinia, MVA and smallpox by genome-wide comparison using bioinformatics and position-specific scoring matrices, and confirmed by T cell functional assays and mass spectrometry. Antigen-specific T memory cells elicited through vaccination will be assessed by pMHC tetramers, conventional and new biomarkers of T cell memory and molecularly detailed T cell memory repertoires as examined by single cell PCR at different times post-vaccination. Likewise, targets and biophysical parameters of human neutralizing antibodies to vaccinia and variola, the latter in conjunction with CDC, will be identified using recombinant orthopox proteins, BIAcore, ELISA and neutralization studies. In Project 3, investigators from the Harvard Skin Disease Research Center will examine human skin elements of orthopox vaccinated normals or atopic dermatitis patients for productive viral infection, and compare and contrast the nature of central memory and skin homing effector T cells therein. Murine models using biologic response modifiers and transgenic mice will be exploited to examine how manipulation of the cutaneous environment alters vaccination efficacy. Project 4 will use contemporary molecular genetics to mutate vaccinia virus-Wyeth strain to lower virulence by deleting immune escape functions but maintaining host range, replication and immunogenicity. Pathogenicity and immunogenicity assessment will be in C57BL/6, transgenic or mutant mice using systematic, mucosal and dermal scarification infectious routes. An Educational Component, Pilot Project Component and Research Resource Technical Development Component are proposed for rapid dissemination of methods and reagents resulting from this Center's effort. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: OUPATIONAL SURVEILLANCE MODULES FOR PREVENTION Principal Investigator & Institution: Bonauto, David; Washington State Dept Lab/Indust of Labor and Industries Olympia, Wa 98504 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 30-JUN-2005 Summary: Through surveillance of several National Occupational Research Agenda (NORA), Healthy People, and Washington State Department of Labor and Industries priority conditions including occupational asthma (OA), adult lead poisoning, musculoskeletal disorders of the upper extremity, low back disorders, dermatitis, hospitalized burns, traumatic head and brain injuries (THBI) as well as assaults, the Safety and Health Assessment and Research for Prevention (SHARP) program will demonstrate the application of a comprehensive, occupational surveillance program. Through demonstration of the proposed surveillance program, SHARP will create a systematic model for adoption by other states. To allow for adaptability, SHARP proposes development of a modular approach which demonstrates several approaches to outcome based surveillance, hazard based surveillance, and subsequent prevention activities. The proposed project will address the following aims: 1) Conduct a survey of state based occupational surveillance programs to determine currently employed

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approaches to surveillance and prevention, program capabilities, and program opinion leaders. 2) Demonstrate a modular approach to occupational surveillance. This modular approach should encompass the use of different data sources for priority conditions selected by an individual program. 3) Develop modules for the creation, dissemination, and evaluation of prevention efforts. 4) Conduct an employer/employee survey to further identify etiologic agents or practices in one identified industry. 5) Develop an Internet based library of surveillance modules and prevention materials. 6) Produce and disseminate three surveillance reports for WA State priority conditions per year. 7) Produce and disseminate two prevention reports to employers or employees per year. Through the proposed project, SHARP will demonstrate the utilization of several data sources for the surveillance of occupational diseases and hazards. Further, SHARP will demonstrate the analysis of such data, the creation of simple public health interventions using surveillance data, the implementation of interventions, and the evaluation of interventions using surveillance data. Finally, SHARP will produce a web accessible library of materials detailing the methodology of the various components of the surveillance program including prevention materials that may be modified and disseminated in other states. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PARALLEL ASSAYS FOR ANTI-RO PEPTIDE DIAGNOSTICS Principal Investigator & Institution: Harley, John B.; Professor; Jk Autoimmunity, Inc. 800 Research Pky, Ste 100 Oklahoma City, Ok 73104 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 30-JUN-2004 Summary: (provided by the applicant): Diagnosis of rheumatic diseases is inefficient, time consuming, and frustrating. Indeed, many patients suffer unnecessarily. We wish to develop a parallel assay system for the serology of autoimmune rheumatic diseases involving multiple analytes (on the order of 1,500 per assay performed) by concentrating upon the anti-Ro autoantibody system. Anti-Ro is associated with systemic lupus erythematosus, Sjogren's syndrome, subacute acute cutaneous lupus, congenital complete heart block, and neonatal lupus dermatitis. In addition, up to 1% of the adult female population has developed these autoantibodies. Anti-Ro autoantibodies are clearly very important. The details of the fine specificity of anti-Ro have great potential to provide information that can help provide diagnostic insight, prognostic evaluation, and assess disease risk. This project has three goals. First, we will adapt anti-Ro detection to a new technology. Second, we will attempt to reproduce our previous data with the new technology. Third, we will exploit the efficiencies of the new technology to much more completely define anti-Ro fine specificity and to use the aggregate data to design useful new products. We will adapt existing technology to detect antibodies against the particular epitopes of Ro, using fiber optic microspheres in parallel array. Compared to currently employed methods, this technology will allow as much as a 1,000-fold increase in throughput, a 1,500-fold decrease in reagents and serum required for assay, and a 500-fold decrease in per analyte cost. Preliminary data have identified a putative initial epitope in the anti-Ro autoimmune response and show a close immunologic relationship to a possible etiologic agent. We will explore the advantages of this technology to reveal the relationships between peptide-defined epitopes of Ro and putative precursor antigens, the progression of the autoimmune response, and the disorders associated with anti-Ro with the hope of developing commercially useful new diagnostics, in addition to the obvious research opportunities that understanding these relationships would offer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: PI3KC2 BETA IN CA2+ SIGNALING VIA SPHINGOSINE KINASE Principal Investigator & Institution: Choi, Oksoon H.; Biochemistry; Meharry Medical College 1005-D B Todd Blvd Nashville, Tn 37208 Timing: Fiscal Year 2002; Project Start 05-FEB-2002; Project End 31-JAN-2006 Summary: Stimulation of mast cells via the high affinity receptor for IgE (FcepsilonRI) leads to the release of inflammatory mediators that are responsible for allergic inflammatory diseases, such as asthma and allergic dermatitis. The release of inflammatory mediators is dependent on the increase in cytosolic free Ca2+ ([Ca2+]i), which is initiated by the mobilization of Ca2+ from the endoplasmic reticulum and followed by influx of Ca2+ from outside of the cell. It is generally believed that inositol 1,4,5-trisphosphate (IP3) is responsible for mobilizing Ca2+ from the intracellular stores. However, we have shown that FcepsilonRI-mediated production of IP3 is not sufficient to account for the increase in [Ca2+]i. This suggests an alternative mechanism for Ca2+ mobilization via sphingosine 1- phosphate, a product of sphingosine kinase. Furthermore, the increase in sphingosine 1-phosphate production and Ca2+ mobilization has been observed in an antigen-stimulated mast cell line, RBL-2H3 cells that has been overexpressed with the beta isoform of Class II phosphoinositide 3-kinase (PI3KC2beta). Our long-range goal is to understand the mechanisms underlying [Ca2+]i increase in mast cells. The objective of this particular application is to understand the role of Class II PI3K in sphingosine kinase activation and Ca2+ mobilization. The central hypothesis for the proposed research is that activation of a Class II PI3K via FcepsilonRI increases production of sphingosine 1-phosphate, which causes Ca2+ mobilization in conjunction with IP3 in RBL-2H3 Cells. We formulated this hypothesis based on strong preliminary findings, which demonstrate that overexpression of PI3KC2beta increases FcepsilonRI-mediated production of sphingosine 1-phosphate and Ca2+ mobilization. In addition, increased production of sphingosine 1-phosphate leads to increased mobilization of Ca2+ only in the presence of IP3. The rationale for the proposed research is that, once the alternative pathway of Ca2+ mobilization is elucidated, it can be targeted as a new approach to treat allergic inflammatory diseases. The central hypothesis will be tested by pursuing three specific aims: 1) Identify initiating biochemical events for FcepsilonRI-mediated Ca2+ mobilization. 2) Identify intermediate signaling molecule(s) in the alternative pathway for FcepsilonRI-mediated Ca2+ mobilization. 3) Determine how FcepsilonRI-mediated Ca2+ mobilization is regulated by sphingosine kinase and phospholipase C pathways in RBL-2H3 cells. It is our expectation that the resultant approach will delineate an alternative Ca2+ signaling pathway that involves the activation of PI3KC2beta, sphingosine kinase and phospholipase C. The research proposed in this application is significant, because the outcomes are expected to provide new targets for therapeutic interventions for the prevention and treatment of allergic inflammatory diseases. In addition, they are expected to offer a better fundamental understanding of how Ca2+ is mobilized in mast cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: PILOT--INTRINSIC PROPERITES PRECURSORS IN ATOPIC DERMATITIS

OF

LANGERHANS

CELL

Principal Investigator & Institution: Gruchalla, Rebecca S.; Assistant Professor; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2002; Project Start 01-JUN-2002; Project End 31-MAY-2006

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Summary: The development of atopic dermatitis (AD), a common chronic inflammatory skin diseases, is thought to be influenced by both environmental factors (allergens) and by genetic factors that control immunological responsiveness to the relevant allergens. Because of their remarkable ability to initiate and regulate cutaneous immune responses, epidermal Langerhans cells (LC), the principal antigen presenting cells (APC) in skin, are thought to play a pivotal role in both the induction and amplification of the inflammation in AD. Moreover, recent evidence show that LC from AD skin differ, both phenotypically and functionally, from those isolated from the skin of normal individuals. These differences may exist at the level of LC precursors as well, since LClike DC precursor CD14+ cells of AD patients are phenotypically and functionally different from LC-like DC generated from counterpart precursors of healthy individuals. The goal of this pilot and feasibility (P&F) study is to characterize the intrinsic properties of LC precursors that govern their differentiation towards the abnormal phenotype characteristic of that seen in patients with AD. The proposed studies are related to, but nonetheless a distinct departure from the PI's previous research focus. The specific aims are: Aim 1. To determine whether phenotypic abnormalities exist at the level of DD14+ LC precursors in AD. Aim 2. To determine whether genetic polymorphisms reported for AD are present in CD14+ LC precursors of AD patients. Aim 3. To determine whether CD14+ precursors from AD patients vs. normal controls are differentially regulated by specific cytokines. Aim 4. To examine whether drugs used for treatment of AD modulate properties of LC CD14+ precursors. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PILOT--LASER ASSISTED THROUGH STRATUM CORNEUM

PENETRATION

OF

ALLERGENS

Principal Investigator & Institution: Nedorost, Susan T.; 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: Clinical diagnosis of allergic contact dermatitis has historically utilized patch testing. This involves applying suspected allergens to the intact skin of a patient's back for 48 hours under occlusion with tape, and then observing the back at intervals for one week after application. Patch testing has good sensitivity and specificity, but there are a number of difficulties with this testing modality. Many patients find it inconvenient or impossible to keep their backs dry for the week-long testing procedure; this is especially difficult for patients whose occupation involves manual labor or those who live in a humid climate. Children find it particularly difficult to tolerate patches on the back due to their high activity levels, and, in young children, the temptation to prematurely remove the patches due to mild itching. Atopy patch testing has been utilized to study allergy to proteins such as dust mite in atopic patients. These proteins are larger molecules that poorly penetrate intact stratum corneum; but may be very relevant to patients with atopic dermatitis who often have non-intact skin barrier due to scratching. Technology that would allow allergens to move through the stratum corneum without prolonged occlusion are desirable. Removal of the stratum corneum with a laser prior to application of test allergens could preclude the need for tape occlusion of the test sites, thus avoiding many of the logistical problems with the current testing methods. Use of the laser may also allow a standardized way to facilitate introduction of protein allergens for atopy patch testing. The purpose of this study is to investigate the utility, safety, and patient satisfaction of laser assisted penetration of allergens in the investigation of contact dermatitis and atopic dermatitis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: PLATELET ACTIVATING FACTOR IN KERATINOCYTE FUNCTION Principal Investigator & Institution: Travers, Jeffrey B.; Associate Professor & Chair; Dermatology; Indiana Univ-Purdue Univ at Indianapolis 620 Union Drive, Room 618 Indianapolis, in 462025167 Timing: Fiscal Year 2001; Project Start 01-JUL-1997; Project End 30-JUN-2002 Summary: Platelet-activating factor(PAF) is a phospholipid-derived mediator which has been implicated in cutaneous inflammation, thus antagonists of PAF could form the basis of novel antiinflammatory treatments. My previous studies have demonstrated that keratinocytes both synthesize and express functional receptors for PAF. This project tests the hypothesis that PAF has proinflammatory effects on keratinocytes through two separate lines of investigation which will be conducted concurrently. First, an in vivo murine model system will be developed to evaluate: 1) the epicutaneous effects of specific PAF receptor (PAF-R) agonists and antagonists; 2) the potential antiinflammatory effects of potent PAF-R antagonists on experimentally-induced dermatitis. Second, an in vitro model system of the PAF-R will be developed through retroviral-mediated gene transfer of both the wild-type and truncated mutant PAF-R (which does not undergo homologous desensitization) into the PAF-R-negative epidermoid cell line KB. This PAF-R model system will allow characterization of the morphological and functional effects of the PAF-R in epidermal cells. These two separate lines of investigation will provide both information as well as tools for future studies to dissects the role of PAR in the complex cytokine network found in the skin, information which could be translated into novel therapeutic strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: PRE-CLINICAL STUDIES ON LUPINUS TERMIS SEEDS EXTRACT Principal Investigator & Institution: Antoun, Mikhail D.; Professor and Faculty Chairperson; Pharmaceutical Sciences; University of Puerto Rico Med Sciences Medical Sciences Campus San Juan, Pr 00936 Timing: Fiscal Year 2002; Project Start 15-FEB-2002; Project End 30-NOV-2003 Summary: (provided by applicant): Atopic dermatitis is a skin condition that affects an estimated 10-20 percent of the population. Aside from Protopic (tacrolimus) ointment, which has been recently approved by the FDA, the main treatment for the past 40 years has been steroids. This proposal is intended to carry out preliminary pharmacologytoxicology studies on an alcoholic extract obtained form the seeds of a plant which, in earlier clinical studies performed outside the US, demonstrated encouraging activity in the management of chronic hand and foot eczema. The results that will be obtained will be used to develop a future R01 grant application that will include a phase II clinical trial to evaluate the extract in the treatment of chronic atopic dermatitis. The studies are intended to 1) assure the quality of the imported seeds, by analyzing different crops obtained from the source country, over a period of two years; 2) develop a standardized reproducible method for the preparation of the extract; 3) determine the stability of the ointments prepared from the extract; 4) carry out a repeat-dose toxicology study of the ointments, for nine months, in pigs; 5) carry out a systemic exposure of rats to the active components of the extract, for 90 days, by oral administration; 6) perform a battery of genetic toxicology studies, and 7) investigate whether the extract and ointment preparations have the potential to induce sensitization. The source material is a commercial cash crop. Experimental procedures approved by the U.S. Pharmacopeia/National Formulary, or well-established published protocols will be used in the quality assurance studies. The animals will be housed in the Animal

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Resources Center of the Medical Sciences Campus of the University of Puerto Rico, throughout the period of the study, under the care of the facility's veterinarian. This facility is accredited by the American Association for the Accreditation of Laboratory Animal Care (AAALAC International) Developing a new herbal treatment for chronic atopic dermatitis will benefit patients who are at risk or who have developed resistance to other therapies, including Protopic. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: VULVODYNIA

PREVALENCE

AND

ETIOLOGICAL

PREDICTORS

OF

Principal Investigator & Institution: Harlow, Bernard L.; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 29-SEP-2000; Project End 31-AUG-2005 Summary: (Adapted from the applicant's description): Vulvodynia is a syndrome of unexplained vulvar itching, burning, and/or pain that causes major physical and psychological distress. It is a diagnosis of exclusion when vulvar discomfort becomes chronic over many months and the presence of any other remediable cause, such as infection or dermatitis, is ruled out. The two major subtypes of vulvodynia -generalized vulvar dysesthesia and vestibulodynia -- are often misclassified. Few descriptive or etiologic epidemiological studies have been performed. Thus, the prevalence and incidence in the general population is unknown and no preventable exposures have been identified. A recent NIH sponsored consensus conference stressed the need to determine the prevalence of vulvodynia and conduct population-based observational studies to identify modifiable risk factors. The applicant has conducted a population-based prevalence survey in more than 400 women that achieved a 70% response rate and found that 18% of women reported a lifetime history of chronic vulvar symptoms that lasted three months or longer. Approximately 8% of all women surveyed were currently experiencing these symptoms. In addition, the applicant conducted a pilot case-control study of 31 women diagnosed with either dysesthetic vulvodynia or vestibulodynia, or a combination of the two within the last five years and compared them to 31 similarly aged healthy women identified from the general population. Cases were, on average, three times more likely to report medical treatments or surgical procedures for conditions that may have influenced perineal pain, or a greater frequency of condom use and use of talcum powder in the genital area that may have lead to mucosal abrasion and inflammation. The applicant now proposes to survey 16,000 women 20-59 years of age from the general population to estimate the agespecific prevalence of vulvodynia. From this sample, the applicant will identify 400 cases of vulvodynia, verified through a two-step screening process, and a sample of 400 frequency matched age and county of residence controls. Structured interviews will assess a wide spectrum of exposures related to trauma. A subsample of 80 cases and 80 controls will receive a clinical examination to confirm the presence or absense of vulvodynia, and also will provide a vaginal lavage and vulvar swab specimen for the assessment of cytokines and the culturing of microbiological organisms. The applicant hypothesizes that various types of vulvar trauma may precede the spontaneous and evoked vulvar pain experienced by women with vulvodynia and that vulvodynia may be a variant of a specific type of Complex Regional Pain Syndrome that is consistent with sensory disturbances such as mechanical allodynia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: PRODERMX: TOPICAL PROTECTOR AGAINST RADIATION DERMATITIS Principal Investigator & Institution: Fahl, William E.; Professor; Procertus Biopharm, Inc. 2800 S Fish Hatchery Rd Madison, Wi 53711 Timing: Fiscal Year 2003; Project Start 13-AUG-2003; Project End 31-JUL-2004 Summary: (provided by applicant): Several recent clinical studies have described the side effect of radiation-induced dermatitis that occurs in the majority of cancer patients who receive radiotherapy. These same studies also report the lack of effective agents to prevent or treat this dermatitis. In some of these patients, the side effects are severe enough that they withdraw from further radiotherapy. Nonetheless, radiotherapy remains a standard and essential part of cancer treatment and cure. ProCertus has developed a topically applied treatment to diminish or eliminate the dermatitis associated with radiotherapy. In current animal proof of concept studies, ProCertus has shown a >90% reduction in radiation-induced dermatitis by pretreating animals with ProDermX, which is currently a research stage human pharmaceutical. This technology consists of a carrier vehicle that delivers a single active agent to the stem cells of the epidermis. The active agent, a proprietary "chemoprotective polyamine," physically protects cellular DNA while also inducing a G1 phase, cell cycle block. This strategy enables the stem cells within the stratum germinativum of the epidermis to survive the radiation exposure, and to continue to replenish the outer layers of the skin and thus maintain a patent skin surface. Though ProCertus scientists have already carried this product through animal model proof of concept, there remain several biological and pharmacological questions that need to be answered before human studies can be initiated. Three Specific Aims have been designed to address and answer these questions during the course of this Phase I SBIR project, which will then enable initial studies in human populations in future research. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: RECONSTRUCTION LANGERHANS CELLS

OF

SKIN

MODEL

CONTAINING

Principal Investigator & Institution: Ayehunie, Seyoum; Mattek Corporation 200 Homer Ave Ashland, Ma 01721 Timing: Fiscal Year 2002; Project Start 30-SEP-1997; Project End 31-AUG-2004 Summary: (provided by applicant): Phase I research demonstrated that a Langerhans cell (LC) containing model of the epidermis is feasible. LC progenitor cells were harvested from peripheral or cord blood samples, cryopreserved, and matured using cytokines into the LC specific CD1a+ phenotype. By modifying the extracellular matrix substrate, these cells were successfully incorporated into a highly differentiated, serumfree epidermal model, albeit at a lower density than in native epidermis. The LC derived from cord blood maintained their dendntic, CD1a+ HLA-DR+/- phenotype and expressed Birbeck granules within the cultures. The exposure of 2 contact allergens resulted in the release of TNF-a and IL-lb. 2 cytokines known to be critically involved in the initial stages of allergic contact dermatitis (ACD). Exposure to the common irritant, on the other hand, did not result in TNF-a or IL- lb release. In addition, following exposure to UV irradiation, immuno-staining showed that LC were migrating out of the tissue, as is known to occur in vivo.Phase II studies will expand on the Phase I results to further develop an epidermal model containing immunologically competent cells. Initial research will focus on the optimization of culture conditions to improve LC incorporation into the tissue model. The effects of allergens on cytokine release and gene

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expression will be investigated. Experiments designed to model LC migration from skin following exposure to allergens or UV light and subsequent T-cell activation will be performed to determine the degree to which the model's behavior corresponds to in vivo ACD reactions. Finally, based on these studies, an assay kit to predict whether a material is likely to act as a contact allergen will be developed. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: REGULATION OF CUTANEOUS INFLAMMATION BY LOCAL GD T CELLS Principal Investigator & Institution: Tigelaar, Robert E.; Professor; Dermatology; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-JUL-2008 Summary: (provided by applicant): In species as diverse as chickens, mice, and humans, substantial numbers of T cells are constitutively associated with body surface epithelia, such as the gut, genitourinary tract, and the skin. Such intraepithelial lymphocytes (IELs) are commonly enriched in T cell receptor (TCR)gamma/delta+ cells, frequently with limited tissue associated antigen receptor diversity; thus, most IELs in mouse skin, also known as dendritic epidermal T cells (DETC), express strikingly homogeneous Vgamma5/Vdelta1 TCRs notable for their lack of junctional (CDR3 region) diversity. Combined use of different strains of TCRd-/- (knockout) mice and selective reconstitution of such mice via adoptive transfer has shown that Vgamma5+ DETC, but not other gamma/delta cells, are potent down-regulators of several physiologically relevant, cutaneous inflammatory responses, including a localized, geneticallydependent, TCRalpha/beta+ T cell-dependent environmentally-dependent, chronic dermatitis that shares several features of human atopic dermatitis. The long-term goal of this project is to utilize this powerful experimental model to define the mechanisms by which local T cells regulate the effects of systemic immune responses within local tissues. The specific aims of this project are: 1. To characterize in detail the cutaneous inflammation normally down-regulated by DETC) using: a) immunohistology, ex vivo flow cytometry, and microarray analysis; b) phenotypic comparisons of susceptible delta-/- mice with delta-/- mice also deficient in selected pro-inflammatory cells and/or molecules by virtue either of treatment with cytokine antagonists or blocking antibodies, or of a second "knockout" genetic mutation 2. To characterize the genes expressed by "resting" DETC and DETC "activated" in vitro by serial analysis of gene expression (SAGE), validate such analyses by quantitative RT-PCR of DETC in various in vivo and in vitro activation states, and compare such gene expression patterns with those both of gut-associated gamma/delta+ and alpha/beta+ IELs, and of systemic CD8+ alpha/beta+ "naive" and "memory" T cells. 3. To investigate selected candidate DETC anti-inflammatory cytokines/effector molecules by reconstituting delta-/- recipients with fetal thymic DETC precursors rendered deficient in candidate anti-inflammatory molecules. 4. To utilize genome-wide microsatellite mapping to identify the genetic interval(s) controlling susceptibility/resistance to the spontaneous dermatitis that develops in some, but not other d-/- mice, followed by additional studies (development of congenic lines, differential expression analyses of genes contained within this interval) directed at definitive identification of the gene(s) that regulate cutaneous inflammation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: SCOR IN CELLULAR AND MOLECULAR MECHANISMS OF ASTHMA Principal Investigator & Institution: Martinez, Fernando D.; Professor of Pediatrics; Pediatrics; University of Arizona P O Box 3308 Tucson, Az 857223308 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 31-AUG-2006 Summary: (Applicant's Abstract) Most cases of asthma begin during the first years of life. This suggests that a significant proportion of the risk for the development of asthma can be attributed to complex gene by environment interactions occurring during these early years. Understanding the developmental alterations of the immune system in early life that are associated with the subsequent development of asthma, is essential to designing a strategy for primary and secondary prevention of the disease. In this SCOR proposal we will integrate molecular, immunologic, genetic, genomic, and epidemiologic approaches to study the immune, genetic, and environmental interactions that occur at the beginning of asthma. In Project 1 we explore the gene by environment interactions that may be involved in the apparent protective effect of an increased microbial burden in early life on the development of early allergic sensitization and asthma. A population sample of children living in rural areas of Europe and in whom exposure to indoor endotoxin has been assessed will be studied. Known or newly discovered polymorphisms in genes coding for the main components of the endotoxin response system will be assessed and related to endotoxin exposure and asthma-related outcomes. In Project 2, the genetic and immune factors that explain the strong and independent relation between atopic dermatitis (eczema) in early life and the subsequent development of asthma will be explored. It is well known that most children who will go on to develop asthma show Th2-deviated responses to local aeroallergens very early in life, but not all children who do show such responses develop the disease. Project 3 will explore the complex molecular mechanisms that determine if a Th2deviated response will result in the synthesis of IgG4, IgE or both in humans. Finally, we have recently described five new polymorphisms in the promoter region of the CD14 gene. We have shown that these polymorphisms are associated with total serum IgE levels in school children. Project 4 will explore the biology of novel proximal and distant regulatory elements of the CD14 gene and will thus provide new insights on the mechanisms by which the innate immune response may influence the susceptibility to early allergies and asthma. Our SCOR offers a unique opportunity to study in a comprehensive manner the way in which environmental factors and genetic background influence the maturation of the immune system during the initial phases of the asthma process. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: SEX DIFFERENCES IN OPIOID-INDUCED IMMUNOMODULATION Principal Investigator & Institution: Elliott, Jay C.; Psychology; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-AUG-2006 Summary: (provided by applicant): There is little extant data concerning how sex may modulate the magnitude of opioid-induced immunomodulation. The present proposal addresses this important issue by extending the recently-identified finding that morphine and other mu-opioids produce significantly greater enhancement in female than male rats, of contact hypersensitivity (CHS), a cutaneous form of delayed-type hypersensitivity. Specific Aim I tests the hypothesis that morphine administered prior to the challenge phase of CHS induces sexually dimorphic effects on key mediators of

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CHS, including cytokine expression and T-lymphocyte infiltration. To that end, animals will be sacrificed at selected times following antigen challenge and the extent of CD4( and CD8( T-lymphocyte infiltration will be quantified by immunohistochemistry. To assess which molecular mediators are differentially expressed in males and females, cytokine levels will be quantified by Real-Time RT-PCR. Specific Aim II tests the hypothesis that kappa and delta opioids also produce differential effects on CHS in males and females through their activity at CNS opioid receptors. This aim will employ intracranial cannulation, drug microinjection techniques, and receptor antagonism to address this important issue. Specific Aim III will assess the role of a putative key hormonal determinant of observed sex differences by determining the effect of estradiol replacement in ovariectomized female rats on morphine's modulation of the CHS response. Together, these investigations will provide novel data concerning mechanisms of sexually dimorphic modulation of the clinically-relevant CHS response by a range of opioid drugs. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: SIGNALING LEUKOCYTES

BY

CYTOPLASMIC

TYROSINE

KINASES

IN

Principal Investigator & Institution: Lowell, Clifford A.; Laboratory Medicine; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 30-JUN-2006 Summary: Cytoplasmic tyrosine kinases initiate intracellular signaling pathways that regulate myeloid leukocyte responses to inflammatory and infectious stimuli. We have studied the Src-family of tyrosine kinases using a panel of knockout mice that lack one or all Src-family members (Hck, Fgr, and Lyn) normally expressed in myeloid cells. Initial work has revealed that the primary functional role of these kinases is regulating the integrin signaling pathway leading to leukocyte adhesion and activation. Neutrophils lacking Hck and Fgr fail to undergo cell spreading, respiratory burst or granule exocytosis following plating on surfaces which crosslink beta2 or beta3 integrins. Similarly, macrophages from these mice manifest alterations in cytoskeletal structure, cell spreading and migration. This integrin signaling pathway involves the adapter protein c-Cbl and the lipid kinase PI-3 kinase. Using Syk-deficient leukocytes generated in bone marrow chimeras with syk-/- fetal liver cells, we have found that this kinase is also critically involved in leukocyte integrin signaling. Defects in myeloid cell function result in altered immune responses in knockout mice in vivo; hck-/- fgr-/mutants suffer reduced tissue damage during endotoxemia and blunted development of inflammatory disease when crossed with motheaten mice. To extend these studies, we propose to examine downstream molecules in the integrin signaling pathway using leukocytes from Src- family or Syk-deficient animals. We will focus on the Rho-family GTPases, which regulate actin cytoskeletal dynamics, using both biochemical and genetic approaches. Biochemical approaches will include direct study of the activation state of these GTPases (and their effectors) using binding or enzymatic assays. Genetic approaches will be carried out by transducing macrophages with retroviral vectors encoding signaling molecules that are predicted to rescue the adhesion/migration phenotype of hck-/- fgr-/- lyn-/- or syk-/- cells. Our goal is to compare and contrast the effects of Src-family versus Syk kinase deficiency on downstream signaling responses. We will study the effects of these mutations in vivo using a series of skin inflammation models, all performed in mixed chimeric mice to allow comparison of mutant and wild type leukocytes in the same animal. We will also test the hypothesis that the hematopoietic phenotype seen in lyn-/- mice may be secondary to impaired integrin-

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mediated adhesion of stem cells. These studies will expand our understanding of the roles of these kinases in hematopoietic cells and will validate whether Src-family or Syk kinases may be potential targets for therapeutics against inflammatory diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: SKIN DISEASES RESEARCH CORE CENTER Principal Investigator & Institution: Bergstresser, Paul R.; Professor and Chairman; Dermatology; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2001; Project Start 01-JUN-1997; Project End 31-MAY-2006 Summary: This application requests competitive renewal of the UT Southwestern SDRC. It is supported by a record of achievement over the past 4 years that includes: (1) 2-fold expansion in the number of research-funded, full- time faculty members in the Department of Dermatology; (2) parallel 2- fold rise in annual competitive funding of dermatology faculty members (from $1.4 to $2.8 M); (3) stable number of active members comprised of a new mix of basic scientists, clinical investigators, and technology experts (achieved in the face of passage of several previous members to the helm of prestigious facilities in other major institutions); (4) 2-fold increase in annual competitive funding for skin disease-related research by SDRC investigators (from $3.5 to $7.4 M); (5) highly successful Core Laboratory Program with 3 components graduating into self-sustained status (Patient Access and Data Management, Photobiology, and Protein Chemistry), 1 component expanded (Tissue Culture and Phenotype), and 3 new components created (Bioinformatics, Skin Engineering and Cutting-Edge Technology); (6) 36-fold return on investment in P&F Projects in just the first half of the current funding period (from $319,253 to $11,488,650); (7) outstanding record of training 28 research fellows (many of whom have become faculty members of academic departments in the U.S. and the world); (8) large number of high quality publications(at least 236 published or in press as a direct result of SDRC funding); (9) enrichment program that has brought distinguished scientists to provide seminars, and co-sponsored an international symposium on contact dermatitis; and (1) endowment that has supplemental SDRC funds, thus partially achieving self-sustenance and greater allocations for Core and P&F Programs, respectively. The SDRC has been the key force in advancing skin and skin disease- related research in the Dept. of NIH funding coupled with proceeds from private benefaction should consolidate the Center into an increasingly effective, fully-sustained unit of biomedical excellence. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: SKIN HOMING T CELLS--MOLECULAR CHARACTERIZATION OF CLA Principal Investigator & Institution: Kupper, Thomas S.; Professor and Chair; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 08-SEP-1997; Project End 31-AUG-2002 Summary: (Adapted from the applicant's abstract) - It has become clear that many chronic skin diseases characterized by cutaneous inflammation, such as psoriasis, cutaneous T cell lymphoma (CTCL), and atopic dermatitis are mediated by T cells. Furthermore, memory T lymphocytes bear cell surface molecules that permit them to home preferentially to various tissues, including skin. A subset of memory T cells bear a marker called cutaneous lymphocyte antigen (CLA) recognized by a unique monoclonal antibody HECA-452. CLA is found on T cells in cutaneous infiltrates in a wide variety of skin diseases including CTCL, psoriasis, atopic dermatitis, and graft versus host disease,

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but is not found on T cells that infiltrate other organs. In vitro, expression of CLA also correlates with binding of T cells to E selectin, perhaps the earliest requisite step in the extravasation of T cells through postcapillary venules walls into the dermis. Beyond the presence of a sLex-related tetrasaccharide structure recognized by HECA-452, the structure of CLA is completely obscure. The applicant has generated significant preliminary data that address the molecular identity of CLA; these data are made possible by the identification of culture conditions that allow for the generation of homogenous populations of CLA-positive T cells (as well as matched control CLAnegative T cells) and the analysis of their tethering and rolling properties in a flow chamber. Western analysis, using antibodies to PSGL-1 and HECA-452 antibody, indicate that both recognize similar, if not identical, antigens on CLA+ and E-selectinbinding T cells. The specific hypotheses that this grant proposal will test are as follows: (i) The protein core of CLA is similar, if not identical, to PSGL-1, a widely expressed leukocyte P-selectin ligand, and (ii) differential post-translational modification of PSGL1 by a specific alpha (1,3) fucosyltransferase, FucTVII, determines both the expression of the CLA/HECA-452 reactive epitope on T cells and their capacity to bind well to Eselectin. A related hypothesis is also adavanced: (iii) T cell expression of FucTVII is a central determinant of whether a T cell that undergoes the naive-to-memory transition becomes a CLA+ skin homing T cell. These hypotheses will be directly tested. If as indicated by preliminary data, FucTVII regulation defines T cell homing to skin, this enzyme and its substrates may represent important targets for drug discovery relevant to diseases such as CTCL, atopic dermatitis, and graft versus host disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: STRESS & ENHANCEMENT OF SKIN IMMUNITY: MOLECULAR MECHANI Principal Investigator & Institution: Dhabhar, Firdaus S.; Oral Biology; Ohio State University 1800 Cannon Dr, Rm 1210 Columbus, Oh 43210 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 31-MAY-2005 Summary: The overall goal of these studies is to elucidate the mechanisms mediating the recent finding that under certain conditions stress can enhance skin immunity. We initially reported that acute of short-duration stress induces a redistribution of immune cells from the blood to organs such as the skin. Since the skin is the body's first line of defense, we examined the functional consequences of this leukocyte trafficking using the delayed type hypersensitivity (DTH) response as an in vivo assay for skin cell mediated immunity. Studies showed that acute stress experienced immediately before primary ( sensitization phase) or secondary (challenge phase) antigen exposure significantly enhanced skin DTH. In contrast, chronic stress suppressed skin DTH. In agreement with these studies, several investigators have reported stress-induced enhancement of DTH to different antigens administered to different sites of sensitization and challenge. The long- term objective of our research program is to elucidate the neuroendocrine and immune mediators and health consequences of the bi-directional effects of acute versus chronic stress on immune function. The overall goal of the proposed studies is to elucidate the mechanisms mediating the effects of acute stress on leukocyte trafficking and skin immunity. These studies will use wild type and gene knockout mice, immunoneutralization, flow cytometry, immunohistochemistry, in situ hybridization, RT-PCR, and ELISA to conduct analyses at the level of the organism, cell, protein, and gene expression. Three specific aims will be addressed: 1)Identify cell adhesion molecules that mediate the stress-induced redistribution of leukocytes. 2) Identify leukocyte subpopulations that mediate a stress-induced enhancement of the

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sensitization and challenge phases of DTH. 3) Identify chemokines and cytokines that mediate a stress-induced enhancement of both phases of DTH. These studies are important because stress is suspected to play a role in the etiology of many diseases and we propose to study the effects of stress on two important immune parameters: Leukocyte trafficking, which is crucial for the surveillance and effector functions of the immune system. And DTH, which mediates aspects of immunoprotection (e.g. resistance to infections and cancer and post-vaccination immunity) and immunopathology (e.g. autoimmune, dermatitis, and granulomatous disorders). It is hoped that the elucidation of mechanisms such as those proposed here will facilitate the development of biomedical treatments designed to harness and individual's physiology to selectively enhance (during surgery, wound healing, infections, or cancer) or suppress (during autoimmune or inflammatory disorders) an immune response depending on the clinical needs to the patient. 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 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)

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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: T CELL DIVERSITY IN THE INDUCTION OF AUTOIMMUNITY Principal Investigator & Institution: Laufer, Terri M.; Medicine; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 15-FEB-2002; Project End 31-JAN-2007 Summary: (provided by applicant): The graft-versus-host-disease (GVHD) which complicates allogeneic bone marrow transplantation is characterized by organ damage including dermatitis, enteritis, and hepatitis. A majority of post-transplant patients also develop antibodies to self-antigens, including anti-dsDNA, which mimic those in systemic lupus erythematosus. The development of both manifestations requires CD4+ T cells; however, the specificity of the inciting T cells is largely unknown. We propose to utilize transgenic models to examine the CD4 cell-antigen presenting cell (APC) interactions which initiate murine GVHD. K14 mice are a model of abnormal thymic development in which CD4+ T cells are autoreactive due to a failure of negative selection. H2-DM-deficient thymi select autoreactive CD4+ cells on restricted class IIassociated peptides. K14 CD4 cells induce anti-dsDNA antibodies in syngeneic hosts; H2-DM-deficient CD4+ do not. 2-2-3 mice carry transgenes for the TCR genes from a B6reactive K14 T cell hybridoma, 2-2-3. Double transgenic 2-2-3/K14 mice spontaneously develop skin disease which histologically resembles cutaneous GVHI); however, 2-231K14 CD4+ cells cannot induce autoantibodies in syngeneic mice. Thus, cutaneous GVHD is induced by monoclonal T cells which interact with keratinocytes; whereas, the production of autoantibodies during GVHD requires the activation of a diverse repertoire of T cells. In Specific Aim I, we will ask why K14, H2-DM, and 2-2-3/K14 CD4 cells induce different spectrums of autoantibodies after transfer to syngeneic hosts. We will examine the localization, division, and cytokine production of transferred CD4+ cells and B cell activation and germinal center production. Specific Aim II will extend these studies to investigate anti-DNA Ab production during GVHD in a mouse transgenic for the heavy chain of an anti-DNA antibody. In Specific Aim III, the keratinocyte/CD4+ cell interactions required for cutaneous GVHD in 2-2-3/K14 mice will be dissected. Temporal requirement for hematopoietic APC, inflammatory cytokines, and MHC class II expression in skin will be determined. Finally, in Specific Aim IV, we will identify the peptide specificity of the autoreactive 2-2-3 CD4 cell response to APC and keratinocytes in GVHD. Understanding the requirements for T cell diversity and the interactions between "graft" T cells and host antigen presenting cells offers improved immunologic targets for preventing GVHD following bone marrow transplant. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: TEC INHIBITORS- A NEW THERAPEUTIC FOR ALLERGIC DISEASES Principal Investigator & Institution: Kawakami, Yuko; Allimmune, Llc 10355 Science Center Dr San Diego, Ca 92121

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Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-JUL-2004 Summary: (provided by applicant): The incidence of allergic diseases such as atopic dermatitis (AD) has been dramatically increasing in the US and other industrialized countries for the past two decades. We and others have demonstrated that Tec family protein-tyrosine kinases have crucial roles in the activation of immune cells elicited by the engagement of antigen receptors or Fc receptors. As such, these kinases are supposed to play critical roles in the pathogenesis of AD and other allergic diseases that involve the activation of T and B lymphocytes, mast cells, and eosinophils. We recently identified a small-molecule compound, terreic acid (TA), as a selective inhibitor of Tec family kinases. In addition, we recently established highly efficient experimental conditions to rapidly induce skin lesions in AD-prone NC/Nga mice. Using this mouse model, we propose to explore whether TA or related compounds are therapeutically efficacious as a treatment of AD. Since we have a screening method for searching for Tec inhibitors whose usefulness has been proven, we will also expand our search for better compounds. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: TH2-MEDIATED INFLAMMATORY RESPONSES IN THE SKIN AND LUNG Principal Investigator & Institution: Herrick, Christina A.; Assistant Professor of Dermatology; Dermatology; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2001; Project Start 30-SEP-2000; Project End 31-AUG-2003 Summary: (Adapted from Applicant's Abstract) This is a four year mentored training program under the direction of Dr. Kim Bottomly, Professor of Immunobiology at Yale School of Medicine. After completing a residency in Dermatology at Yale, I joined Dr. Bottomly's lab as a postdoctoral fellow, studying Th2-mediated lung inflammation in a mouse model of Asthma. My interest in this project was a natural outgrowth of my doctoral studies involving regulation of IgE responses and my clinical interest in atopic dermatitis. I established a novel method of inducing strongly biased Th2 responses in vivo by epicutaneously (e.c.) exposing mice to soluble protein. Upon airway challenge, these e.c. sensitized mice develop lung inflammatory responses with features of human allergic asthma, including high numbers of eosinophils and mucus hypersecretion. We have shown that: 1) these e.c.- induced Th2 responses are IL-4 independent, but STAT6 dependent; 2) IL-4 independent Th2 responses in e.c. sensitized C57BL/6 mice are dependent on IL- 13; and 3) eosinophil migration from lung into airway in e.c. sensitized mice is IL-4 dependent in BALB/c, but not in C57BL/6, mice. It is our hypothesis that recruitment of eosinophils to the airway of e.c. sensitized mice is differentially regulated in these two strains because of differences in IL-13 production or receptivity. This will be tested in the following specific aims: 1) definition of the role of IL-13 during e.c. sensitization in BALB/c and C57BL/6 mice; and 2) determination of the cellular, molecular, and genetic factors that regulate airway eosinophilia in e.c. sensitized mice. In the third specific aim, the mechanisms put forth to explain the genetic difference in regulation of Th2 lung inflammation will be extended to the skin. This will involve establishing a new model of Th2-mediated skin inflammation by secondary antigen challenge in the skin (rather than the airway) of e.c. sensitized mice. Questions to be answered in this aim include: 1) is cutaneous inflammation governed by the same factors operating in the lung? 2) is eosinophil recruitment to skin IL-4 dependent in BALB/c mice, but not in C57BL/6 mice?; and 3) what is the role of IL-13 in skin inflammation? My plan is to continue working with Dr. Bottomly over the next several

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years to answer these questions. During this time, establishment of a novel model of Th2- mediated skin inflammation will provide me with a unique system in which to pursue future inquiries, facilitating my transition to an independent investigator. My goal is to continue basic science investigation of atopic skin disease as a junior faculty member in the Department of Dermatology at Yale School of Medicine. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

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

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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

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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: TRIAL OF PAROXETINE AS ADJUVANT TREATMENT FOR ATOPIC DERMATITIS SYMPTOMS Principal Investigator & Institution: Mccall, Calvin; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2002; Project Start 01-MAY-2002; Project End 30-APR-2004 Summary: Atopic dermatitis (AD) is a common dermatologic condition often associated with significant pruritus. The pruritus and associated scratching can be the most debilitating aspects of AD and exacerbate the dermatitis. Patients often report that current treatments for pruritus in AD are ineffective. An agent that would provide relief of the pruritus associated with AD would be very important in the control of the disease. Recent studies suggest that serotonin has a role in causing pruritus, and that serotonin antagonists may be beneficial in the treatment of pruritus. Serotonin reuptake inhibitors (SSRIs) may also prove to be effective in the treatment of pruritus. The goals of this investigation are to determine if 12 weeks of paroxetine will 1a) diminish the pruritus associated with moderate to severe AD, 1b) diminish AD associated skin severity, 1c) diminish AD-associated impairment of quality of life, 2a) diminish ADassociated potential co-morbid depression and anxiety, 2b) diminish AD- associated specific neuropsychiatric and bodily symptoms related to imbalances in cytokines that are modulated by anti-depressant therapy, 2c) reduce excessive, habitual, or obsessivecompulsive traits of scratching associated with moderate to severe AD. The study will be a double-blind, placebo-controlled, randomized, single-site study of 40-60 adult subjects with moderate-to severe AD. Patients will receive paroxetine or placebo for 12 weeks followed by a two-week dose taper. Efficiency of treatment will be assessed based on the improvement in itching as measured by the pruritus Visual Analog Scale, improvement in the Physician's Global Assessment of skin symptoms, improvement in the Eczema Area and Severity Index, serial photography, improvement in the subject's Quality of Life in Atopic Dermatitis survey, improvement in the Atopic DermatitisInventory Trait for Compulsive, Habitual, and Excessive Scratching survey, improvement in the Structured Clinical Interview for DSM-IV and the Beck's Depression and Speilberger State- Trait Anxiety Inventory scales, and improvement in the Neurotoxicity Rating Scale of neuro-psychiatric and bodily symptoms.

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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: WETLAND URBANIZATION GRADIENTS AND VECTOR BORNE DISEASES Principal Investigator & Institution: Kiesecker, Joseph; Biology; Pennsylvania State University-Univ Park 201 Old Main University Park, Pa 16802 Timing: Fiscal Year 2001; Project Start 15-SEP-2000; Project End 31-AUG-2005 Summary: A great variety of parasites are dependent on freshwater environments. The digenetic trematodes, or flukes, are a prominent example whose members usually have free-swimming aquatic forms and whose hosts are often freshwater organisms. Digeneans are the agents of several well-known human diseases including schistosoniiasis, echinostomiasis, and cercarial dermatitis. The diseases of wildlife are generally less known. However, digeneans have received close attention recently because of their suspected role in outbreaks of amphibian deformities. We propose a multi-tier approach to understanding the influence of human induced changes on vector borne disease in host amphibians. Our goal is understand key forms of anthropogenic: change that influence disease outbreaks and to develop predictive models for the emergence and dynamics of amphibian trematode parasites in anthropogenicallyinfluenced environments. We propose to complete a large-scale, multi-regional survey of wetlands across the northeastern United States and a set of long-term experiments involving manipulation of whole wetlands. The survey will be conducted in 4 regions and, in each, will be stratified across a gradient of human development. In each wetland surveyed we willcollect information on physical and chemical conditions and will sample resident snails and amphibians. The identity and burden of trematodes will be determined for each animal collected. Experiments will be conducted simultaneously in two regions with each experiment lasting for five years. In one experiment, we will alter the light environment. In a second, we will manipulate nutrient concentrations. In a third experiment, we will alter wetland hydro-period. Each manipulation will mimic changes believed to be associated with anthropogenic disturbances of wetlands. In each experiment, we will alter a subset of entire ponds from baseline conditions and compare the dynamics of snails, trematodes, and amphibians subsequently. Finally we plan to develop quantitative models in order to make predictions about the effects of urbanization on the disease dynamics. Development of mathematical models for these trematode systems will provide a template for studies of other snail borne diseases with similar community modules, for example, schistosomiasis. 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 “dermatitis” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for dermatitis in the PubMed Central database: •

Atopic Dermatitis and Fungi. by Faergemann J.; 2002 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126862

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Ceramidase Activity in Bacterial Skin Flora as a Possible Cause of Ceramide Deficiency in Atopic Dermatitis. by Ohnishi Y, Okino N, Ito M, Imayama S.; 1999 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=95668

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Early inflammatory markers in elicitation of allergic contact dermatitis. by Martin A, Gallino N, Gagliardi J, Ortiz S, Lascano AR, Diller A, Daraio MC, Kahn A, Mariani AL, Serra HM.; 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=122084

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Fever associated with cyclosporin for treating atopic dermatitis. by Thomas MD, Cook LJ.; 1998 Nov 7; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28712

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IkappaBalpha deficiency results in a sustained NF-kappaB response and severe widespread dermatitis in mice. by Klement JF, Rice NR, Car BD, Abbondanzo SJ, Powers GD, Bhatt PH, Chen CH, Rosen CA, Stewart CL.; 1996 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=231222

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IL-10 is critical for Th2 responses in a murine model of allergic dermatitis. by Laouini D, Alenius H, Bryce P, Oettgen H, Tsitsikov E, Geha RS.; 2003 Oct 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=198527

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IL-18 contributes to the spontaneous development of atopic dermatitis-like inflammatory skin lesion independently of IgE /stat6 under specific pathogen-free conditions. by Konishi H, Tsutsui H, Murakami T, Yumikura-Futatsugi S, Yamanaka KI, Tanaka M, Iwakura Y, Suzuki N, Takeda K, Akira S, Nakanishi K, Mizutani H.; 2002 Aug 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123258

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Modulation of cathepsin G expression in severe atopic dermatitis following mediumdose UVA1 phototherapy. by Breuckmann F, von Kobyletzki G, Avermaete A, Kreuter A, Altmeyer P, Gambichler T.; 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126230

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Molecular Analysis of Malassezia Microflora on the Skin of Atopic Dermatitis Patients and Healthy Subjects. by Sugita T, Suto H, Unno T, Tsuboi R, Ogawa H, Shinoda T, Nishikawa A.; 2001 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=88376

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Molecular Typing of Papillomatous Digital Dermatitis-Associated Treponema Isolates Based on Analysis of 16S-23S Ribosomal DNA Intergenic Spacer Regions. by Stamm LV, Bergen HL, Walker RL.; 2002 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130723

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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.

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New Yeast Species, Malassezia dermatis, Isolated from Patients with Atopic Dermatitis. by Sugita T, Takashima M, Shinoda T, Suto H, Unno T, Tsuboi R, Ogawa H, Nishikawa A.; 2002 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=140359

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Oral corticosteroids for poison ivy dermatitis. by Goodall J.; 2002 Feb 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=99302

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Oral corticosteroids for poison ivy dermatitis. by McKee MD, Schemitsch EH, Waddell JP, Richards RR, Kudo PA.; 2002 Feb 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=99303

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Twice weekly fluticasone propionate added to emollient maintenance treatment to reduce risk of relapse in atopic dermatitis: randomised, double blind, parallel group study. by Berth-Jones J, Damstra RJ, Golsch S, Livden JK, Van Hooteghem O, Allegra F, Parker CA.; 2003 Jun 21; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=162129

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Two cases of occupational allergic contact dermatitis from a cycloaliphatic epoxy resin in a neat oil: Case Report. by Jensen CD, Andersen KE.; 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=153490

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Typing of Pasteurella multocida Isolated from Pigs with and without Porcine Dermatitis and Nephropathy Syndrome. by Lainson FA, Aitchison KD, Donachie W, Thomson JR.; 2002 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=153357

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 dermatitis, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “dermatitis” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for dermatitis (hyperlinks lead to article summaries): •

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A review of recent journal highlights focusing on atopic dermatitis. Author(s): Allam JP, Bieber T. Source: Clinical and Experimental Dermatology. 2003 September; 28(5): 577-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12950368&dopt=Abstract

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 second step of chemotaxis after transendothelial migration: keratinocytes undergoing apoptosis release IFN-gamma-inducible protein 10, monokine induced by IFN-gamma, and IFN-gamma-inducible alpha-chemoattractant for T cell chemotaxis toward epidermis in atopic dermatitis. Author(s): Klunker S, Trautmann A, Akdis M, Verhagen J, Schmid-Grendelmeier P, Blaser K, Akdis CA. Source: Journal of Immunology (Baltimore, Md. : 1950). 2003 July 15; 171(2): 1078-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847282&dopt=Abstract

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Acrodermatitis continua of Hallopeau: was it an outcome of a surgical trauma or initially misdiagnosed as onychomycosis? Author(s): Sahin MT, Ozturkcan S, Turel A, Kandiloglu AR. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2003 March; 17(2): 236-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12705767&dopt=Abstract

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Acute pigmentation due to minocycline therapy in atopic dermatitis. Author(s): Nakamura S, Yokozeki H, Nishioka K. Source: The British Journal of Dermatology. 2003 May; 148(5): 1073-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12786854&dopt=Abstract

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Addition of fexofenadine to a topical corticosteroid reduces the pruritus associated with atopic dermatitis in a 1-week randomized, multicentre, double-blind, placebocontrolled, parallel-group study. Author(s): Kawashima M, Tango T, Noguchi T, Inagi M, Nakagawa H, Harada S. Source: The British Journal of Dermatology. 2003 June; 148(6): 1212-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828751&dopt=Abstract

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Adults with atopic dermatitis and herpes simplex and topical therapy with tacrolimus: what kind of prevention? Author(s): Lubbe J, Sanchez-Politta S, Tschanz C, Saurat JH. Source: Archives of Dermatology. 2003 May; 139(5): 670-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756112&dopt=Abstract

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Airborne allergic contact dermatitis from 3-iodo-2-propynyl-butylcarbamate at a paint factory. Author(s): Jensen CD, Thormann J, Andersen KE. Source: Contact Dermatitis. 2003 March; 48(3): 155-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12755730&dopt=Abstract

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Allergic contact dermatitis due to DL-alpha-tocopheryl nicotinate. Author(s): Oshima H, Tsuji K, Oh-I T, Koda M. Source: Contact Dermatitis. 2003 March; 48(3): 167-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12755738&dopt=Abstract

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Allergic contact dermatitis from etofenamate without cross-sensitization to other anthranilic acid derivatives. Author(s): Chu CY, Chen YL, Lin LJ, Sun CC. Source: Dermatology (Basel, Switzerland). 2003; 206(4): 341-2. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771478&dopt=Abstract

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Allergic contact dermatitis from formaldehyde with initially negative repeated open application test. Author(s): Tanglertsampan C. Source: Contact Dermatitis. 2003 March; 48(3): 171-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12755741&dopt=Abstract

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Allergic contact dermatitis from pentylene glycol in an emollient cream, with possible co-sensitization to resveratrol. Author(s): Gallo R, Viglizzo G, Vecchio F, Parodi A. Source: Contact Dermatitis. 2003 March; 48(3): 176-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12755747&dopt=Abstract

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Allergic contact dermatitis in a dental nurse induced by methacrylates. Author(s): Kiec-Swierczynska M, Krecisz B. Source: International Journal of Occupational Medicine and Environmental Health. 2003; 16(1): 73-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12705721&dopt=Abstract

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Allergic contact dermatitis to henna tattoo. Author(s): Baron S, Baxter K, Wilkinson M. Source: Archives of Disease in Childhood. 2003 September; 88(9): 747. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12937089&dopt=Abstract

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Allergic hyperreactivity to microbial components: a trigger factor of “intrinsic” atopic dermatitis? Author(s): Novak N, Allam JP, Bieber T. Source: The Journal of Allergy and Clinical Immunology. 2003 July; 112(1): 215-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847506&dopt=Abstract

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Alteration in the production of IL-10 and IL-12 and aberrant expression of CD23, CD83 and CD86 by monocytes or monocyte-derived dendritic cells from atopic dermatitis patients. Author(s): Aiba S, Manome H, Yoshino Y, Tagami H. Source: Experimental Dermatology. 2003 February; 12(1): 86-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12631251&dopt=Abstract

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An epidemic of contact dermatitis at the University of Hawaii Manoa. Author(s): Ning L. Source: Journal of American College Health : J of Ach. 2002 May; 50(6): 299-301. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12701655&dopt=Abstract

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An open pilot study using tacrolimus ointment in the treatment of seborrheic dermatitis. Author(s): Meshkinpour A, Sun J, Weinstein G. Source: Journal of the American Academy of Dermatology. 2003 July; 49(1): 145-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12833030&dopt=Abstract

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An open trial of calcium dobesilate in patients with venous ulcers and stasis dermatitis. Author(s): Kaur C, Sarkar R, Kanwar AJ, Attri AK, Dabra AK, Kochhar S. Source: International Journal of Dermatology. 2003 February; 42(2): 147-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709007&dopt=Abstract

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An overview of atopic dermatitis. Author(s): Hanifin JM. Source: Dermatology Nursing / Dermatology Nurses' Association. 2003 August; Suppl: 6-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14520891&dopt=Abstract

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Analysis of gene expression in peripheral blood eosinophils from patients with atopic dermatitis by differential display. Author(s): Hashida R, Ogawa K, Miyagawa M, Sugita Y, Takahashi E, Nagasu T, Katsunuma T, Akasawa A, Tsujimoto G, Matsumoto K, Saito H. Source: International Archives of Allergy and Immunology. 2003 June; 131 Suppl 1: 2633. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771546&dopt=Abstract

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Animal models of atopic dermatitis. Author(s): Marsella R, Olivry T. Source: Clinics in Dermatology. 2003 March-April; 21(2): 122-33. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12706330&dopt=Abstract

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Association between novel GM-CSF gene polymorphisms and the frequency and severity of atopic dermatitis. Author(s): Rafatpanah H, Bennett E, Pravica V, McCoy MJ, David TJ, Hutchinson IV, Arkwright PD. Source: The Journal of Allergy and Clinical Immunology. 2003 September; 112(3): 593-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=13679820&dopt=Abstract

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Association of SPINK5 gene polymorphisms with atopic dermatitis in the Japanese population. Author(s): Kato A, Fukai K, Oiso N, Hosomi N, Murakami T, Ishii M. Source: The British Journal of Dermatology. 2003 April; 148(4): 665-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12752122&dopt=Abstract

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Atopic dermatitis. Author(s): Sankar R. Source: Indian Pediatrics. 2003 August; 40(8): 793. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12951386&dopt=Abstract

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Atopic dermatitis: a new treatment paradigm using pimecrolimus. Author(s): Weinberg JM, Bowerman JG, Brown SM, Gerstein D, Kane KS, Selevan J, Virdee S. Source: J Drugs Dermatol. 2003 April; 2(2): 131-40. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12852364&dopt=Abstract

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Atopic dermatitis: molecular mechanisms, clinical aspects and new therapeutical approaches. Author(s): Galli E, Cicconi R, Rossi P, Casati A, Brunetti E, Mancino G. Source: Current Molecular Medicine. 2003 March; 3(2): 127-38. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12630559&dopt=Abstract

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Atopic dermatitis-like eruption precipitated by infliximab. Author(s): Wright RC. Source: Journal of the American Academy of Dermatology. 2003 July; 49(1): 160-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12833036&dopt=Abstract

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Atopy patch test reactions show a rapid influx of inflammatory dendritic epidermal cells in patients with extrinsic atopic dermatitis and patients with intrinsic atopic dermatitis. Author(s): Kerschenlohr K, Decard S, Przybilla B, Wollenberg A. Source: The Journal of Allergy and Clinical Immunology. 2003 April; 111(4): 869-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12704371&dopt=Abstract

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Atypical and unusual clinical manifestations of contact dermatitis to clothing (textile contact dermatitis): case presentation and review of the literature. Author(s): Lazarov A, Cordoba M, Plosk N, Abraham D. Source: Dermatology Online Journal [electronic Resource]. 2003 August; 9(3): 1. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12952748&dopt=Abstract

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Autoimmune progesterone dermatitis and its manifestation as anaphylaxis: a case report and literature review. Author(s): Snyder JL, Krishnaswamy G. Source: Annals of Allergy, Asthma & Immunology : Official Publication of the American College of Allergy, Asthma, & Immunology. 2003 May; 90(5): 469-77; Quiz 477, 571. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775127&dopt=Abstract

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Baseball pitcher's friction dermatitis. Author(s): Inui S, Yamamoto S, Ikegami R, Ozawa K, Itami S, Yoshikawa K. Source: Contact Dermatitis. 2002 September; 47(3): 176-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492562&dopt=Abstract

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Benzoyl peroxide as a cause of airborne contact dermatitis in an orthopaedic technician. Author(s): Forschner K, Zuberbier T, Worm M. Source: Contact Dermatitis. 2002 October; 47(4): 241. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492531&dopt=Abstract

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Berloque dermatitis mimicking child abuse. Author(s): Gruson LM, Chang MW. Source: Archives of Pediatrics & Adolescent Medicine. 2002 November; 156(11): 1091-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12413335&dopt=Abstract

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Bilateral chondrodermatitis nodularis chronica helicis on the free border of the helix in a woman. Author(s): Oelzner S, Elsner P. Source: Journal of the American Academy of Dermatology. 2003 October; 49(4): 720-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14512925&dopt=Abstract

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Bingo-hall worker's occupational copper contact dermatitis from coins. Author(s): Suarez CP, Fernandez-Redondo V, Toribio J. Source: Contact Dermatitis. 2002 September; 47(3): 182. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492566&dopt=Abstract

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Biochemist's occupational allergic contact dermatitis from iodoacetamide and acrylamide. Author(s): Aalto-Korte K, Jolanki R, Suuronen K, Estlander T. Source: Contact Dermatitis. 2002 December; 47(6): 361-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581285&dopt=Abstract

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Blue jean button dermatitis. Nickel allergy presenting as a periumbilical rash. Author(s): Cerveny KA Jr, Brodell RT. Source: Postgraduate Medicine. 2002 November; 112(5): 79-80, 83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12462187&dopt=Abstract

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Bullous autoimmune estrogen dermatitis. Author(s): Mutasim DF, Baumbach JL. Source: Journal of the American Academy of Dermatology. 2003 July; 49(1): 130-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12833026&dopt=Abstract

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Candida--agent of the diaper dermatitis? Author(s): Dorko E, Viragova S, Pilipcinec E, Tkacikova L. Source: Folia Microbiol (Praha). 2003; 48(3): 385-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12879751&dopt=Abstract

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Cardiac catheterization-induced acute radiation dermatitis presenting as a fixed drug eruption. Author(s): Schecter AK, Lewis MD, Robinson-Bostom L, Pan TD. Source: J Drugs Dermatol. 2003 August; 2(4): 425-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12884469&dopt=Abstract

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Case report: allergic contact dermatitis and new-onset asthma. Chromium exposure during leather tanning. Author(s): Lockman LE. Source: Can Fam Physician. 2002 December; 48: 1907-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12520790&dopt=Abstract

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Cellular phone dermatitis with chromate allergy. Author(s): Seishima M, Oyama Z, Oda M. Source: Dermatology (Basel, Switzerland). 2003; 207(1): 48-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835548&dopt=Abstract

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Central nervous system involvement in a child with polyarteritis nodosa and severe atopic dermatitis. Author(s): Morfin-Maciel B, Medina A, Espinosa Rosales F, Berron R, Huerta Lopez J. Source: Rev Alerg Mex. 2002 November-December; 49(6): 189-95. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12561651&dopt=Abstract

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Characterization of monocyte subtypes in the allergic form of atopic eczema/dermatitis syndrome. Author(s): Novak N, Allam P, Geiger E, Bieber T. Source: Allergy. 2002 October; 57(10): 931-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12269940&dopt=Abstract

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Childhood atopic dermatitis: 1. Author(s): Moffat L. Source: Prof Nurse. 2003 September; 19(1): 15-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14515815&dopt=Abstract

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Chronic actinic dermatitis as the presenting feature of HIV infection in three Chinese males. Author(s): Wong SN, Khoo LS. Source: Clinical and Experimental Dermatology. 2003 May; 28(3): 265-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12780709&dopt=Abstract

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Chronic actinic dermatitis secondary to simvastatin. Author(s): Holme SA, Pearse AD, Anstey AV. Source: Photodermatology, Photoimmunology & Photomedicine. 2002 December; 18(6): 313-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12535029&dopt=Abstract

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Chronic radiodermatitis following percutaneous coronary interventions: a report of two cases. Author(s): Aerts A, Decraene T, van den Oord JJ, Dens J, Janssens S, Guelinckx P, Flour M, Degreef H, Garmyn M. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2003 May; 17(3): 340-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12702082&dopt=Abstract

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Ciclopiroxolamine cream for treating seborrheic dermatitis: a double-blind parallel group comparison. Author(s): Unholzer A, Varigos G, Nicholls D, Schinzel S, Nietsch KH, Ulbricht H, Korting HC. Source: Infection. 2002 December; 30(6): 373-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12478328&dopt=Abstract

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Clinical and immunologic reactivity to aeroallergens in “intrinsic” atopic dermatitis patients. Author(s): Kerschenlohr K, Decard S, Darsow U, Ollert M, Wollenberg A. Source: The Journal of Allergy and Clinical Immunology. 2003 January; 111(1): 195-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12532120&dopt=Abstract

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Clinical dose and adverse effects of topical steroids in daily management of atopic dermatitis. Author(s): Furue M, Terao H, Rikihisa W, Urabe K, Kinukawa N, Nose Y, Koga T. Source: The British Journal of Dermatology. 2003 January; 148(1): 128-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534606&dopt=Abstract

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Combined skin prick and patch testing enhances identification of peanut-allergic patients with atopic dermatitis. Author(s): Seidenari S, Giusti F, Bertoni L, Mantovani L. Source: Allergy. 2003 June; 58(6): 495-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12757450&dopt=Abstract

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Comparison of epidermal hydration and skin surface lipids in healthy individuals and in patients with atopic dermatitis. Author(s): Sator PG, Schmidt JB, Honigsmann H. Source: Journal of the American Academy of Dermatology. 2003 March; 48(3): 352-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12637914&dopt=Abstract

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Comparison of transepidermal water loss, capacitance and pH values in the skin between intrinsic and extrinsic atopic dermatitis patients. Author(s): Choi SJ, Song MG, Sung WT, Lee DY, Lee JH, Lee ES, Yang JM. Source: Journal of Korean Medical Science. 2003 February; 18(1): 93-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12589094&dopt=Abstract

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Confocal histopathology of irritant contact dermatitis in vivo and the impact of skin color (black vs white). Author(s): Hicks SP, Swindells KJ, Middelkamp-Hup MA, Sifakis MA, Gonzalez E, Gonzalez S. Source: Journal of the American Academy of Dermatology. 2003 May; 48(5): 727-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12734502&dopt=Abstract

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Confocal laser scanning microscopic observation of glycocalyx production by Staphylococcus aureus in skin lesions of bullous impetigo, atopic dermatitis and pemphigus foliaceus. Author(s): Akiyama H, Hamada T, Huh WK, Yamasaki O, Oono T, Fujimoto W, Iwatsuki K. Source: The British Journal of Dermatology. 2003 March; 148(3): 526-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12653745&dopt=Abstract

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Contact dermatitis from a dry stick deodorant. Author(s): Devos SA, Constandt L. Source: Contact Dermatitis. 2002 September; 47(3): 170-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492555&dopt=Abstract

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Contact dermatitis from electrocardiograph-monitoring electrodes: role of p-tertbutylphenol-formaldehyde resin. Author(s): Avenel-Audran M, Goossens A, Zimerson E, Bruze M. Source: Contact Dermatitis. 2003 February; 48(2): 108-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12694215&dopt=Abstract

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Contact dermatitis to Shiitake mushroom. Author(s): Curnow P, Tam M. Source: The Australasian Journal of Dermatology. 2003 May; 44(2): 155-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12752194&dopt=Abstract

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Contact hypersensitivity in hand dermatitis. Author(s): Li LF, Wang J. Source: Contact Dermatitis. 2002 October; 47(4): 206-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492518&dopt=Abstract

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Contact irritant dermatitis and anti-pruritic agents: the need to address the itch. Author(s): Burkhart CG, Burkhart HR. Source: J Drugs Dermatol. 2003 April; 2(2): 143-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12852365&dopt=Abstract

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Correlation of the density of yeast Malassezia with the clinical severity of seborrhoeic dermatitis. Author(s): Zaidi Z, Wahid Z, Cochinwala R, Soomro M, Qureishi A. Source: J Pak Med Assoc. 2002 November; 52(11): 504-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12585368&dopt=Abstract

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Cost of illness of atopic dermatitis in children: a societal perspective. Author(s): Kemp AS. Source: Pharmacoeconomics. 2003; 21(2): 105-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12515572&dopt=Abstract

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Cost-effectiveness analysis of tacrolimus ointment versus high-potency topical corticosteroids in adults with moderate to severe atopic dermatitis. Author(s): Ellis CN, Drake LA, Prendergast MM, Abramovits W, Boguniewicz M, Daniel CR, Lebwohl M, Paller AS, Stevens SR, Whitaker-Worth DL, Tong KB. Source: Journal of the American Academy of Dermatology. 2003 April; 48(4): 553-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664019&dopt=Abstract

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Cough sensitivity in atopic dermatitis. Author(s): Pecova R, Frlickova Z, Pec J, Tatar M. Source: Pulmonary Pharmacology & Therapeutics. 2003; 16(4): 203-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12850122&dopt=Abstract

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Cutaneous field stimulation of sensory nerve fibers reduces itch without affecting contact dermatitis. Author(s): Wallengren J. Source: Allergy. 2002 December; 57(12): 1195-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12464050&dopt=Abstract

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Cytokine gene polymorphisms in allergic contact dermatitis. Author(s): Westphal GA, Schnuch A, Moessner R, Konig IR, Kranke B, Hallier E, Ziegler A, Reich K. Source: Contact Dermatitis. 2003 February; 48(2): 93-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12694213&dopt=Abstract

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Cytokine gene polymorphisms in atopic dermatitis. Author(s): Reich K, Westphal G, Konig IR, Mossner R, Schupp P, Gutgesell C, Hallier E, Ziegler A, Neumann C. Source: The British Journal of Dermatology. 2003 June; 148(6): 1237-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828754&dopt=Abstract

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Dead Sea treatment - principle for outpatient use in atopic dermatitis: safety and efficacy of synchronous balneophototherapy using narrowband UVB and bathing in Dead Sea salt solution. Author(s): Schiffner R, Schiffner-Rohe J, Gerstenhauer M, Landthaler M, Hofstadter F, Stolz W. Source: Eur J Dermatol. 2002 November-December; 12(6): 543-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12459524&dopt=Abstract

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79

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Decompensation of chronic stable alcoholic liver disease by severe exfoliative dermatitis. Author(s): Shawcross DL, Mookerjee RP, Jalan R. Source: European Journal of Gastroenterology & Hepatology. 2003 April; 15(4): 433-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12655267&dopt=Abstract

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Decreased frequency of intracellular IFN-gamma producing T cells in whole blood preparations from patients with atopic dermatitis. Author(s): Kallstrom E, Roscher I, Andreasson A, Back O, van Hage-Hamsten M. Source: Experimental Dermatology. 2002 December; 11(6): 556-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12473063&dopt=Abstract

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Decreasing allergic contact dermatitis frequency through dermatotoxicologic and epidemiologic based intervention? Author(s): Wesley NO, Maibach HI. Source: Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association. 2003 June; 41(6): 857-60. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738190&dopt=Abstract

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Delayed diagnosis of occupational contact dermatitis from sodium pyrithione in a metalworking fluid. Author(s): Isaksson M. Source: Contact Dermatitis. 2002 October; 47(4): 248-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492539&dopt=Abstract

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Demonstration of TARC and CCR4 mRNA expression and distribution using in situ RT-PCR in the lesional skin of atopic dermatitis. Author(s): Zheng X, Nakamura K, Furukawa H, Nishibu A, Takahashi M, Tojo M, Kaneko F, Kakinuma T, Tamaki K. Source: The Journal of Dermatology. 2003 January; 30(1): 26-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12598706&dopt=Abstract

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Dermatitis herpetiformis and a gluten-free diet. Author(s): Lovett W. Source: American Family Physician. 2003 February 1; 67(3): 470; Author Reply 470. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12588069&dopt=Abstract

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Dermatitis herpetiformis with flame figures mimicking an arthropod bite. Author(s): Rose C, Brocker EB, Krahl D. Source: The American Journal of Dermatopathology. 2003 June; 25(3): 277-8; Author Reply 278. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775996&dopt=Abstract

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Dermatitis herpetiformis: problems, progress and prospects. Author(s): Fry L. Source: Eur J Dermatol. 2002 November-December; 12(6): 523-31. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12459520&dopt=Abstract

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Dermatitis in humans associated with the mites Pyemotes tritici, Dermanyssus gallinae, Ornithonyssus bacoti and Androlaelaps casalis in Israel. Author(s): Rosen S, Yeruham I, Braverman Y. Source: Medical and Veterinary Entomology. 2002 December; 16(4): 442-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12510897&dopt=Abstract

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Detection of cytotoxic anti-LEDGF autoantibodies in atopic dermatitis. Author(s): Ayaki M, Ohoguro N, Azuma N, Majima Y, Yata K, Ibaraki N, Singh DP, Ko V, Shinohara T. Source: Autoimmunity. 2002 August; 35(5): 319-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12515286&dopt=Abstract

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Diagnosis and treatment of chronic actinic dermatitis. Author(s): Dawe RS, Ferguson J. Source: Dermatologic Therapy. 2003; 16(1): 45-51. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12919126&dopt=Abstract

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Diagnostic accuracy of the atopy patch test and the skin-prick test for the diagnosis of food allergy in young children with atopic eczema/dermatitis syndrome. Author(s): Stromberg L. Source: Acta Paediatrica (Oslo, Norway : 1992). 2002; 91(10): 1044-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12434888&dopt=Abstract

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Diaper dermatitis--an overview. Author(s): Prasad HR, Srivastava P, Verma KK. Source: Indian J Pediatr. 2003 August; 70(8): 635-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14510084&dopt=Abstract

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Dichotomic nature of atopic dermatitis reflected by combined analysis of monocyte immunophenotyping and single nucleotide polymorphisms of the interleukin4/interleukin-13 receptor gene: the dichotomy of extrinsic and intrinsic atopic dermatitis. Author(s): Novak N, Kruse S, Kraft S, Geiger E, Kluken H, Fimmers R, Deichmann KA, Bieber T. Source: The Journal of Investigative Dermatology. 2002 October; 119(4): 870-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12406333&dopt=Abstract

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Differences between intrafollicular microorganism profiles in perioral and seborrhoeic dermatitis. Author(s): Takiwaki H, Tsuda H, Arase S, Takeichi H. Source: Clinical and Experimental Dermatology. 2003 September; 28(5): 531-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12950346&dopt=Abstract

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Differences in fecal microflora between patients with atopic dermatitis and healthy control subjects. Author(s): Watanabe S, Narisawa Y, Arase S, Okamatsu H, Ikenaga T, Tajiri Y, Kumemura M. Source: The Journal of Allergy and Clinical Immunology. 2003 March; 111(3): 587-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12642841&dopt=Abstract

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Differential susceptibility to staphylococcal superantigen (SsAg)-induced apoptosis of CD4+ T cells from atopic dermatitis patients and healthy subjects: the inhibitory effect of IL-4 on SsAg-induced apoptosis. Author(s): Lin YT, Wang CT, Hsu CT, Wang LF, Shau WY, Yang YH, Chiang BL. Source: Journal of Immunology (Baltimore, Md. : 1950). 2003 July 15; 171(2): 1102-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847285&dopt=Abstract

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Dirt, worms and atopic dermatitis. Author(s): Flohr C. Source: The British Journal of Dermatology. 2003 May; 148(5): 871-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12786815&dopt=Abstract

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Disease severity and associated family impact in childhood atopic dermatitis. Author(s): Balkrishnan R, Housman TS, Carroll C, Feldman SR, Fleischer AB. Source: Archives of Disease in Childhood. 2003 May; 88(5): 423-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716715&dopt=Abstract

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Distinct TCR delta repertoires are present in the cutaneous lesions and inflamed duodenum of patients with dermatitis herpetiformis. Author(s): Holtmeier W, Pfander M, Zollner TM, Kaufmann R, Caspary WF. Source: Experimental Dermatology. 2002 December; 11(6): 527-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12473060&dopt=Abstract

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Do oral antihistamines stop the itch of atopic dermatitis? Author(s): Dimson S, Nanayakkara C. Source: Archives of Disease in Childhood. 2003 September; 88(9): 832-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12937115&dopt=Abstract

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Down-regulation of vasoactive intestinal polypeptide receptor expression in atopic dermatitis. Author(s): Groneberg DA, Welker P, Fischer TC, Dinh QT, Grutzkau A, Peiser C, Wahn U, Henz BM, Fischer A. Source: The Journal of Allergy and Clinical Immunology. 2003 May; 111(5): 1099-105. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12743576&dopt=Abstract

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Drug-induced reversible lymphoid dyscrasia: a clonal lymphomatoid dermatitis of memory and activated T cells. Author(s): Magro CM, Crowson AN, Kovatich AJ, Burns F. Source: Human Pathology. 2003 February; 34(2): 119-29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12612879&dopt=Abstract

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Dyshidrotic-like spongiotic dermatitis after intravenous immunoglobulin therapy. Author(s): Uyttendaele H, Obadiah J, Grossman M. Source: J Drugs Dermatol. 2003 June; 2(3): 337-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12848120&dopt=Abstract

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Earlobe dermatitis. Author(s): Ozkaya-Bayazit E, Baykal C, Buyukbabani N, Hafiz G. Source: Archives of Dermatology. 2002 December; 138(12): 1607-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12472356&dopt=Abstract

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Early sensitization to house dust mite is a major risk factor for subsequent development of bronchial asthma in Japanese infants with atopic dermatitis: results of a 4-year followup study. Author(s): Ohshima Y, Yamada A, Hiraoka M, Katamura K, Ito S, Hirao T, Akutagawa H, Kondo N, Morikawa A, Mayumi M. Source: Annals of Allergy, Asthma & Immunology : Official Publication of the American College of Allergy, Asthma, & Immunology. 2002 September; 89(3): 265-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12269646&dopt=Abstract

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Effect of exclusive breast-feeding and early solid food avoidance on the incidence of atopic dermatitis in high-risk infants at 1 year of age. Author(s): Schoetzau A, Filipiak-Pittroff B, Franke K, Koletzko S, Von Berg A, Gruebl A, Bauer CP, Berdel D, Reinhardt D, Wichmann HE; German Infant Nutritional Intervention Study Group. Source: Pediatric Allergy and Immunology : Official Publication of the European Society of Pediatric Allergy and Immunology. 2002 August; 13(4): 234-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390439&dopt=Abstract

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Effect of oral cyclosporin A in children with Staphylococcus aureus-colonized vs S aureus-infected severe atopic dermatitis. Author(s): Bunikowski R, Mielke M, Brautigam M, Renz H, Wahn U. Source: Pediatric Allergy and Immunology : Official Publication of the European Society of Pediatric Allergy and Immunology. 2003 February; 14(1): 55-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12603712&dopt=Abstract

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Effect of probiotic Lactobacillus strains in children with atopic dermatitis. Author(s): Rosenfeldt V, Benfeldt E, Nielsen SD, Michaelsen KF, Jeppesen DL, Valerius NH, Paerregaard A. Source: The Journal of Allergy and Clinical Immunology. 2003 February; 111(2): 389-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12589361&dopt=Abstract

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Effect of staphylococcal enterotoxin B on specific antibody production in children with atopic dermatitis. Author(s): Sohn MH, Kim CH, Kim WK, Jang GC, Kim KE. Source: Allergy and Asthma Proceedings : the Official Journal of Regional and State Allergy Societies. 2003 January-February; 24(1): 67-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635580&dopt=Abstract

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Effects of an episode of specialist care on the impact of childhood atopic dermatitis on the child's family. Author(s): Balkrishnan R, Manuel J, Clarke J, Carroll CL, Housman TS, Fleischer AB Jr. Source: Journal of Pediatric Health Care : Official Publication of National Association of Pediatric Nurse Associates & Practitioners. 2003 July-August; 17(4): 184-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847428&dopt=Abstract

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Efficacy and safety of topically applied tacrolimus ointment in patients with moderate to severe atopic dermatitis. Author(s): Wong WR, Tsai HJ, Hong HS. Source: Chang Gung Med J. 2003 July; 26(7): 485-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14515971&dopt=Abstract

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Efficacy and tolerability of montelukast as a therapeutic agent for severe atopic dermatitis in adults. Author(s): Nettis E, Pannofino A, Fanelli M, Ferrannini A, Tursi A. Source: Acta Dermato-Venereologica. 2002; 82(4): 297-8. Erratum In: Acta Derm Venereol. 2003; 83(1): 79. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12361137&dopt=Abstract

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Efficacy evaluation of an oil-in-water emulsion (Dermoflan) in atopic dermatitis. Author(s): Peris K, Valeri P, Altobelli E, Fargnoli MC, Carrozzo AM, Chimenti S. Source: Acta Dermato-Venereologica. 2002; 82(6): 465-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12575858&dopt=Abstract

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Efficacy of ultraviolet A1 phototherapy on the expression of bcl-2 in atopic dermatitis and cutaneous T-cell lymphoma in vivo: a comparison study. Author(s): Breuckmann F, von Kobyletzki G, Avermaete A, Kreuter A, Altmeyer P. Source: Photodermatology, Photoimmunology & Photomedicine. 2002 October; 18(5): 217-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390661&dopt=Abstract

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Electrical impedance as a potential tool to distinguish between allergic and irritant contact dermatitis. Author(s): Nyren M, Kuzmina N, Emtestam L. Source: Journal of the American Academy of Dermatology. 2003 March; 48(3): 394-400. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12637919&dopt=Abstract

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Elidel (pimecrolimus) cream 1%: a nonsteroidal topical agent for the treatment of atopic dermatitis. Author(s): Eichenfield LF, Beck L. Source: The Journal of Allergy and Clinical Immunology. 2003 May; 111(5): 1153-68. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12743593&dopt=Abstract

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Endogenous antimicrobial peptides and skin infections in atopic dermatitis. Author(s): Ong PY, Ohtake T, Brandt C, Strickland I, Boguniewicz M, Ganz T, Gallo RL, Leung DY. Source: The New England Journal of Medicine. 2002 October 10; 347(15): 1151-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12374875&dopt=Abstract

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Enhancement of allergic skin wheal responses and in vitro allergen-specific IgE production by computer-induced stress in patients with atopic dermatitis. Author(s): Kimata H. Source: Brain, Behavior, and Immunity. 2003 April; 17(2): 134-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12676575&dopt=Abstract

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Enhancement of allergic skin wheal responses by microwave radiation from mobile phones in patients with atopic eczema/dermatitis syndrome. Author(s): Kimata H. Source: International Archives of Allergy and Immunology. 2002 December; 129(4): 34850. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12483040&dopt=Abstract

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Enhancement of allergic skin wheal responses in patients with atopic eczema/dermatitis syndrome by playing video games or by a frequently ringing mobile phone. Author(s): Kimata H. Source: European Journal of Clinical Investigation. 2003 June; 33(6): 513-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12795649&dopt=Abstract

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Eotaxin gene single nucleotide polymorphisms in the promoter and exon regions are not associated with susceptibility to atopic dermatitis, but two of them in the promoter region are associated with serum IgE levels in patients with atopic dermatitis. Author(s): Tsunemi Y, Saeki H, Nakamura K, Sekiya T, Hirai K, Fujita H, Asano N, Tanida Y, Kakinuma T, Wakugawa M, Torii H, Tamaki K. Source: Journal of Dermatological Science. 2002 September; 29(3): 222-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12234713&dopt=Abstract

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Epoxy contact dermatitis due to pacemaker compounds. Author(s): Skoet R, Tollund C, Bloch-Thomsen PE. Source: Cardiology. 2003; 99(2): 112. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12711888&dopt=Abstract

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Erythema multiforme-like molluscum dermatitis. Author(s): Lee HJ, Kwon JA, Kim JW. Source: Acta Dermato-Venereologica. 2002; 82(3): 217-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12353720&dopt=Abstract

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Ethnicity as a possible endogenous factor in irritant contact dermatitis: comparing the irritant response among Caucasians, blacks, and Asians. Author(s): Modjtahedi SP, Maibach HI. Source: Contact Dermatitis. 2002 November; 47(5): 272-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534531&dopt=Abstract

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Eumovate (clobetasone butyrate) 0.05% cream with its moisturizing emollient base has better healing properties than hydrocortisone 1% cream: a study in nickelinduced contact dermatitis. Author(s): Parneix-Spake A, Goustas P, Green R. Source: The Journal of Dermatological Treatment. 2001 December; 12(4): 191-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12241627&dopt=Abstract

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Evolution in the treatment of atopic dermatitis: new approaches to managing a chronic skin disease. Author(s): Nicol NH. Source: Dermatology Nursing / Dermatology Nurses' Association. 2003 August; Suppl: 4-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14520890&dopt=Abstract

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Expansion and proliferation of skin-homing T cells in atopic dermatitis as assessed at the single cell level. Author(s): Jung T, Schulz S, Zachmann K, Neumann C. Source: International Archives of Allergy and Immunology. 2003 February; 130(2): 143-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673068&dopt=Abstract

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Exposure to pets and atopic dermatitis during the first two years of life. A cohort study. Author(s): Zirngibl A, Franke K, Gehring U, von Berg A, Berdel D, Bauer CP, Reinhardt D, Wichmann HE, Heinrich J; GINI study group. Source: Pediatric Allergy and Immunology : Official Publication of the European Society of Pediatric Allergy and Immunology. 2002 December; 13(6): 394-401. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12485314&dopt=Abstract

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Extrafacial and generalized granulomatous periorificial dermatitis. Author(s): Urbatsch AJ, Frieden I, Williams ML, Elewski BE, Mancini AJ, Paller AS. Source: Archives of Dermatology. 2002 October; 138(10): 1354-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12374542&dopt=Abstract

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Exudative hyponychial dermatitis associated with capecitabine and docetaxel combination chemotherapy for metastatic breast carcinoma: report of three cases. Author(s): Chen GY, Chang TW, Chen WC. Source: The British Journal of Dermatology. 2003 May; 148(5): 1071-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12786853&dopt=Abstract

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Exudative retinal detachment due to methicillin-resistant Staphylococcus aureus infection after scleral buckling in the treatment of retinal detachment accompanied by atopic dermatitis. Author(s): Osawa S, Sasoh M, Ito K, Matsui K, Yoshida S, Uji Y. Source: Retina (Philadelphia, Pa.). 2002 October; 22(5): 649-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12441736&dopt=Abstract

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Eyelid dermatitis: experience in 203 cases. Author(s): Guin JD. Source: Journal of the American Academy of Dermatology. 2002 November; 47(5): 75565. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12399770&dopt=Abstract

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Failure of an ointment based on IR3535 (ethyl butylacetylaminopropionate) to prevent an outbreak of cercarial dermatitis during swimming races across Lake Annecy, France. Author(s): Caumes E, Felder-Moinet S, Couzigou C, Darras-Joly C, Latour P, Leger N. Source: Annals of Tropical Medicine and Parasitology. 2003 March; 97(2): 157-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12803871&dopt=Abstract

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Fluocinolone acetonide 0.01% in peanut oil: therapy for childhood atopic dermatitis, even in patients who are peanut sensitive. Author(s): Paller AS, Nimmagadda S, Schachner L, Mallory SB, Kahn T, Willis I, Eichenfield LF. Source: Journal of the American Academy of Dermatology. 2003 April; 48(4): 569-77. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664021&dopt=Abstract

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Food hypersensitivity in two groups of children and young adults with atopic dermatitis evaluated a decade apart. Author(s): Ellman LK, Chatchatee P, Sicherer SH, Sampson HA. Source: Pediatric Allergy and Immunology : Official Publication of the European Society of Pediatric Allergy and Immunology. 2002 August; 13(4): 295-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390446&dopt=Abstract

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Framing the future of antifungals in atopic dermatitis. Author(s): Nikkels AF, Pierard GE. Source: Dermatology (Basel, Switzerland). 2003; 206(4): 398-400. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771497&dopt=Abstract

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Frequency and intensity of responses to mite patch tests are lower in nonatopic subjects with respect to patients with atopic dermatitis. Author(s): Seidenari S, Giusti F, Pellacani G, Bertoni L. Source: Allergy. 2003 May; 58(5): 426-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12752330&dopt=Abstract

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Frequency of contact allergy to Compositae extracts in patients with atopic dermatitis. Author(s): Nettis E, Giordano D, Soccio A, Ferrannini A, Tursi A. Source: Contact Dermatitis. 2002 September; 47(3): 169-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492554&dopt=Abstract

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Gamma-linolenic acid supplementation for prophylaxis of atopic dermatitis--a randomized controlled trial in infants at high familial risk. Author(s): van Gool CJ, Thijs C, Henquet CJ, van Houwelingen AC, Dagnelie PC, Schrander J, Menheere PP, van den brandt PA. Source: The American Journal of Clinical Nutrition. 2003 April; 77(4): 943-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663296&dopt=Abstract

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Generalized seborrheic dermatitis in an immunodeficient newborn. Author(s): Bykowsky MJ. Source: Cutis; Cutaneous Medicine for the Practitioner. 2002 December; 70(6): 324; Author Reply 324. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12502120&dopt=Abstract

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Genetic association analysis using microsatellite markers in atopic dermatitis. Author(s): Iizuka M, Katsuyama Y, Mabuchi T, Umezawa Y, Matsuyama T, Ozawa A, Kawada H, Inoko H, Morita E, Ota M. Source: Tokai J Exp Clin Med. 2002 August; 27(2): 51-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12472170&dopt=Abstract

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Genetic dissection between coeliac disease and dermatitis herpetiformis in sib pairs. Author(s): Karell K, Korponay-Szabo I, Szalai Z, Holopainen P, Mustalahti K, Collin P, Maki M, Partanen J. Source: Annals of Human Genetics. 2002 November; 66(Pt 5-6): 387-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12485471&dopt=Abstract

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Genital swelling caused by octyldodecanol contact dermatitis. Author(s): Dawn G, Forsyth A. Source: Clinical and Experimental Dermatology. 2003 March; 28(2): 228-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12653724&dopt=Abstract

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Ghost anemone dermatitis. Author(s): Freudenthal AR, Barbagallo JS. Source: Journal of the American Academy of Dermatology. 2002 November; 47(5): 722-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12399764&dopt=Abstract

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Glutaraldehyde-induced and formaldehyde-induced allergic contact dermatitis among dental hygienists and assistants. Author(s): Ravis SM, Shaffer MP, Shaffer CL, Dehkhaghani S, Belsito DV. Source: The Journal of the American Dental Association. 2003 August; 134(8): 1072-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12956347&dopt=Abstract

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Hand dermatitis as an unsuspected presentation of textile dye contact sensitivity. Author(s): Giusti F, Mantovani L, Martella A, Seidenari S. Source: Contact Dermatitis. 2002 August; 47(2): 91-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12423406&dopt=Abstract

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Heliotherapy in atopic dermatitis: a prospective study on climatotherapy using the SCORAD index. Author(s): Autio P, Komulainen P, Larni HM. Source: Acta Dermato-Venereologica. 2002; 82(6): 436-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12575850&dopt=Abstract

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High incidence of adverse reactions to egg challenge on first known exposure in young atopic dermatitis children: predictive value of skin prick test and radioallergosorbent test to egg proteins. Author(s): Monti G, Muratore MC, Peltran A, Bonfante G, Silvestro L, Oggero R, Mussa GC. Source: Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology. 2002 October; 32(10): 1515-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12372134&dopt=Abstract

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High-density oligonucleotide array analysis of mRNA transcripts in peripheral blood cells of severe atopic dermatitis patients. Author(s): Heishi M, Kagaya S, Katsunuma T, Nakajima T, Yuki K, Akasawa A, Maeda M, Gunji S, Sugita Y, Tsujimoto G, Saito H. Source: International Archives of Allergy and Immunology. 2002 September; 129(1): 5766. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12372999&dopt=Abstract

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HLA-DR-dependent increased mannan-induced lymphoproliferative response in atopic eczema dermatitis syndrome. Author(s): Savolainen J, Kosonen J, Kortekangas-Savolainen O, Yssel H, Bousquet J. Source: Allergy. 2003 January; 58(1): 72-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12580811&dopt=Abstract

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Homeopathic treatment of Japanese patients with intractable atopic dermatitis. Author(s): Itamura R, Hosoya R. Source: Homeopathy. 2003 April; 92(2): 108-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12725253&dopt=Abstract

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Human T lymphotrophic virus-I (HTLV-I) infection in patients with unclassifiable dermatitis in central Kerala, south India: a preliminary study. Author(s): Ajithkumar K, Ramalingam S, Kannangai R, Prakash KJ. Source: Sexually Transmitted Infections. 2002 December; 78(6): E7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12473822&dopt=Abstract

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Hypoproteinemia in severe childhood atopic dermatitis: a serious complication. Author(s): Nomura I, Katsunuma T, Tomikawa M, Shibata A, Kawahara H, Ohya Y, Abe J, Saito H, Akasawa A. Source: Pediatric Allergy and Immunology : Official Publication of the European Society of Pediatric Allergy and Immunology. 2002 August; 13(4): 287-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390445&dopt=Abstract

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Identification of highly expressed genes in peripheral blood T cells from patients with atopic dermatitis. Author(s): Matsumoto Y, Oshida T, Obayashi I, Imai Y, Matsui K, Yoshida NL, Nagata N, Ogawa K, Obayashi M, Kashiwabara T, Gunji S, Nagasu T, Sugita Y, Tanaka T, Tsujimoto G, Katsunuma T, Akasawa A, Saito H. Source: International Archives of Allergy and Immunology. 2002 December; 129(4): 32740. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12483038&dopt=Abstract

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IgE-mediated hypersensitivity against human sweat antigen in patients with atopic dermatitis. Author(s): Hide M, Tanaka T, Yamamura Y, Koro O, Yamamoto S. Source: Acta Dermato-Venereologica. 2002; 82(5): 335-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12430731&dopt=Abstract

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Immediate-type hypersensitivity and allergic contact dermatitis due to paraphenylenediamine in hair dye. Author(s): Wong GA, King CM. Source: Contact Dermatitis. 2003 March; 48(3): 166. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12755736&dopt=Abstract

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Impaired sweating function in adult atopic dermatitis: results of the quantitative sudomotor axon reflex test. Author(s): Eishi K, Lee JB, Bae SJ, Takenaka M, Katayama I. Source: The British Journal of Dermatology. 2002 October; 147(4): 683-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12366413&dopt=Abstract

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91

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Impaired thymic output and restricted T-cell repertoire in two infants with immunodeficiency and early-onset generalized dermatitis. Author(s): Pirovano S, Mazzolari E, Pasic S, Albertini A, Notarangelo LD, Imberti L. Source: Immunology Letters. 2003 March 3; 86(1): 93-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12600751&dopt=Abstract

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Improvement of skin symptoms and mineral imbalance by drinking deep sea water in patients with atopic eczema/dermatitis syndrome (AEDS). Author(s): Kimata H, Tai H, Nakagawa K, Yokoyama Y, Nakajima H, Ikegami Y. Source: Acta Medica (Hradec Kralove). 2002; 45(2): 83-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12325458&dopt=Abstract

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In patients with dermatitis herpetiformis distribution of transglutaminase in cutaneous tissue does not differ from controls. Author(s): Biagi F, Bassi E, Ardigo M, Vignini MA, Caravaggi M, Borroni G, Corazza GR. Source: Dig Liver Dis. 2003 January; 35(1): 41-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12725607&dopt=Abstract

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Increased acetylcholine levels in skin biopsies of patients with atopic dermatitis. Author(s): Wessler I, Reinheimer T, Kilbinger H, Bittinger F, Kirkpatrick CJ, Saloga J, Knop J. Source: Life Sciences. 2003 March 28; 72(18-19): 2169-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12628475&dopt=Abstract

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Increased frequency of intracellular interleukin (IL)-13 and IL-10, but not IL-4, expressing CD4+ and CD8+ peripheral T cells of patients with atopic dermatitis. Author(s): Aleksza M, Lukacs A, Antal-Szalmas P, Hunyadi J, Szegedi A. Source: The British Journal of Dermatology. 2002 December; 147(6): 1135-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12452862&dopt=Abstract

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Increased S100B serum levels in diffuse dermatitis. Author(s): Guidi B, Diociaiuti A, Capizzi R, Forni F, Scribano D, Vultaggio P, Zappacosta B, Amerio PL. Source: Melanoma Research. 2002 December; 12(6): 633. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12459654&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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Influence of age on the outcome of the atopy patch test with food in children with atopic dermatitis. Author(s): Perackis K, Celik-Bilgili S, Staden U, Mehl A, Niggemann B. Source: The Journal of Allergy and Clinical Immunology. 2003 September; 112(3): 625-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=13679826&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-13 gene polymorphism G4257A is associated with atopic dermatitis in Japanese patients. Author(s): Tsunemi Y, Saeki H, Nakamura K, Sekiya T, Hirai K, Kakinuma T, Fujita H, Asano N, Tanida Y, Wakugawa M, Torii H, Tamaki K. Source: Journal of Dermatological Science. 2002 November; 30(2): 100-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12413765&dopt=Abstract

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International Consensus Conference on Atopic Dermatitis II (ICCAD II): Chairman's introduction and overview. Author(s): Ellis C, Luger T. Source: The British Journal of Dermatology. 2003 May; 148 Suppl 63: 1-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12694267&dopt=Abstract

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International Consensus Conference on Atopic Dermatitis II (ICCAD II): clinical update and current treatment strategies. Author(s): Ellis C, Luger T, Abeck D, Allen R, Graham-Brown RA, De Prost Y, Eichenfield LF, Ferrandiz C, Giannetti A, Hanifin J, Koo JY, Leung D, Lynde C, Ring J, Ruiz-Maldonado R, Saurat JH; ICCAD II Faculty. Source: The British Journal of Dermatology. 2003 May; 148 Suppl 63: 3-10. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12694268&dopt=Abstract

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Interstitial granulomatous dermatitis with histiocytic pseudorosettes: a new histopathologic pattern in cutaneous borreliosis. Detection of Borrelia burgdorferi DNA sequences by a highly sensitive PCR-ELISA. Author(s): Moreno C, Kutzner H, Palmedo G, Goerttler E, Carrasco L, Requena L. Source: Journal of the American Academy of Dermatology. 2003 March; 48(3): 376-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12637917&dopt=Abstract

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Interstitial granulomatous dermatitis with plaques and arthritis. Author(s): Banuls J, Betlloch I, Botella R, Jimenez MJ, Blanes M, Pascual JC, Belinchon I, Silvestre JF. Source: Eur J Dermatol. 2003 May-June; 13(3): 308-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12804998&dopt=Abstract

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Investigation of an outbreak of cercarial dermatitis. Author(s): Levesque B, Giovenazzo P, Guerrier P, Laverdiere D, Prud'Homme H. Source: Epidemiology and Infection. 2002 October; 129(2): 379-86. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12403114&dopt=Abstract

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IP-10 in atopic dermatitis. Author(s): Yamashita T, Akamatsu H, Tomitaka A, Ogawa Y, Sugawara N, Matsunaga K. Source: Allergy. 2003 March; 58(3): 261. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12653804&dopt=Abstract

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Irritant contact dermatitis after use of Bispectral Index sensor in prone position. Author(s): Pousman RM, Eilers WA 3rd, Johns B, Jung H. Source: Anesthesia and Analgesia. 2002 November; 95(5): 1337-8, Table of Contents. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12401622&dopt=Abstract

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Irritant dermatitis due to prolonged contact with Oilatum Plus. Author(s): Loo WJ. Source: The British Journal of Dermatology. 2003 January; 148(1): 171-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534617&dopt=Abstract

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Irritant dermatitis to detergents in textiles. Author(s): Matthies W. Source: Current Problems in Dermatology. 2003; 31: 123-38. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12882025&dopt=Abstract

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Is atopic dermatitis a risk factor for intervertebral disc degeneration? A preliminary clinical and MRI study. Author(s): Ito S, Hattori T, Fukutake T, Sugimoto K. Source: Journal of the Neurological Sciences. 2003 January 15; 206(1): 39-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12480083&dopt=Abstract

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Is tacrolimus the best therapy for atopic dermatitis? Author(s): Mcauliffe EP. Source: American Family Physician. 2003 May 1; 67(9): 1874. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12751651&dopt=Abstract

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Isolation of Borrelia burgdorferi sensu lato from a fibrous nodule in a patient with acrodermatitis chronica atrophicans. Author(s): Maraspin V, Ruzic-Sabljic E, Strle F. Source: Wiener Klinische Wochenschrift. 2002 July 31; 114(13-14): 533-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12422596&dopt=Abstract

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Lack of effect of cyclosporine in lichen amyloidosis associated with atopic dermatitis. Author(s): Akar A, Tastan HB, Demiriz M, Erbil H. Source: Eur J Dermatol. 2002 November-December; 12(6): 612-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12459544&dopt=Abstract

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Lithium gluconate 8% vs ketoconazole 2% in the treatment of seborrhoeic dermatitis: a multicentre, randomized study. Author(s): Dreno B, Chosidow O, Revuz J, Moyse D; THE STUDY INVESTIGATOR GROUP. Source: The British Journal of Dermatology. 2003 June; 148(6): 1230-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828753&dopt=Abstract

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Lithium gluconate in the treatment of seborrhoeic dermatitis: a multicenter, randomised, double-blind study versus placebo. Author(s): Dreno B, Moyse D. Source: Eur J Dermatol. 2002 November-December; 12(6): 549-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12459525&dopt=Abstract

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Long-term treatment with cetirizine of infants with atopic dermatitis: a multi-country, double-blind, randomized, placebo-controlled trial (the ETAC trial) over 18 months. Author(s): Diepgen TL; Early Treatment of the Atopic Child Study Group. Source: Pediatric Allergy and Immunology : Official Publication of the European Society of Pediatric Allergy and Immunology. 2002 August; 13(4): 278-86. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390444&dopt=Abstract

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Lymphomatoid allergic contact dermatitis from para-phenylenediamine. Author(s): Calzavara-Pinton P, Capezzera R, Zane C, Brezzi A, Pasolini G, Ubiali A, Facchetti F. Source: Contact Dermatitis. 2002 September; 47(3): 173-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492559&dopt=Abstract

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Lymphomatoid contact dermatitis to para-tertyl-butyl phenol resin. Author(s): Evans AV, Banerjee P, McFadden JP, Calonje E. Source: Clinical and Experimental Dermatology. 2003 May; 28(3): 272-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12780711&dopt=Abstract

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Management of chondrodermatitis helicis by protective padding: a series of 12 cases and a review of the literature. Author(s): Timoney N, Davison PM. Source: British Journal of Plastic Surgery. 2002 July; 55(5): 387-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12372366&dopt=Abstract

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Management of severe atopic dermatitis with thymostimulin. Author(s): Wisuthsarewong W, Viravan S. Source: J Med Assoc Thai. 2002 August; 85 Suppl 2: S749-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12403256&dopt=Abstract

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Managing a common disorder in children: Atopic dermatitis. Author(s): Cheigh NH. Source: Journal of Pediatric Health Care : Official Publication of National Association of Pediatric Nurse Associates & Practitioners. 2003 March-April; 17(2): 84-8; Quiz 89-90. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12665731&dopt=Abstract

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Managing childhood atopic dermatitis. Author(s): Leung AK, Barber KA. Source: Adv Ther. 2003 May-June; 20(3): 129-37. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12956254&dopt=Abstract

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Measurement of electrical current perception threshold of sensory nerves for pruritus in atopic dermatitis patients and normal individuals with various degrees of mild damage to the stratum corneum. Author(s): Kobayashi H, Kikuchi K, Tsubono Y, Tagami H. Source: Dermatology (Basel, Switzerland). 2003; 206(3): 204-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673076&dopt=Abstract

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Measuring atopic dermatitis severity in randomized controlled clinical trials: what exactly are we measuring? Author(s): Charman C, Chambers C, Williams H. Source: The Journal of Investigative Dermatology. 2003 June; 120(6): 932-41. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12787117&dopt=Abstract

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Microbiological aspects of diaper dermatitis. Author(s): Ferrazzini G, Kaiser RR, Hirsig Cheng SK, Wehrli M, Della Casa V, Pohlig G, Gonser S, Graf F, Jorg W. Source: Dermatology (Basel, Switzerland). 2003; 206(2): 136-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592081&dopt=Abstract

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Myelogenous leukemia cutis resembling stasis dermatitis. Author(s): Chang HY, Wong KM, Bosenberg M, McKee PH, Haynes HA. Source: Journal of the American Academy of Dermatology. 2003 July; 49(1): 128-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12833025&dopt=Abstract

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Narrowband UV-B vs medium-dose UV-A1 phototherapy in chronic atopic dermatitis. Author(s): Legat FJ, Hofer A, Brabek E, Quehenberger F, Kerl H, Wolf P. Source: Archives of Dermatology. 2003 February; 139(2): 223-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12588233&dopt=Abstract

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Natural course of cow's milk allergy in childhood atopic eczema/dermatitis syndrome. Author(s): Oranje AP, Wolkerstorfer A, de Waard-van der Spek FB. Source: Annals of Allergy, Asthma & Immunology : Official Publication of the American College of Allergy, Asthma, & Immunology. 2002 December; 89(6 Suppl 1): 52-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12487205&dopt=Abstract

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Natural killer and dendritic cell contact in lesional atopic dermatitis skin-Malassezia-influenced cell interaction. Author(s): Buentke E, Heffler LC, Wilson JL, Wallin RP, Lofman C, Chambers BJ, Ljunggren HG, Scheynius A. Source: The Journal of Investigative Dermatology. 2002 October; 119(4): 850-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12406330&dopt=Abstract

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Neutrophil CD11b, L-selectin and Fc IgA receptors in patients with dermatitis herpetiformis. Author(s): Smith AD, Streilein RD, Hall RP 3rd. Source: The British Journal of Dermatology. 2002 December; 147(6): 1109-17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12452859&dopt=Abstract

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Nickel sensitization in adolescents and association with ear piercing, use of dental braces and hand eczema. The Odense Adolescence Cohort Study on Atopic Diseases and Dermatitis (TOACS). Author(s): Mortz CG, Lauritsen JM, Bindslev-Jensen C, Andersen KE. Source: Acta Dermato-Venereologica. 2002; 82(5): 359-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12430735&dopt=Abstract

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Nickel-elicited systemic contact dermatitis. Author(s): Dou X, Liu LL, Zhu XJ. Source: Contact Dermatitis. 2003 March; 48(3): 126-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12755723&dopt=Abstract

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Novel SLC39A4 mutations in acrodermatitis enteropathica. Author(s): Nakano A, Nakano H, Nomura K, Toyomaki Y, Hanada K. Source: The Journal of Investigative Dermatology. 2003 June; 120(6): 963-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12787121&dopt=Abstract

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Occlusive treatment of chronic hand dermatitis with pimecrolimus cream 1% results in low systemic exposure, is well tolerated, safe, and effective. An open study. Author(s): Thaci D, Steinmeyer K, Ebelin ME, Scott G, Kaufmann R. Source: Dermatology (Basel, Switzerland). 2003; 207(1): 37-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835546&dopt=Abstract

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Occupational airborne allergic contact dermatitis from 2-aminothiophenol. Author(s): Bonamonte D, Carino M, Mundo L, Foti C. Source: Eur J Dermatol. 2002 November-December; 12(6): 592-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12459537&dopt=Abstract

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Occupational airborne allergic contact dermatitis from mesna. Author(s): Kiec-Swierczynska M, Krecisz B. Source: Contact Dermatitis. 2003 March; 48(3): 171. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12755742&dopt=Abstract

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Occupational airborne and hand dermatitis to hop (Humulus lupulus) with nonoccupational relapses. Author(s): Spiewak R, Dutkiewicz J. Source: Annals of Agricultural and Environmental Medicine : Aaem. 2002; 9(2): 249-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12498595&dopt=Abstract

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Occupational allergic contact dermatitis caused by isocyanates. Author(s): Goossens A, Detienne T, Bruze M. Source: Contact Dermatitis. 2002 November; 47(5): 304-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534536&dopt=Abstract

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Occupational allergic contact dermatitis from falcarinol. Author(s): Machado S, Silva E, Massa A. Source: Contact Dermatitis. 2002 August; 47(2): 113-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12423414&dopt=Abstract

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Occupational allergic contact dermatitis from PEG-4 rapeseed amide in a massage oil. Author(s): Isaksson M. Source: Contact Dermatitis. 2002 September; 47(3): 175-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492561&dopt=Abstract

98

Dermatitis

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Occupational allergic contact dermatitis in hospital workers caused by methyldibromo glutaronitrile in a work soap. Author(s): Diba VC, Chowdhury MM, Adisesh A, Statham BN. Source: Contact Dermatitis. 2003 February; 48(2): 118-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12694221&dopt=Abstract

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Occupational allergic contact dermatitis to nitromethane. Author(s): Webb KG, Fowler JF Jr. Source: American Journal of Contact Dermatitis : Official Journal of the American Contact Dermatitis Society. 2002 December; 13(4): 201-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12478536&dopt=Abstract

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Occupational contact dermatitis from canary-grass seed. Author(s): Monteseirin J, Perez-Formoso JL, Sanchez-Hernandez MC, Hernandez M, Bonilla I, Camacho MJ, Guardia P, Conde J. Source: Contact Dermatitis. 2002 October; 47(4): 247. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492538&dopt=Abstract

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Occupational contact dermatitis in the textile industry. Author(s): Wigger-Alberti W, Elsner P. Source: Current Problems in Dermatology. 2003; 31: 114-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12882024&dopt=Abstract

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Occupational contact dermatitis to hydrangea. Author(s): Rademaker M. Source: The Australasian Journal of Dermatology. 2003 August; 44(3): 220-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12869051&dopt=Abstract

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Occupational contact dermatitis. Author(s): Antezana M, Parker F. Source: Immunol Allergy Clin North Am. 2003 May; 23(2): 269-90, Vii. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12803363&dopt=Abstract

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Occupational irritant contact dermatitis from synthetic mineral fibres according to Finnish statistics. Author(s): Jolanki R, Makinen I, Suuronen K, Alanko K, Estlander T. Source: Contact Dermatitis. 2002 December; 47(6): 329-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581277&dopt=Abstract

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Occupational irritant contact dermatitis. Author(s): Gould D. Source: Nursing Standard : Official Newspaper of the Royal College of Nursing. 2003 April 16-22; 17(31): 53-6, 58, 60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12739293&dopt=Abstract

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Occupational protein contact dermatitis due to Calliphora vomitoria larvae (maggots) bred as fishing bait. Author(s): Pazzaglia M, Tullo S, Tosti A. Source: Contact Dermatitis. 2003 March; 48(3): 176. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12755746&dopt=Abstract

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Occurrence of patchy parakeratosis in normal-appearing skin in patients with active atopic dermatitis and in patients with healed atopic dermatitis: a cause of impaired barrier function of the atopic skin. Author(s): Sakurai K, Sugiura H, Matsumoto M, Uehara M. Source: Journal of Dermatological Science. 2002 October; 30(1): 37-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12354418&dopt=Abstract

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On Zimmerman's “Dermatitis factitia as a war weapon”. Author(s): Taieb A. Source: Archives of Dermatology. 2003 May; 139(5): 666-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756109&dopt=Abstract

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Optimal management of atopic dermatitis in infancy. Author(s): Moneret-Vautrin DA. Source: Allerg Immunol (Paris). 2002 November; 34(9): 325-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12512191&dopt=Abstract

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Oral terbinafine for the treatment of seborrheic dermatitis in adults. Author(s): Cassano N, Amoruso A, Loconsole F, Vena GA. Source: International Journal of Dermatology. 2002 November; 41(11): 821-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12453014&dopt=Abstract

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Oxidative stress and altered antioxidant defenses in children with acute exacerbation of atopic dermatitis. Author(s): Tsukahara H, Shibata R, Ohshima Y, Todoroki Y, Sato S, Ohta N, Hiraoka M, Yoshida A, Nishima S, Mayumi M. Source: Life Sciences. 2003 April 18; 72(22): 2509-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12650859&dopt=Abstract

100 Dermatitis

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Paediatric atopic dermatitis in Perth general practice. Author(s): Thom GA, Halbert AR. Source: The Australasian Journal of Dermatology. 2003 February; 44(1): 28-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581078&dopt=Abstract

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Palmar-plantar keratoderma of Unna Thost associated with atopic dermatitis: an underrecognized entity? Author(s): Loh TH, Yosipovitch G, Tay YK. Source: Pediatric Dermatology. 2003 May-June; 20(3): 195-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12787265&dopt=Abstract

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Parental knowledge of topical therapies in the treatment of childhood atopic dermatitis. Author(s): Beattie PE, Lewis-Jones MS. Source: Clinical and Experimental Dermatology. 2003 September; 28(5): 549-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12950351&dopt=Abstract

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Patch testing for allergic contact dermatitis in the allergist office. Author(s): Fonacier L, Charlesworth EN. Source: Curr Allergy Asthma Rep. 2003 July; 3(4): 283-90. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12791205&dopt=Abstract

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Patch testing in allergic contact dermatitis caused by topical Chinese herbal medicine. Author(s): Li LF, Wang J. Source: Contact Dermatitis. 2002 September; 47(3): 166-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492552&dopt=Abstract

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Pathophysiology of atopic dermatitis. Author(s): Kang K, Stevens SR. Source: Clinics in Dermatology. 2003 March-April; 21(2): 116-21. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12706329&dopt=Abstract

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Peristomal allergic contact dermatitis caused by Stomahesive paste: An additional case. Author(s): Gallo R, Ciambellotti A, Cozzani E, Parodi A. Source: Journal of the American Academy of Dermatology. 2002 October; 47(4): 633. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12271318&dopt=Abstract

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Pet hamsters as a source of rat mite dermatitis. Author(s): Creel NB, Crowe MA, Mullen GR. Source: Cutis; Cutaneous Medicine for the Practitioner. 2003 June; 71(6): 457-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12839256&dopt=Abstract

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Photoaggravated allergic contact dermatitis due to Rosmarinus officinalis crossreactive with Thymus vulgaris. Author(s): Armisen M, Rodriguez V, Vidal C. Source: Contact Dermatitis. 2003 January; 48(1): 52-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12641580&dopt=Abstract

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Photoallergic contact dermatitis due to diclofenac. Author(s): Montoro J, Rodriguez M, Diaz M, Bertomeu F. Source: Contact Dermatitis. 2003 February; 48(2): 115. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12694217&dopt=Abstract

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Photodermatitis in a patient with HIV infection. Author(s): Lopez-Lerma I, Alsina MM, Blanco JL, Lecha M. Source: Journal of the American Academy of Dermatology. 2003 July; 49(1): 159-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12833035&dopt=Abstract

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Phototherapy of atopic dermatitis. Author(s): Scheinfeld NS, Tutrone WD, Weinberg JM, DeLeo VA. Source: Clinics in Dermatology. 2003 May-June; 21(3): 241-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781441&dopt=Abstract

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Plasma IL-13 levels in patients with atopic dermatitis. Author(s): Terao H, Koga T, Urabe K, Moroi Y, Furue M. Source: The Journal of Dermatology. 2003 January; 30(1): 76-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12598715&dopt=Abstract

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Platelet-activating factor antagonist WEB 2086 inhibits ultraviolet-B radiationinduced dermatitis in the human skin. Author(s): Baltas E, Trach V, Dobozy A, Kemeny L. Source: Skin Pharmacology and Applied Skin Physiology. 2003 July-August; 16(4): 25962. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12784066&dopt=Abstract

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Premenstrual deterioration of skin symptoms in female patients with atopic dermatitis. Author(s): Kiriyama K, Sugiura H, Uehara M. Source: Dermatology (Basel, Switzerland). 2003; 206(2): 110-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592076&dopt=Abstract

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Prevalence and correlates of hand dermatitis among nurses in a Japanese teaching hospital. Author(s): Smith DR, Ohmura K, Yamagata Z. Source: J Epidemiol. 2003 May; 13(3): 157-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12749603&dopt=Abstract

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Prevalence of asthma, allergic rhinitis and dermatitis in primary school children in Uasin Gishu district, Kenya. Author(s): Esamai F, Ayaya S, Nyandiko W. Source: East Afr Med J. 2002 October; 79(10): 514-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635755&dopt=Abstract

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Prevalence of atopic dermatitis in Japanese adults. Author(s): Muto T, Hsieh SD, Sakurai Y, Yoshinaga H, Suto H, Okumura K, Ogawa H. Source: The British Journal of Dermatology. 2003 January; 148(1): 117-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534604&dopt=Abstract

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Prevalence of hypertension among patients with atopic dermatitis. Author(s): Abramovits W, Stevenson L, Prendergast MM, Tong K. Source: The British Journal of Dermatology. 2003 February; 148(2): 380; Author Reply 380. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12588411&dopt=Abstract

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Protein oxidative damage in the stratum corneum: Evidence for a link between environmental oxidants and the changing prevalence and nature of atopic dermatitis in Japan. Author(s): Niwa Y, Sumi H, Kawahira K, Terashima T, Nakamura T, Akamatsu H. Source: The British Journal of Dermatology. 2003 August; 149(2): 248-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932228&dopt=Abstract

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Psoriasiform dermatitis susceptibility in Itgb2(tm1Bay) PL/J mice requires low-level CD18 expression and at least two additional loci for progression to severe disease. Author(s): Barlow SC, Collins RG, Ball NJ, Weaver CT, Schoeb TR, Bullard DC. Source: American Journal of Pathology. 2003 July; 163(1): 197-202. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12819024&dopt=Abstract

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Quantitative analysis of bikunin-laden mast cells in follicular eruptions and chronic skin lesions of atopic dermatitis. Author(s): Isogai R, Matsukura A, Aragane Y, Maeda A, Matsukura M, Yudate T, Sugihara K, Takahashi M, Aisu K, Tezuka T. Source: Archives of Dermatological Research. 2002 December; 294(9): 387-92. Epub 2002 October 11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12522575&dopt=Abstract

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Radiation recall dermatitis from docetaxel. Author(s): Piroth MD, Krempien R, Wannenmacher M, Zierhut D. Source: Onkologie. 2002 October; 25(5): 438-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12415198&dopt=Abstract

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Radiation recall dermatitis may represent the Koebner phenomenon. Author(s): Camidge R, Price A. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 October 1; 20(19): 4130; Author Reply 4130. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12351618&dopt=Abstract

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Randomized, double-blind, placebo-controlled trial of autologous blood therapy for atopic dermatitis. Author(s): Pittler MH, Armstrong NC, Cox A, Collier PM, Hart A, Ernst E. Source: The British Journal of Dermatology. 2003 February; 148(2): 307-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12588384&dopt=Abstract

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Randomized, open-labeled, non-inferiority study between ciclopiroxolamine 1% cream and ketoconazole 2% foaming gel in mild to moderate facial seborrheic dermatitis. Author(s): Chosidow O, Maurette C, Dupuy P. Source: Dermatology (Basel, Switzerland). 2003; 206(3): 233-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673081&dopt=Abstract

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Recalcitrant atopic dermatitis due to allergy to Compositae. Author(s): Wintzen M, Donker AS, van Zuuren EJ. Source: Contact Dermatitis. 2003 February; 48(2): 87-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12694211&dopt=Abstract

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Recurrent staphylococcal infections and chronic dermatitis in a 45-year-old man. Author(s): De Vera M, Yu BH. Source: Annals of Allergy, Asthma & Immunology : Official Publication of the American College of Allergy, Asthma, & Immunology. 2003 September; 91(3): 244-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14533655&dopt=Abstract

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Regional variation in prevalence and etiology of allergic contact dermatitis. Author(s): Thompson TR, Belsito DV. Source: American Journal of Contact Dermatitis : Official Journal of the American Contact Dermatitis Society. 2002 December; 13(4): 177-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12478532&dopt=Abstract

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Reiter's syndrome-like pattern in AIDS-associated psoriasiform dermatitis. Author(s): Utikal J, Beck E, Dippel E, Klemke CD, Goerdt S. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2003 January; 17(1): 114-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12602996&dopt=Abstract

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Relapsing Kaposi's varicelliform eruption and herpes simplex following facial tacrolimus treatment for atopic dermatitis. Author(s): Ambo M. Source: Acta Dermato-Venereologica. 2002; 82(3): 224-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12353724&dopt=Abstract

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Relation between vesicular eruptions on the hands and tinea pedis, atopic dermatitis and nickel allergy. Author(s): Bryld LE, Agner T, Menne T. Source: Acta Dermato-Venereologica. 2003; 83(3): 186-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12816153&dopt=Abstract

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Relationship of occupation to contact dermatitis: evaluation in patients tested from 1998 to 2000. Author(s): Rietschel RL, Mathias CG, Fowler JF Jr, Pratt M, Taylor JS, Sherertz EF, Marks JG Jr, Belsito DV, Storrs FJ, Maibach HI, Fransway AF, Deleo VA; North American Contact Dermatitis Group. Source: American Journal of Contact Dermatitis : Official Journal of the American Contact Dermatitis Society. 2002 December; 13(4): 170-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12478531&dopt=Abstract

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Reliance on erythema scores may mask severe atopic dermatitis in black children compared with their white counterparts. Author(s): Ben-Gashir MA, Hay RJ. Source: The British Journal of Dermatology. 2002 November; 147(5): 920-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12410701&dopt=Abstract

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Re-patch testing patients with long-term contact dermatitis. Author(s): Rebandel P, Rudzki E. Source: Contact Dermatitis. 2002 October; 47(4): 234. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492524&dopt=Abstract

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Results of atopy patch tests with house dust mites in adults with 'intrinsic' and'extrinsic' atopic dermatitis. Author(s): Ingordo V, D'Andria G, D'Andria C, Tortora A. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2002 September; 16(5): 450-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12428836&dopt=Abstract

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Rheumatoid neutrophilic dermatitis, rheumatoid papules, and rheumatoid nodules in a patient with seronegative rheumatoid arthritis. Author(s): Yamamoto T, Matsunaga T, Nishioka K. Source: Journal of the American Academy of Dermatology. 2003 April; 48(4): 634-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664038&dopt=Abstract

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Rheumatoid neutrophilic dermatitis. Author(s): Yoshida Y, Kiryu H, Furue M, Nakayama J, Matsuda T. Source: The Journal of Dermatology. 2003 March; 30(3): 255-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12692368&dopt=Abstract

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Risk: benefit ratio is important in treating atopic dermatitis. Author(s): Allen BR, Luger TA. Source: Bmj (Clinical Research Ed.). 2002 October 26; 325(7370): 970. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12399360&dopt=Abstract

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Role of different valence states of chromium in the elicitation of allergic contact dermatitis. Author(s): Iyer VJ, Banerjee G, Govindram CB, Kamath V, Shinde S, Gaikwad A, Jerajani HR, Raman G, Cherian KM. Source: Contact Dermatitis. 2002 December; 47(6): 357-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581283&dopt=Abstract

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Role of foods in irregular aggravation of atopic dermatitis. Author(s): Uenishi T, Sugiura H, Uehara M. Source: The Journal of Dermatology. 2003 February; 30(2): 91-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12692374&dopt=Abstract

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Routine patch testing with frullanolide mix: an European Environmental and Contact Dermatitis Research Group multicentre study. Author(s): Ducombs G, Lepoittevin JP, Berl V, Andersen KE, Brandao FM, Bruynzeel DP, Bruze M, Camarasa JG, Frosch PJ, Goossens A, Lachapelle JM, Lahti A, Le Coz CJ, Maibach HI, Menne T, Seidenari S, Shaw S, Tosti A, Wilkinson JD; European Environmental and Contact Dermatitis Research Group multicentre Study. Source: Contact Dermatitis. 2003 March; 48(3): 158-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12755731&dopt=Abstract

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Safety and efficacy of nonsteroid pimecrolimus cream 1% in the treatment of atopic dermatitis in infants. Author(s): Ho VC, Gupta A, Kaufmann R, Todd G, Vanaclocha F, Takaoka R, FolsterHolst R, Potter P, Marshall K, Thurston M, Bush C, Cherill R. Source: The Journal of Pediatrics. 2003 February; 142(2): 155-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12584537&dopt=Abstract

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Sanichlor-induced atopic dermatitis and asthma in ophthalmologists. Author(s): Goverdhan S, Gaston H. Source: Eye (London, England). 2003 January; 17(1): 108-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12579187&dopt=Abstract

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Seborrheic dermatitis today, gone tomorrow? The link between the biocene and treatment. Author(s): Pierard GE. Source: Dermatology (Basel, Switzerland). 2003; 206(3): 187-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673072&dopt=Abstract

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Seborrheic dermatitis. Author(s): Gupta AK, Bluhm R, Cooper EA, Summerbell RC, Batra R. Source: Dermatologic Clinics. 2003 July; 21(3): 401-12. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12956195&dopt=Abstract

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Septic arthritis as a complication of allergic contact dermatitis. Author(s): Saunders H, Nixon R. Source: Contact Dermatitis. 2003 February; 48(2): 116-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12694219&dopt=Abstract

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Sequence diversity of the intergenic spacer region of the rRNA gene of Malassezia globosa colonizing the skin of patients with atopic dermatitis and healthy individuals. Author(s): Sugita T, Kodama M, Saito M, Ito T, Kato Y, Tsuboi R, Nishikawa A. Source: Journal of Clinical Microbiology. 2003 July; 41(7): 3022-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12843037&dopt=Abstract

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Severe allergic contact eyelid dermatitis caused by swimming goggles. Author(s): Vaswani SK, Collins DD, Pass CJ. Source: Annals of Allergy, Asthma & Immunology : Official Publication of the American College of Allergy, Asthma, & Immunology. 2003 June; 90(6): 672-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12839329&dopt=Abstract

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Severe refractory chronic actinic dermatitis successfully treated with tacrolimus ointment. Author(s): Abe R, Shimizu T, Tsuji A, Matsumura T, Shimizu H. Source: The British Journal of Dermatology. 2002 December; 147(6): 1273-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12452891&dopt=Abstract

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Shiitake dermatitis. Author(s): Lippert U, Martin V, Schwertfeger C, Junghans V, Ellinghaus B, Fuchs T. Source: The British Journal of Dermatology. 2003 January; 148(1): 178-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534625&dopt=Abstract

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Skin lipids and epidermal differentiation in atopic dermatitis. Author(s): Proksch E, Jensen JM, Elias PM. Source: Clinics in Dermatology. 2003 March-April; 21(2): 134-44. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12706331&dopt=Abstract

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Soluble CD30 plasma concentrations correlate with disease activity in patients with atopic dermatitis. Author(s): Folster-Holst R, Henseler T, Wehde J, Lemke H, Weichenthal M, Christophers E, Hansen HP. Source: Acta Dermato-Venereologica. 2002; 82(4): 245-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12361126&dopt=Abstract

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Specific patterns of responsiveness to microbial antigens staphylococcal enterotoxin B and purified protein derivative by cord blood mononuclear cells are predictive of risk for development of atopic dermatitis. Author(s): Sharp MJ, Rowe J, Kusel M, Sly PD, Holt PG. Source: Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology. 2003 April; 33(4): 435-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12680857&dopt=Abstract

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Sphingosylphosphorylcholine is upregulated in the stratum corneum of patients with atopic dermatitis. Author(s): Okamoto R, Arikawa J, Ishibashi M, Kawashima M, Takagi Y, Imokawa G. Source: Journal of Lipid Research. 2003 January; 44(1): 93-102. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12518027&dopt=Abstract

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Stereochemical considerations on concomitant allergic contact dermatitis to ester of the cis-trans isomeric compounds maleic acid and fumaric acid. Author(s): Hansson C, Thorneby-Andersson K. Source: Skin Pharmacology and Applied Skin Physiology. 2003 March-April; 16(2): 11722. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12637787&dopt=Abstract

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Subclinical activation of latent cytomegalovirus (CMV) infection and anti-CMV immune response in patients with atopic dermatitis. Author(s): Docke WD, Kiessling C, Worm M, Friedrich M, Pruss A, Weitz M, Prosch S, Kern F, Volk HD, Sterry W, Asadullah K. Source: The British Journal of Dermatology. 2003 May; 148(5): 954-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12786826&dopt=Abstract

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Surface expression of Fc epsilon RI on Langerhans' cells of clinically uninvolved skin is associated with disease activity in atopic dermatitis, allergic asthma, and rhinitis. Author(s): Semper AE, Heron K, Woollard AC, Kochan JP, Friedmann PS, Church MK, Reischl IG. Source: The Journal of Allergy and Clinical Immunology. 2003 August; 112(2): 411-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12897750&dopt=Abstract

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Surveillance of allergic contact dermatitis: epoxy resin and microscopic immersion oil. Author(s): Hughes R, Taylor JS. Source: Journal of the American Academy of Dermatology. 2002 December; 47(6): 965-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12451390&dopt=Abstract

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Systemic contact dermatitis from ethylenediamine in an aminophylline preparation presenting as the baboon syndrome. Author(s): Isaksson M, Ljunggren B. Source: Acta Dermato-Venereologica. 2003; 83(1): 69-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12636035&dopt=Abstract

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Systemic contact dermatitis to doxepin. Author(s): Brancaccio RR, Weinstein S. Source: J Drugs Dermatol. 2003 August; 2(4): 409-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12884464&dopt=Abstract

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Systemic contact dermatitis to gentamicin. Author(s): Paniagua MJ, Garcia-Ortega P, Tella R, Gaig P, Richart C. Source: Allergy. 2002 November; 57(11): 1086-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12359018&dopt=Abstract

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T cell phenotype in allergic asthma and atopic dermatitis. Author(s): Wohlfahrt JG, Kunzmann S, Menz G, Kneist W, Akdis CA, Blaser K, SchmidtWeber CB. Source: International Archives of Allergy and Immunology. 2003 August; 131(4): 272-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915770&dopt=Abstract

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Tacrolimus 0.1% ointment for seborrhoeic dermatitis: an open-label pilot study. Author(s): Braza TJ, DiCarlo JB, Soon SL, McCall CO. Source: The British Journal of Dermatology. 2003 June; 148(6): 1242-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828755&dopt=Abstract

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Tacrolimus ointment 0.1% in the treatment of nickel-induced allergic contact dermatitis. Author(s): Saripalli YV, Gadzia JE, Belsito DV. Source: Journal of the American Academy of Dermatology. 2003 September; 49(3): 47782. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12963912&dopt=Abstract

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Tacrolimus ointment for the treatment of atopic dermatitis is not associated with an increase in cutaneous infections. Author(s): Fleischer AB Jr, Ling M, Eichenfield L, Satoi Y, Jaracz E, Rico MJ, Maher RM; Tacrolimus Ointment Study Group. Source: Journal of the American Academy of Dermatology. 2002 October; 47(4): 562-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12271302&dopt=Abstract

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Tacrolimus ointment for the treatment of atopic dermatitis: report of first clinical experience in Taiwan. Author(s): Lan CC, Huang CC, Chen YT, Wang LF, Lin CT, Chen GS. Source: Kaohsiung J Med Sci. 2003 June; 19(6): 296-304. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12873038&dopt=Abstract

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Test your knowledge. Patient with a skin rash. Author(s): Tan E, Teixeira F. Source: Aust Fam Physician. 2003 May; 32(5): 351-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12772369&dopt=Abstract

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The atopic eczema/dermatitis syndrome. Epidemiology, natural course, and immunology of the IgE-associated (“extrinsic”) and the nonallergic (“intrinsic”) AEDS. Author(s): Wuthrich B, Schmid-Grendelmeier P. Source: J Investig Allergol Clin Immunol. 2003; 13(1): 1-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861844&dopt=Abstract

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The presence of surface CD30 on T cells in atopic dermatitis. Author(s): Lipozencic J, Bobek D, Jakic-Razumovic J. Source: Acta Dermatovenerol Croat. 2003; 11(3): 145-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12967506&dopt=Abstract

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The role of the dermatology nurse in atopic dermatitis management. Author(s): Tofte S. Source: Dermatology Nursing / Dermatology Nurses' Association. 2003 August; Suppl: 10-1, 18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14520892&dopt=Abstract

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The unfavorable effects of concomitant asthma and sleeplessness due to the atopic eczema/dermatitis syndrome (AEDS) on quality of life in subjects allergic to housedust mites. Author(s): Terreehorst I, Duivenvoorden HJ, Tempels-Pavlica Z, Oosting AJ, de Monchy JG, Bruijnzeel-Koomen CA, Post MW, Gerth van Wijk R. Source: Allergy. 2002 October; 57(10): 919-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12269938&dopt=Abstract

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Topical calcipotriol is not effective in facial seborrhoeic dermatitis. Author(s): Berth-Jones J, Adnitt PI. Source: The Journal of Dermatological Treatment. 2001 September; 12(3): 179. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12243712&dopt=Abstract

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Topical corticosteroids in atopic dermatitis. Author(s): Atherton DJ. Source: Bmj (Clinical Research Ed.). 2003 October 25; 327(7421): 942-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14576221&dopt=Abstract

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Topical pimecrolimus in the treatment of seborrheic dermatitis. Author(s): Brownell I, Quan LT, Hsu S. Source: Dermatology Online Journal [electronic Resource]. 2003 August; 9(3): 13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12952760&dopt=Abstract

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Topical treatment of atopic dermatitis with St. John's wort cream--a randomized, placebo controlled, double blind half-side comparison. Author(s): Schempp CM, Windeck T, Hezel S, Simon JC. Source: Phytomedicine : International Journal of Phytotherapy and Phytopharmacology. 2003; 10 Suppl 4: 31-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12807340&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 actinic dermatitis with tacrolimus ointment. Author(s): McCall CO. Source: Journal of the American Academy of Dermatology. 2003 October; 49(4): 775; Author Reply 775-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14512946&dopt=Abstract

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Treatment options and new therapeutic approaches in atopic dermatitis. Author(s): Boguniewicz M. Source: Dermatology Nursing / Dermatology Nurses' Association. 2003 August; Suppl: 12-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14520893&dopt=Abstract

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Twice weekly fluticasone propionate added to emollient maintenance treatment to reduce risk of relapse in atopic dermatitis: randomised, double blind, parallel group study. Author(s): Berth-Jones J, Damstra RJ, Golsch S, Livden JK, Van Hooteghem O, Allegra F, Parker CA; Multinational Study Group. Source: Bmj (Clinical Research Ed.). 2003 June 21; 326(7403): 1367. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12816824&dopt=Abstract

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Two unusual cases of diffuse acrodermatitis chronica atrophicans seronegative for Lyme borreliosis. Author(s): Berger TG, Schoerner C, Schell H, Simon M, Schuler G, Rollinghoff M, Gessner A. Source: European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology. 2003 June; 22(6): 392-5. Epub 2003 May 29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12783283&dopt=Abstract

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Type I sensitization in adolescents: prevalence and association with atopic dermatitis. The Odense Adolescence Cohort Study on Atopic Diseases and Dermatitis (TOACS). Author(s): Mortz CG, Lauritsen JM, Andersen KE, Bindslev-Jensen C. Source: Acta Dermato-Venereologica. 2003; 83(3): 194-201. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12816155&dopt=Abstract

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Up-regulated expression of MICA and proinflammatory cytokines in skin biopsies from patients with seborrhoeic dermatitis. Author(s): Molinero LL, Gruber M, Leoni J, Woscoff A, Zwirner NW. Source: Clinical Immunology (Orlando, Fla.). 2003 January; 106(1): 50-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12584051&dopt=Abstract

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Use of Wau Wa in dermatitis patients. Author(s): Daniels J, Shaw D, Atherton D. Source: Lancet. 2002 September 28; 360(9338): 1025. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12383696&dopt=Abstract

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Validation of expert opinion in identifying comorbidities associated with atopic dermatitis/eczema. Author(s): Ellis CN, Drake LA, Prendergast MM, Abramovits W, Boguniewicz M, Daniel CR, Lebwohl M, Stevens SR, Whitaker-Worth DL, Tong KB. Source: Pharmacoeconomics. 2003; 21(12): 875-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12908843&dopt=Abstract

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Validation of the Dermatology Life Quality Index and the Work Productivity and Activity Impairment-Chronic Hand Dermatitis questionnaire in chronic hand dermatitis. Author(s): Reilly MC, Lavin PT, Kahler KH, Pariser DM. Source: Journal of the American Academy of Dermatology. 2003 January; 48(1): 128-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12522383&dopt=Abstract

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Viral infections in atopic dermatitis: pathogenic aspects and clinical management. Author(s): Wollenberg A, Wetzel S, Burgdorf WH, Haas J. Source: The Journal of Allergy and Clinical Immunology. 2003 October; 112(4): 667-74. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14564342&dopt=Abstract

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What do trainee hairdressers know about hand dermatitis? Author(s): Ling TC, Coulson IH. Source: Contact Dermatitis. 2002 October; 47(4): 227-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492522&dopt=Abstract

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What is your diagnosis? Bacterial dermatitis due to Corynebacterium species. Author(s): Pichardo RO, Lu D, Sangueza OP, Prieto VG. Source: The American Journal of Dermatopathology. 2002 December; 24(6): 510-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12481775&dopt=Abstract

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CHAPTER 2. NUTRITION AND DERMATITIS Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and dermatitis.

Finding Nutrition Studies on Dermatitis 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 “dermatitis” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.

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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 information is typical of that found when using the “Full IBIDS Database” to search for “dermatitis” (or a synonym): •

Allergic contact dermatitis following exposure to essential oils. Author(s): Skin and Cancer Foundation, Carlton, Victoria, Australia, and Health Waikato, Hamilton, New Zealand. Source: Bleasel, N Tate, B Rademaker, M Australas-J-Dermatol. 2002 August; 43(3): 211-3 0004-8380

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Alternative treatments for atopic dermatitis: a selected review. Author(s): Dept. of Medicine, McMaster University, Hamilton, Ontario, Canada. Source: Vender, R B Skin-Therapy-Lett. 2002 February; 7(2): 1-5 1201-5989

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An integrative approach to eczema (atopic dermatitis). Author(s): Certified Nutritional Consultant Faculty, Drexel University Nursing and Health Professions CE, Philadelphia, Pennsylvania, USA. Source: Ross, S M Holist-Nurs-Pract. 2003 Jan-February; 17(1): 56-62 0887-9311

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Antihistamines in the management of canine atopic dermatitis: a retrospective study of 171 dogs (1992-1998). Author(s): Koret Veterinary Teaching Hospital, School of Veterinary Medicine, The Hebrew University of Jerusalem, Rehovot, Israel. Source: Zur, Gila Ihrke, Peter J White, Stephen D Kass, Philip H Vet-Ther. 2002 Spring; 3(1): 88-96 1528-3593

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Association of a new-type prostaglandin D2 receptor CRTH2 with circulating T helper 2 cells in patients with atopic dermatitis. Author(s): Department of Molecular Biology, Toho University School of Medicine, Tokyo, Japan. Source: Iwasaki, M Nagata, K Takano, S Takahashi, K Ishii, N Ikezawa, Z J-InvestDermatol. 2002 September; 119(3): 609-16 0022-202X

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Biphasic cytokine expression by T cell clones from patients with atopic dermatitis with different incubation periods and strengths of stimuli. Author(s): Department of Dermatology, Fukushima Medical University School of Medicine, Fukushima City, Japan. Source: Kanek, R Matsu, T Iwatsuki, K Motok, Y Oyama Kaneko, F Fukushima-J-MedSci. 2001 December; 47(2): 51-62 0016-2590

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Blue jean button dermatitis. Nickel allergy presenting as a periumbilical rash. Author(s): Department of Internal Medicine, Akron General Medical Center, Akron, Ohio, USA. Source: Cerveny, K A Jr Brodell, R T Postgrad-Med. 2002 November; 112(5): 79-80, 83 0032-5481

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Bullous phytophotodermatitis associated with high natural concentrations of furanocoumarins in limes. Author(s): Department of Pediatrics, Northwestern University Medical School, Chicago, IL, USA. [email protected] Source: Wagner, Annette M Wu, Jashin J Hansen, Ronald C Nigg, Herbert N Beiere, Ross C Am-J-Contact-Dermat. 2002 March; 13(1): 10-4 1046-199X

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Can zinc be used for the treatment of Microsporum gypseum dermatitis in man as well as in sheep? Source: Xylouri Frangiadaki, E Papadopoulou, C V Bryoni, G Int-J-Antimicrob-Agents. 2002 September; 20(3): 230-1 0924-8579

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Cashew nut dermatitis in a returned traveler. Author(s): Division of Infectious Disease, University of Alabama at Birmingham, 1530 3rd Ave. S BBRB 203, Birmingham, AL 35294-2170, USA. Source: Maje, H A Freedman, D O J-Travel-Med. 2001 Jul-August; 8(4): 213-5 1195-1982

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Comparison of valnemulin and lincomycin in the treatment of digital dermatitis by individually applied topical spray. Author(s): Bridgets Diary Research Centre, Martyr Worthy, Hampshire. Source: Laven, R A Hunt, H Vet-Rec. 2001 September 8; 149(10): 302-3 0042-4900

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Contact dermatitis to botanical extracts. Author(s): Department of Dermatology, New York University School of Medicine, New York, NY, USA. Source: Kiken, D A Cohen, D E Am-J-Contact-Dermat. 2002 September; 13(3): 148-52 1046-199X

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Cost of illness of atopic dermatitis in children: a societal perspective. Author(s): Department of Immunology, Royal Children's Hospital, Melbourne, Australia. [email protected] Source: Kemp, A S Pharmacoeconomics. 2003; 21(2): 105-13 1170-7690

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Cutaneous lymphocyte-associated antigen expression in children with atopic dermatitis and non-atopic healthy children. Author(s): Department of Immunology, Royal Children's Hospital, Melbourne, Parkville, Victoria, Australia. Source: Campbell, D E Kemp, A S Pediatr-Allergy-Immunol. 1999 November; 10(4): 2537 0905-6157

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Cytokine network and dysregulated apoptosis in atopic dermatitis. Author(s): Swiss Institute of Allergy and Asthma Research, Davos, Switzerland. [email protected] Source: Akdis, M Trautmann, A Klunker, S Blaser, K Akdis, C A Acta-Odontol-Scand. 2001 June; 59(3): 178-82 0001-6357

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Deficiency of epidermal protein-bound omega-hydroxyceramides in atopic dermatitis. Author(s): Kekule-Institut fur Organische Chemie und Biochemie, Universitaet Bonn, Gerhard-Domagk-Strasse 1, D-53121 Bonn, Germany. Source: Macheleidt, O Kaiser, H W Sandhoff, K J-Invest-Dermatol. 2002 July; 119(1): 16673 0022-202X

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Dermatitis associated with Dirofilaria (Nochtiella) repens microfilariae in dogs from central Italy. Author(s): [email protected] Source: Tarello, W Acta-Vet-Hung. 2002; 50(1): 63-78 0236-6290

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Dermatitis to captopril. Author(s): Department of Allergy, Hospital Rio Hortega. Valladolid, Spain. Source: Martinez, J C Fuentes, M J Armentia, A Vega, J M Fernandez, A AllergolImmunopathol-(Madr). 2001 Nov-December; 29(6): 279-80 0301-0546

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Effect and correlation of serum total IgE, eosinophil granule cationic proteins and sensitized allergens in atopic dermatitis patients with or without rhinitis. Author(s): School of Medical Technology, Kaohsiung Medical University, No. 100, ShihChuan 1st Road, Kaohsiung, Taiwan 80708. Source: Wu, C S Yu, C L Chang, C H Kuo, W R Lin, H J Yu, H S Kaohsiung-J-Med-Sci. 2002 May; 18(5): 229-35 1607-551X

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Effective treatment of seborrheic dermatitis using a low dose, oral homeopathic medication consisting of potassium bromide, sodium bromide, nickel sulfate, and sodium chloride in a double-blind, placebo-controlled study. Author(s): Loma Lux Laboratories, Tulsa, OK, USA. [email protected] Source: Smith, Steven A Baker, Ardith E Williams, John H Altern-Med-Revolume 2002 February; 7(1): 59-67 1089-5159

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Efficacy of corticosteroids in acute experimental irritant contact dermatitis? Author(s): Department of Dermatology, University of California at San Francisco Medical Center, CA 94143-0989, USA. Source: Levin, C Zhai, H Bashir, S Chew, A L Anigbogu, A Stern, R Maibach, H SkinRes-Technol. 2001 November; 7(4): 214-8 0909-752X

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Five cases of livedo-like dermatitis (Nicolau's syndrome) due to bismuth salts and various other non-steroidal anti-inflammatory drugs. Author(s): Dipartimento di Medicina Clinica e Sperimentale-Sezione Dermatologia, Universita di Ferrara, Italy. Source: Corazza, M Capozzi, O Virgilit, A J-Eur-Acad-Dermatol-Venereol. 2001 November; 15(6): 585-8 0926-9959

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Improvement of skin symptoms and mineral imbalance by drinking deep sea water in patients with atopic eczema/dermatitis syndrome (AEDS). Author(s): Department of Allergy, Unitika Central Hospital, Uji-City, Kyoto Prefecture, Japan. [email protected] Source: Kimata, H Tai, H Nakagawa, K Yokoyama, Y Nakajima, H Ikegami, Y ActaMedica-(Hradec-Kralove). 2002; 45(2): 83-4 1211-4286

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Liver X receptor activators display anti-inflammatory activity in irritant and allergic contact dermatitis models: liver-X-receptor-specific inhibition of inflammation and primary cytokine production. Author(s): Department of Dermatology, University of California, San Francisco, USA. Source: Fowler, A J Sheu, M Y Schmuth, M Kao, J Fluhr, J W Rhein, L Collins, J L Willson, T M Mangelsdorf, D J Elias, P M Feingold, K R J-Invest-Dermatol. 2003 February; 120(2): 246-55 0022-202X

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Occupational allergic contact dermatitis to silver and colophonium in a jeweler. Author(s): Royal Hallamshire Hospital, Sheffield, England. Source: Agarwal, S Gawkrodger, D J Am-J-Contact-Dermat. 2002 June; 13(2): 74 1046199X

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Phytotherapy of chronic dermatitis and pruritus of dogs with a topical preparation containing tea tree oil (Bogaskin). Author(s): Department of Internal Medicine/Naturheilkunde, University of Zurich. [email protected] Source: Fitzi, J Furst Jucker, J Wegener, T Saller, R Reichling, J Schweiz-Arch-Tierheilkd. 2002 May; 144(5): 223-31 0036-7281

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Positive skin and oral challenge responses to potato and occurrence of immunoglobulin E antibodies to patatin (Sol t 1) in infants with atopic dermatitis. Author(s): Department of Dermatology, Tampere University Hospital and University of Tampere, Finland. [email protected] Source: Majamaa, H Seppala, U Palosuo, T Turjanmaa, K Kalkkinen, N Reunala, T Pediatr-Allergy-Immunol. 2001 October; 12(5): 283-8 0905-6157

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Probiotics and atopic dermatitis. A new strategy in atopic dermatitis. Author(s): Department of Paediatrics, Second University, Naples, Italy. [email protected] Source: Miraglia del Giudice, M Jr De Luca, M G Capristo, C Dig-Liver-Dis. 2002 September; 34 Suppl 2: S68-71 1590-8658

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Proteolytic activity of Staphylococcus aureus strains isolated from the colonized skin of patients with acute-phase atopic dermatitis. Author(s): Institute of Molecular Biology and Biotechnology, Jagiellonian University, ul. Gronostajowa 7, 30-387 Krakow, Poland. [email protected] Source: Miedzobrodzki, J Kaszycki, P Bialecka, A Kasprowicz, A Eur-J-Clin-MicrobiolInfect-Dis. 2002 April; 21(4): 269-76 0934-9723

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Steroid dermatitis resembling rosacea: aetiopathogenesis and treatment. Author(s): Department of Dermatology and Venereology, Zagreb University Hospital Center, Croatia. [email protected] Source: Ljubojeviae, S Basta Juzbasiae, A Lipozeneiae, J J-Eur-Acad-Dermatol-Venereol. 2002 March; 16(2): 121-6 0926-9959

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The antibacterial-corticosteroid combination. What is its role in atopic dermatitis? Author(s): Glan Clwyd Hospital, Bodelwyddan, Rhyl, Wales. Source: Williams, R E Am-J-Clin-Dermatol. 2000 Jul-August; 1(4): 211-5 1175-0561

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The relationship between HIV infection and atopic dermatitis. Author(s): Mount Sinai School of Medicine, 1 Gustave L. Levy Place, Box 1048, New York, NY 10029, USA. [email protected] Source: Rudikoff, D Curr-Allergy-Asthma-Repage 2002 July; 2(4): 275-81 1529-7322

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Treatment principles of atopic dermatitis. Author(s): Department of Dermatology, University of Aarhus, Marselisborg Hospital, Denmark. [email protected] Source: Thestrup Pedersen, K J-Eur-Acad-Dermatol-Venereol. 2002 January; 16(1): 1-9 0926-9959

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Vegetarian diet ameliorates symptoms of atopic dermatitis through reduction of the number of peripheral eosinophils and of PGE2 synthesis by monocytes. Author(s): Department III of Internal Medicine, Osaka University Medical School. [email protected] Source: Tanaka, T Kouda, K Kotani, M Takeuchi, A Tabei, T Masamoto, Y Nakamura, H Takigawa, M Suemura, M Takeuchi, H Kouda, M J-Physiol-Anthropol-Appl-Human-Sci. 2001 November; 20(6): 353-61 1345-3475

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/

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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WebMDHealth: 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 dermatitis; 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 Niacin Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,892,00.html

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Riboflavin Source: Integrative Medicine Communications; www.drkoop.com Vitamin A Source: Prima Communications, Inc.www.personalhealthzone.com Vitamin B Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10067,00.html Vitamin B12 Source: Healthnotes, Inc.; www.healthnotes.com Vitamin B2 (riboflavin) Source: Integrative Medicine Communications; www.drkoop.com Vitamin B3 Source: Healthnotes, Inc.; www.healthnotes.com Vitamin B6 Source: Healthnotes, Inc.; www.healthnotes.com Vitamin E Source: Healthnotes, Inc.; www.healthnotes.com •

Minerals Acetyl-l-carnitine Source: Healthnotes, Inc.; www.healthnotes.com Betaine Hydrochloride Source: Healthnotes, Inc.; www.healthnotes.com Biotin Source: Healthnotes, Inc.; www.healthnotes.com Biotin Source: Integrative Medicine Communications; www.drkoop.com Iron Source: Healthnotes, Inc.; www.healthnotes.com Selenium Source: Healthnotes, Inc.; www.healthnotes.com Sulfur Source: Integrative Medicine Communications; www.drkoop.com Vitamin H (biotin) Source: Integrative Medicine Communications; www.drkoop.com

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Zinc Source: Healthnotes, Inc.; www.healthnotes.com Zinc Source: Integrative Medicine Communications; www.drkoop.com •

Food and Diet Brazil Nuts Source: Healthnotes, Inc.; www.healthnotes.com Cinnamon Alternative names: Cinnamomum zeylanicum Source: Healthnotes, Inc.; www.healthnotes.com Corn-free Diet Source: Healthnotes, Inc.; www.healthnotes.com Dairy-free Diet Source: Healthnotes, Inc.; www.healthnotes.com Egg-free Diet Source: Healthnotes, Inc.; www.healthnotes.com Gluten-free Diet Source: Healthnotes, Inc.; www.healthnotes.com Mushrooms Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10046,00.html Octopus Source: Healthnotes, Inc.; www.healthnotes.com Pecans Source: Healthnotes, Inc.; www.healthnotes.com Pumpkin Seeds Source: Healthnotes, Inc.; www.healthnotes.com Soy-free Diet Source: Healthnotes, Inc.; www.healthnotes.com Wheat Source: Healthnotes, Inc.; www.healthnotes.com Wheat-free Diet Source: Healthnotes, Inc.; www.healthnotes.com

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CHAPTER 3. ALTERNATIVE MEDICINE AND DERMATITIS Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to dermatitis. 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 dermatitis 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 “dermatitis” (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 dermatitis: •

A double-blind, randomized, placebo-controlled trial of n-3 versus n-6 fatty acidbased lipid infusion in atopic dermatitis. Author(s): Mayser P, Mayer K, Mahloudjian M, Benzing S, Kramer HJ, Schill WB, Seeger W, Grimminger F. Source: Jpen. Journal of Parenteral and Enteral Nutrition. 2002 May-June; 26(3): 151-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12005454&dopt=Abstract

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A phase III trial comparing an anionic phospholipid-based (APP) cream and aloe vera-based gel in the prevention and treatment of radiation dermatitis. Author(s): Bosley C, Smith J, Baratti P, Pritchard DL, Xiong X, Li C, Merchant TE. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 October 1; 57(2 Suppl): S438. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12965848&dopt=Abstract

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A randomized comparison of an emollient containing skin-related lipids with a petrolatum-based emollient as adjunct in the treatment of chronic hand dermatitis. Author(s): Kucharekova M, Van De Kerkhof PC, Van Der Valk PG. Source: Contact Dermatitis. 2003 June; 48(6): 293-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14531866&dopt=Abstract

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A randomized, double-blind, placebo-controlled trial to investigate the efficacy and safety of a Chinese herbal product (P07P) for the treatment of canine atopic dermatitis. Author(s): Nagle TM, Torres SM, Horne KL, Grover R, Stevens MT. Source: Veterinary Dermatology. 2001 October; 12(5): 265-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11906651&dopt=Abstract

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A review of recent journal highlights focusing on atopic dermatitis. Author(s): Allam JP, Bieber T. Source: Clinical and Experimental Dermatology. 2003 September; 28(5): 577-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12950368&dopt=Abstract

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A trial of oolong tea in the management of recalcitrant atopic dermatitis. Author(s): Uehara M, Sugiura H, Sakurai K. Source: Archives of Dermatology. 2001 January; 137(1): 42-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11176659&dopt=Abstract

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Accuracy of questions related to allergic contact dermatitis. Author(s): Fleming CJ, Burden AD, Forsyth A. Source: American Journal of Contact Dermatitis : Official Journal of the American Contact Dermatitis Society. 2000 December; 11(4): 218-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11123414&dopt=Abstract

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Acrodermatitis enteropathica: case report and review of the literature. Author(s): Perafan-Riveros C, Franca LF, Alves AC, Sanches JA Jr. Source: Pediatric Dermatology. 2002 September-October; 19(5): 426-31. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12383101&dopt=Abstract

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Acute necrotizing dermatitis and septicemia after application of a d-limonene-based insecticidal shampoo in a cat. Author(s): Lee JA, Budgin JB, Mauldin EA. Source: J Am Vet Med Assoc. 2002 July 15; 221(2): 258-62, 239-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12118590&dopt=Abstract

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Allergic and irritant occupational contact dermatitis from Alstroemeria. Author(s): Mascarenhas R, Robalo-Cordeiro M, Fernandes B, Oliveira HS, Goncalo M, Figueiredo A.

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Source: Contact Dermatitis. 2001 March; 44(3): 196-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11218006&dopt=Abstract •

Allergic contact dermatitis at the application site of an electrosurgical earthing plate occurring in a windscreen repairer. Author(s): Banerjee P, White IR. Source: Contact Dermatitis. 2001 February; 44(2): 97. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11205413&dopt=Abstract

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Allergic contact dermatitis due to avena extract. Author(s): Pazzaglia M, Jorizzo M, Parente G, Tosti A. Source: Contact Dermatitis. 2000 June; 42(6): 364. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10871113&dopt=Abstract

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Allergic contact dermatitis due to Icelandic poppy (Papaver nudicaule). Author(s): Jury CS, Lever R. Source: Contact Dermatitis. 2000 May; 42(5): 300-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10789861&dopt=Abstract

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Allergic contact dermatitis elicitation thresholds of potent allergens in humans. Author(s): Jerschow E, Hostynek JJ, Maibach HI. Source: Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association. 2001 November; 39(11): 1095-108. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11527569&dopt=Abstract

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Allergic contact dermatitis following exposure to essential oils. Author(s): Bleasel N, Tate B, Rademaker M. Source: The Australasian Journal of Dermatology. 2002 August; 43(3): 211-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12121401&dopt=Abstract

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Allergic contact dermatitis from camomile used in phytotherapy. Author(s): Giordano-Labadie F, Schwarze HP, Bazex J. Source: Contact Dermatitis. 2000 April; 42(4): 247. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10750867&dopt=Abstract

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Allergic contact dermatitis from ciclopirox olamine. Author(s): Foti C, Diaferio A, Bonamonte D. Source: The Australasian Journal of Dermatology. 2001 May; 42(2): 145. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11309043&dopt=Abstract

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Allergic contact dermatitis from diallyl disulfide. Author(s): Fernandez-Vozmediano JM, Armario-Hita JC, Manrique-Plaza A. Source: Contact Dermatitis. 2000 February; 42(2): 108-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10703639&dopt=Abstract

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Allergic contact dermatitis from mastic in compound mastic paint. Author(s): Wakelin SH. Source: Contact Dermatitis. 2001 August; 45(2): 118. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11553130&dopt=Abstract

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Allergic contact dermatitis from Mentha spicata (spearmint). Author(s): Bonamonte D, Mundo L, Daddabbo M, Foti C. Source: Contact Dermatitis. 2001 November; 45(5): 298. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11722493&dopt=Abstract

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Allergic contact dermatitis from pentylene glycol in an emollient cream, with possible co-sensitization to resveratrol. Author(s): Gallo R, Viglizzo G, Vecchio F, Parodi A. Source: Contact Dermatitis. 2003 March; 48(3): 176-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12755747&dopt=Abstract

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Allergic contact dermatitis from pine tar. Author(s): Iorizzo M, Lucente P, Pazzaglia M. Source: Contact Dermatitis. 2000 August; 43(2): 125. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10945763&dopt=Abstract

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Allergic contact dermatitis from shellac in mascara. Author(s): Le Coz CJ, Leclere JM, Arnoult E, Raison-Peyron N, Pons-Guiraud A, Vigan M; Members of Revidal-Gerda. Source: Contact Dermatitis. 2002 March; 46(3): 149-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12000323&dopt=Abstract

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Allergic contact dermatitis from sodium dihydroxycetyl phosphate, a new cosmetic allergen? Author(s): Lomholt H, Rastogi SC, Andersen KE. Source: Contact Dermatitis. 2001 September; 45(3): 143-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11553139&dopt=Abstract

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Allergic contact dermatitis in children: a practical approach to management. Author(s): Bruckner AL, Weston WL.

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Source: Skin Therapy Letter. 2002 October; 7(8): 3-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12548328&dopt=Abstract •

Allergic contact dermatitis to propolis in a violin maker. Author(s): Lieberman HD, Fogelman JP, Ramsay DL, Cohen DE. Source: Journal of the American Academy of Dermatology. 2002 February; 46(2 Suppl Case Reports): S30-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11807465&dopt=Abstract

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Allergic contact dermatitis to tea tree oil with erythema multiforme-like id reaction. Author(s): Khanna M, Qasem K, Sasseville D. Source: American Journal of Contact Dermatitis : Official Journal of the American Contact Dermatitis Society. 2000 December; 11(4): 238-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11123417&dopt=Abstract

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Allergic contact dermatitis. Author(s): Kimbe I, Basketter DA, Gerberick GF, Dearman RJ. Source: International Immunopharmacology. 2002 February; 2(2-3): 201-11. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11811925&dopt=Abstract

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Alternative treatments for atopic dermatitis: a selected review. Author(s): Vender RB. Source: Skin Therapy Letter. 2002 February; 7(2): 1-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12007013&dopt=Abstract

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An integrative approach to eczema (atopic dermatitis). Author(s): Ross SM. Source: Holistic Nursing Practice. 2003 January-February; 17(1): 56-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12597676&dopt=Abstract

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An unexpected occurrence of acute contact dermatitis during rhinoplasty. Author(s): Mabrie DC, Papel ID. Source: Archives of Facial Plastic Surgery : Official Publication for the American Academy of Facial Plastic and Reconstructive Surgery, Inc. and the International Federation of Facial Plastic Surgery Societies. 1999 October-December; 1(4): 320-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10937124&dopt=Abstract

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Antibacterial effect of beta-thujaplicin on staphylococci isolated from atopic dermatitis: relationship between changes in the number of viable bacterial cells and clinical improvement in an eczematous lesion of atopic dermatitis. Author(s): Arima Y, Nakai Y, Hayakawa R, Nishino T.

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Source: The Journal of Antimicrobial Chemotherapy. 2003 January; 51(1): 113-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12493795&dopt=Abstract •

Antimicrobial effects of acidic hot-spring water on Staphylococcus aureus strains isolated from atopic dermatitis patients. Author(s): Akiyama H, Yamasaki O, Tada J, Kubota K, Arata J. Source: Journal of Dermatological Science. 2000 November; 24(2): 112-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11064246&dopt=Abstract

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Antipruritic and antidermatitic effect of extract and compounds of Impatiens balsamina L. in atopic dermatitis model NC mice. Author(s): Oku H, Ishiguro K. Source: Phytotherapy Research : Ptr. 2001 September; 15(6): 506-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11536380&dopt=Abstract

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Atopic dermatitis management: comparing the treatment patterns of dermatologists in Japan, U.S.A. and U.K. Author(s): Baron ED, Barzilai D, Johnston G, Kawashima M, Takigawa M, Nakagawa H, Graham-Brown RA, Stevens SR. Source: The British Journal of Dermatology. 2002 October; 147(4): 710-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12366417&dopt=Abstract

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Azathioprine as a corticosteroid sparing agent for the treatment of dermatitis caused by the weed Parthenium. Author(s): Verma KK, Manchanda Y, Pasricha JS. Source: Acta Dermato-Venereologica. 2000 January-February; 80(1): 31-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10721830&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. 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

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Balsam-related systemic contact dermatitis. Author(s): Salam TN, Fowler JF Jr. Source: Journal of the American Academy of Dermatology. 2001 September; 45(3): 37781. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11511833&dopt=Abstract

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Basal cell carcinoma on nickel dermatitis after leech applying. Author(s): Shamsaddini S, Dabiri S.

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Source: East Mediterr Health J. 2000 January; 6(1): 197-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11370335&dopt=Abstract •

Berloque dermatitis induced by “Florida water”. Author(s): Wang L, Sterling B, Don P. Source: Cutis; Cutaneous Medicine for the Practitioner. 2002 July; 70(1): 29-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12184670&dopt=Abstract

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Bullous phytophotodermatitis associated with high natural concentrations of furanocoumarins in limes. Author(s): Wagner AM, Wu JJ, Hansen RC, Nigg HN, Beiere RC. Source: American Journal of Contact Dermatitis : Official Journal of the American Contact Dermatitis Society. 2002 March; 13(1): 10-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11887098&dopt=Abstract

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Can zinc be used for the treatment of Microsporum gypseum dermatitis in man as well as in sheep? Author(s): Xylouri-Frangiadaki E, Papadopoulou CV, Bryoni G. Source: International Journal of Antimicrobial Agents. 2002 September; 20(3): 230-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12385705&dopt=Abstract

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Clinical efficacy and immunoregulatory and neurohumoral effects of MM therapy in patients with atopic dermatitis. Author(s): Adaskevich VP. Source: Crit Rev Biomed Eng. 2000; 28(5-6): 11-21. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11211977&dopt=Abstract

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Clinical features of 31 patients with systemic contact dermatitis due to the ingestion of Rhus (lacquer). Author(s): Park SD, Lee SW, Chun JH, Cha SH. Source: The British Journal of Dermatology. 2000 May; 142(5): 937-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10809851&dopt=Abstract

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Combined contact and photocontact allergic dermatitis to etofenamate in flogoprofen gel. Author(s): Sanchez-Perez J, Sanchez TS, Garcia-Diez A. Source: American Journal of Contact Dermatitis : Official Journal of the American Contact Dermatitis Society. 2001 December; 12(4): 215-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11753896&dopt=Abstract

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Comparison of skin prick test results between crude allergen extracts from foods and commercial allergen extracts in atopic dermatitis by double-blind placebo-controlled

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food challenge for milk, egg, and soybean. Author(s): Kim TE, Park SW, Noh G, Lee S. Source: Yonsei Medical Journal. 2002 October; 43(5): 613-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12402374&dopt=Abstract •

Contact dermatitis associated with an erythema multiforme-like eruption. Author(s): Veien NK, Hausen BM. Source: American Journal of Contact Dermatitis : Official Journal of the American Contact Dermatitis Society. 2000 December; 11(4): 235-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11187214&dopt=Abstract

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Contact dermatitis complicated by environment. Author(s): O'Connell-Gifford E. Source: Ostomy Wound Manage. 2000 September; 46(9): 16-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11189537&dopt=Abstract

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Contact dermatitis from Chelidonium majus (greater celandine). Author(s): Etxenagusia MA, Anda M, Gonzalez-Mahave I, Fernandez E, Fernandez de Corres L. Source: Contact Dermatitis. 2000 July; 43(1): 47. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10902593&dopt=Abstract

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Contact dermatitis from soybean extract in a cosmetic cream. Author(s): Shaffrali FC, Gawkrodger DJ. Source: Contact Dermatitis. 2001 January; 44(1): 51-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11156026&dopt=Abstract

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Contact dermatitis from tosylamide/formaldehyde resin with photosensitivity. Author(s): Vilaplana J, Romaguera C. Source: Contact Dermatitis. 2000 May; 42(5): 311-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10789873&dopt=Abstract

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Contact dermatitis from white flower embrocation. Author(s): Saary MJ, Holness DL. Source: Contact Dermatitis. 2001 February; 44(2): 100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11205379&dopt=Abstract

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Contact dermatitis in students practicing sports: incidence of rubber sensitisation. Author(s): Ventura MT, Dagnello M, Matino MG, Di Corato R, Giuliano G, Tursi A. Source: British Journal of Sports Medicine. 2001 April; 35(2): 100-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11273970&dopt=Abstract

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Contact dermatitis to Asparagus officinalis. Author(s): Rademaker M, Yung A. Source: The Australasian Journal of Dermatology. 2000 November; 41(4): 262-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11105376&dopt=Abstract

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Contact dermatitis to botanical extracts. Author(s): Kiken DA, Cohen DE. Source: American Journal of Contact Dermatitis : Official Journal of the American Contact Dermatitis Society. 2002 September; 13(3): 148-52. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12165936&dopt=Abstract

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Contact leukoderma following nickel dermatitis elicited by TENS electrode plates. Author(s): Al'Ajlan A, Thestrup-Pedersen K, Al'Eisa A. Source: Contact Dermatitis. 2000 March; 42(3): 172-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10727175&dopt=Abstract

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Control of digital dermatitis. Author(s): Blowey RW. Source: The Veterinary Record. 2000 March 4; 146(10): 295. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10749046&dopt=Abstract

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Cost of illness of atopic dermatitis in children: a societal perspective. Author(s): Kemp AS. Source: Pharmacoeconomics. 2003; 21(2): 105-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12515572&dopt=Abstract

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Dead Sea treatment - principle for outpatient use in atopic dermatitis: safety and efficacy of synchronous balneophototherapy using narrowband UVB and bathing in Dead Sea salt solution. Author(s): Schiffner R, Schiffner-Rohe J, Gerstenhauer M, Landthaler M, Hofstadter F, Stolz W. Source: Eur J Dermatol. 2002 November-December; 12(6): 543-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12459524&dopt=Abstract

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Dermatitis caused by electromagnetic radiation. Author(s): Morris SD, McGibbon DH, Rycroft RJ. Source: Contact Dermatitis. 2001 September; 45(3): 188. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11553161&dopt=Abstract

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Dermatitis caused by radio-frequency electromagnetic radiation. Author(s): Strobos MA, Coenraads PJ, De Jongste MJ, Ubels FL.

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Source: Contact Dermatitis. 2001 May; 44(5): 309. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11379983&dopt=Abstract •

Dietary habits among patients with atopic dermatitis. Author(s): Solvoll K, Soyland E, Sandstad B, Drevon CA. Source: European Journal of Clinical Nutrition. 2000 February; 54(2): 93-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10694778&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 monoterpenes released from feverfew (Tanacetum parthenium) plants cause airborne Compositae dermatitis? Author(s): Paulsen E, Christensen LP, Andersen KE. Source: Contact Dermatitis. 2002 July; 47(1): 14-8. Erratum In: Contact Dermatitis. 2003 March; 48(3): 179-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12225407&dopt=Abstract

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Docetaxel-induced radiation recall dermatitis and successful rechallenge without recurrence. Author(s): Camidge DR, Kunkler IH. Source: Clin Oncol (R Coll Radiol). 2000; 12(4): 272-3. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11005698&dopt=Abstract

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Dose-response in double-blind, placebo-controlled oral food challenges in children with atopic dermatitis. Author(s): Sicherer SH, Morrow EH, Sampson HA. Source: The Journal of Allergy and Clinical Immunology. 2000 March; 105(3): 582-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10719311&dopt=Abstract

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Effect of probiotic Lactobacillus strains in children with atopic dermatitis. Author(s): Rosenfeldt V, Benfeldt E, Nielsen SD, Michaelsen KF, Jeppesen DL, Valerius NH, Paerregaard A. Source: The Journal of Allergy and Clinical Immunology. 2003 February; 111(2): 389-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12589361&dopt=Abstract

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Effective treatment of seborrheic dermatitis using a low dose, oral homeopathic medication consisting of potassium bromide, sodium bromide, nickel sulfate, and

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sodium chloride in a double-blind, placebo-controlled study. Author(s): Smith SA, Baker AE, Williams JH. Source: Alternative Medicine Review : a Journal of Clinical Therapeutic. 2002 February; 7(1): 59-67. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11896746&dopt=Abstract •

Effects of dietary restriction on spontaneous dermatitis in NC/Nga mice. Author(s): Fan W, Kouda K, Nakamura H, Takeuchi H. Source: Experimental Biology and Medicine (Maywood, N.J.). 2001 December; 226(11): 1045-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11743141&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 n-3 polyunsaturated fatty acids on dermatitis in NC/Nga mice. Author(s): Suzuki R, Shimizu T, Kudo T, Ohtsuka Y, Yamashiro Y, Oshida K. Source: Prostaglandins, Leukotrienes, and Essential Fatty Acids. 2002 April; 66(4): 43540. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12054914&dopt=Abstract

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Efficacy evaluation of an oil-in-water emulsion (Dermoflan) in atopic dermatitis. Author(s): Peris K, Valeri P, Altobelli E, Fargnoli MC, Carrozzo AM, Chimenti S. Source: Acta Dermato-Venereologica. 2002; 82(6): 465-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12575858&dopt=Abstract

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Evaluation of dietary intake of vitamin E in the treatment of atopic dermatitis: a study of the clinical course and evaluation of the immunoglobulin E serum levels. Author(s): Tsoureli-Nikita E, Hercogova J, Lotti T, Menchini G. Source: International Journal of Dermatology. 2002 March; 41(3): 146-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12010339&dopt=Abstract

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Evidence-based veterinary dermatology: a systematic review of the pharmacotherapy of canine atopic dermatitis. Author(s): Olivry T, Mueller RS; The International Task Force on Canine Atopic Dermatitis. Source: Veterinary Dermatology. 2003 June; 14(3): 121-46. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12791047&dopt=Abstract

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Exposure to pets and atopic dermatitis during the first two years of life. A cohort study. Author(s): Zirngibl A, Franke K, Gehring U, von Berg A, Berdel D, Bauer CP, Reinhardt D, Wichmann HE, Heinrich J; GINI study group. Source: Pediatric Allergy and Immunology : Official Publication of the European Society of Pediatric Allergy and Immunology. 2002 December; 13(6): 394-401. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12485314&dopt=Abstract

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Exudative hyponychial dermatitis associated with capecitabine and docetaxel combination chemotherapy for metastatic breast carcinoma: report of three cases. Author(s): Chen GY, Chang TW, Chen WC. Source: The British Journal of Dermatology. 2003 May; 148(5): 1071-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12786853&dopt=Abstract

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Frequency of contact allergy to Compositae extracts in patients with atopic dermatitis. Author(s): Nettis E, Giordano D, Soccio A, Ferrannini A, Tursi A. Source: Contact Dermatitis. 2002 September; 47(3): 169-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492554&dopt=Abstract

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Frequency of textile dye and resin sensitization in patients with contact dermatitis in Israel. Author(s): Lazarov A, Trattner A, Abraham D, David M. Source: Contact Dermatitis. 2002 February; 46(2): 119-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11918613&dopt=Abstract

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Gamma-linolenic acid supplementation for prophylaxis of atopic dermatitis--a randomized controlled trial in infants at high familial risk. Author(s): van Gool CJ, Thijs C, Henquet CJ, van Houwelingen AC, Dagnelie PC, Schrander J, Menheere PP, van den brandt PA. Source: The American Journal of Clinical Nutrition. 2003 April; 77(4): 943-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663296&dopt=Abstract

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Heliotherapy in atopic dermatitis: a prospective study on climatotherapy using the SCORAD index. Author(s): Autio P, Komulainen P, Larni HM. Source: Acta Dermato-Venereologica. 2002; 82(6): 436-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12575850&dopt=Abstract

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Hochu-ekki-to suppresses development of dermatitis and elevation of serum IgE level in NC/Nga mice. Author(s): Kobayashi H, Mizuno N, Kutsuna H, Teramae H, Ueoku S, Onoyama J, Yamanaka K, Fujita N, Ishii M.

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Source: Drugs Exp Clin Res. 2003; 29(2): 81-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12951838&dopt=Abstract •

Homeopathic treatment of Japanese patients with intractable atopic dermatitis. Author(s): Itamura R, Hosoya R. Source: Homeopathy. 2003 April; 92(2): 108-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12725253&dopt=Abstract

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Hyperpigmentation and contact dermatitis due to Juglans regia. Author(s): Bonamonte D, Foti C, Angelini G. Source: Contact Dermatitis. 2001 February; 44(2): 101-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11205381&dopt=Abstract

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Inhibitory effect of Byakko-ka-ninjin-to on itch in a mouse model of atopic dermatitis. Author(s): Tohda C, Sugahara H, Kuraishi Y, Komatsu K. Source: Phytotherapy Research : Ptr. 2000 May; 14(3): 192-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10815013&dopt=Abstract

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Irritant contact dermatitis due to Indian God lotion. Author(s): Lee TY, Lam TH. Source: Contact Dermatitis. 2001 October; 45(4): 237. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11683838&dopt=Abstract

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Lack of effect of the abnormal fatty acid metabolism in NC/Nga mice on their atopic dermatitis. Author(s): Kawamoto S, Kita M, Hamada M, Aki T, Shigeta S, Suzuki O, Ono K. Source: Bioscience, Biotechnology, and Biochemistry. 2001 February; 65(2): 431-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11302182&dopt=Abstract

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Local erythematous dermatitis after intravenous docetaxel. Author(s): Hirai K, Ishiko O, Nakajima S, Kanaoka Y, Nakamura Y, Oiso N, Ishii M, Ogita S. Source: Gynecologic and Obstetric Investigation. 2002; 53(2): 118-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11961387&dopt=Abstract

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Management of severe atopic dermatitis with thymostimulin. Author(s): Wisuthsarewong W, Viravan S. Source: J Med Assoc Thai. 2002 August; 85 Suppl 2: S749-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12403256&dopt=Abstract

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Mastix is another allergen causing bone-setter's herbs dermatitis. Author(s): Lee TY, Lam TH. Source: Contact Dermatitis. 2001 May; 44(5): 312-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11380086&dopt=Abstract

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Non-eczematous pigmented interface dermatitis from para-tertiary-butylphenolformaldehyde resin in a watchstrap adhesive. Author(s): Ozkaya-Bayazit E, Buyukbabani N. Source: Contact Dermatitis. 2001 January; 44(1): 45-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11156020&dopt=Abstract

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Nonoccupational allergic contact dermatitis to cashew nut simulating photosensitivity eczema. Author(s): Criado RF, Criado PR, Malaman F, Ensina LF, Vasconcellos C, Aun WT, Mello JF, Pires MC. Source: American Journal of Contact Dermatitis : Official Journal of the American Contact Dermatitis Society. 2002 June; 13(2): 85-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12053904&dopt=Abstract

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Occupational airborne allergic contact dermatitis from sawdust in livestock sheds. Author(s): de Cock P, van Ginkel CJ, Faber WR, Bruynzeel DP. Source: Contact Dermatitis. 2000 February; 42(2): 113. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10703644&dopt=Abstract

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Occupational airborne and hand dermatitis to hop (Humulus lupulus) with nonoccupational relapses. Author(s): Spiewak R, Dutkiewicz J. Source: Annals of Agricultural and Environmental Medicine : Aaem. 2002; 9(2): 249-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12498595&dopt=Abstract

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Occupational allergic contact dermatitis from formaldehyde resin in clothing. Author(s): Cockayne SE, McDonagh AJ, Gawkrodger DJ. Source: Contact Dermatitis. 2001 February; 44(2): 109-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11205387&dopt=Abstract

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Occupational allergic contact dermatitis from PEG-4 rapeseed amide in a massage oil. Author(s): Isaksson M. Source: Contact Dermatitis. 2002 September; 47(3): 175-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492561&dopt=Abstract

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Occupational allergic contact dermatitis in two aromatherapists. Author(s): Keane FM, Smith HR, White IR, Rycroft RJ.

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Source: Contact Dermatitis. 2000 July; 43(1): 49-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10902596&dopt=Abstract •

Occupational allergic contact dermatitis to silver and colophonium in a jeweler. Author(s): Agarwal S, Gawkrodger DJ. Source: American Journal of Contact Dermatitis : Official Journal of the American Contact Dermatitis Society. 2002 June; 13(2): 74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12022124&dopt=Abstract

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Occupational contact dermatitis from a garlic and herb mixture. Author(s): Hughes TM, Varma S, Stone NM. Source: Contact Dermatitis. 2002 July; 47(1): 48. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12225414&dopt=Abstract

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Occupational contact dermatitis from colophonium in a dental technician. Author(s): Cockayne SE, Murphy R, Gawkrodger DJ. Source: Contact Dermatitis. 2001 January; 44(1): 42-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11156017&dopt=Abstract

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Occupational contact dermatitis from propolis. Author(s): Henschel R, Agathos M, Breit R. Source: Contact Dermatitis. 2002 July; 47(1): 52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12225418&dopt=Abstract

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Occupational contact dermatitis from ylang-ylang oil. Author(s): Romaguera C, Vilaplana J. Source: Contact Dermatitis. 2000 October; 43(4): 251. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11011949&dopt=Abstract

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Occupational contact dermatitis to Phaseolus vulgaris in a farmer - a case report. Author(s): Spiewak R, Dutkiewicz J. Source: Annals of Agricultural and Environmental Medicine : Aaem. 2000; 7(1): 55-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10865246&dopt=Abstract

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Optimal management of atopic dermatitis. Author(s): Abeck D, Strom K. Source: American Journal of Clinical Dermatology. 2000 January-February; 1(1): 41-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11702304&dopt=Abstract

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Oral administration of persimmon leaf extract ameliorates skin symptoms and transepidermal water loss in atopic dermatitis model mice, NC/Nga.

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Author(s): Matsumoto M, Kotani M, Fujita A, Higa S, Kishimoto T, Suemura M, Tanaka T. Source: The British Journal of Dermatology. 2002 February; 146(2): 221-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11903231&dopt=Abstract •

Oral hyposensitization in patients with contact dermatitis from Parthenium hysterophorus. Author(s): Handa S, Sahoo B, Sharma VK. Source: Contact Dermatitis. 2001 May; 44(5): 279-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11298693&dopt=Abstract

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Outbreak of caterpillar dermatitis caused by airborne hairs of the mistletoe browntail moth (Euproctis edwardsi). Author(s): Balit CR, Ptolemy HC, Geary MJ, Russell RC, Isbister GK. Source: The Medical Journal of Australia. 2001 December 3-17; 175(11-12): 641-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11837874&dopt=Abstract

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Paediatric atopic dermatitis in Perth general practice. Author(s): Thom GA, Halbert AR. Source: The Australasian Journal of Dermatology. 2003 February; 44(1): 28-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581078&dopt=Abstract

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Patch testing in allergic contact dermatitis caused by topical Chinese herbal medicine. Author(s): Li LF, Wang J. Source: Contact Dermatitis. 2002 September; 47(3): 166-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492552&dopt=Abstract

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Patch testing with the European standard series and Compositae extracts in patients with airborne contact dermatitis. Author(s): Sharma VK. Source: Contact Dermatitis. 2001 January; 44(1): 49-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11156024&dopt=Abstract

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Patient and physician perspectives vary on atopic dermatitis. Author(s): McAlister RO, Tofte SJ, Doyle JJ, Jackson A, Hanifin JM. Source: Cutis; Cutaneous Medicine for the Practitioner. 2002 June; 69(6): 461-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12078849&dopt=Abstract

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Perceptions of physicians and pediatric patients about atopic dermatitis, its impact, and its treatment. Author(s): Paller AS, McAlister RO, Doyle JJ, Jackson A.

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Source: Clinical Pediatrics. 2002 June; 41(5): 323-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12086198&dopt=Abstract •

Peristomal allergic contact dermatitis caused by Stomahesive paste: An additional case. Author(s): Gallo R, Ciambellotti A, Cozzani E, Parodi A. Source: Journal of the American Academy of Dermatology. 2002 October; 47(4): 633. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12271318&dopt=Abstract

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Photocontact dermatitis and chloracne: two major occupational and environmental skin diseases induced by different actions of halogenated chemicals. Author(s): Yamamoto O, Tokura Y. Source: Journal of Dermatological Science. 2003 August; 32(2): 85-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12850300&dopt=Abstract

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Photosensitivity from colophony in a case of chronic actinic dermatitis associated with contact allergy from colophony. Author(s): Kuno Y, Kato M. Source: Acta Dermato-Venereologica. 2001 November-December; 81(6): 442-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11859957&dopt=Abstract

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Phototherapy of atopic dermatitis. Author(s): Scheinfeld NS, Tutrone WD, Weinberg JM, DeLeo VA. Source: Clinics in Dermatology. 2003 May-June; 21(3): 241-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781441&dopt=Abstract

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Phytodermatitis from Ranunculus damascenus. Author(s): Metin A, Calka O, Behcet L, Yildirim E. Source: Contact Dermatitis. 2001 March; 44(3): 183. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11217994&dopt=Abstract

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Phytotherapy of chronic dermatitis and pruritus of dogs with a topical preparation containing tea tree oil (Bogaskin). Author(s): Fitzi J, Furst-Jucker J, Wegener T, Saller R, Reichling J. Source: Schweiz Arch Tierheilkd. 2002 May; 144(5): 223-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12070906&dopt=Abstract

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Probiotics and atopic dermatitis. A new strategy in atopic dermatitis. Author(s): Miraglia del Giudice M Jr, De Luca MG, Capristo C. Source: Dig Liver Dis. 2002 September; 34 Suppl 2: S68-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12408445&dopt=Abstract

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Propolis-induced granulomatous contact dermatitis accompanied by marked lymphadenopathy. Author(s): Teraki Y, Shiohara T. Source: The British Journal of Dermatology. 2001 June; 144(6): 1277-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11422066&dopt=Abstract

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Prurigo-nodularis-like lesion in parthenium dermatitis. Author(s): Sharma VK, Sahoo B. Source: Contact Dermatitis. 2000 April; 42(4): 235. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10750856&dopt=Abstract

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Psychobiological aspects of atopic dermatitis: an overview. Author(s): Buske-Kirschbaum A, Geiben A, Hellhammer D. Source: Psychotherapy and Psychosomatics. 2001 January-February; 70(1): 6-16. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11150933&dopt=Abstract

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Purpuric contact dermatitis in patients with allergic reaction to textile dyes and resins. Author(s): Lazarov A, Cordoba M. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2000 March; 14(2): 101-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10972094&dopt=Abstract

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Radiation recall dermatitis from docetaxel. Author(s): Piroth MD, Krempien R, Wannenmacher M, Zierhut D. Source: Onkologie. 2002 October; 25(5): 438-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12415198&dopt=Abstract

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Shoe dermatitis due to colophonium used as leather tanning or finishing agent in Portuguese shoes. Author(s): Strauss RM, Wilkinson SM. Source: Contact Dermatitis. 2002 July; 47(1): 59. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12225424&dopt=Abstract

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Systemic therapy of atopic dermatitis. Author(s): Sidbury R, Hanifin JM. Source: Clinical and Experimental Dermatology. 2000 October; 25(7): 559-66. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11122228&dopt=Abstract

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Tea tree oil dermatitis associated with linear IgA disease. Author(s): Perrett CM, Evans AV, Russell-Jones R.

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Source: Clinical and Experimental Dermatology. 2003 March; 28(2): 167-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12653706&dopt=Abstract •

The effect of a newly developed ointment containing eicosapentaenoic acid and docosahexaenoic acid in the treatment of atopic dermatitis. Author(s): Watanabe T, Kuroda Y. Source: J Med Invest. 1999 August; 46(3-4): 173-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10687312&dopt=Abstract

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The effect of antibacterial soap with 1.5% triclocarban on Staphylococcus aureus in patients with atopic dermatitis. Author(s): Breneman DL, Hanifin JM, Berge CA, Keswick BH, Neumann PB. Source: Cutis; Cutaneous Medicine for the Practitioner. 2000 October; 66(4): 296-300. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11109156&dopt=Abstract

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The therapeutic effect of evening primrose oil in atopic dermatitis patients with dry scaly skin lesions is associated with the normalization of serum gamma-interferon levels. Author(s): Yoon S, Lee J, Lee S. Source: Skin Pharmacology and Applied Skin Physiology. 2002 January-February; 15(1): 20-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11803254&dopt=Abstract

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The treatment of atopic dermatitis with licorice gel. Author(s): Saeedi M, Morteza-Semnani K, Ghoreishi MR. Source: The Journal of Dermatological Treatment. 2003 September; 14(3): 153-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14522625&dopt=Abstract

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The use of complementary medicine in children with atopic dermatitis in secondary care in Leicester. Author(s): Johnston GA, Bilbao RM, Graham-Brown RA. Source: The British Journal of Dermatology. 2003 September; 149(3): 566-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14510990&dopt=Abstract

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Topical treatment of atopic dermatitis with St. John's wort cream--a randomized, placebo controlled, double blind half-side comparison. Author(s): Schempp CM, Windeck T, Hezel S, Simon JC. Source: Phytomedicine : International Journal of Phytotherapy and Phytopharmacology. 2003; 10 Suppl 4: 31-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12807340&dopt=Abstract

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Treatment of atopic dermatitis and impact on quality of life: a review with emphasis on topical non-corticosteroids. Author(s): Schiffner R, Schiffner-Rohe J, Landthaler M, Stolz W. Source: Pharmacoeconomics. 2003; 21(3): 159-79. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12558467&dopt=Abstract

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Treatment of canine atopic dermatitis with a commercial homeopathic remedy: a single-blinded, placebo-controlled study. Author(s): Scott DW, Miller WH Jr, Senter DA, Cook CP, Kirker JE, Cobb SM. Source: Can Vet J. 2002 August; 43(8): 601-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12170834&dopt=Abstract

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Use of an antibiotic footbath in the treatment of bovine digital dermatitis. Author(s): Laven RA, Proven MJ. Source: The Veterinary Record. 2000 October 28; 147(18): 503-6. Erratum In: Vet Rec 2000 December 2; 147(23): 660. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11110490&dopt=Abstract

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Vegetarian diet ameliorates symptoms of atopic dermatitis through reduction of the number of peripheral eosinophils and of PGE2 synthesis by monocytes. Author(s): Tanaka T, Kouda K, Kotani M, Takeuchi A, Tabei T, Masamoto Y, Nakamura H, Takigawa M, Suemura M, Takeuchi H, Kouda M. Source: Journal of Physiological Anthropology and Applied Human Science. 2001 November; 20(6): 353-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11840688&dopt=Abstract

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Vitamin E ointment at high dose levels suppresses contact dermatitis in rats by stabilizing keratinocytes. Author(s): Kuriyama K, Shimizu T, Horiguchi T, Watabe M, Abe Y. Source: Inflammation Research : Official Journal of the European Histamine Research Society. [et Al.]. 2002 October; 51(10): 483-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12477076&dopt=Abstract

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What is the cost of atopic dermatitis in preschool children? Author(s): Emerson RM, Williams HC, Allen BR. Source: The British Journal of Dermatology. 2001 March; 144(3): 514-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11260008&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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WebMDHealth: 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 dermatitis; 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: Integrative Medicine Communications; www.drkoop.com Acne Source: Prima Communications, Inc.www.personalhealthzone.com Acrodermatitis Enteropathica Source: Healthnotes, Inc.; www.healthnotes.com Allergic Rhinitis Source: Integrative Medicine Communications; www.drkoop.com Allergies and Sensitivities Source: Healthnotes, Inc.; www.healthnotes.com Asthma Source: Healthnotes, Inc.; www.healthnotes.com Benign Prostatic Hyperplasia Alternative names: Prostate Enlargement Source: Prima Communications, Inc.www.personalhealthzone.com Candidiasis Source: Integrative Medicine Communications; www.drkoop.com

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Celiac Disease Source: Healthnotes, Inc.; www.healthnotes.com Cellulitis Source: Integrative Medicine Communications; www.drkoop.com Chronic Candidiasis Source: Healthnotes, Inc.; www.healthnotes.com Congestive Heart Failure Source: Prima Communications, Inc.www.personalhealthzone.com Cystic Fibrosis Source: Healthnotes, Inc.; www.healthnotes.com Dermatitis Herpetiformis Source: Healthnotes, Inc.; www.healthnotes.com Eczema Source: Healthnotes, Inc.; www.healthnotes.com Eczema Source: Integrative Medicine Communications; www.drkoop.com Eczema Source: Prima Communications, Inc.www.personalhealthzone.com Food Allergy Source: Integrative Medicine Communications; www.drkoop.com Hay Fever Source: Integrative Medicine Communications; www.drkoop.com Hives Source: Healthnotes, Inc.; www.healthnotes.com Inflammatory Bowel Disease Source: Integrative Medicine Communications; www.drkoop.com Lupus Source: Integrative Medicine Communications; www.drkoop.com Malabsorption Source: Healthnotes, Inc.; www.healthnotes.com Msg Sensitivity Source: Healthnotes, Inc.; www.healthnotes.com Night Vision (impaired) Source: Prima Communications, Inc.www.personalhealthzone.com

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Osteoarthritis Source: Healthnotes, Inc.; www.healthnotes.com Osteoarthritis Source: Integrative Medicine Communications; www.drkoop.com Phenylketonuria Source: Healthnotes, Inc.; www.healthnotes.com Photodermatitis Source: Integrative Medicine Communications; www.drkoop.com Photosensitivity Source: Healthnotes, Inc.; www.healthnotes.com Rheumatoid Arthritis Source: Healthnotes, Inc.; www.healthnotes.com Schizophrenia Source: Healthnotes, Inc.; www.healthnotes.com Seborrheic Dermatitis Source: Healthnotes, Inc.; www.healthnotes.com Shingles and Postherpetic Neuralgia Source: Healthnotes, Inc.; www.healthnotes.com Skin Infection Source: Integrative Medicine Communications; www.drkoop.com Sleep Apnea Source: Integrative Medicine Communications; www.drkoop.com Sunburn Source: Integrative Medicine Communications; www.drkoop.com Systemic Lupus Erythematosus Source: Healthnotes, Inc.; www.healthnotes.com Systemic Lupus Erythematosus Source: Integrative Medicine Communications; www.drkoop.com Ulcerative Colitis Source: Integrative Medicine Communications; www.drkoop.com Varicose Veins Source: Prima Communications, Inc.www.personalhealthzone.com Yeast Infection Source: Integrative Medicine Communications; www.drkoop.com

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Alternative Therapy Aromatherapy Source: Integrative Medicine Communications; www.drkoop.com Hypnotherapy Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,706,00.html Massage Source: Integrative Medicine Communications; www.drkoop.com Mind & Body Medicine Source: Integrative Medicine Communications; www.drkoop.com Native American Medicine Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,721,00.html Traditional Chinese Medicine Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10085,00.html

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Chinese Medicine Mubiezi Alternative names: Cochinchina Momordica Seed; Semen Momordicae Source: Chinese Materia Medica Songhuafen Alternative names: Pine Pollen; Pollen Pini Source: Chinese Materia Medica

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Herbs and Supplements Achillea Alternative names: Yarrow; Achillea millefolium L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Adenosine Monophosphate (AMP) Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10106,00.html Aesculus Alternative names: Horse Chestnut; Aesculus hippocastanum L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org

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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 Source: Prima Communications, Inc.www.personalhealthzone.com Alpha Lipoic Acid Source: Healthnotes, Inc.; www.healthnotes.com Alpha-Lipoic Acid Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10002,00.html Arctium Alternative names: Burdock, Gobo; Arctium lappa L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Arnica Alternative names: Arnica montana L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Arnica Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,753,00.html AVA Source: Integrative Medicine Communications; www.drkoop.com Betula Alternative names: Birch; Betula sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Bilberry Source: Prima Communications, Inc.www.personalhealthzone.com Borago Alternative names: Borage; Borago officinalis Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Boric Acid Source: Healthnotes, Inc.; www.healthnotes.com Boswellia Alternative names: Boswellia serrata Source: Healthnotes, Inc.; www.healthnotes.com

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Boswellia Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,759,00.html Bromelain Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,760,00.html Bryonia Bryony Alternative names: Bryony; Bryonia sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Burdock Blend Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Calendula Alternative names: Calendula officinalis Source: Healthnotes, Inc.; www.healthnotes.com Calendula (Pot Marigold) Alternative names: Calendula officinalis Source: Integrative Medicine Communications; www.drkoop.com Calendula Officinalis Source: Integrative Medicine Communications; www.drkoop.com Centella Alternative names: Gotu Kola; Centella asiatica (Linn.) Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Chamomile Source: Prima Communications, Inc.www.personalhealthzone.com Chamomile Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,766,00.html Chasteberry Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,767,00.html Cinnamomum Alternative names: Cinnamon; Cinnamomum zeylanicum Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org

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Coleus Forskohlii Source: Prima Communications, Inc.www.personalhealthzone.com Colloidal Oatmeal Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10107,00.html Curcuma Alternative names: Turmeric; Curcuma longa L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Cynara Artichoke Alternative names: Artichoke; Cynara scolymus L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Cynara C Alternative names: Cardoon; Cynara cardunculus L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Cyproheptadine Source: Healthnotes, Inc.; www.healthnotes.com Dandelion Alternative names: Taraxacum officinale Source: Integrative Medicine Communications; www.drkoop.com Dandelion Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10021,00.html Dapsone Source: Healthnotes, Inc.; www.healthnotes.com Digestive Enzymes Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10051,00.html Dong Quai (Angelica) Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,774,00.html Echinacea Alternative names: Echinacea purpurea, Echinacea angustifolia, Echinacea pallida Source: Healthnotes, Inc.; www.healthnotes.com

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Echinacea Alternative names: Echinacea angustifolia, Echinacea pallida, Echinacea purpurea, Purple Coneflower Source: Integrative Medicine Communications; www.drkoop.com Echinacea Angustifolia Source: Integrative Medicine Communications; www.drkoop.com Echinacea Pallida Source: Integrative Medicine Communications; www.drkoop.com Echinacea Purpurea Source: Integrative Medicine Communications; www.drkoop.com Equisetum Alternative names: Horsetail; Equisetum arvense L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Eugenia Clove Alternative names: Cloves; Eugenia sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Evening Primrose Alternative names: Oenothera biennis, Sun Drop Source: Integrative Medicine Communications; www.drkoop.com Fenofibrate Source: Healthnotes, Inc.; www.healthnotes.com Fo-Ti Alternative names: Polygonum multiflorum Source: Healthnotes, Inc.; www.healthnotes.com Gamma-Linolenic Acid (GLA) Source: Integrative Medicine Communications; www.drkoop.com Ginkgo Alternative names: Ginkgo biloba Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Ginkgo Biloba Source: Integrative Medicine Communications; www.drkoop.com GLA Source: Integrative Medicine Communications; www.drkoop.com GLA (Gamma-Linolenic Acid) Source: Prima Communications, Inc.www.personalhealthzone.com Glycyrrhiza1 Alternative names: Licorice; Glycyrrhiza glabra L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org

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Gotu Kola Source: Prima Communications, Inc.www.personalhealthzone.com Gotu Kola Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10031,00.html Greater Celandine Alternative names: Chelidonium majus Source: Healthnotes, Inc.; www.healthnotes.com Green-lipped Mussel Source: Healthnotes, Inc.; www.healthnotes.com Grindelia Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Guggul Alternative names: Commiphora mukul Source: Healthnotes, Inc.; www.healthnotes.com Hawthorn Source: Prima Communications, Inc.www.personalhealthzone.com Hops Alternative names: Humulus lupulus Source: Healthnotes, Inc.; www.healthnotes.com Hypericum Perforatum Source: Integrative Medicine Communications; www.drkoop.com Illicium Alternative names: Star Anise; Illicium verum (Hook, F.) Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Isoniazid Source: Healthnotes, Inc.; www.healthnotes.com Ivy Leaf Alternative names: Hedera helix Source: Healthnotes, Inc.; www.healthnotes.com Kava Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,798,00.html

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Kava Kava Alternative names: Piper methysticum, Ava Source: Integrative Medicine Communications; www.drkoop.com Klamathweed Source: Integrative Medicine Communications; www.drkoop.com Lavandula Alternative names: Lavender; Lavandula sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Maidenhair Tree Source: Integrative Medicine Communications; www.drkoop.com Matricaria Alternative names: Chamomile; Matricaria chamomilla Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Melaleuca Alternative names: Tea Tree Oil; Melaleuca alternifolia Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Mentha X Piperita Source: Integrative Medicine Communications; www.drkoop.com Methylsulfonylmethane Source: Healthnotes, Inc.; www.healthnotes.com MSM Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,807,00.html Nettle Source: Prima Communications, Inc.www.personalhealthzone.com Ocimum Alternative names: Basil, Albahaca; Ocimum basilicum Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Oenothera Biennis Source: Integrative Medicine Communications; www.drkoop.com Olive Leaf Alternative names: Olea europa Source: Healthnotes, Inc.; www.healthnotes.com Paba Source: Healthnotes, Inc.; www.healthnotes.com Paba (Para-Aminobenzoic Acid) Source: Prima Communications, Inc.www.personalhealthzone.com

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Peppermint Alternative names: Mentha x piperita Source: Integrative Medicine Communications; www.drkoop.com Peppermint Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,812,00.html Piper Alternative names: Kava; Piper methysticum Forst.f Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Piper Methysticum Source: Integrative Medicine Communications; www.drkoop.com Plantago Psyllium Alternative names: Psyllium, Ispaghula; Plantago psyllium/ovata Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Plantain Alternative names: Plantago lanceolata, Plantago major Source: Healthnotes, Inc.; www.healthnotes.com Pot Marigold Alternative names: Calendula officinalis Source: Integrative Medicine Communications; www.drkoop.com Purple Coneflower Source: Integrative Medicine Communications; www.drkoop.com Reishi Source: Prima Communications, Inc.www.personalhealthzone.com Rosmarinus Alternative names: Rosemary; Rosmarinus officinalis L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Royal Jelly Source: Healthnotes, Inc.; www.healthnotes.com Ruta Alternative names: Rue; Ruta graveolens L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Schisandra Alternative names: Schisandra chinensis Source: Healthnotes, Inc.; www.healthnotes.com

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St. John’s Wort Alternative names: Hypericum perforatum Source: Healthnotes, Inc.; www.healthnotes.com St. John's Wort Alternative names: Hypericum perforatum, Klamathweed Source: Integrative Medicine Communications; www.drkoop.com Sun Drop Source: Integrative Medicine Communications; www.drkoop.com Tanacetum Alternative names: Feverfew; Tanacetum parthenium (L.) Schultz-Bip. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Taraxacum Alternative names: Dandelion; Taraxacum officinale (Dhudhal) Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Taraxacum Officinale Source: Integrative Medicine Communications; www.drkoop.com Tea Tree Alternative names: Melaleuca alternifolia Source: Healthnotes, Inc.; www.healthnotes.com Terminalia Alternative names: Myrobalans; Terminalia arjuna Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Tetracycline Source: Healthnotes, Inc.; www.healthnotes.com Thuja Occid Alternative names: Arbor Vitae; Thuja occidentalis Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Thuja Plicata Alternative names: Western Red Cedar Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Thymus Extracts Source: Healthnotes, Inc.; www.healthnotes.com Tylophora Alternative names: Tylophora indica, Tylophora asthmatica Source: Healthnotes, Inc.; www.healthnotes.com Verbascum Alternative names: Mullein; Verbascum thapsus L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org

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Vitex Alternative names: Vitex agnus-castus Source: Healthnotes, Inc.; www.healthnotes.com Willow Bark Alternative names: There are several species of willow includingSalix alba, Salix nigra, Salix fragilis, Salix purpurea, Salix babylonica, White Willow, European Willow, Black Willow, Pussy Willow, Crack Willow, Purple Willow, Weeping Willow, Liu-zhi Source: Integrative Medicine Communications; www.drkoop.com Witch Hazel Alternative names: Hamamelis virginiana Source: Healthnotes, Inc.; www.healthnotes.com Zingiber Alternative names: Ginger; Zingiber officinale Roscoe 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 DERMATITIS Overview In this chapter, we will give you a bibliography on recent dissertations relating to dermatitis. 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 “dermatitis” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on dermatitis, we have not necessarily excluded non-medical dissertations in this bibliography.

Dissertations on Dermatitis 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 dermatitis. 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: •

Art Therapy and Atopic Dermatitis: Making the Invisible Visible by Marchand, Sylvie; Ma from Concordia University (canada), 2002, 89 pages http://wwwlib.umi.com/dissertations/fullcit/MQ72968

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Botulinum Toxin in the Treatment of Focal Hyperhidrosis and Dyshidrotic Hand Dermatitis by Swartling, Carl Fredrik; Ph.D from Uppsala Universitet (sweden), 2002, 67 pages http://wwwlib.umi.com/dissertations/fullcit/f721713

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Dissecting Genetic Susceptibility to Gluten Sensitivity: HLA-linked Risk Factors in Coeliac Disease and Dermatitis Herpetiformis by Karell, Kati Annika; Ph.D from Helsingin Yliopisto (finland), 2003, 103 pages http://wwwlib.umi.com/dissertations/fullcit/f24193

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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 DERMATITIS Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning dermatitis.

Recent Trials on Dermatitis The following is a list of recent trials dedicated to dermatitis.8 Further information on a trial is available at the Web site indicated. •

Induction of Suction Blisters in Patients with Urticaria, Blistering Diseases, Inflammatory Dermatoses and Neoplastic Disorders, and in Normal Volunteers Condition(s): Dermatitis; Healthy; Neoplasm; Urticaria; Vesiculobullous Skin Disease Study Status: This study is currently recruiting patients. Sponsor(s): National Cancer Institute (NCI) Purpose - Excerpt: The use of a suction blister apparatus has facilitated study of the immunologic capacity of human epidermal cells. We have been able to prepare purified populations of these cells after blister formation. Specifically, using the blister tops, we are able to enrich for epidermal Langerhans cells which are very potent stimulators in antigen presenting assays. Thus, this normal volunteer study provides an important source of fresh epidermal tissue from which we can study normal epidermal Langerhans cell function. In addition, we have recently used blister roofs in important experimental models of HIV-1 transmission. There is no other method available for assessing the biologic function of freshly isolated Langerhans cells without altering their milieu. It is a very safe and effective way to obtain human epidermal samples. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001150

8

These are listed at www.ClinicalTrials.gov.

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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

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Cytokine Production Patterns in Patients with Systemic Mastocytosis Compared with Atopic Dermatitis and Healthy Individuals Condition(s): Atopic Dermatitis; Healthy; Mastocytosis Study Status: This study is completed. Sponsor(s): National Institute of Allergy and Infectious Diseases (NIAID) Purpose - Excerpt: Cytokine Production Patterns in Patients with Systemic Mastocytosis Compared with Atopic Dermatitis and Healthy Individuals Summary: This study will examine how mast cells (cells involved in allergic reactions) migrate and multiply in the skin of patients with mastocytosis, a condition characterized by too many mast cells in the body. The mast cells tend to multiply in the skin, causing dark, itchy skin spots known as urticaria pigmentosa. This study will determine if the skin of patients with mastocytosis produces chemicals called cytokines that cause mast cells to migrate to the skin and multiply. The findings will be compared with those from normal volunteers and patients with atopic dermatitis, a skin disease characterized by recurrent itchy rash usually seen in people with a family history of allergies. Healthy volunteers, patients with mastocytosis and patients with atopic dermatitis 18 years of age and older may be eligible for this study. Participants will have the following tests and procedures: Suction blisters - Two to eight small blisters will be raised on the forearm using gentle suction. The fluid in the blisters will be collected with a syringe to study the chemicals produced by the skin. The tops of the blisters may be removed for research. - Template study - Patients with high cytokine content in the blister fluid may have a template study. For this procedure, a plastic block (template) with holes matching the blister sites is placed over the blistered area. The wells of the template are filled with salt water and the fluid is removed with a syringe at 3, 8 and/or 24 hours. Patients are hospitalized for 24 hours for this study. - Skin biopsy - A skin biopsy will be done to correlate cytokine levels with the number of mast cells in the skin. An area of skin is numbed with an

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anesthetic and a small circular area about the size of a pencil eraser is removed, using a sharp cookie cutter-type instrument. - Blood draw - About 4 tablespoons of blood will be drawn to compare the chemicals in the blood with those in the blister fluid. The blood will also be analyzed for a complete blood count, clotting factors and substances that may be elevated in people with allergies. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001760

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. 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 “dermatitis” (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 DERMATITIS 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 “dermatitis” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on dermatitis, we have not necessarily excluded non-medical patents in this bibliography.

Patents on Dermatitis By performing a patent search focusing on dermatitis, 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 will tell you how to obtain this information later in the chapter. The following is an 9Adapted

from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.

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example of the type of information that you can expect to obtain from a patent search on dermatitis: •

1, 3-bis-(substituted-phenyl)-2-propen-1-ones and their use to treat VCAM-1 mediated disorders Inventor(s): Hoong; Lee K. (Suwanee, GA), Meng; Charles Q. (Alpharetta, GA), Ni; Liming (Duluth, GA), Sikorski; James A. (Alpharetta, GA) Assignee(s): Atherogenics, Inc. (Alpharetta, GA) Patent Number: 6,608,101 Date filed: June 20, 2001 Abstract: It has been discovered certain 1,3-bis-(substituted-phenyl)-2-propen-1-ones, including compounds of formula (I) inhibit the expression of VCAM-1, and thus can be used to treat a patient with a disorder mediated by VCAM-1. Examples of inflammatory disorders that are mediated by VCAM-1 include, but are not limited to arthritis, asthma, dermatitis, cystic fibrosis, post transplantation late and chronic solid organ rejection, multiple sclerosis, systemic lupus erythematosis, inflammatory bowel diseases, autoimmune diabetes, diabetic retinopathy, rhinitis, ischemia-reperfusion injury, postangioplasty restenosis, chronic obstructive pulmonary disease (COPD), glomerulonephritis, Graves disease, gastrointestinal allergies, conjunctivitis, atherosclerosis, coronary artery disease, angina and small artery disease. Excerpt(s): The present invention includes novel heteroaryl or heterocyclic 1,3-bis(substituted-phenyl)-2-propen-1-ones as well as methods and compositions for the treatment of disorders mediated by VCAM-1 or MCP-1 and for the treatment of inflammatory disorders generally that include the administration of a 1,3-bis(substituted-phenyl)-2-propen-1-one that has at least one phenyl substituent that is an aryl, heteroaryl or heterocyclic moiety. Adhesion of leukocytes to the endothelium represents a fundamental, early event in a wide variety of inflammatory conditions, autoimmune disorders and bacterial and viral infections. Leukocyte recruitment to endothelium is mediated in part by the inducible expression of adhesion molecules on the surface of endothelial cells that interact with counterreceptors on immune cells. Endothelial cells determine which types of leukocytes are recruited by selectively expressing specific adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin. VCAM-1 binds to the integrin VLA-4 expressed on lymphocytes, monocytes, macrophages, eosinophils, and basophils but not neutrophils. This interaction facilitates the firm adhesion of these leukocytes to the endothelium. VCAM-1 is an inducible gene that is not expressed, or expressed at very low levels, in normal tissues. VCAM-1 is upregulated in a number of inflammatory diseases, including arthritis, asthma, dermatitis, psoriasis, cystic fibrosis, post transplantation late and chronic solid organ rejection, multiple sclerosis, systemic lupus erythematosis, inflammatory bowel diseases, autoimmune diabetes, diabetic retinopathy, rhinitis, ischemia-reperfusion injury, post-angioplasty restenosis, chronic obstructive pulmonary disease (COPD), glomerulonephritis, Graves disease, gastrointestinal allergies, conjunctivitis, atherosclerosis, coronary artery disease, angina and small artery disease. Coronary heart disease (CHD), primarily as a result of atherosclerosis, remains the leading cause of death in industrialized countries. Atherosclerosis is a disease characterized by vascular inflammation, deposition of lipids in the arterial vessel wall and smooth muscle cell proliferation resulting in a narrowing of the vessel passages. In advanced stages of the disease atherosclerotic lesions can become unstable resulting in plaque rupture, thrombosis, myocardial infarction and

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ischemic heart disease. It is now well accepted that the initiating events in atherosclerosis are local injury to the arterial endothelium that results in the induction of VCAM-1 and recruitment of mononuclear leukocytes that express the integrin counterreceptor, VLA-4, (O'Brien, et al., J. Clin. Invest., 92: 945-951, 1993). Subsequent conversion of leukocytes to foamy macrophages results in the synthesis of a wide variety of inflammatory cytokines, growth factors, and chemoattractants that help propagate formation of the mature atheromatous plaque by further inducing endothelial activation, leukocyte recruitment, smooth muscle cell proliferation, and extracellular matrix deposition. Pharmacological inhibition of VCAM-1 expression has been shown to inhibit atherosclerosis in several animal models (Sundell et al., Circulation, 100: 42, 1999). A monoclonal antibody against VCAM-1 has also been shown to inhibit neointimal formation in a mouse model of arterial wall injury (Oguchi, S., et al., Arterioscler. Thromb. Vasc. Biol., 20: 1729-1736, 2000). Web site: http://www.delphion.com/details?pn=US06608101__ •

4-phenylpiperidines for the treatment of pruritic dermatoses Inventor(s): Armer; Richard Edward (Sandwich, GB), Dutton; Christopher James (Sandwich, GB), Gethin; David Morris (Sandwich, GB), Gibson; Stephen Paul (Sandwich, GB), Smith; Julian Duncan (Sandwich, GB), Tommasini; Ivan (Sandwich, GB) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 6,610,711 Date filed: May 11, 2000 Abstract: Novel compounds having general formula (I), and pharmaceutically and veterinarily acceptable salts thereof wherein R.sup.1, R.sup.2, R.sup.3, W, Y.sup.1, Y.sup.2, X, n and y are as defined above and processes for their preparation and intermediate compounds prepared therein. The novel compounds are useful for having utility in the treatment of pruritic dermatoses including allergic dermatitis and atopy in animals and humans. Excerpt(s): This invention relates to novel 4-phenylpiperidines having utility in the treatment of pruritic dermatoses including allergic dermatitis and atopy in animals and humans, and processes for the preparation of and intermediates used in the preparation of such compounds. Itching or pruritus is a common dermatological symptom which can give rise to considerable distress, in both humans and animals. Pruritus is often associated with inflammatory skin disease which can commonly be caused by hypersensitivity reactions, such as reaction to insect bites e.g. flea bites, or to environmental allergens such as house dust mite or pollen; or by bacterial and fungal infections of the skin or ectoparasite infections. Previous treatments for pruritus include the use of corticosteroids and antihistamines, however both have undesired side effects. Other therapies include the use of essential fatty acid dietary supplements which are slow to act and offer only limited efficacy against allergic dermatitis. A variety of emollients such as soft paraffin, glycerine and lanolin are also employed but with limited success and there is a continuing need for an effective remedy. Certain 1,3,4trisubstituted 4-aryl-piperidine derivatives are disclosed in GB-A-1525584 as potent narcotic antagonists which also display analgesic properties. These compounds are also claimed in EP-B-0287339 as opioid antagonists which block the effect of agonists at the mu or kappa receptors having potential utility in treating a variety of disorders associated with these receptors such as eating disorders, opiate overdose, depression, smoking, alcoholism, sexual dysfunction, shock, stroke, spinal damage and head

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trauma; utility as an appetite suppressant for weight loss has also been suggested. Further related 1-N-substituted-4-aryl piperidines are disclosed in EP-A-0506468 and EP-A-0506478. Potential utility is suggested in preventing peripherally mediated undesired opiate effects and in relieving the symptoms of idiopathic constipation and irritable bowel syndrome. Web site: http://www.delphion.com/details?pn=US06610711__ •

Anti-irritant compositions containing a cyclic nucleotide Inventor(s): Goyarts; Earl C. (Commack, NY), Mammone; Thomas (Farmingdale, NY), Muizzuddin; Neelam (Bethpage, NY) Assignee(s): E-L Management (New York, NY) Patent Number: 6,531,140 Date filed: May 4, 1999 Abstract: The present invention relates to cosmetic or pharmaceutical topical compositions containing at least one cyclic nucleotide having its 2' hydroxyl group replaced by a hydrogen atom for inhibiting phosphodiesterase activity. The phosphodiesterase inhibitor is in combination with a magnesium buffer and a cosmetically or pharmaceutically acceptable carrier. The invention also includes methods for treating or preventing inflammation or irritation such as is common in the skin disease, atopic dermatitis, which is known to be related to the uncontrolled activity of phosphodiesterase. Excerpt(s): The present invention relates to topical anti-irritant compositions which contain a phosphodiesterase inhibitor. In particular, the invention relates to topical skin care compositions containing 2'-deoxy adenosine 3 '5' cyclic monophosphate which exhibit inhibitory action toward phosphodiesterase. Irritation and inflammation are complex processes that involve various factors such as, for example, prostaglandins, leukotrines, cytokines, proteases. Another factor is the intracellular level of cyclic adenosine monophosphate (hereinafter referred to as "cAMP"), and therefore, it is possible to control inflammation and irritation by modulating the levels of cAMP. Modulation can be achieved by employing one of two methods. One method involves the inhibition of new cAMP synthesis and the other method entails the removal of existing cAMP. One known removal method involves the use of an enzyme, cyclic nucleotide phosphodiesterase (hereinafter referred to as "PDE"). This isoenzyme is the catalyst for the hydrolytic reaction whereby cAMP is converted to adenosine 5' monophosphate (hereinafter referred to as "AMP"). A family of isoenyzmes is formed by various PDEs and is categorized into seven types, known as Types I-VII whereby the type is determined by the inhibitor sensitivity. Human epidermal keratinocytes have been shown to contain both Type IV and Type V phosphodiesterase activity. As a result of its relationship with cAMP, it is also known in the prior art that PDE plays a role in inflammatory response. There is an abnormal elevated activity of PDE in leukocytes of patients with skin disorders such as atopic dermatitis. The presence of elevated PDE activity causes a deficiency in cAMP control and results in exaggerated immune and inflammatory responses in the blood and tissue. Since elevated PDE activity is known to have a correlation with irritation and inflammation, means of inhibiting PDE activity have, therefore, been sought. Web site: http://www.delphion.com/details?pn=US06531140__

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Ceramidase gene Inventor(s): Ito; Makoto (Fukuoka, JP), Okino; Nozomu (Fukuoka, JP) Assignee(s): Takara Shuzo Co., Ltd. (Kyoto-fu, JP) Patent Number: 6,489,117 Date filed: February 7, 2001 Abstract: To provide a polypeptide having ceramidase activity, and a gene encoding thereof useful as an reagent for lipid engineering and as indices for diagnosis of atopic dermatitis, an easy method for detecting the polypeptide and method for detecting the gene as well as a method for detecting atopic dermatitis. A polypeptide having an amino acid sequence as shown in SEQ ID NO: 1 in Sequence Listing, or a polypeptide having an amino acid sequence which has substitution, deletion, addition or insertion of one or more amino acids in the amino acid sequence of SEQ ID NO: 1 and having ceramidase activity; a gene encoding the polypeptide; a gene capable of hybridizing with the above genes under stringent conditions, and encoding a polypeptide having ceramidase activity; an oligonucleotide probe or primer, which is capable of hybridizing under stringent conditions with the above genes or with a gene having a nucleotide sequence complementary thereto; a method for detecting a gene encoding a polypeptide having ceramidase activity, by using the oligonucleotide probe and/or primer; an antibody or a fragment thereof, which is capable of specifically binding to the polypeptide; a method for detecting a polypeptide having ceramidase activity, by using the above antibody or fragment thereof; a method for detecting atopic dermatitis, by the methods. Excerpt(s): The present invention relates to a polypeptide having ceramidase activity, and a gene encoding said polypeptide. More particularly, the present invention relates to an amino acid sequence of ceramidase as well as a nucleotide sequence encoding the amino acid sequence which are useful as an reagent for lipid engineering for analyzing structure and action of ceramide and as an index for diagnosis of atopic dermatitis. In addition, the present invention relates to a method for producing a polypeptide having ceramidase activity by gene engineering. Further, the present invention relates to a method for detecting the polypeptide, and a method for detecting a gene encoding the polypeptide. Further, the present invention relates to a method for detecting atopic dermatitis by utilizing the above method for detecting the polypeptide and the above method for detecting the gene. Ceramidase is an enzyme that hydrolyses ceramide, which is one of sphingolipids, into sphingosine and a fatty acid. Sphingosine formed by hydrolysis of ceramide by ceramidase has various physiological activities, such as inhibition of protein kinase C, activation of phospholipase D, inhibition of a calmodulindependent enzyme, and the like, and is an important substance which is considered to have a role in regulating cellular functions through its involvement in cell proliferation and intracellular signal transduction. The regulation of the level of such sphingosine is an important role played by ceramidase. Ceramidases are classified on the basis of its optimum pH into an acidic ceramidase and a neutral/alkaline ceramidase. There have been reported that ceramidases having optimum pH in an acidic region are present in mammalian tissues such as rat brain [Biochemistry, 8, 1692-1698 (1969)], guinea pig epithelial cell [J. Biol. Chem., 270, 12677-12684 (1995)], human kidney [Biochim. Biophys. Acta, 398, 125-131 (1975)], spleen [Biochim. Biophys. Acta, 1004, 245-251 (1989)], fibroblast [Biochem. J., 205, 419-425 (1982)] and epithelium [FEBS Lett., 268, 110-112 (1990)]; human urine [J. Biol. Chem., 270, 11098-11102 (1995)], and the like. Web site: http://www.delphion.com/details?pn=US06489117__

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Chemical compounds having ion channel blocking activity for the treatment of immune dysfunction Inventor(s):.O slashed.dum; Niels (K.o slashed.benhavn, DK), Christophersen; Palle (Ballerup, DK), J.o slashed.rgensen; Tino D. (Solr.o slashed.d Strand, DK), Jensen; Bo S. (K.o slashed.benhavn S, DK), Olsen; S.o slashed.ren-Peter (Klampenborg, DK), Str.o slashed.b.ae butted.k; Dorte (Farum, DK) Assignee(s): NeuroSearch A/S (Ballerup, DK) Patent Number: 6,545,028 Date filed: April 14, 2000 Abstract: This invention relates to treatment or alleviation of a disease, condition or disorder selected from inflammatory bowel disease, Chron's disease, colitis ulcerosa, Coeliac disease, dermatitis herpetiformis, dermatomyositis, enteritis allergia, erytherma nodosum leprosum, ileitis regionalis, psoriasis, purpura, scleritis or scleroderma by administering to a living body certain imidazole, triazole, or 1,4-dihydropyridine derivatives. Excerpt(s): The present invention relates to chemical compounds having inhibitory activity on an intermediate conductance Ca.sup.2+ activated potassium channel (IK.sub.Ca), and the use of such compounds for the treatment or alleviation of diseases or conditions relating to immune dysfunction. Moreover, the invention relates to a method of screening a chemical compound for inhibitory activity on an intermediate conductance Ca.sup.2+ activated potassium channel (IK.sub.Ca). Ion channels are transmembrane proteins, which catalyse the transport of inorganic ions across cell membranes. The ion channels participate in processes as diverse as the generation and timing of action potentials, synaptic transmissions, secretion of hormones, contraction of muscles, etc. Web site: http://www.delphion.com/details?pn=US06545028__

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Composition and method for hair and scalp treatment Inventor(s): Nguyen; Carolina (Garden Grove, CA), Parr; James W. (San Juan Capistrano, CA), Sun; Ziming (Fountain Valley, CA), Travaline; Darcy (Coto De Caza, CA) Assignee(s): Amitee Cosmetics, Inc. (Costa Mesa, CA) Patent Number: 6,455,058 Date filed: September 13, 2000 Abstract: A hair and scalp treatment composition containing (1) an anti-dandruff agent such as salicylic acid, (2) a polyethylenimine, and (3) an amphoteric surfactant. The composition provides superior effects for repairing damaged hair, protecting hair against chemical and mechanical damage. In addition, the composition also provides scalp treatment for against dandruff, seborrheic dermatitis and psoriasis. The composition could be incorporated into either aqueous or anhydrous solvent systems. Excerpt(s): This invention is directed to the field of hair and scalp treatments. The following is intended to provide a background of the inventive composition and method of this patent; however, this discussion is not intended to suggest that the information set forth is prior art. In today's hair care market, there continues to be a long-felt need for hair care products effective to facilitate the prevention of hair damage and also to

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repair damaged hair. There are many different products in the market and most of them target specific problems. Since most people have an accelerated life pace, they are looking for multi-functional products that can simplify their daily routine. Web site: http://www.delphion.com/details?pn=US06455058__ •

Composition for the topical treatment of poison ivy and other forms of contact dermatitis Inventor(s): McCadden; Michael E. (121 Whitebridge Meadows La., St. Louis, MO 63141) Assignee(s): none reported Patent Number: 6,479,058 Date filed: August 31, 2000 Abstract: Composition for topical administration comprising (a) a corticosteroid, and (b) a drying agent. Excerpt(s): The present invention relates to a composition for the treatment of rashes, dermatoses or skin eruptions, which are known to be treated topically to improve or favorably alter the disease condition. Such rashes, dermatoses or skin eruptions include acute, inflammatory reactions of the skin caused by an allergic or irritant reaction (such as that caused by poison ivy, poison oak or poison sumac, or other forms of allergic or irritant contact dermatitis), other forms of eczema, lichen simplex chronicus, rashes, dermatoses or skin eruptions of a chronic nature (e.g. seborrheic dermatitis, psoriasis, atopic dermatitis) or caused by infection, irritation or aggravation of another condition such as occurs with acne, and other rashes, dermatoses or skin eruptions. Contact dermatitis may be produced by primary irritants or allergic sensitizes. Irritant contact dermatitis is a nonallergic reaction of the skin caused by exposure to irritating substances. Any person would react to an irritant if the concentration and duration of contact were sufficient. Most primary irritants are chemical substances, although physical and biologic (infectious) agents may produce the same reaction. Irritants account for 80% of occupational contact dermatitis and also cause the most frequent type of nonindustrial contact reaction. Allergic contact dermatitis is a manifestation of delayed hypersensitivity and results from the exposure of sensitized individuals to contact allergens. Poison ivy and poison oak induce sensitization in more than 70% of the population, thereby causing allergic contact dermatitis (Arndt, Kenneth A., Manual of Dermatologic Therapeutics, 5.sup.th edition, 1995, Little, Brown and Co., page 49). Irritants will cause an inelastic and stiff-feeling skin, discomfort due to dryness, pruritus secondary to inflammation, and pain due to fissures, blisters, and ulcers. Mild irritants produce erythema, microvesiculation, and oozing that may be indistinguishable from allergic contact dermatitis. Chronic exposure to mild irritants or allergens results in dry, thickened, and fissured skin. Strong irritants cause blistering, erosion, and ulcers of the skin. Allergic contact dermatitis, in its mild form, is similar in appearance to the irritant eruption. A more typical allergic contact reaction will consist of grouped or linear tense vesicles and blisters. If involvement is severe there may be marked edema, particularly of the face and in the periorbital and genital areas. Web site: http://www.delphion.com/details?pn=US06479058__

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Composition having bactericidal action, cosmetics containing said composition and ultraviolet ray screening agent Inventor(s): Ozeki; Hiroshi (Koshigaya, JP) Assignee(s): Huziwara; Noboru (Tokyo, JP), Sato; Yuko (Saitama, JP), Yamazaki; Takeshi (Urawa, JP) Patent Number: 6,482,420 Date filed: December 27, 2000 Abstract: A composition having a bactericidal action is provided which has no toxicity to the human body, and particularly a composition having a bactericidal action is provided which exhibit an excellent therapeutic effect for skin diseases such as atopic dermatitis, acne or the like.A composition, in which an extract from a silk gland and/or a liquid silk is an active ingredient, has a bactericidal action to make renewal of a skin cell, exhibiting an excellent therapeutic effect for skin diseases. Excerpt(s): This invention relates to a composition having a bactericidal action having an excellent effect on beauty and health for a skin or the like, a cosmetics containing the composition, and a ultraviolet ray screening agent. It has been well known that a vitamin, a Chinese milk vetch, hyaluronic acid, and other various additives are added into a skin cosmetics in order to maintain a healthy physical function of the skin and to maintain a healthy clear skin. A medicinal cosmetics has been also proposed, in which where it is coated, as a medicine for external application, on the skin directly, function of the skin is activated to help regeneration of the skin. Web site: http://www.delphion.com/details?pn=US06482420__

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Compounds and methods Inventor(s): Blaney; Frank E. (Harlow, GB), Bondinell; William E (Wayne, PA), Chan; James A. (West Chester, PA) Assignee(s): SmithKline Beecham Corporation (Philadelphia, PA) Patent Number: 6,506,790 Date filed: August 29, 2001 Abstract: This invention relates to substituted benzo[1,2-b:5,4-b']dipyran-4-amines which are modulators, agonists or antagonists, of the CCR5 receptor. In addition, this invention relates to the treatment and prevention of disease states mediated by CCR5, including, but not limited to, asthma and a topic disorders (for example, a topic dermatitis and allergies), rheumatoid arthritis, sarcoidosis and other fibrotic diseases, atherosclerosis, psoriasis, autoimmune diseases such as multiple sclerosis, and inflammatory bowel disease, all in mammals, by the use of substituted benzo[1,2-b:5,4b']dipyran-4-amines which are CCR5 receptor antagonists. Furthermore, since CD8+T cells have been implicated in COPD, CCR5 may play a role in their recruitment and therefore antagonists to CCR5 could provide potential therpeutic in the treatment of COPD. Also, since CCR5 is a co-receptor for the entry of HIV into cells, selective receptor modulators may be useful in the treatment of HIV infection. Excerpt(s): This invention relates to substituted benzo[1,2-b:5,4-b']dipyran4-amines which are modulators, agonists or antagonists, of the CC chemokine receptor CC-CKR5 now designated as CCR5 (Nature Medicine, 2: 1174-8, 1996). In addition, this invention relates to the treatment and prevention of disease states mediated by CCR5. T cells are

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not only key regulators of the immune response to infectious agents but are believed critical for the initiation and maintenance of the inflammatory reaction in a variety of chronic diseases. Increased numbers or enhanced activation state of T cells, especially CD4+ T cells, have been demonstrated in the synovium of individuals with rheumatoid arthritis (M. J. Elliott and R. N. Maini, Int. Arch. Allergy Immunol. 104: 112-1125, 1994), in the bronchial mucosa of asthmatics (C. J. Corrigan and A. B. Kay, Immunol. Today 13: 501-506, 1992), in the lesions of multiple sclerosis (R. Martin and H. F. McFarland, Crit. Rev. Clin. Lab. Sci. 32: 121-182, 1995), in psoriatic lesions (J. L. Jones, J. Berth-Jone, A. Fletcher and P. E. Hutchinson, J. Pathol. 174: 77-82, 1994) and in the fatty streaks of atherosclerosis (R. Ross, Annu. Rev. Physiol. 57: 791-804, 1995). T cells, as well as other inflammatory cells, will migrate into tissues in response to the production of a variety chemotactic factors. Among these factors are a superfamily of 8-12 kDa proteins known as the chemokines. These proteins share structural features such as the presence of 3-4 conserved cysteine residues. RANTES, which stands for Regulated upon Activation Normal T cell Expressed and Secreted, is a 8 kDa protein member of CC branch of the chemokine family. These proteins recruit and activate immune and inflammatory cells through an interaction with G-protein coupled receptors. The CC branch is defined by the absence of an intervening amino acid residue between the first two cysteine residues and members of this family predominately elicit the migration of mononuclear cells, eosinophils and basophils (M. Baggiolini, B. Dewald, and B. Moser, Adv. Immunol. 55: 97-179, 1994; and J. J. Oppenheim, C. O. C. Zachariae, N. Mukaida, and K. Matsushima, Annu. Rev. Immunol. 9: 617-648, 1991). Web site: http://www.delphion.com/details?pn=US06506790__ •

Condensed pyridazine compounds, their production and use Inventor(s): Gyoten; Michiyo (Daito, JP), Kawano; Yasuhiko (Suita, JP), Nagaya; Hideaki (Toyonaka, JP) Assignee(s): Takeda Chemical Industries, Ltd. (Osaka, JP) Patent Number: 6,610,694 Date filed: April 2, 2001 Abstract: A condensed pyridazine derivative which exhibits anti-allergic activity, antihistaminic activity and/or eosinophil chemotaxis-inhibiting activity, anti-inflammatory activity, anti-PAF (platelet-activating factor) activity, and the like, and is useful as an agent for preventing or treating asthma, allergic conjunctivitis, allergic rhinitis, urticaria, atopic dermatitis, and the like. Excerpt(s): This application is the National Stage of International Application No. PCT/JP99/05469, filed on Oct. 5, 1999. The present invention relates to novel condensed pyridazine derivatives exhibiting an excellent anti-allergic, anti-histaminic, antiinflammatory or eosinophil chemotaxis-inhibiting activity, or other activities, and useful as agents for preventing or treating atopic dermatitis, allergic rhinitis, bronchial asthma, allergic conjunctivitis, chronic urticaria, etc., their pro-drugs, methods of their production, and their use in medicaments. wherein R represents a hydrogen atom, a phenyl group or a lower alkylcarbonylamino group; R.sup.1 represents morpholino or piperidino; R.sup.2 represents a hydrogen atom or a lower alkyl group (at least one of R and R.sup.2 is a group other than a hydrogen atom; when R is a phenyl group, R.sup.1 is morpholino and R.sup.2 is a lower alkyl group); or a salt thereof, is useful as a bronchodilator for mitigating bronchial spasms.

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Web site: http://www.delphion.com/details?pn=US06610694__ •

Cream composition comprising Dead Sea Mud Inventor(s): Efron; Dov (Jerusalem, IL), Gavrieli; Yona (Tivon, IL), Gilad; Zivn (Dead Sea, IL), Magdassi; Shlomo (Jerusalem, IL), Maor; Zeev (Dead Sea, IL), MeshulamSimon; Galit (Tivon, IL), Yehuda; Shaul (Dead Sea, IL) Assignee(s): Dead Sea Laboratories Ltd. (Dead Sea, IL) Patent Number: 6,582,709 Date filed: October 15, 2001 Abstract: The preset invention relates to a pharmaceutical cream composition for topical application for the treatment of skin disorders and skin diseases, comprising 1-6 wt. % Dead Sea Mud as an active ingredient. Said composition is for use in treating skin disorders and skin diseases such as psoriasis, saborrehic dermatitis, xerosis, attopic dermatitis, eczema, diaper rush, skin burns of stage I and sensitive skin. Said cream composition is also for use as a leave-on cosmetic cream for beautifying and enhancing the skin appearance. In addition to Dead Sea Mud said composition comprises ingredients suitable for the preparation of cosmetic cream. Said cream can further comprises up to 4 wt % Dead Sea water. Excerpt(s): The present invention relates to pharmaceutical and cosmetic cream compositions containing Dead Sea Mud for topical skin application. More specifically, the present invention relates to compositions for prevention and treatment of skin related disorders such as saborrehic dermatitis, xerosis, eczema, psoriasis and skin burns and for cosmetic use for retaining skin moisture and repairing of impaired skin. The skin is the largest organ in the body, serving as a protective barrier from the external environment. As such it is susceptible to various disorders and diseases caused by microorganisms, exposure to radiation, contact with irritating materials and loss of water. Dead Sea mud and water are known for their therapeutic and cosmetic properties (for example see Ma'or Z. and Yehuda S. (1997) International Journal of Cosmetic Science 19: 105-110). Various cosmetic products based on these properties exist in the market. For example, Japanese application JP 96011775 discloses a beauty plaster, comprising among other ingredients, natural salt and mud from the Dead Sea. PCT application No. PCT/IL98/00311 (applicant: Dead Sea Laboratories Ltd.) discloses a composition for skin care and protection comprising 10-15% of Dead Sea water. Web site: http://www.delphion.com/details?pn=US06582709__

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Desmethylolanzapine compositions and methods Inventor(s): Yelle; William E. (Littleton, MA) Assignee(s): Sepracor Inc. (Marlborough, MA) Patent Number: 6,468,997 Date filed: December 19, 2001 Abstract: Methods and compositions are disclosed utilizing N-desmethylolanzapine for the treatment of psychosis in humans. N-Desmethylolanzapine exhibits a lessened liability toward drug-drug interactions than olanzapine and a more predictable dosing regimen than olanzapine. N-Desmethylolanzapine is also useful for the treatment of

Patents 171

acute mania, mild anxiety states, anxiety disorders, schizophrenia, bipolar disorder, attention deficit hyperactivity disorder, autistic disorder, excessive aggression, substance abuse, depressive signs and symptoms, tic disorder, functional bowel disorder and fungal dermatitis. Excerpt(s): The invention relates to methods of treating psychosis, acute mania, mild anxiety states, schizophrenia, bipolar disorder, autistic disorder, excessive aggression, substance abuse, depressive signs and symptoms, tic disorder, functional bowel disorder and fungal dermatitis. It is commercially available as Zyprexa.RTM. from Eli Lilly Co. The antipsychotic effect of olanzapine is ascribed by the literature to blocking of the dopamine D.sub.2 receptor and to 5-HT antagonism. Formation of desmethylolanzapine occurs in the liver through the enzymes of the P450 system, specifically CYP1A2. Other drugs which inhibit the CYP1A2 isoenzyme may interfere with the formation of this metabolite. In addition, coadministration of drugs also metabolized by CYP1A2 may lead to elevated blood concentrations of one or both drugs through competitive inhibition. Specifically, known inhibitors of CYP1A2 such as fluvoxamine and quinoline antibiotics (ciprofloxacin) may interfere with the demethylation of olanzapine. Compounds which are inducers of CYP1A2 may cause faster metabolism of olanzapine in exposed persons. In addition, men appear to exhibit higher CYP1A2 activity than women, resulting in gender-related differences in olanzapine metabolism. Web site: http://www.delphion.com/details?pn=US06468997__ •

Diaper dermatitis preventative medication and a method for making and using same Inventor(s): Moehring; Richard J. (Houston, TX) Assignee(s): Mentis Technologies, L.C. (Houston, TX) Patent Number: 6,464,994 Date filed: May 24, 2000 Abstract: The invention discloses a composition for the prevention and treatment of diaper dermatitis which includes an effective amount of an anti-lipase agent and/or an anti-protease agent in a suitable vehicle. The composition is designed to maintain an effective amount of the lipase and/or protease inhibitors and to be applied to tissues susceptible to fecal enzyme insult. The invention also discloses a composition for the prevention and treatment of diaper dermatitis which includes an effective amount of a sacrificial lipase substrate and/or, a sacrificial protease substrate in a suitable vehicle. The composition is designed to maintain an effective amount of the substrates and to be applied to tissues susceptible to fecal enzyme insult. The present invention also discloses a combination or mixtures of an effective amount of an anti-lipase agent and/or an antiprotease agent in a suitable vehicle and an effective amount of a sacrificial lipase substrate and/or a sacrificial protease substrate in a suitable vehicle. Excerpt(s): The present invention relates to a composition for the prophylaxis and/or treatment of diaper dermatitis or similar dermal irritation and methods for making and using the composition. More particularly, the present invention relates to a composition including an enzyme inhibitor system, a sacrificial substrate system or a combined system for the prophylaxis and/or treatment of tissue irritation due to enzyme activity, especially protease and lipase enzyme activity, and methods for making and using such compositions. The compositions of the present invention are especially useful in inhibiting the activity of lipase and protease enzymes present in expressed feces that

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cause diaper dermatitis or similar dermal conditions or in tissues exposed to bodily fluids or any fluid containing lipase and protease enzymes or the exposure of tissues to any composition (solid, liquid, emulsion, dispersion, etc.) containing lipase and protease enzymes. Diaper dermatitis is a phenomenon frequently encountered by parents of small children or by patients in nursing homes who are required to wear a diaper. Although the dermatitis is treatable, occurrence and persistence often results in unhappy children and sleep deprived parents. In severe cases, it results in painful decubitus ulcers. Many ointments and powders exist on the market for treating and preventing diaper dermatitis, but most function by merely forming a barrier between the skin and expressed feces. Web site: http://www.delphion.com/details?pn=US06464994__ •

Ectoparasite saliva proteins and apparatus to collect such proteins Inventor(s): Frank; Glenn Robert (Wellington, CO), Hunter; Shirley Wu (Fort Collins, CO), Sim; Gek-Kee (Fort Collins, CO), Wallenfels; Lynda (St. George, UT), Weber; Eric R. (Ft. Collins, CO) Assignee(s): Heska Corporation (Fort Collins, CO) Patent Number: 6,485,968 Date filed: January 8, 1998 Abstract: The present invention is directed to a novel product and method for isolating ectoparasite saliva proteins, and a novel product and method for detecting and/or treating allergic dermatitis in an animal. The present invention also relates to ectoparasite saliva proteins, nucleic acid molecules having sequences that encode such proteins, and antibodies raised against such proteins. The present invention also includes methods to obtain such proteins and to use such proteins to identify animals susceptible to or having allergic dermatitis. The present invention also includes therapeutic compositions comprising such proteins and their use to treat animals susceptible to or having allergic dermatitis. Excerpt(s): The present invention relates to a novel product and method for isolating ectoparasite saliva proteins, and a novel product and method for detecting and/or treating allergic dermatitis in an animal. Bites from ectoparasites, in particular fleas, can cause a hypersensitive response in animals. In particular, hypersensitive responses to fleabites is manifested in a disease called flea allergy dermatitis (FAD). Hypersensitivity refers to a state of altered reactivity in which an animal, having be n previously exposed to a compound, exhibits an allergic response to the compound upon subsequent exposures. Hypersensitive responses include immediate and delayed-type hypersensitivity, and in particular Type I, Type II, Type III and Type IV hypersensitivities (described in detail in Janeway et al., Immunobiology, Garland Publishing, New York, 1994, which is incorporated in its entirety by this reference). Foreign compounds that induce symptoms of immediate and/or delayed hypersensitivity are herein referred to as allergens. The term "allergen" primarily refers to foreign compounds capable of causing an allergic response. The term can be used interchangeably with the term "antigen," especially with respect to a foreign compound capable of inducing symptoms of immediate and/or delayed hypersensitivity. Factors that influence an animal's susceptibility to an allergen can include a genetic component and/or environmental exposure to an allergen. Animals can be de-sensitized to an allergen by repeated injections of the allergen to which an animal is hypersensitive.

Patents 173

Web site: http://www.delphion.com/details?pn=US06485968__ •

Herbal compositions for treating immunological disorders Inventor(s): Sheu; Shuenn-Jyi (Taipei, TW) Assignee(s): GloboAsia, L.L.C. (Hanover, MD) Patent Number: 6,503,542 Date filed: September 12, 2001 Abstract: The present invention provides a pharmaceutical composition which comprises water extracts of Tuber ophiopogon, Tuber pinelliae, Radix glycyrrhizae, and Radix pancis quinquefoli, and 50% alcohol extraction of Herba tridacis procumbentis. The pharmaceutical compositions are especially effective in treating patients with immunological disorders, such as asthma, atopic eczema, atopic dermatitis, allergic rhinitis and rheumatoid arthritis. Excerpt(s): The present invention relates to a novel medicinal herbal composition and its use for treating patients with immunological disorders, particularly IgE mediated diseases, which include, but are not limited to, allergic rhinitis, allergic conjunctivitis, allergic asthma, atopic eczema, atopic dermatitis, food allergy, hyper IgE syndrome, and rheumatoid arthritis. The novel medicinal herbal composition contains aqueous extracts of Tuber ophiopogon, Tuber pinelliae, Radix glycyrrhizae, Herba tridacis procumbentis, and Radix pancis quinquefolii. The present invention also relates to a method for making the medicinal herbal composition and methods for treating patients with the medicinal herbal composition. Antigen-induced, particularly allergen-induced immunological disorders, such as asthma, has long been known as one of the serious health problems in the world. Allergy in one form or another afflicts more than 20% of the world population. In recent years, statistics shows that the onset of the allergicrelated immunological disorders has shifted to the younger population, which means that more children and/or adolescents have developed symptoms of allergen-induced immunological disorders. For instance, in Taiwan, the prevalence of childhood asthma increased from 1.3% in 1974, to 5.07% in 1985, and to 5.8% in 1991. Also, allergic rhinitis increased from 7.84% in 1985 to 20.67% in 1991. Furthermore, atopic eczema was 1.43% in 1974 and 1.23% in 1985, in 1991, it was 3.84%. It is believed that the early onset of allergen-related immunological disorders are likely due to environmental pollution. Respiratory allergies are immunoglobulin E (IgE)-mediated immune response. (See Brinker, J. Naturopathic Medicine, (1993):4:64-68). There are two major types of respiratory allergic reactions: The immediate hypersensitivity reactions include allergic rhinitis (hay fever) and allergic (extrinsic) bronchial asthma. Allergic rhinitis is brought on by antigen/IgE binding to sensitized mast cells and basophils, causing a decrease in cAMP which leads to release of esosinophil chemotactic factor and histamine. Histamine binding to H1-receptors has several results. It increases vasodilation, capillary permeability, and smooth muscle contraction, manifesting as nasal congestion with watery discharge, sneezing, and itching eyes. Web site: http://www.delphion.com/details?pn=US06503542__

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Infant skin care composition Inventor(s): Harbeck; Marie (3202 Clumpgrass Cove, Austin, TX 78735) Assignee(s): none reported Patent Number: 6,589,537 Date filed: January 3, 2001 Abstract: A resistant to body fluids, organic oil-based topical transdermal composition for the alleviation and treatment of infant skin conditions, including, dry, sensitive, chapped, cracked, itching reddened, and flaking skin, as well as infant skin infirmities associated with eczema, dermatitis, and diaper rash, which has as main constituents, organic oil lipids, vitamin A, tocopheral linoleate, and tincture of benzoin, in an organic beeswax emulsifying base. Excerpt(s): This invention relates to an improved and useful organic oil-based topical transdermal composition for the alleviation and treatment of infant skin conditions, including, dry, sensitive, chapped, cracked, itching, reddened, and flaking skin, as well as infant skin infirmities associated with eczema, dermatitis, and diaper rash, which has as its main constituents, safflower oil, flaxseed oil, vitamin A, tocopheral linoleate, sweet almond oil, apricot kernel oil, essential oil of lavender, and tincture of benzoin, in an organic beeswax emulsifying base. The pharmaceutical industry is continually expanding its efforts in order to provide infant topical preparations which will eliminate and prevent diaper rash, cracking, chapping, chaffing, redness and restore the skin to its natural healthy condition, thus the combinations of skin aggravating synthetic compositions employed continue to increase yearly. Thus, synthetic surfactants, silicones, ammonia, alcohol's, solvents, acids, artificial colors, animal oils, mineral oils, petrolatum derivatives, fungicides, plant resins, oxides, plus cadmium, cobalt, lead, mercury, molybdenum, nickel, silver, tin, zinc and iron salts, nitrates, chlorides, and fragrances, and the like are being incorporated into the compositions of the cited prior art compositions that are supplied to stores and supermarkets. Web site: http://www.delphion.com/details?pn=US06589537__

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Inhibitor of replicative senescence of human keratinocytes containing retinoic acid as active ingredients Inventor(s): Min; Byung-Moo (#13-501 Rex Apt., 300-3 Ichon-dong, Yongsan-ku, Seoul 140-030, KR) Assignee(s): none reported Patent Number: 6,566,399 Date filed: August 3, 2001 Abstract: Disclosed is an inhibitor of replicative senescence of human keratinocytes containing retinoic acid, including all-trans retinoic acid, 3,4-didehydroretinoic acid, and 9-cis retinoic acid, as active ingredients. The retinoic acid plays an important role in extending the in vitro life span and inhibiting replicative senescence of the human mucosal keratinocytes and the human epidermal keratinocytes, thereby being used for a prophylactic or therapeutic agent of various diseases attributed to replicative senescence of the human oral keratinocytes. In addition, the inhibitor containing the retinoic acid can be used for a cosmetic purpose and as a prophylactic or therapeutic agent for wound-caused dermatitis and ski senescence.

Patents 175

Excerpt(s): This patent application claims a benefit of priority from Korean Patent Application No. 2000-44972 filed Aug. 3, 2000 and Korean Patent Application No. 200146911 filed Aug. 3, 2001, the contents of each of which are incorporated herein by reference. The present invention relates to an inhibitor against replicative senescence of human keratinocytes. The inhibitor against replicative senescence of human keratinocytes can extend the in vitro life span and inhibit replicative senescence. Therefore, the inhibitor containing retinoic acid as active ingredients of the present invention can be used for a prophylactic or therapeutic agent of various oral diseases, such as trauma-caused inflammation, exelcymosis-caused inflammation, burn-caused inflammation, traumatic ulcer, and angular cheilosis, for a cosmetic purpose and for a prophylactic or therapeutic agent for wound-caused dermatitis and skin senescence. Replicative senescence is regarded to be an essential causative element of organismic aging (Wantanabe Y. et al. Oncogene, 1997, 14, 2025-2032). It is assumed that such senescent cells are accumulated in the living body and the phenotype expressed from the cells alters thereby accumulating in age-related pathology (Dimri G. D., et al., Proc. Natl. Acad. Sci., 1995, 92, 9363-9367). Web site: http://www.delphion.com/details?pn=US06566399__ •

Inhibitors of transcription factor-NF-.kappa.B Inventor(s): Callahan; James F. (Philadelphia, PA), Chabot-Fletcher; Marie C. (Phoenixville, PA) Assignee(s): SmithKline Beecham Corporation (Philadelphia, PA) Patent Number: 6,492,425 Date filed: December 19, 2000 Abstract: The present invention provides pharmaceutical compositions of salicylanilide inhibitors of transcription factor NF-.kappa.B, and methods for treating diseases in which activation of NF-.kappa.B is implicated. More specifically, the present invention provides methods of treatment of a variety of diseases associated with NF-.kappa.B activation including inflammatory disorders; particularly rheumatoid arthritis, inflammatory bowel disease, and asthma; dermatosis, including psoriasis and atopic dermatitis; autoimmune diseases; tissue and organ rejection; Alzheimer's disease; stroke; atherosclerosis; restenosis; cancer, including Hodgkin's disease; certain viral infections, including AIDS; osteoarthritis; osteoporosis; and Ataxia Telangiestasia by administering to a patient in need thereof a compound of the present invention. Excerpt(s): This invention relates in general to salicylanilide inhibitors of transcription factor NF-.kappa.B. Such compounds are particularly useful for treating diseases in which activation of NF-.kappa.B is implicated. More specifically, these compounds inhibit I.kappa.B phosphorylation and subsequent degradation. Such compounds are useful in the treatment of a variety of diseases associated with NF-.kappa.B activation including inflammatory disorders; particularly rheumatoid arthritis, inflammatory bowel disease, and asthma; dermatosis, including psoriasis and atopic dermatitis; autoimmune diseases; tissue and organ rejection; Alzheimer's disease; stroke; atherosclerosis; restenosis; cancer, including Hodgkins disease; and certain viral infections, including AIDS; osteoarthritis; osteoporosis; and Ataxia Telangiestasia. Recent advances in scientific understanding of the mediators involved in acute and chronic inflammatory diseases and cancer have led to new strategies in the search for effective therapeutics. Traditional approaches include direct target intervention such as the use of specific antibodies, receptor antagonists, or enzyme inhibitors. Recent

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breakthroughs in the elucidation of regulatory mechanisms involved in the transcription and translation of a variety of mediators have led to increased interest in therapeutic approaches directed at the level of gene transcription. The activity of NF-.kappa.B is regulated by its interaction with a member of the inhibitor I.kappa.B family of proteins. This interaction effectively blocks the nuclear localization sequence on the NF-.kappa.B proteins, thus preventing-migration-of the dimer to the nucleus. A wide variety of stimuli activate NF-.kappa.B through what are likely to be multiple signal transduction pathways. Included are bacterial products (LPS), some viruses (HIV-1, HTLV-1), inflammatory cytokines (TNF.alpha., IL-1), and environmental stress. Apparently common to all stimuli however, is the phosphorylation and subsequent degradation of I.kappa.B. I.kappa.B is phosphorylated on two N-terminal serines by the recently identified I.kappa.B kinases (IKK-.alpha. and IKK-.beta.). Site-directed mutagenesis studies indicate that these phosphorylations are critical for the subsequent activation of NF-.kappa.B in that once phosphorylated the protein is flagged for degradation via the ubiquitin-proteasome pathway. Free from I.kappa.B, the active NF-.kappa.B complexes are able to translocate to the nucleus where they bind in a selective manner to preferred gene-specific enhancer sequences. Included in the genes regulated by NF-.kappa.B are a number of cytokines, cell adhesion molecules, and acute phase proteins. Web site: http://www.delphion.com/details?pn=US06492425__ •

Isoxazole derivatives to be used as phosphodiesterase VII inhibitors Inventor(s): Eggenweiler; Hans-Michael (Weiterstadt, DE), Gassen; Michael (Griesheim, DE), Jonas; Rochus (Darmstadt, DE), Welge; Thomas (Alsbach, DE), Wolf; Michael (Darmstadt, DE) Assignee(s): Merck Patentgesellschaft (Darmstadt, DE) Patent Number: 6,531,498 Date filed: May 3, 2002 Abstract: The invention relates to compounds of formula I and to their physiologically acceptable salts and solvates which act as phosphodiesterse VII inhibitors and are thus useful for the treatment of allergic disorders, asthma, chronic bronchitis, atopic dermatitis, psoriasis and other skin disorders, inflammatory disorders, autoimmune diseases, rheumatoid arthritis, multiple sclerosis, Crohn's disease, diabetes mellitus or ulcerative colitis, osteoporosis, transplant rejection reactions, cachexia, tumor growth, tumor metastases, sepsis, memory disturbances, atherosclerosis and AIDS. Excerpt(s): and their physiologically acceptable salts and/or solvates as phosphodiesterase VII inhibitors. The invention further relates to the use of the compounds of the formula I for producing a pharmaceutical for controlling allergic disorders, asthma, chronic bronchitis, atopic dermatitis, psoriasis and other skin disorders, inflammatory disorders, autoimmune diseases such as, for example, rheumatoid arthritis, multiple sclerosis, Crohn's disease, diabetes mellitus or ulcerative colitis, osteoporosis, transplant rejection reactions, cachexia, tumour growth or tumour metastases, sepsis, memory disturbances, atherosclerosis and AIDS. Compounds of the formula I are described by Bionet. Web site: http://www.delphion.com/details?pn=US06531498__

Patents 177

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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 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__

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Method for treating inflammation using soluble receptors to interleukin-20 Inventor(s): Blumberg; Hal (Seattle, WA), Chandrasekher; Yasmin A. (Mercer Island, WA), Foster; Donald C. (Lake Forest Park, WA), Kelly; James D. (Mercer Island, WA), Thompson; Penny (Snohomish, WA), Xu; Wenfeng (Mukilteo, WA) Assignee(s): ZymoGenetics, Inc. (Seattle, WA) Patent Number: 6,610,286 Date filed: December 22, 2000

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Abstract: A method for treating IL-20 induced inflammation. An antagonist to IL-20 is administered to treat inflammation and associated diseases. The antagonist can be an antibody that binds to IL-20 or its receptor or a soluble receptor that binds to IL-20. Examples of such diseases are adult respiratory disease, psoriasis, eczema, contact dermatitis, atopic dermatitis, septic shock, multiple organ failure, inflammatory lung injury, bacterial pneumonia, inflammatory bowel disease, rheumatoid arthritis, asthma, ulcerative colitis and Crohn's disease. Excerpt(s): The teachings of all of the references cited herein are incorporated in their entirety herein by reference. Inflammation normally is a localized, protective response to trauma or microbial invasion that destroys, dilutes, or walls-off the injurious agent and the injured tissue. It is characterized in the acute form by the classic signs of pain, heat, redness, swelling, and loss of function. Microscopically, it involves a complex series of events, including dilation of arterioles, capillaries, and venules, with increased permeability and blood flow, exudation of fluids, including plasma proteins, and leukocyte migration into the area of inflammation. Diseases characterized by inflammation are significant causes of morbidity and mortality in humans. Commonly, inflammation occurs as a defensive response to invasion of the host by foreign, particularly microbial, material. Responses to mechanical trauma, toxins, and neoplasia also may results in inflammatory reactions. The accumulation and subsequent activation of leukocytes are central events in the pathogenesis of most forms of inflammation. Deficiencies of inflammation compromise the host. Excessive inflammation caused by abnormal recognition of host tissue as foreign or prolongation of the inflammatory process may lead to inflammatory diseases as diverse as diabetes, arteriosclerosis, cataracts, reperfusion injury, and cancer, to post-infectious syndromes such as in infectious meningitis, rheumatic fever, and to rheumatic diseases such as systemic lupus erythematosus and rheumatoid arthritis. The centrality of the inflammatory response in these varied disease processes makes its regulation a major element in the prevention control or cure of human disease. Web site: http://www.delphion.com/details?pn=US06610286__ •

Method of treating inflammatory bowel disease using a topical formulation of IL-11 Inventor(s): Bedrosian; Camille L. (Belmont Hills, MA), Keith, Jr.; James C. (Andover, MA), Schendel; Paul F. (Wayland, MA), Schwerschlag; Ullrich S. (Beverly Farms, MA), Warne; Nicholas W. (Andover, MA) Assignee(s): Wyeth (Madison, NJ) Patent Number: 6,540,993 Date filed: September 15, 2000 Abstract: Provided by the present invention are topical formulations of Interleukin-11 and methods for treating a variety of disorders, including inflammatory bowel diseases (e.g., Crohn's disease, ulcerative colitis, indeterminate colitis, and infectious colitis), mucositis (e.g., oral mucositis, gastrointestinal mucositis, nasal mucositis, and proctitis), necrotizing enterocolitis, inflammatory skin disorders (e.g., psoriasis, atopic dermatitis, and contact hypersensitivity), aphthous ulcers, pharyngitis, esophagitis, peptic ulcers, gingivitis, periodontitis, and ocular diseases (e.g., conjunctivitis, retinitis, and uveitis). Excerpt(s): The present invention relates generally to novel compositions and methods for topical delivery of interleukin-11 (IL-11). In preferred embodiments, patients are treated employing topical delivery of recombinant human IL-11 for inflammatory bowel

Patents 179

diseases (e.g., Crohn's disease, ulcerative colitis, indeterminate colitis, and infectious colitis), mucositis (e.g., oral mucositis, gastrointestinal mucositis, nasal mucositis, and proctitis), necrotizing enterocolitis, inflammatory skin disorders (e.g., psoriasis, atopic dermatitis, and contact hypersensitivity), aphthous ulcers, pharyngitis, esophagitis, peptic ulcers, gingivitis, periodontitis, and ocular diseases (e.g., conjunctivitis, retinitis, and uveitis). Inflammatory responses include a broad range of host reaction to a variety of insults, such as injury, infection, or rejection. It is the overproduction 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, multiple sclerosis, osteoporosis, gingivitis, peptic ulcer disease, esophagitis, diabetes, retinitis, uveitis, reperfusion injury after myocardial infarction, cerebral vascular accident, aphthous ulcers (oral), atherosclerosis, tumor metastases, asthma, preeclampsia, pancreatitis, psoriasis, infertility and allergic disorders such as rhinitis, conjunctivitis, and urticaria. Some of these disorders and their symptoms are briefly summarized below. According to the methods of the present invention, IL-11 is administered topically to modulate the host's over reaction at the site of insult, thereby treating the following disorders. Web site: http://www.delphion.com/details?pn=US06540993__ •

Methods for managing scalp conditions Inventor(s): Murad; Howard (4265 Marina City Dr., Penthouse 11, Marina del Rey, CA 90292) Assignee(s): none reported Patent Number: 6,515,007 Date filed: August 3, 2001 Abstract: This application relates to a pharmaceutical composition for the prevention, treatment, and management of scalp conditions, such as dandruff, seborrheic dermatitis, psoriasis, folliculitis, and hair thinning including a therapeutically effective amount of an acidic component of a hydroxyacid or tannic acid, or a pharmaceutically acceptable salt thereof. A preferred anti-dandruff composition and method of managing dandruff includes a therapeutically effective amount of the acid component, a vitamin A component, and an anti-growth agent. A preferred anti-hair thinning composition and method of managing thinning hair includes a therapeutically effective amount of the acidic component, a niacin component present in an amount sufficient to locally increase blood circulation, and a 5-.alpha. reductase inhibitor. The invention also relates to a method of treating chemically processed hair by administering to a patient an amount of an acidic component of a hydroxy acid or tannic acid, or a pharmaceutically acceptable salt thereof, in an amount sufficient to essentially close the cuticle and inhibit modification of the chemically processed hair. Excerpt(s): The application relates to pharmaceutical compositions, as well as methods, to normalize skin for the prevention, treatment and management of scalp conditions. Human skin is a composite material of the epidermis and the dermis. The topmost part of the epidermis is the stratum corneum. This layer is the stiffest layer of the skin, as well as the one most affected by the surrounding environment. Below the stratum corneum is the internal portion of the epidermis. Below the epidermis, the topmost layer of the dermis is the papillary dermis, which is made of relatively loose connective tissues that define the micro-relief of the skin. The reticular dermis, disposed beneath the papillary dermis, is tight, connective tissue that is spatially organized. The reticular

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dermis is also associated with coarse wrinkles. At the bottom of the dermis lies the subcutaneous layer. The principal functions of the skin include protection, excretion, secretion, absorption, thermoregulation, pigmentogenesis, accumulation, sensory perception, and regulation of immunological processes. These functions are detrimentally affected by, for example, dryness, yeast, and structural changes in the skin, such as due to aging and excessive sun exposure. Web site: http://www.delphion.com/details?pn=US06515007__ •

Monocyclic-7H-pyrrolo[2,3-d]pyrimidine compounds, compositions, and methods of use Inventor(s): Blumenkopf; Todd A. (Old Lyme, CT), Brown; Matthew F. (Pawcatuck, CT), Changelian; Paul S. (E. Greenwich, CT), Flanagan; Mark E. (Gales Ferry, CT) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 6,635,762 Date filed: June 17, 1999 Abstract: Novel pyrrolo[2,3-d]pyrimidine compounds useful as inhibitors of the enzyme protein tyrosine kinases such as Janus Kinase 3 as well as immunosuppressive agents for organ transplants, lupus, multiple sclerosis, rheumatoid arthritis, psoriasis, Type I diabetes and complications from diabetes, cancer, asthma, atopic dermatitis, autoimmune thyroid disorders, ulcerative colitis, Crohn's disease, Alzheimer's disease, Leukemia and other autoimmune diseases are described. Excerpt(s): The present invention relates to pyrrolo[2,3-d]pyrimidine compounds which are inhibitors of protein tyrosine kinases, such as the enzyme Janus Kinase 3 (hereinafter also referred to as JAK3) and as such are useful therapy as immunosuppressive agents for organ transplants, lupus, multiple sclerosis, rheumatoid arthritis, psoriasis, Type I diabetes and complications from diabetes, cancer, asthma, atopic dermatitis, autoimmune thyroid disorders, ulcerative colitis, Crohn's disease, Alzheimer's disease, Leukemia and other indications where immunosuppression would be desirable. This invention also relates to a method of using such compounds in the treatment of the above indications in mammals, especially humans, and the pharmaceutical compositions useful therefor. with the proviso that the groups of formulas IV, V, VI or XIII do not contain two or more oxygens, sulfurs or combinations thereof in adjacent positions. Web site: http://www.delphion.com/details?pn=US06635762__

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Peanut allergens and methods Inventor(s): Bannon; Gary A. (LIttle Rock, AR), Burks, Jr.; A. Wesley (Little Rock, AR), Cockrell; Gael (Cabot, AR), Helm; Ricki M. (LIttle Rock, AR), King; Nina E. (Little Rock, AR), Sampson; Hugh A. (Larchmont, NY), Stanley; J. Steven (North Little Rock, AR) Assignee(s): Mt. Sinai School of Medicine (New York, NY), University of Arkansas (Littlerock, AR) Patent Number: 6,486,311 Date filed: June 29, 1998

Patents 181

Abstract: Peanuts are a common cause of food hypersensitivity reactions. The sera of 10 patients who had atopic dermatitis and a positive double-blind placebo-controlled food challenge to peanut were used to investigate the major allergens of peanut. Crude Florunner extracts were fractionated by anion-exchange chromatography using a step gradient (limit buffer, 0.05M BisTris/1.5M NaCl). A protein peak (OD 280) which eluted at 10% NaCl and demonstrated intense IgE-binding was further analyzed by twodimensional SDS-PAGE/immunoblot analysis. The majority of this fraction is a protein which has a molecular weight of 17 kD and a pI of 5.2. Sequencing data from the Nterminus revealed the following initial 9 amino acids: (*)-Q-Q-(*)-E-L-Q-D-L. Based on IgE-binding activity and no known amino acid sequence identity to other allergens, this allergen is designated Ara h II. Ara h II may be used to detect and quantify peanut allergens in foodstuffs. Serum IgE from patients with documented peanut hypersensitivity reactions and a peanut cDNA expression library were used to identify clones that encode peanut allergens. Excerpt(s): To elucidate the exact mechanism of IgE-mediated reactions, the identification and purification of the precise allergens are necessary. Significant information has accumulated in allergen C characterization from a wide variety of sources, including pollens, dust mite, animal danders, and insects.sup.5 In comparison, allergen characterization for even the most common food allergens is much less defined. Despite the significant prevalence of peanut hypersensitivity reactions and several deaths annually, the identification of the clinically relevant antigens and an understanding of the immunobiology of peanut hypersensitivity is just beginning. Monoclonal antibodies are being increasingly used to define and characterize the allergenic epitopes of many allergens. Multiple allergens including the dust mite allergen, Der f I,.sup.6 and the grass pollen allergen, Lol p I,.sup.7 have been studied by using monoclonal antibodies. Murine monoclonal antibodies to these allergens have been shown to be quite effective in defining their allergenic epitopes. In this report we have investigated the epitope specificity of Ara h II,.sup.8 a major peanut allergen, by using monoclonal antibodies as probes for mapping the possible antigenic determinants. We have produced and characterized a panel of monoclonal antibodies specific to Ara h II. The Ara h II monoclonal antibodies allowed us to define at least two antigenic sites on Ara h II. Inhibition assays were used to determine the IgE-binding sites on Ara h II. Web site: http://www.delphion.com/details?pn=US06486311__ •

Pharmaceutical composition for preventing and treating allergic diseases and a method for preparation thereof Inventor(s): Hwang; Woo-Jun (Cheollabook-do, KR), Jang; Chul-Ho (Jeollabook-do, KR), Kim; Hyung-Min (Cheollabook-do, KR), Park; Eun-Jeung (Cheollabook-do, KR) Assignee(s): Biomedpark Co., Ltd. (Yongin, KR), Daehan Biolink Co., Ltd. (Chungbuk, KR) Patent Number: 6,524,627 Date filed: March 20, 2002 Abstract: This invention relates to a pharmaceutical composition comprising Platycodi Radix, Scutellariae Radix, Ponciri Fructus, Schizonepetae Herba, Bupleuri Radix, Angelicae dahuricae Radix, Paeoniae Radix alba, Cnidii Rhizoma, Angelicae gigantis Radix, Ledebouriellae Radix, Forsythiae Fructus, Glycyrrhizae Radix, Lonicerae Flos, Taraxaci Herba, Trichosanthis Radix, Ulmi Cortex Radicis, Astragali Radix, Atractylodis Rhizoma alba, Rehmanniae Rhizoma, Zanthoxyli Fructus, Magnoliae Flos, Xanthii

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Fructus, Mori Cortex Radicis, Pinelliae Tuber, Cimicifugae Rhizoma, Puerariae Radix and Menthae Herba as the active ingredients for preventing and/or treating acute and/or chronic allergic nasal diseases (including chronic paranasal sinusitis), allergic dermatitis, allergic otitis media (including recurrent otitis media with effusions), allergic conjunctivitis, allergic asthma, etc., and to a method for preparation thereof. Excerpt(s): This invention relates to a pharmaceutical composition for preventing and treating allergic diseases and to a method for preparation thereof. Specifically, the present invention relates to a pharmaceutical composition comprising Platycodi Radix, Scutellariae Radix, Ponciri Fructus, Schizonepetae Herba, Bupleuri Radix, Angelicae dahuricae Radix, Paeoniae Radix alba, Cnidii Rhizoma, Angelicae gigantis Radix, Ledebouriellae Radix, Forsythiae Fructus, Glycyrrhizae Radix, Lonicerae Flos, Taraxaci Herba, Trichosanthis Radix, Ulmi Cortex Radicis, Astragali Radix, Atractylodis Rhizoma alba, Rehmanniae Rhizoma, Zanthoxyli Fructus, Magnoliae Flos, Xanthii Fructus, Mori Cortex Radicis, Pinelliae Tuber, Cimicifugae Rhizoma, Puerariae Radix and Menthae Herba as the active ingredients for preventing and/or treating acute and/or chronic allergic nasal diseases (including chronic paranasal sinusitis), allergic dermatitis, allergic otitis media (including recurrent otitis media with effusions), allergic conjunctivitis, allergic asthma, etc., and to a method for preparation thereof. A normal immune reaction may cause local inflammations or eliminate foreign substance without damaging tissues of their hosts by stimulating effective molecules to remove attacks from allergen through various mechanisms. However, the term of hypersensitivity or allergy is used when an immune reaction is excessively activated or progressed in an undesirable direction to harm the human body. Today, allergic diseases cost a lot of money, because they tend to be more severe in civilized societies. According to a literature [Scientific American, September, 1993], more than 20% of American people are suffering from various allergic symptoms, and allergic rhinitis is the most common form of allergy. The attack of allergen can sometimes be fatal. According to the statistical data of 1990, it was reported that 3.6 billion dollars had been spent to the direct medical cost for asthma. As to the number of patients who are suffering from these allergic diseases, Korea is also on the similar level to the developed countries. The number is increasing every year. In particular, young child patients are on rapid increase. Thus, many researchers are devoting themselves in developing a drastic cure to reduce economic, biological and physical burden of the patient from such allergic diseases. It might be said that diversity and complexity of allergic diseases are from the exposure to many kinds of allergen in the modern life. Synthetic fibers such as nylon and Teflon, and synthetic resins such as polyethylene, polyester and epoxy resin, which brought innovation to the textile industry, cause anaphylactic contact dermatitis at skin or mucous membrane by various chemical substances like monomer and polymer that are produced in the manufacturing process. On the other hand, allergic inflammations on the skin are caused by contact with glass frames, artificial teeth, wrist watch chains, plastic raincoats, umbrella handles, etc. The substances such as polyurethane, which are widely used as paints for cars, furniture and musical instruments, are the main cause of bronchial asthma. Rubber, leather, cement, and metals such as platinum, gold, mercury and nickel may cause allergic contact dermatitis. Accessories, such as earrings, necklace and finger rings, or rubber products, may also cause allergy. It is well known that fast food, antiseptic, synthetic sweetening, and additives including food colors may also cause food allergy. Web site: http://www.delphion.com/details?pn=US06524627__

Patents 183

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Topical formulation of alkyl-, phenyl-pyridone Inventor(s): Scheiwe; Max Werner (Maulburg, DE), Yamauchi; Shitotomo (Tokyo, JP) Assignee(s): Mepha AG (Aesch, CH) Patent Number: 6,492,395 Date filed: May 23, 2001 Abstract: A pharmaceutically acceptable topical formulation for the treatment and/or prevention of skin ailments, more particularly of fibriotic nature such as fibriotic lesional tissues, contiguous warts, contact dermatitis, and keloids, and to assist the healing of burns after surgery, comprising as active ingredient a substituted pyridone of the formula: n-(R.sup.1)-R.sup.2 -2-(1H)pyridone or a pharmaceutically acceptable salt or ester thereof, where R.sup.1 is selected from methyl, ethyl, propyl, carboxyl and a carboxymethyl or carboxyethyl ester group, R.sup.2 is selected from phenyl, methylphenyl, ethylphenyl, propylphenyl, and a carboxyphenyl or carboxyethylphenyl ester group, and n is 3, 4 or 5, together with an excipient, characterized in that the excipient comprises, one or more plasticisers, one or more antioxidants, one or more gelforming agents and sufficient pH adjusting agent to bring the pH of the formulation to a value from 4 to 8. The preferred active ingredient is 5-methyl-1-phenyl-2-(1H)pyridone (Pirfenidone). Excerpt(s): or a pharmaceutically acceptable salt or ester thereof, where R.sup.1 is selected from methyl, ethyl, propyl, carboxyl and a carboxymethyl or carboxyethyl ester group, R.sup.2 is selected from phenyl, methylphenyl, ethylphenyl, propylphenyl, and a carboxyphenyl or carboxyethylphenyl ester group, and n is 3, 4 or 5 (position of substitution). The preferred active ingredient is Pirfenidone (CAS 53179-13-8, 5-methyl1-phenyl-2-(1H)-pyridone). As described in U.S. Pat. No. 5,310,562 and EP 0 383 591, Pirfenidone has a broad spectrum of applications in the prevention and treatment of fibrotic diseases, especially for the reparation and prevention of fibrotic lesional tissues, contiguous warts, contact dermatitis, keloids, fibrosis of the lung, fibrosis of the prostate, sclerosis, the healing of burns after surgery and Alzheimer disease. Although the possibility of topical application is mentioned, there is no description of any specific formulation. The application of active ingredients of the class mentioned, (hereafter called alkyl,phenyl pyridones) e.g. Pirfenidone for e.g. the treatment of burns and keloids may possibly be carried out using a solution or a suspension of the agent in aqueous or oily excipient such as emulsions, creams, ointments, gels, microemulsions, liquid emulsions, nanocapsule suspensions, liposome formulations, lotions and the like; however, an ointment, cream or gel formulation is preferable because of their soothing effect and easy application. Because these formulations are used in the treatment of humans they are considered to be pharmaceutical preparations, and as thus have to be proven to be physically and chemically stable before they are permitted on the market. For this reason, each formulation must undergo a stability test. Without the necessary data on stability and shelf life, the formulation cannot be approved by any health authority. Web site: http://www.delphion.com/details?pn=US06492395__

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Treated disposable articles for reducing skin breakdown Inventor(s): Sheridan; Christopher H. (114-14 St., Cress Kill, NJ 07626) Assignee(s): none reported Patent Number: 6,559,353 Date filed: January 19, 1995 Abstract: A disposable waste containment composite is disclosed for fabrication into baby diapers, incontinent briefs, feminine hygiene pads, incontinent under pads and sheets, wound dressings and the like. The composite is formed from a liquid permeable topsheet, an absorbent core and an impermeable backing sheet unified by the use of adhesives, heat and pressure, ultra sonic welding and the like. The composite is characterized in that its topsheet has been treated with a non-aqueous composition comprising propylene glycol, a non-water soluble protectant, and a surface active agent. The treatment composition can also preferably include an emollient an anti-odorant, a healing agent or the like. A unique feature of the treatment is that the non-water soluble components do not restrict or interfere with the passage of bodily waste into the absorbent core. The top sheet so treated delivers in use the protectant and other agents such as the healing agent, to the surface of the skin so that when the fabricated article is employed, the incidence of contact dermatitis, skin irritations, maceration and pressure ulcers are reduced. In addition, the use of this unique topsheet treatment reduces friction which, along with the other benefits, can virtually eliminate the need for separately using medicated creams, ointments or powders. Excerpt(s): The present invention relates to treated disposable absorbent articles such as diapers, incontinent briefs, incontinent pads, bandages, dressings and the like which are effective in preventing or reducing diaper rash (contact irritant dermatitis) particularly in infants and the occurrence of bed sores and ulcerations in non-ambulatory, incontinent subjects. More particularly, the invention relates to the dry treated cover sheet useful in the fabrication of such articles. Existing absorbent articles such as diapers, incontinent briefs, feminine hygiene pads and incontinent under pads conventionally include a topsheet or cover sheet. The topsheet is that part of the absorbent article which is in direct contact with the skin of the user. Chemical treatment of these topsheets has heretofore been limited to the addition of surface active agents to facilitate the transfer of liquid waste through the topsheet and into an absorbent core. To date, attempts to incorporate skin softeners and protectants, and/or friction reducing emollients into the topsheet has resulted in the repelling of the body fluids, rendering the absorbent articles non-functional for their intended purpose. One object of the invention is to apply skin softeners, protectants and friction reducing emollients to a topsheet in a manner that will be effective to transfer these softeners, protectants and emollients to the skin by contact, without affecting the functionality of the absorbent article. Web site: http://www.delphion.com/details?pn=US06559353__

Patents 185

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Treating eczema with a combination of isotonic saline ocean.RTM. and nasal mast cell stabilizers Inventor(s): Feller; Theodore H. (11834 Conway Rd., St. Louis, MO 63131), Fleming; Thomas E. (24 Bopp Ln, St. Louis, MO 63131) Assignee(s): none reported Patent Number: 6,596,284 Date filed: April 30, 2002 Abstract: The present invention relates to the prevention and treatment of atopic dermatitis and treatment of atopic dermatitis and other eczematous disorders by application of topical mast cell stabilizers including cromolyn sodium, nedocromil or lodoxamide, in a vehicle of a buffered isotonic saline solution (OCEAN.RTM.). Excerpt(s): The present invention relates to prevention and treatment of eczema and atopic dermatitis. More particularly, the present invention relates to the prevention and treatment of atopic dermatitis and other eczematous disorders by the application of a combination of topical isotonic saline OCEAN.RTM. and topical nasal mast cell stabilizers. Atopic dermatitis is a chronic inflammatory skin disorder, also known by terms used to describe the disorder as neurodermatitis, disseminated lichen simplex chronicus, or atopic eczema. The prevalence of atopic dermatitis among persons one year to seventy four years of age ranges from seven to twenty four cases per one thousand. Atopic dermatitis is most prevalent in infancy and childhood, less prevalent in puberty, and often persists into adulthood. Horan R F, Schneider L C, Sheffer A L, JAMA 268:2858(1992). Atopic dermatitis is not a primary allergic disorder per se but appears to be inherited in association with certain allergic disorders. Environmental stimuli can trigger the disease in genetically predisposed individuals. The increased prevalence of atopic dermatitis since the 1990s has been attributed to environmental irritants, infections, previous exposure to allergic foods, and airborne allergens such as dust, mites, animal dander and pollens. Web site: http://www.delphion.com/details?pn=US06596284__

Patent Applications on Dermatitis 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 dermatitis:

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This has been a common practice outside the United States prior to December 2000.

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3-Azabicyclo[3.1.0]hexane derivatives useful in therapy Inventor(s): Banks, Bernard Joseph; (County of Kent, GB), Critcher, Douglas James; (County of Kent, GB), Fenwick, Ashley Edward; (County of Kent, GB), Gethin, David Morris; (County of Kent, GB), Gibson, Stephen Paul; (County of Kent, GB) Correspondence: Pfizer Inc; 150 East 42nd Street; 5th Floor - Stop 49; New York; NY; 10017-5612; US Patent Application Number: 20030207876 Date filed: April 8, 2002 Abstract: Compounds of formula I, 1where the substituents are as defined herein, and the pharmaceutically or veterinarily acceptable derivatives or prodrugs thereof, are pharmaceutically and veterinarily useful, in particular they bind to opiate receptors (e.g. mu, kappa and delta opioid receptors). They are likely to be useful in the treatment of diseases or conditions modulated by opiate receptors, for example irritable bowel syndrome; constipation; nausea; vomiting; pruritic dermatoses, such as allergic dermatitis and atopy; eating disorders; opiate overdoses; depression; smoking and alcohol addiction; sexual dysfunction; shock; stroke; spinal damage; and head trauma. Excerpt(s): This claims application claims priority under 35 U.S.C. 120 of U.S. Ser. No. 09/883,567, filed Jun. 18, 2001. This invention relates to pharmaceutically useful compounds, in particular compounds that bind to opiate receptors (e.g. mu, kappa and delta opioid receptors). Compounds that bind to such receptors are likely to be useful in the treatment of diseases modulated by opiate receptors, for example irritable bowel syndrome; constipation; nausea; vomiting; and pruritic dermatoses, such as allergic dermatitis and atopy in animals and humans. Compounds that bind to opiate receptors have also been indicated in the treatment of eating disorders, opiate overdoses, depression, smoking and alcohol addiction, sexual dysfunction, shock, stroke, spinal damage and head trauma. There is a particular need for an improved treatment of itching. Itching, or pruritus, is a common dermatological symptom that can give rise to considerable distress in both humans and animals. Pruritus is often associated with inflammatory skin diseases which may be caused by hypersensitivity reactions, including reactions to insect bites, such as flea bites, and to environmental allergens, such as house dust mite or pollen; by bacterial and fungal infections of the skin; or by ectoparasite infections. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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5-Arylsulfonyl-imidazo[1',2':1,6]pyrido[2,3-b]pyrazine-6-amines compounds

and

related

Inventor(s): Kleinman, Edward F.; (Pawcatuck, CT) Correspondence: Pfizer INC.; Patent Department, Ms8260-1611; Eastern Point Road; Groton; CT; 06340; US Patent Application Number: 20030203911 Date filed: April 28, 2003 Abstract: A compound of the formula 1wherein a, X, R.sup.1, R.sup.2, R.sup.3 and R.sup.4 are as defined above, useful in the treatment of respiratory, allergic, rheumatoid, body weight regulation, inflammatory and central nervous system disorders such as asthma, chronic obstructive pulmonary disease, adult respiratory diseases syndrome,

Patents 187

shock, fibrosis, pulmonary hypersensitivity, allergic rhinitis, atopic dermatitis, psoriasis, weight control, rheumatoid arthritis, cachexia, crohn's disease, ulcerative colitis, arthritic conditions and other inflammatory diseases, depression, multi-infarct dementia and AIDS. Excerpt(s): This non-provisional patent application is based upon and claims priority from U.S. patent application Ser. No. 09/918,099, filed Jul. 30, 2001, which claims priority from United States non-provisional application Ser. No. 09/489,689, filed Jan. 24, 2000, which claims priority from U.S. provisional patent application No. 60/117,875, filed Jan. 29, 1999. This invention relates to 5-arylsulfonyl-imidazo[1',2':1,6]pyrido[2- ,3b]pyrazine-6-amines and related compounds. The compounds are selective inhibitors of phosphodiesterase type 4 (PDE4) and the production of tumor necrosins factor (TNF), and as such are useful in the treatment of respiratory, allergic, rheumatoid, body weight regulation, inflammatory and central nervous system disorders such as asthma, chronic obstructive pulmonary disease, adult respiratory diseases syndrome, shock, fibrosis, pulmonary hypersensitivity, allergic rhinitis, atopic dermatitis, psoriasis, weight control, rheumatoid arthritis, cachexia, Crohn's disease, ulcerative colitis, arthritic conditions and other inflammatory diseases, depression, multi-infarct dementia, and AIDS. This invention also relates to a method of using such compounds in the treatment of the foregoing diseases in mammals, especially humans, and to pharmaceutical compositions containing such compounds. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Antiallergic agent, anti-inflammatory agent, anti-atopic dermatitis agent and antipsoriatic agent Inventor(s): Jujii, Wataru; (Osaka, JP), Sugiura, Hisashi; (Shiga-ken, JP), Suwa, Yoshihide; (Osaka, JP), Uehara, Masami; (Shiga-ken, JP), Yang, Zhibo; (Shiga-ken, JP) Correspondence: Manelli Denison & Selter; 2000 M Street NW Suite 700; Washington; DC; 20036-3307; US Patent Application Number: 20030096025 Date filed: September 30, 2002 Abstract: The antiallergic agent, antiinflammatory agent, anti-atopic dermatitis agent or antipsoriatic agent of the present invention is efficacious in preventing, reducing or relieving symptoms due to inflammation or allergic reactions, and in particular, it is useful in preventing, reducing or relieving the symptoms of atopic dermatitis and psoriasis.The agent of the present invention, which contains oolong tea extract as the active ingredient, is excellent in safety and exerts no side-effect even over continuous and prolonged administration. Excerpt(s): This invention relates to an agent containing oolong tea extract as the active ingredient. More particularly, it relates to an agent having antiinflammatory, antiallergic, anti-atopic dermatitis or antipsoriatic effects and foods, beverages and cosmetics containing the same. Various epidemiological surveys indicate that allergic diseases continue to increase in recent years. In particular, cedar pollen hypersensitivity and atopic dermatitis have been on the remarkable increase and thus even brought about a social problem. It is estimated that the increase in these allergic diseases is caused by not only increase in allergens but also changes in our environment such as air pollution, use of food additives and changes in eating habits. It is the fundamental method for treating allergic diseases to eliminate or not take the causative allergens. It

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has been a practice to administer drugs appropriately selected depending on the severity of the symptoms or the onset mechanism of the disease. Allergic reactions are classified into four groups, i.e., the types I to IV depending on the causative immunoglobulins and cells participating therein. The types I to III allergies are immunological reactions in which humoral antibodies participate. They are called immediate-type allergies, since allergic reactions appear quickly therein. On the other hand, the type IV allergy is a cell-mediated immunological reaction in which not any antibody but sensitized lymphocytes participate. It is also called delayed-type allergy. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Antioxidant dermatological composition Inventor(s): Bhagwat, Dileep; (Bronxville, NY), Glassman, Bradley P.; (Fairfield, NJ), Glassman, Daniel; (Fairfield, NJ) Correspondence: Merchant & Gould PC; P.O. Box 2903; Minneapolis; MN; 55402-0903; US Patent Application Number: 20030138466 Date filed: November 28, 2001 Abstract: Enhanced dermatological compositions are described herein using from about 21 to about 40 wt-% urea with antioxidant skin protectants suitable for the treatment of icthyosis, xerosis, severely dry skin, dermatitis, eczema, debridement and tissue suffering and other similar skin conditions. Excerpt(s): This invention relates to a semi-solid composition containing antioxidants and urea for treating and protecting the skin. As the outermost layer of skin, the stratum corneum (SC) is continuously exposed to an oxidative environment, including air pollutants, ultraviolet radiation, chemical oxidants, and aerobic microorganisms. Human SC reveals characteristic antioxidant and protein oxidation gradients with increasing antioxidant depletion and protein oxidation towards the outer layers. SC antioxidants, lipids, and proteins are oxidatively modified upon treatments with ultraviolet A/ultraviolet B, ozone, and benzoyl peroxide. Thiele J. J., Schroeter C., Hsieh S. N., Podda M., Packer L., Curr Probl Dermatol. 2001;29:26-42. The importance of antioxidants is their role in scavenging free radicals, which are created by natural oxidative process occurring in the environment. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Caspase 1 gene transfer animal Inventor(s): Mizutani, Hitoshi; (Tsu-shi, JP) Correspondence: Oblon, Spivak, Mcclelland, Maier & Neustadt, P.C.; 1940 Duke Street; Alexandria; VA; 22314; US Patent Application Number: 20030159163 Date filed: December 16, 2002 Abstract: A transgenic non-human mammal or its offspring which carries DNA having exogenous caspase 1 gene integrated thereinto in such a manner as to express the gene specifically to skin.In view that the transgenic non-human mammal of the present invention spontaneously develops atopic dermatitis in the absence of any specific

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pathogenic microorganism, the mammal is useful as a disease model animal. Use of the transgenic animal of the present invention enables development of preventive and/or therapeutic drugs for atopic dermatitis based on natural immunity and to clarify the onset mechanism of atopic diseases. Excerpt(s): The present invention relates to a transgenic animal useful as an animal model for atopic dermatitis. Atopic diseases, including atopic dermatitis, asthma, allergic rhinitis, and allergic conjuctivitis, are pathological conditions which permit the subject's own immune system to destroy, and cause disturbance of organs as a result of hyper-responses to environmental antigens to which healthy subjects usually exhibit no response. A conceivable mechanism of development of these diseases includes contribution of Th2 cytokine, which promotes allergic responses. The induction mechanism and regulatory mechanism, which are crucial from the physiological and pharmacological viewpoints, have not yet been completely elucidated. At present, mainstream treatments of atopic diseases include avoidance of antigens; administration of antihistaminic agents which serve as antagonists against binding of a mediator such as histamine to a receptor; and administration of anti-inflammatory steroids. However, development of improved therapies targeting more specific action mechanisms remains hindered, because no suitable test animals have been provided. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Composition and method for prevention, reduction and treatment of radiation dermatitis Inventor(s): Rosenbloom, Richard Allen; (Elkins Park, PA) Correspondence: Knoble & Yoshida; Eight Penn Center; Suite 1350, 1628 John F Kennedy Blvd; Philadelphia; PA; 19103; US Patent Application Number: 20030103953 Date filed: November 6, 2001 Abstract: A composition for the preventing, reducing or treating radiation dermatitis includes a mixture of one or more compounds that regulates cell differentiation and/or cell proliferation, and one or more antioxidants formulated in a pharmaceutically acceptable carrier. The composition of the present invention may further include a flavonoid. A method for the topical administration of the composition in accordance with the present invention for the purpose of preventing, reducing or treating radiation dermatitis involves topically administering an effective amount of the composition of the invention an area of skin which has been or will be exposed to radiation. The composition and method can be employed to prevent, reduce or treat radiation dermatitis caused by a wide variety of types of radiation exposure and is particularly useful for the prevention, reduction or treatment of radiation recall dermatitis. Excerpt(s): The present invention relates to a composition and method for preventing, reducing and treating radiation dermatitis. One common effect of radiation exposure is a condition called radiation dermatitis, in which the skin in the exposed area begins to look reddened, irritated or burned. The exposed skin may also develop a moist reaction, especially where there are skin folds, and may become very sore. Patients receiving radiation therapy are especially at risk for radiation dermatitis. Radiation recall dermatitis has been identified as a particularly bad problem for patients receiving a combination of radiation therapy and chemotherapy to treat cancer. Many attempts have been made to reduce, control or cure radiation dermatitis. U.S. Pat. No. 4,617,187

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to Okuyama, et al. discloses a method for treating radiation dermatitis by topically applying ubidecarenone. However, ubidecarenone might be toxic and can cause many side effects during the treatment. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Compositions for prevention and treatment of dementia Inventor(s): Bain, Allen I; (Vancouver, CA), Zolotoy, Alexander; (Richmond, CA) Correspondence: Kevin S Lemack; Nields & Lemack; 176 E Main Street; Westboro; MA; 01581; US Patent Application Number: 20030144255 Date filed: December 17, 2002 Abstract: 4,4'-diaminodiphenylsulphone is a bactericide and anti-inflammatory agent. It is known to have therapeutic activity against leprosy, dermatitis herpetiformis, actinomycotic mycetoma, asthma, malaria, rheumatoid arthritis, Kaposiis sarcoma, pneumocystis carinii (pneumonia), subcorneal pustular dermatosis and cystic acne, in patients in need of such therapy. It is also known to have therapeutic activity against memory loss in patients in need of such therapy, including patients suffering from Alzheimer disease and related neurodegenerative disorders. Donepezil hydrochloride (donepezil) is an acetylcholinesterase inhibitor that is currently used for the symptomatic treatment of Alzheimer disease in patients in need of such therapy. It has now been found that combinations of 4,4'-diaminodiphenylsulphone and cholinesterase inhibitors unexpectedly show synergistic effects in the prevention and/or treatment of dementia. The present invention relates to novel compositions and methods of preventing and/or treating dementia using combinations of 4,4'diaminodiphenylsulphone and a cholinesterase inhibitor (preferably donepezil). The method involves the administration to such individuals a drug composition of 4,4'diaminodiphenylsulphone and a cholinesterase inhibitor. The invention also relates to a method of preventing and/or treating dementia including senile dementia, that involves the use of this combination of drugs. Excerpt(s): The present invention is generally directed toward a pharmaceutical composition and method for the prevention and treatment of dementia which comprises a fixed combination of at least one 4,4'-diaminodiphenylsulphon- e compound with a cholinesterase inhibitor, although separate compositions of 4,4'diaminodiphenylsulphone and a cholinesterase inhibitor may be administered together or consecutively or separately to the patient. 4,4'-diaminodiphenylsulphone compounds, especially 4,4'-diaminodiphenylsulfone, are widely used in the pharmaceutical industry. The list of diseases responding to 4,4'-diaminodiphenylsulphone includes dermatitis herpertiformis, leprosy, asthma, malaria, rheumatoid arthritis, pneumonia and pneumocyctis carinii. Recently, it has been reported that 4,4'-diaminodiphenylsulphone is also effective in the prevention and treatment of Alzheimer disease and senile dementia (Lang P. G. J. Am. Acad. Dermatol. 1979, 1, 6: 479-492; McGeer P. L. et al., M. Dementia 1992, 3: 146-149; Coleman M. D. Br. J Dermatology 1993; 129: 507-513.). In addition to the 4,4'-diaminodiphenylsulphone compounds, a few cholinesterase inhibitors have also been studied for use in the treatment of the symptoms of Alzheimer disease. Two such compounds having cholinesterase inhibitory activity, donepezil and tacrine, are currently prescribed for the symptomatic treatment of patients with mild to moderate symptoms of dementia. These two drugs, however, only offer symptomatic relief of Alzheimer disease and do not stop the progression of the illness; they also have

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the drawback of hepatotoxicity and/or other cholinergic side effects. The present invention shows that by combining a cholinesterase inhibitor and 4,4'diaminodiphenylsulphone, an unexpected, synergistic effect is achieved towards the prevention and treatment of dementia. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Cosmetic uses of 3beta-acetoxy-7-oxo-DHEA Inventor(s): Burnier, Veronique; (Paris, FR), Courchay, Guy; (Sucy-en-Brie, FR), PicardLesboueyries, Elisabeth; (Velizy, FR), Renault, Beatrice; (Saint Maurice, FR), Roguet, Roland; (Paris, FR) Correspondence: Thomas L. Irving; Finnegan, Henderson, Farabow,; Garrett & Dunner, L.L.P.; 1300 I Street, N.W.; Washington; DC; 20005-3315; US Patent Application Number: 20030165547 Date filed: May 17, 2002 Excerpt(s): The present invention relates to the cosmetic use of 3.beta.-acetoxy-7-oxoDHEA to improve the appearance of keratin materials, with the exception of the treatment of wrinkles and fine lines, dry skin and dermatitis. This use is intended in particular for preventing or treating the loss of firmness of the skin and/or a dull complexion and/or dilation of the pores and/or skin or hair pigmentation disorders and/or hyperseborrhea and/or hyperseborrhea-related imperfections and/or sensitive skin and/or hair loss and/or baldness. The invention also relates to a cosmetic composition containing, in a physiologically acceptable medium, 3.beta.-acetoxy-7-oxoDHEA in combination with at least one other compound. DHEA, or dehydroepiandrosterone, is a natural steroid produced essentially by the adrenal glands. Exogenous DHEA, administered topically or orally, is known for its capacity to promote epidermal keratinization (JP-07 196 467) and to treat dry skin by increasing the endogenous production and secretion of sebum and thus reinforcing the skin's barrier effect (U.S. Pat. No. 4,496,556). Patent U.S. Pat. No. 5,843,932 has also described the use of DHEA to remedy dermal atrophy by inhibiting the loss of collagen and connective tissue. Finally, the Applicant has demonstrated the capacity of DHEA to combat the weathered appearance of the skin (FR 00/00349), to modify skin and hair pigmentation (FR 99/12773) and to combat epidermal atrophy (FR 00/06154). These properties of DHEA make it a candidate of choice as an anti-ageing active agent. However, for regulatory reasons, the hormonal nature of DHEA currently prevents it from being used for the manufacture of cosmetic products in certain countries, and there is thus still a need to provide DHEA analogues with properties as advantageous as DHEA itself, but without any hormonal effects. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Crystal form of N-(4-trifluoromethylphenyl)-5-methylisoxazole-4-carboxamid- e Inventor(s): Faasch, Holger; (Hochheim, DE), Hedtmann, Udo; (Frankfurt, DE), Paulus, Erich; (Eppstein, DE), Westenfelder, Uwe; (Frankfurt, DE) Correspondence: Finnegan, Henderson, Farabow, Garrett & Dunner; Llp; 1300 I Street, NW; Washington; DC; 20005; US Patent Application Number: 20030166945 Date filed: November 25, 2002 Abstract: The invention relates to a crystal modification of the compound of the formula I 1and the processes for the preparation of and use that crystal modifications 1. The invention is used for treating acute immunological episodes, such as sepsis, allergies, graft-versus-host and host-versus-graft-reactions, autoimmune diseases, in particular rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, psoriasis, atopic dermatitis, asthma, urticaria, rhinitis, uveitis, type II diabetes, liver fibrosis, cystic fibrosis, colitis, cancers, such as lung cancer, leukemia, ovarian cancer, sarcomas, Kaposi's sarcoma, meningioma, intestinal cancer, lymphatic cancer, brain tumors, breast cancer, pancreatic cancer, prostate cancer, or skin cancer. Excerpt(s): This case claims benefit under 35 U.S.C.sctn.119 of German priority document 19734438.0 filed on Aug. 8, 1997. This document, as well as German priority document 19756093.8, filed Dec. 17, 1997, are hereby incorporated by reference. The compound of formula I crystallizes in the first crystal modification in the space group P2.sub.1/c with 8 molecules in the unit cell. Molecules of the compound of formula I are present as dimers which originate from the individual molecules by formation of a -C.dbd.O. HN hydrogen bridge bond (2.938.ANG.), the two molecular levels being virtually perpendicular to one another (91.2.degree.). The two molecules have very different conformations. The angles made by the five- and six-membered rings with the central carbonyl group are 5.4.degree. and 2.1.degree. and 23.4.degree. and 23.1.degree., respectively. The latter twist creates the steric preconditions permitting the hydrogen bridge bond between the two molecules. Lines of strong intensity: 16.70; 18.90; 23.00; 23.65; and 29.05 degrees. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Disposable absorbent article having a skin care composition containing an enzyme inhibitor Inventor(s): Osborne, Scott Edward; (Middletown, OH), Roe, Donald Carroll; (West Chester, OH), Rourke, Francis James; (Sharonville, OH) Correspondence: The Procter & Gamble Company; Intellectual Property Division; Winton Hill Technical Center - Box 161; 6110 Center Hill Avenue; Cincinnati; OH; 45224; US Patent Application Number: 20030139711 Date filed: December 18, 2002 Abstract: An absorbent article, at least a portion of which comprises a skin care composition that comprises an enzyme inhibitor and is at least partially transferred from the article to the skin of a wearer of the article as a result of normal contact, wearer motion and/or body heat. The enzyme inhibitor is transferred to the skin with the skin care composition and is available at the skin/urine and skin/feces interfaces to inhibit

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enzymatic activity on the skin and to reduce or prevent the occurrence of inflammation. Repeated application of similar treated articles to the wearer's skin provides an available source with which the enzyme inhibitor transfers onto the skin continuously over time and accumulates to provide a proactive defense against harmful enzymes for the treatment and/or prevention of diaper dermatitis. Excerpt(s): This application is a continuation-in-part of U.S. application Ser. No. 09/623,813, filed on Sep. 8, 2000, which is the National Stage of International Application No. PCT/US99/05311, filed on Mar. 11, 1999, which claims the benefit of U.S. application Ser. No. 09/041,266, filed on Mar. 12, 1998. The invention relates to absorbent articles such as diapers, training pants, adult incontinence briefs, feminine hygiene products and the like, that incorporate a skin care composition that comprises an enzyme inhibitor, preferably on a wearer-contacting surface. During normal wear of the article the enzyme inhibitor is transferred with the skin care composition to at least a portion of the wearer's skin where it is available to inactivate fecal enzymes and reduce the redness and inflammation that can occur following prolonged exposure of skin to body wastes. Diaper rash is a common form of irritation and inflammation of those parts of an infant's body normally covered by a diaper. This condition is also referred to as diaper dermatitis, napkin dermatitis, napkin rash and nappy rash. While certainly more common in infants, this condition is not, in fact, limited to infants. Any individual who suffers from incontinence to the extent that the use of absorbent articles is required may develop this condition. Susceptible individuals range from newborns, to the elderly, to critically ill or nonambulatory individuals. 21 C.F.R. 333.503 defines diaper rash as "[a]n inflammatory skin condition in the diaper area (perineum, buttocks, lower abdomen, and inner thighs) caused by one or more of the following factors: moisture, occlusion, chafing, continued contact with urine or feces or both, or mechanical or chemical irritation." It is generally accepted by the medical profession that true diaper rash or diaper dermatitis is a condition which is, in its most simple stages, a contact irritant dermatitis resulting from extended contact of the skin with urine, or feces, or both. Among the most commonly accepted factors linked to diaper rash are ammonia, fecal enzymes, bacteria, the products of bacterial action, urine pH, and Candida albicans. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Emulsified skin care composition containing salicylic acid, lanolin oil, and propylene glycol Inventor(s): Farber, Elliott; (North Mankato, MN) Correspondence: Hogan & Hartson Llp; IP Group, Columbia Square; 555 Thirteenth Street, N.W.; Washington; DC; 20004; US Patent Application Number: 20030157137 Date filed: December 19, 2002 Abstract: A composition comprising an oil-in-water emulsion for skin care containing salicylic acid or another hydroxy acid, and propylene glycol to prevent formation of crystals of the hydroxy acid. The composition includes, as an emulsifier, at least one nonionic polyoxyethylene ether with a HLB of about 15 to about 17; in some embodiments, another nonionic polyoxyethylene ether with a HLB of 10 to 12 is also included. The composition also includes lanolin oil and a complex comprising Vitamin A and Vitamin D.sub.3. Other ingredients, such as a hydrophilic carbohydratecontaining polymer or a quaternary ammonium-containing polymer, can be included.

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Still other ingredients, such as preservatives, chelators, herbal extracts, allantoin and fragrance, can be included. Another aspect of the invention is a method of use of a composition according to the present invention in treating dermatological or systemic inflammatory conditions such as psoriasis, seborrheic dermatitis, and dandruff. Excerpt(s): This invention is directed to an improved emulsified skin care composition containing salicylic acid and propylene glycol that is particularly useful for treatment and/or palliation of dermatological or systemic inflammatory conditions such as psoriasis, seborrheic dermatitis and dandruff. Despite recent improvements in its treatment, psoriasis remains a serious disease of great importance. The lesions of psoriasis can be painful, unsightly, and disfiguring. Patients suffering from psoriasis are reluctant to be seen in public or undertake activities where the nature of their disease becomes manifest to the population as a whole. Accordingly, the lives of such people are impacted and restricted. The pathological mechanisms underlying psoriasis are not completely known, although much has been learned about these applications. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Enzyme treatment of foodstuffs for celiac sprue Inventor(s): Gray, Gary; (Stanford, CA), Hausch, Felix; (Langenselbold, DE), Khosla, Chaitan; (Palo Alto, CA), Shan, Lu; (Stanford, CA) Correspondence: Bozicevic, Field & Francis Llp; 200 Middlefield RD; Suite 200; Menlo Park; CA; 94025; US Patent Application Number: 20030215438 Date filed: February 14, 2003 Abstract: Administering an effective dose of glutenase to a Celiac or dermatitis herpetiformis patient reduces levels of toxic gluten oligopeptides, thereby attenuating or eliminating the damaging effects of gluten. Excerpt(s): This application claims priority to U.S. Provisional application 60/357,238 filed Feb. 14, 2002; to U.S. Provisional Application 60/380,761 filed May 14, 2002; to U.S. Provisional Application 60/392,782 filed Jun. 28, 2002; and to U.S. Provisional application No. 60/422,933, filed Oct. 31, 2002, to U.S. Provisional Application 60/428,033, filed Nov. 20, 2002, and to U.S. Provisional Application 60/435,881, filed Dec. 20, 2002, each of which are herein specifically incorporated by reference. In 1953, it was first recognized that ingestion of gluten, a common dietary protein present in wheat, barley and rye causes disease in sensitive individuals. Gluten is a complex mixture of glutamine- and proline-rich glutenin and prolamine molecules, which is thought to be responsible for disease induction. Ingestion of such proteins by sensitive individuals produces flattening of the normally luxurious, rug-like, epithelial lining of the small intestine known to be responsible for efficient and extensive terminal digestion of peptides and other nutrients. Clinical symptoms of Celiac Sprue include fatigue, chronic diarrhea, malabsorption of nutrients, weight loss, abdominal distension, anemia, as well as a substantially enhanced risk for the development of osteoporosis and intestinal malignancies (lymphoma and carcinoma). The disease has an incidence of approximately 1 in 200 in European populations. A related disease is dermatitis herpetiformis, which is a chronic eruption characterized by clusters of intensely pruritic vesicles, papules, and urticaria-like lesions. IgA deposits occur in almost all normalappearing and perilesional skin. Asymptomatic gluten-sensitive enteropathy is found in 75 to 90% of patients and in some of their relatives. Onset is usually gradual. Itching and

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burning are severe, and scratching often obscures the primary lesions with eczematization of nearby skin, leading to an erroneous diagnosis of eczema. Strict adherence to a gluten-free diet for prolonged periods may control the disease in some patients, obviating or reducing the requirement for drug therapy. Dapsone, sulfapyridine and colchicines are sometimes prescribed for relief of itching. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Galenical preparations of dapsone and related sulphones, and method of therapeutic and preventative treatment of disease Inventor(s): Aberg, A K Gunnar; (Sarasota, FL), Bain, Allen I; (Vancouver, CA), Zolotoy, Alexander; (Richmond, CA) Correspondence: Kevin S Lemack; Neilds & Lemack; 176 E Main Street; Westboro; MA; 01581; US Patent Application Number: 20030092635 Date filed: August 26, 2002 Abstract: Dapsone and related sulfones are known to have therapeutic activity against leprosy, dermatitis herpetiformis, actinomycotic mycetoma, asthma, malaria, rheumatoid arthritis, Kaposis sarcoma, pneumocystis carini (pneumonia), subcorneal pustular dermatosis and cystic acne, in patients in need of such therapy. These sulfones are also known to have therapeutic activity against memory loss in patients in need of such therapy, including patients suffering from Alzheimer's disease and related neurodegenerative disorders. It has now been found that new, modified-release formulations of dapsone and related sulfones may also be used that decrease side effects and increase effectiveness of the drugs. New methods are disclosed utilizing certain formulations of dapsone and related sulfones that improve the therapeutic index of said drugs. Side effects of these drugs are known to those skilled in the art and include, but are not restricted to anorexia, psychosis, agranulocytosis, peripheral neuritis, hemolysis, methemoglobinemia, nausea, vomiting, headache, dizziness, tachycardia, nervousness, insomnia and skin disorders. Modified-release (as defined herein) formulations of dapsone have now been found to avoid some or all of these side effects, and to have more efficacy on potency. Excerpt(s): The object of the present invention pertains to a method of treating or preventing certain diseases in a human being while increasing compliance, reducing side effects and improving efficacy of the active therapeutic ingredient(s) within a large therapeutic range. The method comprises the use of modified-release dosage formulations of sulfone compounds including 4,4'-diaminodiphenylsulfone, its didextrose sulfonate derivative(s), their analogs, metabolites, any enantiomers, any diasteriomers, or mixtures thereof and/or therapeutically acceptable salts thereof. Dapsone is an active substance that is known in the treatment of various infectious diseases and inflammatory conditions. There is a wealth of data and experimental studies regarding the activity of dapsone and related sulfones. In particular, there is a large amount of data regarding the bioavailability and pharmacokinetics of the drug. It is also known in the prior art that dapsone has therapeutic activity against leprosy, dermatitis herpetiformis, actinomycotic mycetoma, asthma, malaria, rheumatoid arthritis, Kaposis sarcoma, pneumocystis carinii (pneumonia), subcorneal pustular dermatosis and cystic acne, in patients in need of such therapy. However, since the acute or chronic toxicity of dapsone is unacceptable at the doses necessary to treat most

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diseases, it is not possible to use this compound for these indications in the presently available formulation(s). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Hair dryer Inventor(s): Park, Su-Hong; (Inchon, KR) Correspondence: Park & Sutton Llp; 3255 Wilshire Blvd; Suite 1110; Los Angeles; CA; 90010; US Patent Application Number: 20030196344 Date filed: April 22, 2003 Abstract: Disclosed is the hair dryer. In the hair dryer, a hollow dryer housing has an inlet port, an outlet port and a front handle. An intake cover is coupled to a rear side of the dryer housing and has a rear handle protruding downwardly from the hollow dryer, for suctioning an outer air into the dryer housing. A nozzle is coupled to the outlet port of the dryer housing. A heating assembly is positioned in the dryer housing and in the intake cover, and includes a hollow assembly body, a support frame, a driving motor, a rotating shaft, and a blowing fan. A shielding member is installed along an inner side of the dryer housing, the intake cover, and the nozzle. Due to this structure, the hair dryer is capable of absorbing and shielding the magnetic wave not to cause human problems such as headache, dermatitis and chronic fatigue. Excerpt(s): The present invention relates to a hair dryer, more particularly, it relates to a hair dryer having a shielding function against magnetic wave, which is used for drying and styling hair. The hair dryer 100 further comprises a heating assembly 140 that is installed at the interior of the dryer housing 110 and the intake cover 120. The heating assembly 140 has an assembly body 142, a driving motor 144, and a blowing fan 148. A support frame 144 protrudes from the front side of the assembly body 142. The driving motor 146 is mounted on the interior of the assembly body 142, and a part of which is inserted into the support frame 144. A rotation shaft (not shown) projects out of the rear side of the driving motor 146. The blowing fan 148 is forcibly inserted into the rotation shaft (not shown) of the driving motor (146) so that the blowing fan 148 blows an outside air out of the inlet port 112 to the outlet port 114 by the rotation of the driving motor 146. Further, the hair dryer 100 includes an electrical cord 150, an electrical switch 152, and a heating wire 154. The electrical cord 150 supplies an electrical power to the driving motor 146. The electrical switch 152 is connected to the electrical cord 150, which controls the opening and closing of the electrical power. The heating wire 154 winds around the support frame 144 for heating a sucked air through the inlet port 112 of the dryer housing 110. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Herbal composition for treating various disorders including psoriasis, a process for preparation thereof and method for treatment of such disorders Inventor(s): Arora, Sudershan Kumar; (Maharashtra, IN), Gupta, Lavleen Kumar; (Maharashtra, IN), Sanganabhatla, Narender; (Maharashtra, IN), Saraf, Dinesh Balakrishna; (Maharashtra, IN), Srivastava, Vandita; (Maharashtra, IN) Correspondence: Ladas & Parry; 26 West 61 Street; New York; NY; 10023; US Patent Application Number: 20030194456 Date filed: January 10, 2003 Abstract: The invention provides a novel herbal composition containing the extracts of the leaves and/or stem of Argemone mexicana plant, optionally containing the extracts of the fruits of Cuminum cyminum, which exhibits useful in vitro, in vivo and interesting immunological and pharmacological activities; a process for preparation thereof; and a method of treatment of psoriasis and related immunological and biological disorders by administration of the said novel herbal composition. The useful in vitro, in vivo and interesting immunological and pharmacological activities exhibited by the extracts and fractions of the leaves and/or stem of Argemone mexicana plant include immunosuppression, lymphoproliferation inhibition, cytokine modulation such as IL-2 inhibition, IFNgamma inhibition, IL-10 induction, keratinocyte proliferation inhibition, keratolytic activity, endothelial cell proliferation inhibition, inhibition of cell adhesion molecule expression such as ICAM-1, MEST inhibition, and enzymes inhibition such as p60src Tyrosine kinase, which are known to be involved in antipsoriatic activity. The novel herbal composition(s) is useful in the treatment of various disorders, such as psoriasis including plaque psoriasis, gutatte psoriasis, pustular psoriasis and psoriasis of the nails; dermatitis and scleroderma; eczema; inflammatory disorders and other autoimmune diseases like psoriatic arthritis, rheumatoid arthritis, Crohn's disease, multiple sclerosis, irritable bowel disease, ankylosing spondilitis, systemic lupus erythremetosus and Sjogren's syndrome; allergies like asthma and chronic obstructive pulmonary disease and is safe, well-tolerated, non-toxic, with minimal and reversible adverse reactions or side effects, and most importantly, with minimal relapse or recurrence of the disease following completion of a treatment regimen. The invention also describes the presence of phosphodiesterase (III, IV and V) inhibition and 5-Lipoxygenase inhibition in the aqueous, ethanolic or aqueous-ethanolic extracts of fruits of Cuminum cyminum plant. Excerpt(s): The present invention relates to a herbal composition comprising aqueous, ethanolic or aqueous-ethanolic extracts obtained from leaves and/or stem of Argemone mexicana plant, containing a mixture of alkaloids, flavonoids, organic acids, amino acids, sugars/glycosides and salts, optionally in combination with an aqueous, ethanolic or aqueous-ethanolic extract obtained from the fruits of Cuminum cyminum plant, which exhibit useful in vitro and in vivo immunological and pharmacological activities, hitherto not known and which provide significant reduction in the rate of PASI score with better tolerability within the range of normal permissible limit. The present invention also relates to a herbal composition comprising fractions of the aqueous, ethanolic and aqueous-ethanolic extracts obtained from leaves and/or stem of Argemone mexicana plant, containing a mixture of alkaloids, flavonoids, organic acids, amino acids, sugars/glycosides and salts, which exhibit useful in vitro and in vivo immunological and pharmacological activities, hitherto not known. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Indole derivatives, process for preparation of the same and use thereof Inventor(s): Kobayashi, Kaoru; (Mishima-gun, JP), Nambu, Fumio; (Mishima-gun, JP), Torisu, Kazuhiko; (Mishima-gun, JP) Correspondence: Sughrue Mion, Pllc; 2100 Pennsylvania Avenue, N.W.; Washington; DC; 20037; US Patent Application Number: 20030176400 Date filed: December 13, 2002 Abstract: Indole derivatives represented by formula (I): 1(wherein all symbols are described in the description), a process for the preparation of the same and a DP receptor antagonist comprising it as an active ingredient. Since the compounds of formula (I) binds to and are antagonistic to a DP receptor, they are useful in for the prevention and/or treatment of diseases, for example, allergic diseases (allergic rhinitis, allergic conjunctivitis, atopic dermatitis, bronchial asthma, food allergy, etc., systemic mastocytosis; disorders due to systemic mastocyte activation, anaphylactic shock, bronchoconstriction, urticaria, eczema, etc.), diseases accompanied with itching (atopic dermatitis, urticaria, etc.), secondary diseases caused by behaviors (scratching behaviors, beating, etc.) (cataract, retinal detachment, inflammation, infection, sleep disorder, etc.), inflammation, chronic obstructive pulmonary disease, ischemic reperfusion disorder, cerebrovascular disorder, pleuritis complicated by rheumatoid arthritis, ulcerative colitis, and the like. Excerpt(s): The present invention relates to indole derivatives. (wherein all symbols have the same meanings as described below), a process for the preparation of the same and use thereof. Prostaglandin D (hereinafter referred to as "PGD") are known as a metabolite in the arachidonic acid cascade, and are known to have effects of bronchoconstriction, vasodilatation or vasoconstriction and platelet aggregation inhibition. PGD is considered to be produced from mast cells, and the increase of PGD concentration has been recognized among systemic mastocytosis patients (New Eng. J. Med., 303, 1400-1404 (1980)). Also, PGD is considered to relate to neuro activities, especially, sleep and hormone secretion. Furthermore, there are reports suggesting participations in platelet aggregation, glycogen metabolism, ocular tension adjustment and the like. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Inhibitors of transcription factor NF-kappaB Inventor(s): Callahan, James F.; (Philadelphia, PA), Chabot-Fletcher, Marie C.; (Phoenixville, PA) Correspondence: Glaxosmithkline; Corporate Intellectual Property - Uw2220; P.O. Box 1539; King OF Prussia; PA; 19406-0939; US Patent Application Number: 20030092771 Date filed: July 31, 2002 Abstract: The present invention provides pharmaceutical compositions of salicylanilide inhibitors of transcription factor NF-.kappa.B, and methods for treating diseases in which activation of NF-.kappa.B is implicated. More specifically, the present invention provides methods of treatment of a variety of diseases associated with NF-.kappa.B activation including inflammatory disorders; particularly rheumatoid arthritis,

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inflammatory bowel disease, and asthma; dermatosis, including psoriasis and atopic dermatitis; autoimmune diseases; tissue and organ rejection; Alzheimer's disease; stroke; atherosclerosis; restenosis; cancer, including Hodgkin's disease; certain viral infections, including AIDS; osteoarthritis; osteoporosis; and Ataxia Telangiestasia by administering to a patient in need thereof a compound of the present invention. Excerpt(s): This invention relates in general to salicylanilide inhibitors of transcription factor NF-.kappa.B. Such compounds are particularly useful for treating diseases in which activation of NF-.kappa.B is implicated. More specifically, these compounds inhibit I.kappa.B phosphorylation and subsequent degradation. Such compounds are useful in the treatment of a variety of diseases associated with NF-.kappa.B activation including inflammatory disorders; particularly rheumatoid arthritis, inflammatory bowel disease, and asthma; dermatosis, including psoriasis and atopic dermatitis; autoimmune diseases; tissue and organ rejection; Alzheimer's disease; stroke; atherosclerosis; restenosis; cancer, including Hodgkins disease; and certain viral infections, including AIDS; osteoarthritis; osteoporosis; and Ataxia Telangiestasia. Recent advances in scientific understanding of the mediators involved in acute and chronic inflammatory diseases and cancer have led to new strategies in the search for effective therapeutics. Traditional approaches include direct target intervention such as the use of specific antibodies, receptor antagonists, or enzyme inhibitors. Recent breakthroughs in the elucidation of regulatory mechanisms involved in the transcription and translation of a variety of mediators have led to increased interest in therapeutic approaches directed at the level of gene transcription. NF-.kappa.B belongs to a family of closely related dimeric transcription factor complexes composed of various combinations of the Rel/NF-.kappa.B family of polypeptides. The family consists of five individual gene products in mammals, RelA (p65), NF-.kappa.B I (p50/p105), NF.kappa.B2 (p49/p100), c-Rel, and RelB, all of which can form hetero- or homodimers. These proteins share a highly homologous 300 amino acid "Rel homology domain" which contains the DNA binding and dimerization domains. At the extreme C-terminus of the Rel homology domain is a nuclear translocation sequence important in the transport of NF-.kappa.B from the cytoplasm to the nucleus. In addition, p65 and cRel possess potent transactivation domains at their C-terminal ends. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Interleukin-4 production inhibitors Inventor(s): Fukuda, Kazuyuki; (Tokyo, JP), Hori, Kimihiko; (Tochigi, JP), Ichikawa, Yoshiaki; (Tochigi, JP), Iwase, Norikazu; (Tokyo, JP), Nonomura, Mami; (Tochigi, JP), Sato, Hirotaka; (Tokyo, JP), Tanaka, Norihiro; (Tokyo, JP) Correspondence: Oblon, Spivak, Mcclelland, Maier & Neustadt, P.C.; 1940 Duke Street; Alexandria; VA; 22314; US Patent Application Number: 20030129265 Date filed: October 25, 2002 Abstract: This invention relates to IL-4 production inhibitors, antiallergic agents and atopic dermatitis preventives and improvers, each of which contains at one or more compounds selected from the group consisting of hydroxyl-containing monoterpenes, hydroxyl-containing sesquiterpenes and their acylated derivatives. This invention is also concerned with IL-4 production inhibitors, antiallergic agents and atopic dermatitis preventives and improvers, each of which contains an essential oil such as cedarwood oil. This invention is also concerned with bath medicine compositions, each of which

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contains one or more ingredients selected from cedrol, cedrenol, farnesol, patchouli alcohol and vetiverol. Excerpt(s): This invention relates to interleukin-4 (hereinafter called "IL-4") production inhibitors, antiallergic agents and atopic dermatitis preventives and improvers, which contain specific monoterpenes, sesquiterpenes or particular essential oils. This invention is also concerned with bath medicine compositions containing specific plant-derived ingredients. IL-4 is a substance produced by T lymphocytes which are human or animal immune response cells, and are known to act on B lymphocytes and to enhance production of an antibody such as IgE [Rinsho Meneki (Clinical Immunology), 27, 45-57 (1995)]. For many years IgE is known to take a significant part in the onset of an atopic disease. Further, IL-4 is known to act as an accelerator of inflammatory cell infiltration at lesions in allergic diseases [Cell, 62, 457-467 (1990)]. From these, it is considered that IL-4 is largely implicated in the onset of an allergic disease. Inhibition of IL-4 production, if successfully achieved, is therefore believed to make it possible to treat and prevent allergic diseases more fundamentally from their cause than conventional treatment and preventive methods making use of histamine release inhibitors, IgE or histamine effect inhibitors or the like. As substances for inhibiting the production of IL-4, a group of sulfonium derivatives including suplatast tosilate is well-known [Japan. J. Pharmacol., 62, 27-30 (1993)]. They are formulated into oral drugs and are used to treat allergic diseases such as atopic dermatitis, itching and pruritus, and the like, but their effects are not sufficient. In addition, their administration routes are limited because they have low percutaneous or transdermal absorption due to their structures. There is hence an outstanding need for IL-4 production inhibitors, antiallergic agents, and atopic dermatitis preventives and improvers, which are excellent in percutaneous or transdermal absorption, stability and safety. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Method for improving morbid dermatitis by inhibiting activity of a plasminogen activator in the skin Inventor(s): Kawai, Eriko; (Yokohama-shi, JP), Yoshida, Yuzo; (Yokohama-shi, JP) Correspondence: Ronald R. Snider; Snider & Associates; P.O. Box 27613; Washington; DC; 20038-7613; US Patent Application Number: 20030099721 Date filed: July 25, 2002 Abstract: The present invention relates to a plasminogen activator inhibitor, an external preparation for skin comprising the same, a method for improving rough skin and in particular, to improvement of an effective inorganic component.A plasminogen activator inhibitor contains a specific zinc oxide which adsorbs a plasminogen activator and effectively inhibits its activity. When it is used as an external preparation for skin, excellent improvement of rough skin is obtainable.Further when silica-coated zinc oxide is applied as an external preparation for skin, excellent improvement effect and prevention effect for rough skin are obtainable without an intolerance sensitivity reaction in the case of morbid dermatitis such as atopic dermatitis. Excerpt(s): This application claims the priority of Japanese Patent Application No. 11367773 filed on Dec. 24, 1999, which is incorporated herein by reference. The present invention relates to a plasminogen activator inhibitor, an external preparation for skin comprising the same, a method for improving rough skin and in particular, to

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improvement of an effective inorganic component. It has been known that various kinds of medicines, external preparations for skin and cosmetics are effective for improvement and prevention of such symptoms as skin disease, rough skin and pimples. As an effective component of these medicines and cosmetics, for example, essences extracted from plants or animals which are effective for anti-inflammation, or those having moisture retaining or water retaining effect such as amino acids, polysaccharide, lipid and natural polymer have been used because these components are effective for prevention of dermatitis or prevention of water volatilization from a horny layer of epidermis. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Method for the treatment or prevention of atopic dermatitis Inventor(s): Komune, Kunihiko; (Hyogo, JP), Ohmura, Tsuyoshi; (Osaka, JP), Satoh, Hisashi; (Osaka, JP) Correspondence: Boehringer Ingelheim Corporation; 900 Ridgebury Road; P. O. Box 368; Ridgefield; CT; 06877; US Patent Application Number: 20030100565 Date filed: September 6, 2002 Abstract: The invention relates to a method for the treatment or prevention of atopic dermatitis, which comprises the administration of an effective amount of an NK-1 receptor antagonist to a patient in need of such treatment, wherein said NK1 receptor antagonist is effective in inhibiting the substance P (SP-)induced scratching in mice and/or guinea pigs. Excerpt(s): This application claims benefit to EP 01 122 730.3 filed Sep. 21, 2001 and U.S. provisional application No. 60/338,416 filed Nov. 15, 2001. Itch is a sensation that provokes a desire to scratch. It is the most common symptom of cutaneous disease (e.g., atopic dermatitis and contact dermatitis) but its underlying mechanisms are far from being understood. This sensation is produced experimentally by several endogenous substances such as histamine, substance P (SP), vasoactive intestinal peptide and neurotensin. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Method for treating or preventing inflammatory diseases Inventor(s): Peterson, Ward M.; (Morrisville, NC), Yerxa, Benjamin R.; (Raleigh, NC) Correspondence: Howrey Simon Arnold & White, Llp; Box 34; 301 Ravenswood AVE.; Menlo Park; CA; 94025; US Patent Application Number: 20030125299 Date filed: November 6, 2002 Abstract: The present invention provides a method of preventing or treating an inflammatory disease, including but not limited to, sinusitis, rhinitis, conjunctivitis, asthma, dermatitis, inflammatory bowel disease, inflammatory collagen vascular diseases, glomerulonephritis, inflammatory skin diseases, and sarcoidosis. The method comprises administrating to a subject a pharmaceutical formulation comprising a nucleotide receptor agonist, such as nucleoside diphosphate, nucleoside triphosphate, or

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dinucleoside polyphosphate, according to general formula Ia, Ib, IIa, IIb, or III. Preferred indications of the present invention are perennial allergic rhinitis, seasonal allergic rhinitis, infectious allergic rhinitis, and allergic conjunctivitis. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/337,828, filed Nov. 6, 2001. This invention relates to a method of treating, preventing and/or alleviating the symptoms and manifestations of inflammatory diseases. This invention also relates to a method of treating, preventing, and/or alleviating the symptoms and manifestation of allergic reactions. Nucleotide receptor agonists are used in the present invention. Studies suggest that activation of P2Y receptors and/or P2X receptors by extracellular nucleotides (such as ATP and UTP) elicit responses from inflammatory cells (such as mast cells, eosinophil, leukocytes, neutrophils) consistent with a pro-inflammatory effect. ATP is required to stimulate histamine release from rat peritoneal mast cells and histamine and prostaglandin D2 in rat serosal mast cells (Jaffar and Pearce, Agents Actions 30(1-2): 64-6 (1990); Izushi and Tasaka, Pharmacology 42(6): 297-308 (1991)). In the latter case, the effects of ATP were inhibited by reactive blue 2 and suramin, two putative antagonists for P2Y receptors. Anti-IgE-induced histamine release from human lung mast cells was significantly enhanced by ATP and UTP at low concentrations (10.sup.-6 to 10.sup.-4 M) but inhibited at high concentrations (10.sup.-3 M), indicating a bimodal action (Schulman, et al., Am. J. Respir. Cell. Mol. Biol. 20(3):530-7(1999)). Adenine and uridine nucleotides (ADP, ATP, and UTP) activate chemotaxic signals on cultured rat bone marrow mast cells and may function to recruit mast cells by intestinal mucosa as part of a parasitic response (Saito, et al., Int. Arch. Allergy Appl. Immunol. 94(1-4): 68-70 (1991); McCloskey, et al., J. Immunol. 163(2): 9707 (1999)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Method of treating anemia Inventor(s): Creasy, Caretha; (Erdenheim, PA), Dillon, Susan B.; (Chester Springs, PA), Lord, Kenneth A.; (Collegeville, PA) Correspondence: Ratner & Prestia; P.O. Box 980; Valley Forge; PA; 19482-0980; US Patent Application Number: 20030176375 Date filed: May 14, 2001 Abstract: hYAK3-2 polypeptides and polynucleotides and methods for producing such polypeptides by recombinant techniques are disclosed. Also disclosed are methods for utilizing hYAK3-2 polypeptides and polynucleotides in the design of protocols for the treatment of bone loss including osteoporosis; inflammatory diseases such as Adult Respiratory Disease Syndrome (ARDS), Rheumatoid arthritis, Osteoarthritis, Inflammatory Bowel Disease (IBD), psoriasis, dermatitis, asthma, allergies; infections such as bacterial, fungal, protozoan and viral infections, particularly infections caused by HIV-1 or HIV-2; HIV-associated cachexia and other immunodeficiency disorders; septic shock; pain; injury; cancers including testicular cancer; anorexia; bulimia; neutropenia; cytopenia; anemias, including anemias due to renal insufficiency or to chronic disease, such as autoimmunity or cancer, and drug-induced anemias; polycythemia; myelosuppression; Parkinson's disease; cardiovascular disease including restenosis, atherosclerosis, acute heart failure, myocardial infarction; hypotension; hypertension; urinary retention; angina pectoris; ulcers; benign prostatic hypertrophy; and psychotic and neurological disorders, including anxiety, schizophrenia, manic depression, delirium, dementia, severe mental retardation and dyskinesias, such as

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Huntington's disease or Gilles dela Tourett's syndrome., among others, and diagnostic assays for such conditions. Excerpt(s): This application claims priority to U.S. Ser. No. 60/118,045 filed Feb. 1, 1999, which is incorporated by reference in its entirety. This invention relates to newly identified polynucleotides, polypeptides encoded by them and to the use of such polynucleotides and polypeptides, and to their production. More particularly, the polynucleotides and polypeptides of the present invention relate to a serine/threonine protein kinase, hereinafter referred to as hYAK3-2. The invention also relates to inhibiting or activating the action of such polynucleotides and polypeptides. A number of polypeptide growth factors and hormones mediate their cellular effects through a signal transduction pathway. Transduction of signals from the cell surface receptors for these ligands to intracellular effectors frequently involves phosphorylation or dephosphorylation of specific protein substrates by regulatory protein serine/threonine kinases (PSTK) and phosphatases. Serine/threonine phosphorylation is a major mediator of signal transduction in multicellular organisms. Receptor-bound, membranebound and intracellular PSTKs regulate cell proliferation, cell differentiation and signalling processes in many cell types. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Method of utilization of zygosaccharomyces rouxii Inventor(s): Ok, Taing; (Jagoshima, JP) Correspondence: Malin Haley And Dimaggio, PA; 1936 S Andrews Avenue; Fort Lauderdale; FL; 33316; US Patent Application Number: 20030219456 Date filed: May 21, 2002 Abstract: The present invention provides commercial utilization of a novel yeast strain Zygosaccharomyces rouxii and its fermented metabolites as probiotic, as an antioxidant and as an antimicrobial agent in foods and cosmetics. The fermented broth and metabolite substance (s) produced by this invention have a wide spectrum antibacterial activity, strong antioxidant activity, cytochalasin-like activity that inhibits cell cleavage, and is expected to be effective in the treatment of allergy, atopic dermatitis, psoriasis and various skin diseases, second degree burns, high blood pressure, diabetes, cancer, AIDS and as an anti-aging agent. Moreover, this invention is expected to lead to industrial utilization of Z.rouxii for manufacturing succinic acid and malic acid from a yeast. Excerpt(s): This invention relates generally to the composition and utilization of yeast strain Zygosaccharomyces rouxii, hereinafter (Z.R. or Z. Rouxii) and its fermented metabolites in the field of human health and, specifically, as a composition for and use as an antioxidant and, independently, as an antimicrobial agent in foods and cosmetics. Yeast Z.rouxii is primarily regarded as a contaminant in high-sugar foods such as fruit and jam. On the other hand, it is a natural inhabitant in honey, wine and Japanese soy paste (miso), traditional foods since ancient times that are recognized for good health and long life. Out of 500 plus species of yeast identified so far, only Saccharomyces cerevisiae has been employed commercially. There is little industry that utilizes Z.rouxii. A patent related to Z.rouxii is concerned only with the aroma of soy sauce (U.S. Pat. No. 5,210,034, issued May 11, 1993). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Nitrogen-containing tricyclic compounds and drugs containing the same Inventor(s): Harada, Kokichi; (Ibaraki, JP), Kaino, Makoto; (Ibaraki, JP), Katayama, Koichi; (Ibaraki, JP), Kobayashi, Seiichi; (Ibaraki, JP), Miyamoto, Mitsuaki; (Ibaraki, JP), Moriya, Katsuhiro; (Ibaraki, JP), Nishizawa, Yukio; (Ibaraki, JP), Okita, Makoto; (Ibaraki, JP), Sakuma, Yoshinori; (Ibaraki, JP), Sato, Keizo; (Ibaraki, JP), Soejima, Motohiro; (Ibaraki, JP), Tanaka, Masayuki; (Ibaraki, JP), Yamada, Koji; (Ibaraki, JP), Yoshiuchi, Tatsuya; (Ibaraki, JP) Correspondence: Birch Stewart Kolasch & Birch; PO Box 747; Falls Church; VA; 220400747; US Patent Application Number: 20030171367 Date filed: July 25, 2002 Abstract: A phenothiazine, acridan, acridone oxime, acridone hydrazone and dibenzodiazepine derivative represented by formula (I) 1effective against diseases in which histamine, leukotrienes, etc. participate and effective in preventing or treating diseases in which chemical mediators such as histamine and leukotrienes participate, for example, asthma, allergic rhinitis, atopic dermatitis, urticaria, hay fever, gastrointestinal allergy and food allergy. Excerpt(s): This application is the national phase under 35 U.S.C.sctn.371 of prior PCT International Application No. PCT/JP97/00789 which has an International filing date of Mar. 13, 1997 which designated the United States of America, the entire contents of which are hereby incorporated by reference. The present invention relates to a nitrogencontaining tricyclic compound useful as a medicine, a medicine containing the same and processes for producing the same. More particularly, it relates to a novel nitrogencontaining tricyclic compound useful as a medicine for diseases against which the effect of inhibiting the binding of IgE receptor.gamma. to a tyrosine kinase of 72 kDa is efficacious. The bronchial asthma and the atopic diseases in human beings appear in consequence of highly intriacate vital reactions. It is suspected that most of these conditions are caused because various chemical mediators liberated from mast cells and basophils, as triggered by antigen-antibody reactions, induce vital disturbances as by contracting such smooth muscles as bronchial muscles and vessels of the pulmonary circulation or enhancing permeability of blood vessels. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Novel 1,2,4-thiadiazolium derivatives as melanocortin receptor modulators Inventor(s): Eisinger, Magdalena; (Demarest, NJ), Fitzpatrick, Louis J.; (Souderton, PA), Lee, Daniel H.; (Sudbury, MA), Pan, Kevin; (Phoenixville, PA), Plata-Salaman, Carlos; (Ambler, PA), Reitz, Allen B.; (Lansdale, PA), Smith-Swintosky, Virginia L.; (Hatfield, PA), Zhao, Boyu; (Lansdale, PA) Correspondence: Audley A. Ciamporcero JR.; Johnson & Johnson; One Johnson & Johnson Plaza; New Brunswick; NJ; 08933-7003; US Patent Application Number: 20030162819 Date filed: November 4, 2002 Abstract: The present invention is directed to novel 1,2,4-thiadiazol-2-ium derivatives useful as agonists or antagonists of the melanocortin receptor. More particularly, the compounds of the present invention are useful for the treatment of metabolic, CNS and

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dermatological disorders such as obesity, impaired oral glucose tolerance, elevated blood glucose levels, type II diabetes, Syndrome X, diabetic retinopathy, spinal cord injury, nerve injury, acute neurodegenerative disorders, chronic neurodegenerative disorders, plexopathies, male erectile dysfunction, dry eyes, acne, dry skin, aged skin, seborrheic dermatitis, rosacea, excessive ear wax, meibomian gland disorder, pseudofolliculitis, yeast infections, dandruff, hidradenitis suppurativa, ocular rosacea and eccrine gland disorder. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/337,762, filed on Nov. 8, 2001, which is incorporated by reference herein in its entirety. The present invention provides novel 1,2,4-thiadiazol-2-ium derivatives useful for the treatment of a disorder mediated by a melanocortin receptor. More particularly, the compounds of the present invention are useful for the treatment of metabolic, CNS and dermatologic disorders such as obesity, impaired oral glucose tolerance, elevated blood glucose levels, type II diabetes, Syndrome X, diabetic retinopathy, acute neurodegenerative disorders, chronic neurodegenerative disorders, plexopathies, male erectile dysfunction, dry eyes, acne, dry skin, aged skin, seborrheic dermatitis, rosacea, excessive ear wax, meibomian gland disorder, pseudofolliculitis, yeast infections, dandruff, hiradenitis suppurativa, ocular rosacea and eccrine gland disorder. Melanocortins are neuropeptides that arise from pro-opiomelanocortin (POMC), which is most prevalently expressed in the arcuate nucleus of the hypothalamus, pituitary lobes, and the nucleus tractus solarius of the brainstem. [Gantz, I., et al., Molecular Cloning, Expression, and Gene Localization of a Fourth Melanocortin Receptor, J. Biolog. Chem., 1993, 268, 15174-15179.] These peptides include ACTH,.alpha.MSH,.beta.-MSH,.gamma.sub.1-3-MSH, and synthetic analogue NDP-.alpha.MSH (Wikberg, J E S, Melanocortin receptors: new opportunities in drug discovery, Exp. Opin. Ther. Patents, 2000, 11(1), 61-76). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Novel antibodies, drugs containing these antibodies and methods for screening compounds by using these antibodies Inventor(s): Furuya, Akiko; (Machida-shi, JP), Hanai, Nobuo; (Sagamihara-shi, JP) Correspondence: Fitzpatrick Cella Harper & Scinto; 30 Rockefeller Plaza; New York; NY; 10112; US Patent Application Number: 20030170758 Date filed: April 4, 2003 Abstract: The present invention provides antibodies which recognize a novel, membrane-type matrix metalloproteinase polypeptide [MT4-MMP(2)] that has, different from the hitherto reported MT4-MMP, physiological activity; prophylactic agents, diagnostic agents and therapeutic agents comprising the antibodies, for various diseases such as arthrosis deformans, rheumatoid arthritis, asthma, autoimmune diseases, or atopic dermatitis; and methods of screening for inhibitors and activators of MT4MMP(2) using the antibodies.The second object of the present invention is to provide antibodies which recognize novel, human and mouse membrane-type matrix metalloproteinase MT5-MMP polypeptides having physiological activity; prophylactic agents, diagnostic agents and therapeutic agents comprising the antibodies, for various diseases such as arthrosis deformans, rheumatoid arthritis, asthma, autoimmune diseases, atopic dermatitis, brain disorders at the time of cerebral apoplexy, or

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Alzheimer's disease; and methods of screening for inhibitors and activators of MT5MMP using the antibodies. Excerpt(s): The present invention relates to antibodies that specifically react with novel membrane-type matrix metalloproteinase polypeptides; pharmaceuticals containing the antibodies; and methods of screening for compounds that modulate the expression of the polypeptides or bind to the polypeptides using the antibodies. A group of enzymes generically termed "matrix metalloproteinases" (hereinafter, abbreviated to MMPs) that have metal ions at the active center are involved in the degradation of extracellular matrix composed of complicated components such as collagens, fibronectin, laminin and proteoglycans. To date, the following MMPs have been reported: interstitial collagenase (MMP-1), gelatinase A (MMP-2), gelatinase B (MMP-9), stromelysin 1 (MMP-3), matrilysin (MMP-7), neutrophil collagenase (MMP-8), stromelysin 2 (MMP-10), stromelysin 3 (MMP-11), metallo-elastase (MMP-12), collagenase 3 (MMP-13), membrane type I MMP (MT1-MMP or MMP-14), membrane type 2 MMP (MT2-MMP or MMP-15), membrane type 3 MMP (MT3-MMP or MMP-16), membrane type 4 MMP (MT4-MMP or MMP-17), etc. (Protein, Nucleic Acid and Enzyme, 42, 2386 (1997)). These MMPs form a family, and each MMP is basically composed of an N-terminal propeptide domain, an active domain to which zinc ions bind, and a hemopexin-like domain. In MMP-7, no hemopexin-like domain is found. Membrane-type MMPs have a transmembrane domain and a intracellular domain at the C-terminal of the hemopexinlike domain. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Pharmaceutical composition Inventor(s): Mayer, Friedrich Karl; (Oberwil, CH), Ryder, Neil Stewart; (Vienna, AT) Correspondence: Thomas Hoxie; Novartis, Patent And Trademark Department; One Health Plaza 430/2; East Hanover; NJ; 07936-1080; US Patent Application Number: 20030100517 Date filed: October 9, 2002 Abstract: Synergistic combinations of a squalene epoxidase inhibitor such as terbinafine and a macrolide T-cell immunomodulator or immunosuppressant such as 33-epichloro, 33-desoxyascomycin are provided, which are useful in particular in the treatment of diseases involving fungal or suspected fungal infection, for immunomodulation or immunosuppression in conditions in which fungal or suspected fungal colonisation of e.g. the skin plays a role, such as atopic dermatitis and seborrhoeic dermatitis, and in situations of fungal resistance. Excerpt(s): The invention relates to pharmaceutical compositions, for use in particular against fungal infections. It concerns a pharmaceutical composition comprising a squalene epoxidase inhibitor in combination with a macrolide T-cell immunomodulator or immunosuppressant. While an antifungal activity is known for various macrolide Tcell immunomodulators and immunosuppressants, and some such macrolides have even first been disclosed in the literature as antifungals, e.g. ascomycin and rapamycin, their antifungal activity has been viewed mostly as being largely coincidental with their immunomodulating properties, and further, no common pattern was known, the structural and mechanistic similarities between these compounds having been discovered only long after their original isolation. In particular, notwithstanding the antifungal heritage of macrolide T-cell immunomodulators and immunosuppressants,

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no significant reports have appeared in the literature on any potentiating effect on the antifungal activity of squalene epoxidase inhibitors, nor are synergistic pharmaceutical compositions comprising these two classes of drugs in combination known. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Pharmaceutical composition for dermal application Inventor(s): Didriksen, Erik Johannes; (Ballerup, DK) Correspondence: Birch Stewart Kolasch & Birch; PO Box 747; Falls Church; VA; 220400747; US Patent Application Number: 20030175314 Date filed: November 18, 2002 Abstract: A pharmaceutical composition for dermal application comprising, as an active component, a 1or a pharmaceutically acceptable salt thereof, and a vehicle comprising a pharmaceutically acceptable, substantially non-aqueous solvent in which the active component has a solubility of at least about 6.0 g/L at ambient temperature, said solvent being capable of effecting penetration of a therapeutically effective amount of the active component into the epidermis, may be used in the prevention or treatment of dermal inflammatory diseases or conditions such as dermatitis. Excerpt(s): The present invention relates to a pharmaceutical composition for dermal application as well as the use of the composition in the prophylaxis and treatment of dermal conditions. Dermal diseases affect a large number of patients with a prevalence (in the UK) of about 20%. Dermal inflammatory diseases are the most common dermal diseases, constituting about 50% of the skin diseases seen in general practice. Skin diseases may have profound psychosocial consequences, e.g. for patients suffering from extensive psoriasis or eczema. Dermal inflammatory conditions include dermatitis (eczema) typically involving redness or swelling of the skin or lesion which may be oozing, scaling or crusting. The inflamed areas of the skin are often also itchy (pruritic). Examples of dermatitis are atopic dermatitis, contact dermatitis or seborrheic dermatitis. Atopic dermatitis is a chronic, relapsing, pruritic inflammatory skin disease occurring in genetically predisposed individuals. The onset of the disease is mostly in infancy or early childhood, 80% of the cases occurring before the age of 1 year. While there is a general tendency towards spontaneous improvement throughout childhood, approximately 60% of patients with severe atopic dermatitis and approximately 40% of patients with moderate atopic dermatitis contend with skin problems as adults, most frequently hand eczema. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Pharmaceutical formulation comprising an immune response modifier Inventor(s): Busch, Terri F.; (St. Paul, MN), Fretland, Mary; (Eagan, MN), Gust-Heiting, Amy L.; (Hudson, WI), Scholz, Matthew T.; (Woodbury, MN), Skwierczynski, Raymond D.; (Oakdale, MN) Correspondence: Attention: Dean A. Ersfeld; Office OF Intellectual Property Counsel; 3M Innovative Properties Company; P.O. Box 33427; ST. Paul; MN; 55133-3427; US Patent Application Number: 20030199538 Date filed: November 27, 2002 Abstract: Pharmaceutical formulations comprising an immune response modifier (IRM) chosen from imidazoquinoline amines, imidazotetrahydroquinoline amines, imidazopyridine amines, 6,7-fused cycloalkylimidazopyridine amines, 1,2-bridged imidazoquinoline amines, thiazolo-quinolineamines, oxazolo-quinolinamines, thiazolopyridinamines, oxazolo-pyridinamines, imidazonaphthyridine amines, tetrahydroimidazonaphthyridine amines, and thiazolonaphthyridine amines; a fatty acid; and a hydrophobic, aprotic component miscible with the fatty acid are useful for the treatment of dermal associated conditions. Novel topical formulations are provided. In one embodiment, the topical formulations are advantageous for treatment of actinic keratosis, postsurgical scars, basal cell carcinoma, atopic dermatitis, and warts. Excerpt(s): This application claims priority to Provisional Patent Application Serial No. 60/340,605, filed Nov. 29, 2001 and Provisional Patent Application Serial No. 60/378,452, filed May 6, 2002. The present invention is directed to pharmaceutical formulations comprising at least one immune response modifier chosen from imidazoquinoline amines, imidazopyridine amines, 6,7-fused cycloalkylimidazopyridine amines, 1,2-bridged imidazoquinoline amines, thiazoloquinoline amines, oxazoloquinoline amines, thiazolopyridine amines, oxazolopyridine amines, imidazonaphthyridine amines, imidazotetrahydronaphthyridine amines, and thiazolonaphthyridine amines. Embodiments of the present invention are directed to topical formulations for application to the skin of a mammal. Other embodiments of the present invention are directed to methods for treating dermal diseases. Many imidazoquinoline amine, imidazopyridine amine, 6,7-fused cycloalkylimidazopyridine amine, 1,2-bridged imidazoquinoline amine, thiazoloquinoline amine, oxazoloquinoline amine, thiazolopyridine amine, oxazolopyridine amine, imidazonaphthyridine amine, imidazotetrahydronaphthyridine amine, and thiazolonaphthyridine amine compounds have demonstrated potent immunostimulating, antiviral and antitumor (including anticancer) activity, and have also been shown to be useful as vaccine adjuvants. These compounds are hereinafter collectively referred to as "IRM" (immune response modifier) compounds. One of these IRM compounds, known as imiquimod, has been commercialized in a topical formulation, Aldara.TM., for the treatment of anogenital warts associated with human papillomavirus. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Pharmacological composition containing yeast cell wall fraction Inventor(s): Nakamura, Tomohiko; (Takasaki-shi, JP), Shirasu, Yoshiharu; (Takasaki-shi, JP), Wakabayashi, Hideyuki; (Takasaki-shi, JP) Correspondence: Venable, Baetjer, Howard And Civiletti, Llp; P.O. Box 34385; Washington; DC; 20043-9998; US Patent Application Number: 20030118607 Date filed: October 10, 2002 Abstract: The present invention provides a pharmacological composition as a composition as a raw material capable of preventing or treating the symptoms of inflammatory bowel diseases such as ulcerative colitis, constipation, allergic diseases such as atopic dermatitis, and so on, and which has little side effect and thereby safe, high water dispersibility, and can be ingested easily.A yeast cell wall fraction, which comprises yeast extracts residue and being superior in water dispersibility and swelling properties, is used as an active constituent. As a yeast cell wall fraction, a yeast cell wall fraction obtained with a simple operation of water cleansing of yeast cell after alkali processing yields superior effects for preventing or treating the symptoms of inflammatory bowel diseases such as ulcerative colitis, constipation, allergic diseases such as atopic dermatitis, and so on, as well as such yeast cell wall fraction without foreign taste and odor characteristic to autolysis and suitable for ingestion. Excerpt(s): The present invention generally relates to a pharmacological composition containing cell residue obtained by removing soluble cell substance from enzymegenated yeast, preferably cell residue obtained by conducting water cleansing after alkali treatment, and having as its active constituent a yeast cell wall fraction containing abundant protein and dietary fiber. Particularly, the present invention relates to an agent and/or a food product having as its active constituent the aforementioned yeast cell wall fraction and capable of preventing and/or treating the symptoms of inflammatory bowel diseases such as ulcerative colitis, constipation, allergic diseases such as atopic dermatitis, and so on. Conventionally, as technology directed to a pharmacological composition having as its active constituent yeast or a yeast cell component substance, known are a manufacturing method of a polysaccharide ester sulfate compound and the alkali metal saline thereof having a anti-digestive ulcer agent effect and an anti-arterial sclerosis effect, obtained by sulfating a yeast cell wall in a basic organic solution with chlorosulphonic acid or sulfur trioxide, or sulfating a yeast cell wall by blending it with cooled and levigated strong sulfuric acid and thereafter making it an alkali salt (Japanese Patent Application Laid-Open No. 49-48894); a manufacturing method of a polysaccharide ester sulfate compound and the alkali metal saline thereof obtained by sulfating a yeast cell wall in a basic organic solution with chlorosulphonic acid or sulfur trioxide, or sulfating a yeast cell wall by blending it with cooled and levigated strong sulfuric acid and thereafter making it an alkali salt (Japanese Patent Application Laid-Open No. 56-31955); a manufacturing method of a new physiologically active substance peptide mannan A which extracts peptide mannan A from a yeast cell belonging to Saccharomyces and ingests peptide mannan A from such extract (Japanese Patent Laid-Open Publication No. 49-69808); a manufacturing method of a compound protein SP-1 having an anti-ulcer effect and containing amino acids and mannose by making the pepsin act upon the yeast cell wall (Japanese Patent Application Laid-Open No. 62-39527); an anti-allergic agent having as its active constituent mannan deriving from yeast and the like (Japanese Patent Application Laid-Open No.63-119427); an antiulcer agent having as its active constituent dried brewer's yeast with no concern of side effects as it is a natural product (Japanese Patent Application Laid-Open No. 1-313434); a

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nutrition supplement composition to be administered to mammals and containing a sufficient amount of.beta.-glucan deriving from yeast for supplying a fiber source in foods, fecal-increasing agent, and short-chain fatty acid, and which improves the digestion in mammals, decreases the serum cholesterol level, and fortifies the decrease in weight (Japanese Patent Application Laid-Open No. 4-505997); food, beverage and medical product containing magnesium supplement material which connotes magnesium salt within a yeast cell wall prepared by eluting and separating intercellular cell constituents (Japanese Patent Application Laid-Open No. 9-107919); an inhibitor of antibody-producing cell containing yeast-related polymer, and a composition such as food or medical product for autoimmune disease containing this inhibitor of antibodyproducing cell (Japanese Patent Laid-Open Publication No. 9-188626); and a skin condition improving composition suitable for preventing and treating the likes of atopic dermatitis and containing protease hydrolysate of brewer's yeast and diuretic (Japanese Patent Laid-Open Publication No. 9-227390). Further, conventionally, as technology directed to making the autolytic residue of yeast tasteless and odorless, known are a method of improving the flavor of brewer's yeast by moisture distillation and organic solvation of brewer's yeast (Japanese Patent Application Laid-Open No. 63-22177), a method of decolorizing and deodorizing yeast extract residue, or yeast autolytic residue, wherein yeast extract residue is processed with alkali and acid, high concentration ozone treatment is conducted thereafter, and ethanol treatment is further implemented (Japanese Patent Application Laid-Open No. 4-248968); a method of reducing the foreign taste and odor characteristic to yeast by conducting acid treatment and heat treatment to yeast or a yeast-processed product (Japanese Patent Application Laid-Open No. 6-70751); and a method of making a yeast autolytic insoluble substance tasteless and odorless by suspending a yeast autolytic insoluble substance in ethanol, carrying the stirring treatment under alkaline conditions and eluting the causative agent of foreign taste and odor thereby, and eliminating the eluted material pursuant to centrifugation and eliminating the foreign taste and odor characteristic to a yeast autolytic insoluble substance thereby (Japanese Patent Application Laid-Open No. 9-103266). In addition, as technology directed to the treatment method of yeast cells and yeast cell walls, known is a manufacturing method of a seasoning wherein yeast cells are crushed with a highpressure spray-impact homogenizer, hot water extraction is conducted thereto, and centrifugation is performed to the yeast cell walls which could not be made into particulates (Japanese Patent Application Laid-Open No. 9-117263). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Polyamine compounds and compositions for use in conjunction with cancer therapy Inventor(s): Copp, Richard R. JR.; (Oregon, WI), Fahl, Kathleen L.; (Madison, WI), Fahl, William E.; (Madison, WI), Ochsner, Cynthia E.; (Madison, WI), Peebles, Daniel D.; (Fond du Lac, WI) Correspondence: Woodcock Washburn Llp; One Liberty Place, 46th Floor; 1650 Market Street; Philadelphia; PA; 19103; US Patent Application Number: 20030185778 Date filed: February 7, 2003 Abstract: The invention provides novel polyamine compounds and pharmaceutical compositions for administration in conjunction with cancer chemotherapy or radiation therapy. The compounds are administered locally to provide protection against the adverse side-effects of chemotherapy or radiation therapy, such as alopecia, mucositis

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and dermatitis. Pharmaceutical preparations comprising one or more chemoprotective polyamines formulated for topical or local delivery to epithelial or mucosal cells are disclosed. Methods of administering the pharmaceutical preparations are also disclosed. Excerpt(s): This application claims benefit of U.S. Provisional Application No.60/355,356, filed Feb. 7, 2002, the entirety of which is incorporated by reference herein. The present invention relates to the field of cancer therapy. In particular, the invention provides novel polyamine compounds and pharmaceutical compositions for reducing or preventing toxic side effects of radiotherapy and cancer chemotherapeutic agents. Various patents and other publications are referenced in this application in order to more fully describe the state of the art to which this invention pertains. The disclosure of each of these publications is incorporated by reference herein, in its entirety. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Preventive or therapeutic agent for pollen allergy, allergic rhinitis, atopic dermatitis, asthma or urticaria, or health food for prevention or improvement or reduction of symptoms thereof Inventor(s): Yoshida, Satoshi; (Tokyo, JP) Correspondence: Finnegan, Henderson, Farabow,; Garrett & Dunner, L.L.P.; 1300 I Street, N.W.; Washington; DC; 20005-3315; US Patent Application Number: 20030198697 Date filed: April 22, 2002 Abstract: A method for prevention or therapy of pollen allergy, allergic rhinitis, atopic dermatitis, asthma or urticaria by administration of two kinds of crude drugs--seeds of Cucurbita moschata and flowers of Carthamus tinotorius--and at least one crude drug selected from Plantago asiatica, Lonicera japonica, Glycyrrhiza uralensis, Coix lachrymal-jobi var, ma-yuen, Zingiber officinale, Curcuma longa, Curcuma zedoaria and Artemisia argyi to a patient; and a health food for prevention, or improvement, or reduction of these symptoms containing the above substances. Excerpt(s): The present invention is a preventive or therapeutic agent for pollen allergy, allergic rhinitis, atopic dermatitis, asthma or urticaria or a health food for prevention, improvement or reduction of symptoms thereof. In recent years, there has been a rapid increase In the number(s) of patients suffering from allergies caused by cedar pollen and by plants such as Ambrosia artesmisiifolia, Dactylis glomerata, Phleumpratense, and birch or their pollen. In pollen allergies, chemical transmitters such as histamine and leukotriene and various enzymes are liberated from mast cells and basophils by pollen entering the body, and the typical symptoms of allergic conjunctivitis and allergic rhinitis (such as sniffles, stuffiness and sneezing) thereby appear, particularly in the nose and eyes. There has been also an increase in allergic rhinitis, atopic dermatitis, asthma, urticaria, etc., caused not only by pollen, but also by house dust, ticks, etc., carrying allergens. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Preventives or remedies for atopic dermatitis Inventor(s): Kobayashi, Asako; (Ibaraki, JP), Takahashi, Tomoya; (Ibaraki, JP), Takekoshi, Yoichiro; (Tokyo, JP) Correspondence: Fitzpatrick Cella Harper & Scinto; 30 Rockefeller Plaza; New York; NY; 10112; US Patent Application Number: 20030185864 Date filed: January 17, 2003 Abstract: The present invention provides skin epidermal ceramide synthesis accelerators, agents for improving skin epidermal barrier function and agents for preventing or improving atopic dermatitis, which each comprises, as an active ingredient, hydroxyproline or an N-acyl derivative of hydroxyproline, or a salt thereof, and cosmetics for improving skin barrier function or improving atopic dermatitis, which comprises the ceramide synthesis accelerator. Excerpt(s): The present invention relates to ceramide synthesis accelerators and cosmetics comprising the ceramide synthesis accelerator. The skin is always exposed to stimuli from various external environments. A stratum corneum of the skin has a barrier function to prevent the stimuli and invasion of foreign matters from the outside and to prevent transpiration of moisture from the body. It is known that the amount of ceramides in the stratum corneum of the skin is decreased in human and animals having impaired barrier function [Journal of Lipid Research, 30, 89 (1989)]. In addition, it has been reported that the amount of ceramides is also decreased in patients of atopic dermatitis having impaired barrier function [Acta Dermato Venereologica, 78, 27 (1998)]. Currently, external use of ceramide has been examined as a means for improving the barrier function, and its efficacy has been confirmed [Fragrance Journal, 10, 29 (1999)]. Also, since it is not easy to obtain a large amount of ceramides, an attempt has been made recently to screen a substance capable of increasing ceramide production in the skin. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Remedies for allergic diseases and process for producing the same Inventor(s): Fukuda, Harui; (Higashishirakawa-gun, JP) Correspondence: John S. Pratt, Esq; Kilpatrick Stockton, Llp; 1100 Peachtree Street; Suite 2800; Atlanta; GA; 30309; US Patent Application Number: 20030096029 Date filed: July 3, 2002 Abstract: Remedies for allergic diseases obtained by mixing shoots of plants belonging to the family Pinaceae with water and saccharides followed by spontaneous fermentation. As the plants belonging to the family Pinaceae, it is preferable to use plants belonging to the genus Pinus. These remedies, which enable complete recovery in a short administration time without showing any side effects, are useful as remedies for allergic diseases, in particular, asthma and atopic dermatitis. Also, a yeast isolated from these remedies for allergic diseases is provided. Excerpt(s): The application has a right of priority based on Japanese Patent Application No. 2000-184541 filed in Japan on Jun. 14, 2000, all of the contents of the application are incorporated as parts of the specification of the instant application by reference. The

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present invention relates to a remedy for allergic diseases, for example, asthma, atopic dermatitis, conjunctivitis, rhinitis and food allergy, and to a method of producing the same. Further, the present invention relates to yeast isolated from the above-mentioned remedy. A human body has an immune system which is a defense mechanism which, when extraneous substances such as bacteria and viruses invade body, antagonizes them and protects body. Allergies are caused due to excess action of this immune system. Recently, increasing number of people are suffering from allergies possibly because of, though the details are not clear, air pollution, change of dietary life, physical or mental stress increase, environmental changes such as room pollution and the like due to change in resident circumstances, or change in human body constitution. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Remedies for external use for allergic skin diseases Inventor(s): Hisaichi, Shin-ichi; (Kagawa-ken, JP), Inamoto, Yukiko; (Kagawa-ken, JP), Kawabata, Seiichiro; (Kagawa-ken, JP), Kawata, Mitsuhiro; (Kagawa-ken, JP), Nakayama, Daisuke; (Takamatsu-shi, JP), Tokuda, Masaaki; (Takamatsu-shi, JP) Correspondence: Birch Stewart Kolasch & Birch; PO Box 747; Falls Church; VA; 220400747; US Patent Application Number: 20030125307 Date filed: June 28, 2002 Abstract: External preparations for allergic dermatitis containing Aspirin alone as the active ingredient, which exert an excellent therapeutic effects on allergic dermatitis with lower side effects; and a method for treating allergic dermatitis by using these agents for external use. Excerpt(s): The present invention relates to external preparations for treating allergic dermatitis and a method for treating allergic dermatitis. In more detail the present invention relates to external preparations for treating allergic dermatitis containing acetylsalicylic acid as the sole active ingredient and a method for treating allergic dermatitis by using an external preparation containing acetylsalicylic acid as the sole active ingredient. Recently according to change of life style and environment, allergic dermatitis, such as bronchial asthma, allergic rhinitis, atopic dermatitis, etc. has rapidly increased. Nowadays many antiallergic agents are sold. In case of an oral preparation thereof it is anxious for its side effects, such as sleepiness, laziness, etc. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Screening process for atopic dermatitis Inventor(s): Chan, Edward K L; (Gainesville, FL), Muro, Yoshinao; (Showa-ku, JP), Ochs, Robert L; (Pittsburg, PA), Tan, Eng M; (La Jolla, CA) Correspondence: The Scripps Research Institute; Office OF Patent Counsel, Tpc-8; 10550 North Torrey Pines Road; LA Jolla; CA; 92037; US Patent Application Number: 20030215875 Date filed: April 24, 2003 Excerpt(s): The field of this invention is diagnosis of atopic dermatitis. Atopic dermatitis (AD) is a chronic, relapsing, pruritic skin disorder that generally first appears

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in childhood and frequently progresses to asthma and/or allergic rhinitis in the adult (Hanifin et al., Acta Dermatovener (Stockholm) Suppl 1980; 92:44-47; Leung et al., Dermatology in General Medicine, 4th edition, 1993, pp. 1543-1564; Cooper, J Invest Dermatol 1994; 102:128-137). There are no reliable laboratory markers for this condition but AD patients often have elevated serum IgE levels, allergic reactivity to foods and to other common allergens such as pollens, molds, and insects. There have also been reports of antinuclear antibodies (ANAs) in this condition (Taniguchi et al., Acta Derm Venereol (Stockh) Suppl 1992; 176:62-64; Tada et al., Dermatol 1994; 189:38-40). The prevalence of AD appears to be on the rise, with 10-15% of the population being affected at some time during childhood (Beltrani, J Allergy Clin Immunol 1999; 104:587-598; Leung, J Allergy Clin Immunol 1999; 104: S99-S108). We now report the finding of an autoantibody-autoantigen system in 30% of patients with AD which is also shared to a lesser extent by patients with asthma and interstitial cystitis (IC). IC is a urinary bladder condition in which the classical pathology is characterized by predominant mononuclear cell infiltration of the lamina propria with lymphocytes, plasma cells and mast cells (Gillenwater, et al., J Urol 1988; 140:203-206). The present invention provides a process of screening patients for atopic dermatitis. The process includes the step of determining, in sera of the patient, the presence of antibodies against nuclear antigens such as transcription co-activator p75, wherein the presence of such antibodies indicates atopic dermatitis. The screening process can be used to detect atopic dermatitis in patients suffering from other conditions such as asthma or interstitial cystitis. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Specific modulation of Th1/Th2 cytokine expression by ribavirin in activated Tlymphocytes Inventor(s): Tam, Robert; (Irvine, CA) Correspondence: Robert D. Fish; Rutan & Tucker, Llp; P.O. Box 1950; 611 Anton BLVD., 14th Floor; Costa Mesa; CA; 92628-1950; US Patent Application Number: 20030212015 Date filed: June 12, 2003 Abstract: Ribavirin is employed in a manner which is effective to modulate lymphokine expression in activated T cells. In particular, Ribavirin is used to suppress Type 2mediated T cell responses and promote Type 1-mediated T cell response. Thus, instead of administering Ribavirin in its well-recognized role as an anti-viral agent, Ribavirin is herein used in the treatment of imbalances in lymphokine expression. Such imbalances may be found to be concomitants of allergic atopic disorders such as allergic asthma and atopic dermatitis, helminth infection and leishmaniasis, and various primary and secondary immunodeficiencies, which may or may not also be associated with viral infection. Excerpt(s): This application is a continuation-in-part of co-pending, allowed U.S. Ser. No. 09/156,646, filed Sep. 18, 1998, which is a continuation in part of U.S. Ser. No. 09/097,450, filed Jun. 15, 1998, issued on May 16, 2000 as U.S. Pat. No. 6,063,772, which is a continuation of U.S. Ser. No. 08/590,449 filed Jan. 23, 1996, issued on Jun. 16, 1998 as U.S. Pat. No. 5,767,097. The field of the invention is immunology. From seminal work by Mossman and Coffman (Mossmann T R, Coffmann R L: Th1 and Th2 cells: different patterns of lymphokine secretion lead to different functional properties. Annu Rev Immunol 1989, 7: 145-173), growth factors known as cytokines produced by T helper or CD4.sup.+ T cells in both human and murine systems were classified into two subsets,

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Th1 and Th2. These were characterized by their functions in regulating various types of immune responses. Cytokines produced by Th1 cells [interleukin (IL)-2, interferon-alpha (IFN.gamma.), tumor necrosis factor-alpha (TNF.alpha.), IL-12] stimulated strong cellular immunity whereas Th2 cytokines [IL-4, IL-5, IL-6, IL-10, IL-13] were important for eliciting humoral (antibody) responses in vivo. Recently cytokines produced by nonCD4.sup.+ T cells have been shown to be important in in vivo responses. In particular, the cytotoxic or CD8.sup.+ T cells can also be subdivided into two subgroups, Tc1 and Tc2, which correspond to the same subsets in T helper cells (Carter L L, Dutton R W: Type 1 and Type 2: a functional dichotomy for all T cell subsets. Curr Opin Immunol 1996, 8: 336-342). This has led to the current nomenclature being generalized from Th1/Th2 to Type 1/Type 2 to reflect more closely the response generated by particular cytokines, rather than the cell types that produces them. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Synergetic composition for the treatment of psoriasis and other skin disorders and method therefor Inventor(s): Carlo, Jaime; (Tampa, FL), Chinea, Nestor; (Bayamon, PR), Franco, Juan; (San Juan, PR), Rivera, Carmelo; (Yauco, 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 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

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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 application of immixture of ascorbic acid + ascorbic acid compounds for augmenting the synthesis of epidermal ceramides Inventor(s): Castiel, Isabelle; (Jouy En Josas, FR), Ferraris, Corinne; (Paris, FR), La ValleBouchard, Armelle; (S/Siene, FR) Correspondence: Burns, Doane, Swecker & Mathis, L.L.P.; P.O. Box 1404; Alexandria; VA; 22313-1404; US Patent Application Number: 20030190338 Date filed: April 30, 2003 Abstract: Synergistic immixtures of ascorbic acid with at least one monosaccharide ester of ascorbic acid and/or at least one metal salt of phosphorylated ascorbic acid more effectively increase the synthesis of epidermal ceramides in human skin, especially types IV to VII ceramides, as well as improve the barrier function, moisture content and/or suppleness/surface appearance of the skin and which otherwise combat/prevent intrinsic aging thereof and are useful for the treatment of dermatitis. Excerpt(s): This application is a continuation of copending U.S. application Ser. No. 09/828,881, filed Apr. 10, 2001, expressly incorporated by reference herein in its entirety and relied upon. This application claims priority under 35 U.S.C.sctn. 119 of FR00/04575, filed Apr. 10, 2000, hereby expressly incorporated by reference. Copending Application No. 09/828,884 (Attorney Docket No. 016800-441), filed concurrently with parent application Ser. No. 09/828,881 on Apr. 10, 2001 and assigned to the assignee hereof. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Topical formulations for delivery of interleukin-11 Inventor(s): Bedrosian, Camille L.; (Belmont Hills, MA), Keith, James C. JR.; (Andover, MA), Schendel, Paul F.; (Wayland, MA), Schwerschlag, Ullrich S.; (Beverly Farms, MA), Warne, Nicholas W.; (Andover, MA) Correspondence: Mintz, Levin, Cohn, Ferris,; Glovsky And Popeo, P.C.; One Financial Center; Boston; MA; 02111; US Patent Application Number: 20030147849 Date filed: February 7, 2003 Abstract: Provided by the present invention are topical formulations of Interleukin-11 and methods for treating a variety of disorders, including inflammatory bowel diseases

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(e.g., Crohn's disease, ulcerative colitis, indeterminate colitis, and infectious colitis), mucositis (e.g., oral mucositis, gastrointestinal mucositis, nasal mucositis, and proctitis), necrotizing enterocolitis, inflammatory skin disorders (e.g., psoriasis, atopic dermatitis, and contact hypersensitivity), aphthous ulcers, pharyngitis, esophagitis, peptic ulcers, gingivitis, periodontitis, and ocular diseases (e.g., conjunctivitis, retinitis, and uveitis). Excerpt(s): This is a continuation-in-part of U.S. patent application Ser. No. 09/179,026 filed Oct. 26, 1998, which is a continuation-in-part of U.S. patent application Ser. No. 08/892,407, filed Jul. 15, 1997, now U.S. Pat. No. 5,948,402, which is a divisional of U.S. patent application Ser. No. 08/495,724, filed Jun. 27, 1995, now U.S. Pat. No. 5,679,339, issued Oct. 21, 1997. The present invention relates generally to novel compositions and methods for topical delivery of interleukin-11 (IL-11). In preferred embodiments, patients are treated employing topical delivery of recombinant human IL-11 for inflammatory bowel diseases (e.g., Crohn's disease, ulcerative colitis, indeterminate colitis, and infectious colitis), mucositis (e.g., oral mucositis, gastrointestinal mucositis, nasal mucositis, and proctitis), necrotizing enterocolitis, inflammatory skin disorders (e.g., psoriasis, atopic dermatitis, and contact hypersensitivity), aphthous ulcers, pharyngitis, esophagitis, peptic ulcers, gingivitis, periodontitis, and ocular diseases (e.g., conjunctivitis, retinitis, and uveitis). Inflammatory responses include a broad range of host reaction to a variety of insults, such as injury, infection, or rejection. It is the overproduction 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, multiple sclerosis, osteoporosis, gingivitis, peptic ulcer disease, esophagitis, diabetes, retinitis, uveitis, reperfusion injury after myocardial infarction, cerebral vascular accident, aphthous ulcers (oral), atherosclerosis, tumor metastases, asthma, preeclampsia, pancreatitis, psoriasis, infertility and allergic disorders such as rhinitis, conjunctivitis, and urticaria. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Topically applied clostridium botulinum toxin compositions and treatment methods Inventor(s): Coleman, William P. III; (Metairie, LA) Correspondence: Durando Birdwell & Janke, P.L.C.; 2929 E. Broadway BLVD.; Tucson; AZ; 85716; US Patent Application Number: 20030113349 Date filed: December 18, 2002 Abstract: Hyperactive glandular conditions are treated using topically formulated botulinum toxin compositions. In the preferred embodiment of the invention, topical botulinum preparations are applied directly to the skin by a patient as needed to suppress his or her hyperhidrosis, bromhidrosis, chromhidrosis, nevus sudoriferous, acne, seborrhiec dermatitis or other glandular condition. In other embodiments, topical botulinum toxins are applied with the aid of mechanical, electrical, and/or chemical transdermal delivery enhancers. Excerpt(s): This application is based on U.S. Provisional Patent Application Serial No. 60/343,389, filed on Dec. 18, 2001, and entitled "Method and Compositions for Treatment of Hyperhidrosis Using Clostridium Botulinum Toxin." The contents of the Provisional Patent Application are incorporated herein by reference. This invention relates generally to the field of medicine. In particular, it relates to methods and compositions that are especially suitable for the treatment of hyperhidrosis, and other

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conditions of the glands, skin, or smooth and skeletal muscle, and involve the topical application of one or more microbial neurotoxins. Traditionally, bacterial toxins, such as those produced by the genus Clostridia, were best known for their wide-ranging pathogenic effects, including food poisoning, tetanus, and botulism. Virulent botulinum strains are divided into seven groups, with each group producing an antigenically distinct toxin (the so-called types A-G toxins). While the potency of these toxins differ somewhat (and their physiological modes of action vary), they all result in chemodenervation. 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 dermatitis, 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 “dermatitis” (or synonyms) into the “Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on dermatitis. You can also use this procedure to view pending patent applications concerning dermatitis. 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 DERMATITIS Overview This chapter provides bibliographic book references relating to dermatitis. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on dermatitis 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 “dermatitis” (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 dermatitis: •

Under My Skin: A Kid's Guide to Atopic Dermatitis Source: Deerfield, IL: Fujisawa Healthcare, Inc. 2000. 48 p. Contact: Available from Fujisawa Healthcare, Inc. Three Parkway North Center, Deerfield, IL. 60015-2548. (800) 727-7003. Website: www.fujisawa.com. Summary: This book presents information about atopic dermatitis (AD), or eczema, to children. The book is divided into four sections discussing the physical and emotional aspects of AD, healing, and common triggers of AD. Topics within these sections include causes of itching; identifying irritants; the role of stress, allergens, and weather in flare-ups; infections; understanding feelings; struggling with scratching; having a healthy attitude; working with a doctor; flare care; and side effects of medications. Tips for controlling and coping with AD from children with the condition are included. A place for the child to write down questions for their doctor and a sample daily routine are appended. Numerous illustrations.

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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 “dermatitis” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “dermatitis” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “dermatitis” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •

Allergic Contact Dermatitis to Ingredients Used in Topically Applied Pharmaceutical Products & Cosme by A. Dooms-Goossens (1993); ISBN: 9061861470; http://www.amazon.com/exec/obidos/ASIN/9061861470/icongroupinterna

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Allergic Contact Dermatitis to Simple Chemicals by Gilles Dupuis; ISBN: 0824714687; http://www.amazon.com/exec/obidos/ASIN/0824714687/icongroupinterna

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Allergic Contact Dermatitis: Chemical and Metabolic Mechanisms by Camilla K. Smith, et al (2001); ISBN: 0415250471; http://www.amazon.com/exec/obidos/ASIN/0415250471/icongroupinterna

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Allergies: Asthma Hay Fever Dermatitis Migraine and Others by Graham-Bonnalie; ISBN: 0877490392; http://www.amazon.com/exec/obidos/ASIN/0877490392/icongroupinterna

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An Illustrated Pocketbook of Contact Dermatitis by L. Fry; ISBN: 1842140590; http://www.amazon.com/exec/obidos/ASIN/1842140590/icongroupinterna

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Atlas of Contact Dermatitis by Robert L. Rietschel, et al; ISBN: 1853175544; http://www.amazon.com/exec/obidos/ASIN/1853175544/icongroupinterna

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Atopic Dermatitis by Thomas Bieber (Editor), Donald Y. M. Leung (Editor) (2002); ISBN: 0824707427; http://www.amazon.com/exec/obidos/ASIN/0824707427/icongroupinterna

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Atopic Dermatitis by Kristian Thestrup-Pedersen, et al; ISBN: 185317145X; http://www.amazon.com/exec/obidos/ASIN/185317145X/icongroupinterna

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Atopic dermatitis by Georg Rajka; ISBN: 0721674488; http://www.amazon.com/exec/obidos/ASIN/0721674488/icongroupinterna

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Atopic Dermatitis - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet Ref by Health Publica Icon Health Publications (2003); ISBN: 0597835640; http://www.amazon.com/exec/obidos/ASIN/0597835640/icongroupinterna

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Atopic Dermatitis: The Epidemiology, Causes and Prevention of Atopic Eczema by Hywel C. Williams (Editor); ISBN: 0521570751; http://www.amazon.com/exec/obidos/ASIN/0521570751/icongroupinterna

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Botulinum Toxin in the Treatment of Focal Hyperhidrosis & Dyshidrotic Hand Dermatitis (Comprehensive Summaries of Uppsala Dissertations from the Faculty of mediciNe, 1164) by Carl Swartling (2002); ISBN: 9155453406; http://www.amazon.com/exec/obidos/ASIN/9155453406/icongroupinterna

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Color Atlas of Plant Contact Dermatitis by Claude Benezra; ISBN: 0801605911; http://www.amazon.com/exec/obidos/ASIN/0801605911/icongroupinterna

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Color Text of Contact Dermatitis by Walter G. Larsen (Editor), et al; ISBN: 0721635180; http://www.amazon.com/exec/obidos/ASIN/0721635180/icongroupinterna

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Contact Dermatitis by Alexander A. Fisher; ISBN: 0812109716; http://www.amazon.com/exec/obidos/ASIN/0812109716/icongroupinterna

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Contact Dermatitis by Etain. Cronin; ISBN: 0443020140; http://www.amazon.com/exec/obidos/ASIN/0443020140/icongroupinterna

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Current Concepts in Contact Dermatitis by Julian L. Verbov (Editor) (1988); ISBN: 085200687X; http://www.amazon.com/exec/obidos/ASIN/085200687X/icongroupinterna

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Current topics in contact dermatitis; ISBN: 0387505687; http://www.amazon.com/exec/obidos/ASIN/0387505687/icongroupinterna

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Dermatitis herpetiformis by John O'Donel Alexander; ISBN: 0721611052; http://www.amazon.com/exec/obidos/ASIN/0721611052/icongroupinterna

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Dermatitis in machinists : causes and solutions by E. O. Bennett; ISBN: 1880319098; http://www.amazon.com/exec/obidos/ASIN/1880319098/icongroupinterna

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DR V COLEMANS ECZEMA DERMATITIS by COLEMAN; ISBN: 0727820575; http://www.amazon.com/exec/obidos/ASIN/0727820575/icongroupinterna

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Eczema and Dermatitis by Coleman; ISBN: 072782077X; http://www.amazon.com/exec/obidos/ASIN/072782077X/icongroupinterna

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ECZEMA AND DERMATITIS - PHG; ISBN: 0132350106; http://www.amazon.com/exec/obidos/ASIN/0132350106/icongroupinterna

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Eczema and Dermatitis: How to Cope With Inflamed Skin by Rona M., M.D. MacKie; ISBN: 0668056290; http://www.amazon.com/exec/obidos/ASIN/0668056290/icongroupinterna

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Epidermal Keratinocytes Studied by X-Ray Microanalysis, With Special Reference to Contact Dermatitis: In Vivo and in Vitro Studies of Functional Changes in Human Cells (Comprehensive Summaries of Uppsala Dissertations, 884) by Anders Grangsjo (1999); ISBN: 9155445985; http://www.amazon.com/exec/obidos/ASIN/9155445985/icongroupinterna

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Essential Aspects of Atopic Dermatitis by Georg Rajka; ISBN: 0387511652; http://www.amazon.com/exec/obidos/ASIN/0387511652/icongroupinterna

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Essential Aspects of Atopic Dermatitis; ISBN: 3540511652; http://www.amazon.com/exec/obidos/ASIN/3540511652/icongroupinterna

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Exogenous Dermatoses: Environmental Dermatitis by Torkil Menne, Howard I. Maibach (Editor); ISBN: 0849359694; http://www.amazon.com/exec/obidos/ASIN/0849359694/icongroupinterna

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Fisher's Contact Dermatitis by Robert L. Rietschel (Editor), Joseph F. Fowler (Editor); ISBN: 0781722527; http://www.amazon.com/exec/obidos/ASIN/0781722527/icongroupinterna

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Handbook of Contact Dermatitis by Matthias, MD Gebhart (Editor), et al; ISBN: 1853178012; http://www.amazon.com/exec/obidos/ASIN/1853178012/icongroupinterna

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Handbook of Contact Dermatitis by Howard Maibach, et al; ISBN: 0849373514; http://www.amazon.com/exec/obidos/ASIN/0849373514/icongroupinterna

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Irritant Contact Dermatitis by Edward M. Jackson, Ronald Goldner (Editor); ISBN: 0824782887; http://www.amazon.com/exec/obidos/ASIN/0824782887/icongroupinterna

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Irritant Dermatitis: New Clinical and Experimental Aspects (Current Problems in Dermatology, Vol 23) by Peter Elsner, Howard I. Maibach (Editor) (1995); ISBN: 3805560834; http://www.amazon.com/exec/obidos/ASIN/3805560834/icongroupinterna

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Manual of contact dermatitis : on behalf of the International Contact Dermatitis Research Group by Sigfrid Fregert; ISBN: 8716016882; http://www.amazon.com/exec/obidos/ASIN/8716016882/icongroupinterna

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MarketLooks: The Global Market for Prescription Dermatitis, Seborrhea, and Psoriasis Drugs [DOWNLOAD: PDF] by MarketLooks - Kalorama Information (Author); ISBN: B000068IXD; http://www.amazon.com/exec/obidos/ASIN/B000068IXD/icongroupinterna

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Occupational Contact Dermatitis: Clinical and Chemical Aspects by Jean Foussereau; ISBN: 0721638260; http://www.amazon.com/exec/obidos/ASIN/0721638260/icongroupinterna

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Plant Contact Dermatitis by Claude Benezra, et al; ISBN: 0941158284; http://www.amazon.com/exec/obidos/ASIN/0941158284/icongroupinterna

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Pocket Guide to Eczema and Contact Dermatitis by Colin Holden, Lucy Ostlere; ISBN: 0632056630; http://www.amazon.com/exec/obidos/ASIN/0632056630/icongroupinterna

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Practical Contact Dermatitis: A Handbook for the Practitioner by Jere D. Guin (Editor); ISBN: 007025169X; http://www.amazon.com/exec/obidos/ASIN/007025169X/icongroupinterna

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Preventing Dermatitis at Work: Advice for Employers and Employees: Pack of 10 (Leaflet); ISBN: 0717612465; http://www.amazon.com/exec/obidos/ASIN/0717612465/icongroupinterna

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Prevention of Contact Dermatitis (Current Problems in Dermatology, Vol. 25) by Peter Elsner (Editor), et al (1996); ISBN: 3805563116; http://www.amazon.com/exec/obidos/ASIN/3805563116/icongroupinterna

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Skin Tests in Dermatitis and Occupational Chest Disease; ISBN: 0118830600; http://www.amazon.com/exec/obidos/ASIN/0118830600/icongroupinterna

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Textbook of Atopic Dermatitis by Sakari Reitamo, et al; ISBN: 184184246X; http://www.amazon.com/exec/obidos/ASIN/184184246X/icongroupinterna

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Textbook of Contact Dermatitis by R. J. G. Rycroft (1995); ISBN: 3540579435; http://www.amazon.com/exec/obidos/ASIN/3540579435/icongroupinterna

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The Gluten-Free Diet Book: A Guide to Glutensensitive Enteropathy, Dermatitis Herpetriformis, and Gluten-Free Cookery (Positive Health Guide) by Peter Rawcliffe, Ruth Rolph (Photographer); ISBN: 0668059737; http://www.amazon.com/exec/obidos/ASIN/0668059737/icongroupinterna

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The Irritant Contact Dermatitis Syndrome by Pieter G. M. Van Der Valk (Editor), et al; ISBN: 0849373549; http://www.amazon.com/exec/obidos/ASIN/0849373549/icongroupinterna

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The Official Patient's Sourcebook on Atopic Dermatitis by Icon Health Publications, et al (2002); ISBN: 0597831599; http://www.amazon.com/exec/obidos/ASIN/0597831599/icongroupinterna

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Toxicology of Contact Dermatitis: Allergy, Irritancy and Urticaria by David Basketter (Editor), et al; ISBN: 0471972010; http://www.amazon.com/exec/obidos/ASIN/0471972010/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 “dermatitis” (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 •

Allergic contact dermatitis in the guinea pig; identifications of contact allergens, by Bertil Magnusson and Albert M. Kligman. Author: Magnusson, Bertil.; Year: 1963; Springfield, Ill., Thomas [c1970]

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Atopic dermatitis and hypnosis: an investigation of physiologic stigmata before, during and after hypnosis. Author: West, James Robert,; Year: 1968; [Minneapolis] 1960

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Canine allergic inhalant dermatitis. Edited by Sue Drum. Author: Anderson, Warren.; Year: 1951; [n. p., c1973]

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Contact dermatitis. Author: Fisher, Alexander A.,; Year: 1968; Philadelphia, Lea; Febiger, 1967

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Industrial dermatitis; precautionary measures. Author: Great Britain. Ministry of Labour.; Year: 1966; [London, 1962]

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Notes on occupational dermatitis. Author: New Zealand. Dept. of Health.; Year: 1964; [Wellington, 1964]

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Occupational arsenical dermatitis; a study among employees at a copper ore smelting work including investigations of skin reactions to contact with arsenic compounds. Author: Holmqvist, Ivar.; Year: 1965; Stockholm, 1951

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Occupational contact dermatitis. Author: Adams, Robert M.,; Year: 1966; Philadelphia, Toronto, Lippincott [c1969]

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Occupational dermatitis in California. Author: California. Bureau of Adult Health.; Year: 1968; Berkeley, 1958

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Occupational poison oak dermatitis in California. Author: California. Bureau of Occupational Health.; Year: 1967; Berkeley, 1961

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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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•

Plant toxicity and dermatitis; a manual for physicians [by] Kenneth F. Lampe [and] Rune Fagerström. Author: Lampe, Kenneth F.; Year: 1965; Baltimore, Williams; Wilkins, 1968

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Soap photodermatitis; photosensitivity to halogenated salicylanilides, by Peter Simon Herman and W. Mitchell Sams, Jr. Author: Herman, Peter Simon.; Year: 1965; Springfield, Ill., Thomas [c1972]; ISBN: 0398023123 http://www.amazon.com/exec/obidos/ASIN/0398023123/icongroupinterna

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Tacrolimus ointment: a topical immunomodulator for atopic dermatitis Author: Ruzicka, Thomas.; Year: 1967; Berlin; New York: Springer, c2004; ISBN: 3540435131 http://www.amazon.com/exec/obidos/ASIN/3540435131/icongroupinterna

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The vascular effects of parenteral mecholyl (acetyl-beta-methylcholine) in atopic dermatitis. Author: Clark, Lealand L.,; Year: 1961; [Minneapolis] 1960

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What to do about dermatitis. Author: Sawyer, William Alfred,; Year: 1969; Washington, International Association of Machinists [c1954]

Chapters on Dermatitis In order to find chapters that specifically relate to dermatitis, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and dermatitis 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 “dermatitis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on dermatitis: •

What Is Celiac Disease? (And Nontropical Sprue, Dermatitis Herpetiformis, GlutenSensitive Enteropathy, and General Gluten Intolerance) Source: in Korn, D. Kids with Celiac Disease: A Family Guide to Raising Happy, Healthy, Gluten-Free Children. Bethesda, MD: Woodbine House. 2001. p. 3-8. Contact: Available from Woodbine House. 6510 Bells Mill Road, Bethesda, MD 20817. (800) 843-7323 or (301) 897-3570. Fax (301) 897-5838. E-mail: [email protected]. Website: www.woodbinehouse.com. PRICE: $17.95 plus shipping and handling. ISBN: 1890627216. Summary: This chapter defining celiac disease is from a practical survival guide for families of children and teenagers with celiac disease, a lifelong digestive disorder that affects nearly two million Americans. Celiac disease results from an intolerance of gluten, a protein found in wheat, rye, barley, and oats, and any food made with these grains. Removing gluten from the diet is the only known treatment for this illness. Left untreated, the disease can lead to serious conditions such as damage to the central nervous system, osteoporosis, and cancer. The chapter begins by defining celiac disease and explaining how gluten damages the villi in the small intestine, resulting in malnutrition and dehydration. The symptoms tend to be varied, which lends to difficulties in diagnosing celiac disease. Classic symptoms include diarrhea, malabsorption, gas, and bloating; other symptoms can include fatigue, anemia, irritability, vomiting, short stature, or difficulty concentrating. Some people with celiac disease show absolutely no symptoms. The author notes that dermatitis herpetiformis is a 'sister' to celiac disease, with a subset of symptoms (primarily a very severe rash on the

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skin) that responds well to the gluten free diet. The author stresses that the good news about celiac disease is the fact that it is so treatable; a complete, strict gluten free diet will result in nearly immediate improvement. After a few weeks on the gluten free diet, most people feel better overall, as their malnutrition and dehydration resolve. •

Chapter 124: Atopic Dermatitis (Atopic Eczema) 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. 1464-1480. 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 historical aspects, epidemiology, genetics, clinical manifestations, differential diagnosis, immunopathogenesis, management, and prognosis of atopic dermatitis (AD). AD is a chronically relapsing skin disease that occurs most often during early infancy and childhood. The increased prevalence of AD is thought to involve factors such as increased exposure to pollutants, indoor allergens, and a decline in breastfeeding. Although the precise means by which AD is familially transmitted remains uncertain, some studies suggest an autosomal dominant inheritance pattern. The diagnosis of AD is based on a constellation of clinical features, including intensive pruritus, cutaneous reactivity, eye problems, and cutaneous infections. The differential diagnosis of AD involves distinguishing AD from other inflammatory skin diseases, immunodeficiencies, skin malignancies, genetic disorders, metabolic disorders, and infectious diseases and infestations. Although serum immunoglobulin (Ig) E levels are elevated in many patients who have AD, a direct relationship of IgE to implicated allergens and the clinical exacerbation of AD has been difficult to establish. Various studies have investigated the role of foods, aeroallergens, and microbial products in AD. Other studies have examined the immunopathogenesis of AD by investigating peripheral blood cells, T helper cells, cytokine expression, and similarities in the allergic inflammation of asthma and AD. Data suggest that antigen or superantigen exposure, allergen-induced IgE synthesis and T helper 2 cell-like expansion, mast cell degranulation, and keratinocyte injury may contribute to chronic AD skin inflammation and possibly to nonspecific cutaneous hyperresponsiveness. Management of AD involves individualizing a treatment plan to address each patient's skin disease reaction pattern. Options include cutaneous hydration; topical glucocorticoid treatment; identification and elimination of triggering factors such as allergens, emotional stress, and infectious agents; and use of antihistamines and tar preparations. Methods of treating poorly controlled AD include wet dressings and occlusion, systemic glucocorticoids, ultraviolet light, and hospitalization. Unproven or evolving treatments include allergen immunotherapy, interferons, cyclosporine and FK-506, extracorporeal photopheresis, and phosphodiesterase inhibitors. Factors that correlate with a poor prognosis include widespread AD in childhood, associated allergic rhinitis and asthma, family history of AD in parents or siblings, early age at onset of AD, and female sex. 10 figures, 3 tables, and 178 references.

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Chapter 194: Dermatitis Source: in Berkow, R., ed. The Merck Manual of Medical Information: Home Edition (online version). Rahway, NJ: Merck and Company, Inc. 2000. 10 p.

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Contact: Available online from Merck and Company, Inc. (800) 819-9456. Website: www.merck.com/pubs/mmanual_home/contents.htm. Also available from your local book store. PRICE: $29.95 plus shipping. Summary: This chapter provides the general public and people who have dermatitis with information on the symptoms, diagnosis, and treatment of contact dermatitis, chronic dermatitis of the hands and feet, and atopic, seborrheic, nummular, generalized exfoliative, stasis, and localized scratch dermatitis. Dermatitis is an inflammation of the upper layers of the skin. Contact dermatitis is inflammation caused by contact with a particular substance that causes either irritation or an allergic reaction. Symptoms range from a mild, brief redness to severe swelling and blisters. The location of the initial rash is often a clue in diagnosing contact dermatitis. Patch testing may also be used in the diagnostic process. Treatment involves removing or avoiding the substance that is causing the dermatitis. Corticosteroid creams or ointments may be used to relieve the symptoms of mild contact dermatitis. Chronic dermatitis of the hands occurs from repetitive tasks and contact with chemicals, whereas chronic dermatitis of the feet results from the warm, moist conditions in socks and shoes. The best treatment is usually removal of the irritant. Corticosteroid creams, antibiotics, and antifungals may be helpful. Atopic dermatitis, which usually develops in people who have many other allergic disorders, is a chronic, itchy inflammation of the upper layers of the skin. The color, intensity, and location of the rash vary, but it always itches. Diagnosis is based on family history and the typical pattern of the rash. Although no cure exists, avoiding contact with irritants can prevent a rash, bathing less often can be helpful, and using corticosteroid creams or ointments and antihistamines can relieve symptoms. Seborrheic dermatitis, an inflammation of the upper layers of the skin, causes scales on the scalp, on the face, and sometimes on other areas. In adults, treatment involves special shampoos and lotions that contain corticosteroids. Nummular dermatitis is a persistent, usually itchy rash and inflammation characterized by round spots of pimples and blisters that later ooze and form crusts. Treatment options include oral antibiotics, corticosteroids, and ultraviolet light therapy. In people who have generalized exfoliative dermatitis, the entire skin surface becomes red, scaly, thickened, and sometimes crusted. The condition may be caused by certain drugs or may be a complication of another skin condition. Treatment involves eliminating any drug or chemical that could be causing the dermatitis. Care may include medications, heated blankets, and cool baths followed by applications of petroleum jelly and gauze. Stasis dermatitis, which usually occurs on the ankles, is characterized by chronic redness, scaling, warmth, and swelling. Treatment is aimed at reducing the chances of blood pooling in the veins around the ankles by using support hose. Various measures may be used to relieve the symptoms. Localized scratch dermatitis, a chronic, itchy inflammation of the top layer of the skin, causes dryness, scaling, and dark, thickened patches. Antihistamines and corticosteroid creams may be prescribed to control the itching.

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CHAPTER 8. MULTIMEDIA ON DERMATITIS Overview In this chapter, we show you how to keep current on multimedia sources of information on dermatitis. 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 dermatitis is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “dermatitis” 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 “dermatitis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on dermatitis: •

Bottom Line on Hemorrhoids Source: Madison, WI: University of Wisconsin Hospitals and Clinics, Department of Outreach Education. 1996. (videocassette). Contact: Available from University of Wisconsin Hospital and Clinics. Picture of Health, 702 North Blackhawk Avenue, Suite 215, Madison, WI 53705-3357. (800) 757-4354 or (608) 263-6510. Fax (608) 262-7172. PRICE: $19.95 plus shipping and handling; bulk copies available. Order number 051997A. Summary: Straining when going to the bathroom, constipation, prolonged sitting, and infection can all contribute to hemorrhoids, defined as enlarged veins around the anus. This videotape is one in a series of health promotion programs called 'Picture of Health,' produced by the University of Wisconsin. In this program, moderated by Mary Lee and featuring gastroenterologist John Wyman, the common symptoms, diagnosis, and management of hemorrhoids are covered. Dr. Wyman explains the difference between internal and external hemorrhoids (merely an anatomical distinction), and prolapsed

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hemorrhoids, which are enlarged internal hemorrhoids that drop (prolapse) outside the anus. Symptoms include pain and bleeding; pain because of blood clots and bleeding due to trauma to the thin walled veins in that area. The causes of hemorrhoids include straining during defecation, pregnancy, prolonged sitting, constipation, childbirth, and obesity. Dr. Wyman recommends that anyone over the age of 40 who experiences rectal bleeding should consult a physician; younger people who experience recurrent bleeding should also see their physician (to rule out inflammatory bowel disease). Treatment options for hemorrhoids include changes in habits, such as not straining, not wiping vigorously, softening the stool with dietary changes (usually the addition of dietary fiber), and not prolonging sitting on the toilet. Surgery is used for external hemorrhoids, to remove the veins and tributaries; for internal hemorrhoids, rubber band ligation is very effective. The program also explores the problem of perianal dermatitis, including its risk factors and treatment options (which focus on keeping the area clean and dry, and not using over the counter creams that are petroleum based). The program reiterates the importance of having any rectal bleeding investigated by one's health care provider. The program concludes by referring viewers to the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK).

Bibliography: Multimedia on Dermatitis 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 dermatitis (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 dermatitis: •

Acne, perioral dermatitis and rosacea; Contact dermatitis; Infestations [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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Allergic contact dermatitis [slide]: examples and approaches Source: presented by Ernst Epstein, Howard I. Maibach, 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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Anogenital dermatitis [videorecording] Source: Orville J. Stone; produced by University of California at Irvine, California College of Medicine; Year: 1976; Format: Videorecording; Irvine: The University; [Glendale, Calif.: for sale by Telephone Marketing Services], c1976

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Atopic dermatitis [slide] Source: Marion B. Sulzberger, Rudolf L. Baer; produced by Institute for Dermatologic Communication and Education; Year: 1975; Format: Slide; San Francisco: The Institute, c1975

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Atopic dermatitis [slide] Source: M. Eric Gershwin. [et al.]; Year: 1982; Format: Slide; [New York]: Medcom, c1982

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Atopic dermatitis [videorecording] Source: Marion B. Sulzberger, Rudolf L. Baer; produced by Institute for Dermatologic Communication and Education; Year: 1975; Format: Videorecording; San Francisco: The Institute, c1975

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Chronic actinic dermatitis [videorecording] Source: Henry W. Lim; Year: 1996; Format: Videorecording; Secaucus, N.J.: Network for Continuing Medical Education, c1996

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Dermatitis herpetiformis [videorecording] Source: presented by the Department of Medicine, Emory University, School of Medicine; Year: 1983; Format: Videorecording; Atlanta, Ga.: Emory Medical Television Network, 1983

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Dermatitis herpetiformis [videorecording] Source: presented by the Department of Medicine, Emory University, School of Medicine [and] the Emory Medical Television Network; Year: 1989; Format: Videorecording; Atlanta, Ga.: The University, c1989

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Management of allergic contact dermatitis [slide] Source: Alexander A. Fisher, Ronald R. Brancaccio; Year: 1979; Format: Slide; [Evanston, Ill.]: American Academy of Dermatology, c1979

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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

•

Skin cancer and dermatitis factitia [videorecording] Source: Dept. of Medicine, Emory University, School of Medicine; Year: 1979; Format: Videorecording; Atlanta: Emory Medical Television Network: [for loan and sale by A. W. Calhoun Medical Library, 1979]

•

The mystery of contact dermatitis [videorecording]: putting the pieces together Source: American Academy of Dermatology; Year: 1988; Format: Videorecording; Schaumberg, IL: The Academy, 1988

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CHAPTER 9. PERIODICALS AND NEWS ON DERMATITIS Overview In this chapter, we suggest a number of news sources and present various periodicals that cover dermatitis.

News Services and Press Releases One of the simplest ways of tracking press releases on dermatitis 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 “dermatitis” (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 dermatitis. 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 “dermatitis” (or synonyms). The following was recently listed in this archive for dermatitis: •

Connetics submits seborrheic dermatitis treatment application to FDA Source: Reuters Industry Breifing Date: July 02, 2003

•

Fluticasone plus emollient therapy reduces risk of dermatitis relapse Source: Reuters Industry Breifing Date: June 19, 2003

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•

Tacrolimus shows promise as treatment for chronic actinic dermatitis Source: Reuters Industry Breifing Date: January 01, 2003

•

SR Pharma starts phase II pediatric dermatitis trial Source: Reuters Industry Breifing Date: November 25, 2002

•

'Decoy' ointment relieves chronic skin rash in mice Source: Reuters Health eLine Date: October 29, 2002

•

Topical pimecrolimus safe for infants with atopic dermatitis Source: Reuters Industry Breifing Date: August 29, 2002

•

Pimecrolimus prevents flares of atopic dermatitis, reduces need for steroids Source: Reuters Industry Breifing Date: July 16, 2002

•

Pimecrolimus shows promise as maintenance therapy for atopic dermatitis Source: Reuters Industry Breifing Date: March 07, 2002

•

Dermatitis drugs' mechanisms of action clarified Source: Reuters Industry Breifing Date: December 20, 2001

•

FDA approves pimecrolimus for treatment of atopic dermatitis Source: Reuters Medical News Date: December 14, 2001

•

Italy: detergents linked with dermatitis and asthma Source: Reuters Medical News Date: October 18, 2001

•

Italy: Detergents linked to dermatitis, asthma Source: Reuters Health eLine Date: October 17, 2001

•

Mycophenolate mofetil shows promise in treatment of atopic dermatitis Source: Reuters Industry Breifing Date: July 26, 2001

•

Study: Arabic men at risk for beard dermatitis Source: Reuters Health eLine Date: May 25, 2001

•

PhotoMedex seeks FDA approval for laser to treat atopic dermatitis Source: Reuters Industry Breifing Date: May 16, 2001

•

Atrix files IND to study Atrisone as atopic dermatitis therapy Source: Reuters Industry Breifing Date: May 07, 2001

•

Topical tacrolimus targets epidermal antigen-presenting cells in atopic dermatitis Source: Reuters Medical News Date: April 06, 2001

Periodicals and News

•

CCR4+ cells increased in blood and lesional skin of atopic dermatitis patients Source: Reuters Medical News Date: March 05, 2001

•

Occlusive bedding reduces eczema severity in patients with atopic dermatitis Source: Reuters Medical News Date: February 23, 2001

•

Distinct immune effects of psychological stress seen in atopic dermatitis patients Source: Reuters Medical News Date: February 16, 2001

•

Oolong tea improves recalcitrant atopic dermatitis in some patients Source: Reuters Medical News Date: January 26, 2001

•

Oolong tea may relieve symptoms of atopic dermatitis Source: Reuters Health eLine Date: January 25, 2001

•

New dermatitis drug recommended for US approval Source: Reuters Health eLine Date: November 17, 2000

•

Nonsteroid drug promising for treatment of atopic dermatitis, psoriasis Source: Reuters Industry Breifing Date: October 16, 2000

•

Serum CD30 levels correlate with disease activity in atopic dermatitis patients Source: Reuters Industry Breifing Date: July 05, 2000

•

Body-weight-independent use of cyclosporine effective for atopic dermatitis Source: Reuters Medical News Date: May 09, 2000

•

Children with atopic dermatitis at high risk of asthma Source: Reuters Medical News Date: April 10, 2000

•

Contact dermatitis begins in infancy Source: Reuters Health eLine Date: January 12, 2000

•

Birth month affects prevalence of atopic dermatitis during school years Source: Reuters Medical News Date: July 19, 1999

•

FDA approves cream for infant atopic dermatitis Source: Reuters Medical News Date: June 21, 1999

•

Asthma risk in children may be predicted by atopic dermatitis in infancy Source: Reuters Medical News Date: September 02, 1998

•

Photopheresis, UVA1 Radiation Effectively Treat Severe Atopic Dermatitis Source: Reuters Medical News Date: April 20, 1998

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•

Pediatric Skin Rash Linked To Food Allergy Source: Reuters Health eLine Date: March 04, 1998

•

Food Hypersensitivity Common In Children With Atopic Dermatitis Source: Reuters Medical News Date: February 18, 1998

•

Tacrolimus Ointment Safe, Effective Against Atopic Dermatitis Source: Reuters Medical News Date: February 06, 1998

•

Cosmetic Preservative Can Cause Contact Dermatitis Source: Reuters Medical News Date: September 30, 1997

•

Tacrolimus Provides Symptomatic Relief In Atopic Dermatitis Patients Source: Reuters Medical News Date: September 18, 1997

•

Thalidomide Effective In Pediatric Atopic Dermatitis Source: Reuters Medical News Date: June 17, 1997

•

Moisturizers Slow Dermatitis Healing Source: Reuters Health eLine Date: May 30, 1997

•

Transplant Rejection Drug Effectively Treats Atopic Dermatitis Source: Reuters Medical News Date: April 22, 1997 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

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Market Wire’s home page at http://www.marketwire.com/mw/home, type “dermatitis” (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 you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “dermatitis” (or synonyms). If you know the name of a company that is relevant to dermatitis, 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 “dermatitis” (or synonyms).

Newsletters on Dermatitis Find newsletters on dermatitis using the Combined Health Information Database (CHID). You will need to use the “Detailed Search” option. To access CHID, go to the following hyperlink: http://chid.nih.gov/detail/detail.html. Limit your search to “Newsletter” and “dermatitis.” 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.” Type “dermatitis” (or synonyms) into the “For these words:” box. The following list was generated using the options described above: •

Dermatitis Herpetiformis: Part I Source: GIG Newsletter. Gluten Intolerance Group of North America Newsletter. 17(2): 9-14. April-June 1993. Contact: Available from Gluten Intolerance Group of North America. P.O. Box 23053, Seattle, WA 98102. (206) 325-6980. Summary: This newsletter article provides an overview of dermatitis herpetiformis (DH), a common complication in people with celiac disease or gluten intolerance. Written in a question-and-answer format, the document discusses the appearance of DH; the body areas most likely to have DH eruptions; variations in severity; relationship between hormone levels and DH eruptions; demographics; how DH is diagnosed; other IgA skin disorders that mimic DH; treatment options for DH; medications used and side effects of each, including dapsone, sulphapyridine, and sulphamethoxy-pyridazine; and choosing diet versus medication. The article was excerpted from a chapter in the text Coeliac Disease (Blackwell Scientific Publications, 1992).

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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 “dermatitis” (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 dermatitis: •

Allergist's View of Atopic Dermatitis Source: The Advocate. 12(4): 1-2,7. 4th Quarter 2000. Contact: Available from National Eczema Association for Science and Education (NEASE). 1220 SW Morrison, Suite 433, Portland, OR 97205. (800) 818-7546 or (503) 2284430. Fax (503) 224-3363. E-mail: [email protected]. Website: www.eczema-assn.com. Summary: This newsletter article provides health professionals with information on atopic dermatitis (AD). This common chronic skin disease, which causes an extremely itchy, red rash, affects 1 in 7 young children. AD and allergy are closely related. Many children first develop AD and then develop asthma and allergic rhinitis. Children with AD frequently develop allergic respiratory disease. About 1 out of 3 children with moderate to severe AD has food allergy. Although some allergic reactions to food, such as hives, wheezing, and vomiting, are obvious, food allergies are usually not easy to detect in most children with AD. Standard allergy tests are only partially helpful. The ultimate confirmation of food allergy is possible only through an oral food challenge. A positive reaction to an oral food challenge usually causes an itchy, raised red rash. More severe reactions, including hives, lip or throat swelling, cough, wheezing, vomiting, or abdominal pain, may also occur. Although eliminating an allergy causing food from a child's diet is preferable, it can be difficult to completely eliminate major foods such as egg, milk, wheat, or soy. The most frequent cause of dietary elimination failures is unknowing exposure to small amounts of the offending ingredient in processed foods. The prognosis for outgrowing food allergies is very good for most children. Environmental allergens such as pollens, animal dander, and dust mites should be suspected in children with asthma or chronic stuffy, itchy, runny nose or eyes. A skin prick test can be used to evaluate allergy to environmental allergens. The identification and removal of specific allergens can improve AD in these patients. Intensive moisturization is also important in the treatment of AD.

•

Phototherapy for Atopic Dermatitis Source: The Advocate. 13(2): 1-2. Second Quarter 2001. Contact: Available from National Eczema Association for Science and Education (NEASE). 1220 SW Morrison, Suite 433, Portland, OR 97205. (800) 818-7546 or (503) 2284430. Fax (503) 224-3363. E-mail: [email protected]. Website: www.eczema-assn.com. Summary: This newsletter article provides people who have atopic dermatitis (AD) with information on the use of phototherapy in the treatment of this skin disorder. Ultraviolet (UV) light is useful for treating skin diseases because it causes chemical changes in skin cells. The idea of treatment is to cause controlled damage to these cells so that the skin's natural healing capacities are activated. Short term adverse effects of UV radiation are

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local inflammation and cell destruction. Long term risks of UV radiation can be cell changes that may cause cancer. Total exposure over time is an important factor. Medical UV therapy is produced by special lamps that emit light of precise wavelengths and energies. People should undergo UV therapy under the close supervision of a physician. Types of UV therapy available include psoralen plus UVA (PUVA) and UVB. Although PUVA or photochemotherapy is very effective for treating psoriasis, it has limited usefulness in treating AD. UVB is shorter than UVA, so it penetrates the skin better and can be used therapeutically without the need for psoralen. Narrow band UVB is the newest approach to UV therapy. Climatotherapy is a special type of phototherapy that uses the natural light of the sun, often in conjunction with special baths and other methods, to treat AD.

Academic Periodicals covering Dermatitis Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to dermatitis. In addition to these sources, you can search for articles covering dermatitis 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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CHAPTER 10. RESEARCHING MEDICATIONS Overview While a number of hard copy or CD-ROM resources are available for researching medications, a more flexible method is to use Internet-based databases. Broadly speaking, there are two sources of information on approved medications: public sources and private sources. We will emphasize free-to-use public sources.

U.S. Pharmacopeia Because of historical investments by various organizations and the emergence of the Internet, it has become rather simple to learn about the medications recommended for dermatitis. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a nonprofit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI Advice for the Patient can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with dermatitis. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.). The

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following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to dermatitis: Bentoquatam •

Topical - U.S. Brands: IvyBlock http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202901.html

Bleomycin •

Systemic - U.S. Brands: Blenoxane http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202093.html

Bronchodilators, Adrenergic •

Oral/Injection - U.S. Brands: Adrenalin; Alupent; Ana-Guard; Brethine; Bricanyl; EpiPen Auto-Injector; EpiPen Jr. Auto-Injector; Isuprel; Proventil; Proventil Repetabs; Ventolin; Volmax http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202096.html

Ciclopirox •

Topical - U.S. Brands: Loprox http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202140.html

Coal Tar •

Topical - U.S. Brands: Alphosyl; Aquatar; Estar; Fototar; Lavatar; Medotar; Psorigel; Taraphilic; Tarbonis http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202158.html

Methoxsalen •

Systemic - U.S. Brands: 8-MOP; Oxsoralen-Ultra http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202357.html

Pyrithione •

Topical - U.S. Brands: Sebulon; XSeb; Zincon http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202495.html

Resorcinol •

Topical - U.S. Brands: RA http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202507.html

Salicylic Acid •

Topical - U.S. Brands: Antinea; Duofilm; Freezone; Gordofilm; Hydrisalic; Keralyt; Lactisol; Mediplast; P&S; Paplex; Salac; Salacid; Saligel; Salonil; Sebucare; Trans-Plantar; Trans-Ver-Sal; Viranol; X-Seb http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202516.html

Salicylic Acid and Sulfur •

Topical - U.S. Brands: Meted; Sebex http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202517.html

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Salicylic Acid, Sulfur, and Coal Tar •

Topical - U.S. Brands: Sebutone; Vanseb-T http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202518.html

Selenium Sulfide •

Topical - U.S. Brands: Glo-Sel; Selsun http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202520.html

Sulfur •

Topical - U.S. Brands: Finac; Sulpho-Lac http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202543.html

Tacrolimus •

Topical - U.S. Brands: Protopic http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500279.html

Zinc Supplements •

Systemic - U.S. Brands: Orazinc; Verazinc; Zinc 15; Zinc-220; Zinca-Pak; Zincate http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202622.html

Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.

Mosby’s Drug Consult Mosby’s Drug Consult database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/. PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html. Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter,

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Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee.

Researching Orphan Drugs Although the list of orphan drugs is revised on a daily basis, you can quickly research orphan drugs that might be applicable to dermatitis by using the database managed by the National Organization for Rare Disorders, Inc. (NORD), at http://www.rarediseases.org/. Scroll down the page, and on the left toolbar, click on “Orphan Drug Designation Database.” On this page (http://www.rarediseases.org/search/noddsearch.html), type “dermatitis” (or synonyms) into the search box, and click “Submit Query.” When you receive your results, note that not all of the drugs may be relevant, as some may have been withdrawn from orphan status. Write down or print out the name of each drug and the relevant contact information. From there, visit the Pharmacopeia Web site and type the name of each orphan drug into the search box at http://www.nlm.nih.gov/medlineplus/druginformation.html. You may need to contact the sponsor or NORD for further information. NORD conducts “early access programs for investigational new drugs (IND) under the Food and Drug Administration’s (FDA’s) approval ‘Treatment INDs’ programs which allow for a limited number of individuals to receive investigational drugs before FDA marketing approval.” If the orphan product about which you are seeking information is approved for marketing, information on side effects can be found on the product’s label. If the product is not approved, you may need to contact the sponsor. The following is a list of orphan drugs currently listed in the NORD Orphan Drug Designation Database for dermatitis: •

Metronidazole (trade name: Metrogel) http://www.rarediseases.org/nord/search/nodd_full?code=12

•

Sulfadiazine http://www.rarediseases.org/nord/search/nodd_full?code=275

•

Sulfapyridine http://www.rarediseases.org/nord/search/nodd_full?code=899

If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.

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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

•

National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/

•

National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html

•

National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25

•

National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm

•

National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm

•

National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375

•

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

•

National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/

•

National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm

•

National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm

•

National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/

•

National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/

•

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm

•

National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html

•

National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm

•

National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm

•

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

•

National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html

•

National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm

•

Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp

•

National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/

•

National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp

•

Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html

•

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

•

HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html

•

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

•

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/

•

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

•

Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html

•

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/

•

Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html

•

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

•

Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html

•

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

•

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 Combined Health Information Database

A comprehensive source of information on clinical guidelines written for professionals is the Combined Health Information Database. You will need to limit your search to one of the following: Brochure/Pamphlet, Fact Sheet, or Information Package, and “dermatitis” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For the publication date, select “All Years.” Select your preferred language and the format option “Fact Sheet.” Type “dermatitis” (or synonyms) into the “For these words:” box. The following is a sample result: •

GIG: Serving Those with Celiac Sprue and Dermatitis Herpetiformis Since 1974 Source: Seattle, WA: Gluten Intolerance Group. 2001. 2 p. Contact: Available from Gluten Intolerance Group of North America. 15110 10 Avenue SW, Suite A, Seattle, WA 98166. (206) 246-6652. Fax (206) 246-6531. E-mail: [email protected]. Website: www.gluten.net. PRICE: Single copy free. Summary: This brochure describes the activities of the Gluten Intolerance Group (GIG) of North America, a support group for persons with celiac sprue and dermatitis herpetiformis, their families, and health professionals. Celiac sprue, also known as gluten-sensitive enteropathy, non-tropical sprue, and celiac disease, is a digestive disease. Its cause, symptoms, diagnosis, and treatment are described. GIG assists persons with celiac disease through frequent updating of gluten-free diet instruction materials, coordinating outreach programs for newly diagnosed persons with celiac sprue, funding research, increasing awareness of the disease, contacting food and drug companies to assess gluten content of foods, and other programs. Information for setting up local support groups is supplied.

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Research Report on Dermatitis Herpetiformis Source: Seattle, WA: Gluten Intolerance Group of North America. 1993. 17 p. Contact: Available from Gluten Intolerance Group of North America. P.O. Box 23053, Seattle, WA 98102-0353. (206) 325-6980. PRICE: $5; plus shipping and handling. Summary: This document provides an overview of dermatitis herpetiformis (DH), a common complication in people with celiac disease or gluten intolerance. Written in a question-and-answer format, the document discusses the appearance of DH; the body areas most likely to have DH eruptions; variations in severity; relationship between hormone levels and DH eruptions; demographics; diagnosis; other IgA skin disorders that mimic DH; treatment options for DH; medications used and side effects of each, including dapsone, sulphapyridine, and sulphamethoxy-pyridazine; choosing diet versus medication; other substances that can trigger an outbreak of DH, including cleaning products; the use of elemental diets in DH; tests for antibodies as diagnostic

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tools; recent research on diagnosis; advances in drug therapy, including the use of cyclosporin; epidemiological information; and disorders or conditions associated with DH, including thyroid disease, other autoimmune disorders, low gastric acid secretion, lymphoma, and dental enamel defects. One chart lists toll-free telephone numbers for the major manufacturers of cleaning products. 21 references.

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 “dermatitis” (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 60021 578 341 125 2 61067

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 “dermatitis” (or synonyms) at the following Web site: http://text.nlm.nih.gov.

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Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.

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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/.

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Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.

The Genome Project and Dermatitis In the following section, we will discuss databases and references which relate to the Genome Project and dermatitis. 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 “dermatitis” (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 dermatitis: •

Acrodermatitis Enteropathica, Zinc-deficiency Type Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?201100

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Deafness, Neural, with Atypical Atopic Dermatitis Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?221700

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Dermatitis Herpetiformis, Familial Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?601230

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Dermatitis, Atopic Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?603165

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Dermatitis, Atopic, 2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605803

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Dermatitis, Atopic, 3 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605804

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Dermatitis, Atopic, 4 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605805

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Dermatitis, Atopic, 5 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605844

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Dermatitis, Atopic, 6 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605845 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

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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

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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

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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

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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

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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

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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 “dermatitis” (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 “dermatitis” (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 dermatitis 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 dermatitis. 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 dermatitis. 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 “dermatitis”:

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Guides on dermatitis Dermatitis http://www.nlm.nih.gov/medlineplus/dermatitis.html

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Other guides Eczema http://www.nlm.nih.gov/medlineplus/eczema.html Impetigo http://www.nlm.nih.gov/medlineplus/impetigo.html Skin Diseases http://www.nlm.nih.gov/medlineplus/skindiseases.html Toilet Training and Bedwetting http://www.nlm.nih.gov/medlineplus/toilettrainingandbedwetting.html

Within the health topic page dedicated to dermatitis, the following was listed: •

General/Overviews Dermatitis Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=DS00339

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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 Itching for a Little Relief? New Therapies Proving Effective for Millions of Adults and Children with Eczema Source: American Academy of Dermatology http://www.aad.org/PressReleases/itchingRelief.html Poison Ivy: Treatment Options Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=AN00539

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Specific Conditions/Aspects Allergic Skin Conditions Source: American Academy of Allergy, Asthma, and Immunology http://www.aaaai.org/patients/publicedmat/tips/allergicskinconditions.stm Cercarial Dermatitis: Swimmer's Itch Source: National Center for Infectious Diseases, Division of Parasitic Diseases http://www.cdc.gov/ncidod/dpd/parasites/schistosomiasis/factsht_cardmermati tis.htm

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Neurodermatitis Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=AN00298 People Who Should NOT Get the Smallpox Vaccine (Unless They Are Exposed to Smallpox) Source: Centers for Disease Control and Prevention http://www.bt.cdc.gov/agent/smallpox/vaccination/contraindications-public.asp Perioral Dermatitis Source: American Academy of Dermatology http://www.aad.org/pamphlets/Perioral.html Poison Ivy: Prevention and Treatment Source: InteliHealth http://www.intelihealth.com/IH/ihtIH?t=8214&p=%7Ebr%2CIHW%7C%7Est%2C 24479%7C%7Er%2CWSIHW000%7C%7Eb%2C%2A%7C Poisonous Plants: How to Recognize, Avoid and Destroy Them Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=FL00080 Pseudomonas Dermatitis / Folliculitis “Hot Tub Rash” Source: National Center for Infectious Diseases, Division of Parasitic Diseases http://www.cdc.gov/healthyswimming/derm.htm Seborrheic Dermatitis: What It Is and How To Treat It Source: American Academy of Family Physicians http://familydoctor.org/handouts/157.html •

Children Atopic Eczema: Ditch the Itch! Source: American Academy of Dermatology http://www.aad.org/Kids/atopiceczema.html Diaper Rash: Tips on Prevention and Treatment Source: American Academy of Family Physicians http://familydoctor.org/healthfacts/051/index.html Eczema/Atopic Dermatitis Source: Nemours Foundation http://kidshealth.org/parent/infections/skin/eczema_atopic_dermatitis.html Pesky Poisonous Plants Source: American Academy of Dermatology http://www.aad.org/Kids/plants.html

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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/

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Pictures/Diagrams Atlas of the Body: The Skin Source: American Medical Association http://www.medem.com/MedLB/article_detaillb.cfm?article_ID=ZZZQYMPCGJC &sub_cat=98

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Research What's Eating You? New Research Finds Link Between Diet and Contact Dermatitis Source: American Academy of Dermatology http://www.aad.org/PressReleases/eating.html

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Statistics FASTATS: Dermatological Conditions Source: National Center for Health Statistics http://www.cdc.gov/nchs/fastats/skin.htm

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 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 dermatitis. 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: •

Dermatitis Herpetiformis Source: Omaha, NE: Celiac Sprue Association/United States of America, Inc. (CSA/USA). 200x. [4 p.]. Contact: Available from Celiac Sprue Association/United States of America, Inc.(CSA/USA). P.O. Box 31700, Omaha, NE 68131-0700. (402) 558-0600. E-mail: [email protected]. Website: www.csaceliacs.org. PRICE: Single copy free. Summary: Dermatitis herpetiformis (DH) is an important associated disorder or complication of celiac disease, a condition of gluten intolerance in which the small intestinal lining is damaged by a protein fraction of gluten called gliadin. DH is characterized as an intensely itchy skin eruption distinguished by the formation of small papules or vesicles. Although its severity may vary, it persists indefinitely and is a lifelong condition. This brochure describes DH, including the genetics, immune system

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changes in CH, treatment strategies, and associated disorders. The brochure emphasizes that the gluten-free diet has distinct advantages for the patient with DH: it reduces the drug therapy necessary and its associated complications; it provides an improvement in gastrointestinal symptoms; and the gluten free diet is a therapy aimed at the cause rather than the symptoms of the disease. The brochure concludes with the contact information for the Celiac Sprue Association/United States of American, Inc., a national support organization that offers information and referral services. (www.csaceliacs.org). •

Food Allergy and Atopic Dermatitis Source: Fairfax, VA: Food Allergy and Anaphylaxis Network. 2000. 12 p. Contact: Available from Food Allergy and Anaphylaxis Network (FAAN). 10400 Eaton Place, Suite 107, Fairfax, VA 22030-2208. (800) 929-4040. Fax (703) 691-2713. E-mail: [email protected]. Website: www.foodallergy.org. PRICE: $3.00 plus shipping and handling. Summary: It is estimated that up to 10 percent of young children have eczema or atopic dermatitis and one in three children with significant atopic dermatitis have food allergies. This booklet discusses food allergies and atopic dermatitis, defined as a nonscarring allergic skin disease caused by a number of factors; food is one factor. This disease is not contagious. With proper management, it can be controlled, and children can grow to be self confident and enjoy the friendship of others. This booklet offers tips and other sources of information to help parents of the child with food allergy and atopic dermatitis. The booklet covers symptoms, causes, drug therapy, complications, prevention strategies, what happens as the child gets older, and tips for keeping atopic dermatitis under control in the areas of general management, school, baths, laundry, and food allergy. Atopic dermatitis is caused by inflammation of the skin and the skin's inability to retain adequate moisture. Certain substances or factors can cause atopic dermatitis to flare, including irritants such as wool, skin infections, dry skin, low humidity, heat, sweating, or emotional stress; and allergens, such as dust mites, pollens and molds, or foods. Atopic dermatitis cannot be cured, but can be controlled with consistent treatment and avoidance of substances or factors that cause it to flare. Prescription antihistamines can be used to help treat the itching that accompanies this disease, and steroid ointments can help stop the inflammation in the skin. To keep atopic dermatitis under control it is important to avoid or reduce exposure to irritants and allergens, and to moisturize the skin. The booklet stresses that raising a child with atopic dermatitis and food allergies requires extra time, planning, and the help of a doctor that the parent feels comfortable talking with. The booklet concludes with a list of additional sources of information, including the Food Allergy Network, and organizations through which readers can locate a board certified allergist, find allergy free food products, and get information about other allergy products.

•

Handout on Health: Atopic Dermatitis Source: Bethesda, MD: National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 1999. 40 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-68 HH (booklet), or AR-68L HH (large print).

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Summary: This booklet provides people who have atopic dermatitis and their families and caregivers with information on the symptoms, diagnosis, and treatment of this chronic skin disease, which makes the skin extremely itchy and inflamed. Atopic dermatitis most often affects infants and young children, but it can continue into adulthood. It affects males and females equally, and its onset decreases substantially with age. Atopic dermatitis is the most common of the many types of eczema. Although the cause is unknown, the disease seems to result from a combination of genetic and environmental factors. Symptoms vary from person to person, but the most common symptoms are dry, itchy skin; cracks behind the ears; and rashes on the cheeks, arms, and legs. Other common features of atopic dermatitis include lichenification, papules, ichthyosis, keratosis pilaris, hyperlinear palms, urticaria, cheilitis, atopic pleat, and hyperpigmented eyelids. The features of atopic dermatitis depend on whether an infant, a child, or an adult is affected. Diagnosis involves obtaining a thorough medical history and observing symptoms. Skin scratch/prick tests and blood tests for airborne allergens may occasionally help the doctor rule out or confirm a specific allergen that might be important in diagnosis. Many factors can make atopic dermatitis symptoms worse. These factors can be classified as irritants or allergens. Irritants are substances that directly affect the skin, whereas allergens are substances from foods, plants, or animals that inflame the skin. Other factors, including emotional issues, temperature and climate, and skin infections, also have a role in atopic dermatitis. Treatment involves proper skin care, lifestyle changes, and medications and phototherapy. People who have atopic dermatitis can maintain a high quality of life despite their symptoms. Research supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases and other components of the National Institutes of Health focuses on genetics, biochemical abnormalities, faulty regulation of immunoglobulin E, immune system imbalance, and treatment. The booklet also lists additional resources. •

Eczema/Atopic Dermatitis Source: American Academy of Dermatology. 2001. 8 p. Contact: Available from American Academy of Dermatology. 930 N. Beacham Rd., P.O. Box 4014, Schaumberg, IL 60168-4014. (888) 462-DERM ext. 22. Website: www.aad.org. PRICE: Single copies free; bulk prices available. Summary: This brochure describes atopic dermatitis (AD), a common, chronic condition of the skin that is characterized by redness, itching, oozing, and crusting. It may be hereditary and can occur at any age. In infancy it is usually referred to as infantile eczema and is characterized by an itchy, oozing, or crusting rash usually on the face and scalp. Most babies improve by the age of 2. In older children with AD, the skin is still itchy but patches are dry and darker in color. The patches usually occur on the hands and feet in teens and young adults. Sometimes AD is associated with food allergies. Creams, ointments, lotions, and tars are used to treat AD. Antihistamines can help with the itching. Ultraviolet light may be recommended in severe cases of AD. Topical immunomodulators are a new class of drugs that may be helpful in treating moderate to severe AD. 3 figures.

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Gluten Intolerance Group of North America: Serving Those with Celiac Sprue and Dermatitis Herpetiformis Source: Seattle, WA: Gluten Intolerance Group of North America. 199x. 2 p. Contact: Available from Gluten Intolerance Group of North America. P.O. Box 23053, Seattle, WA 98102-0353. (206) 325-6980. PRICE: Single copy free.

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Summary: This brochure describes gluten sensitive enteropathy (GSE), a group of hereditary immune system disorders that includes celiac sprue (CS), dermatitis herpetiformis (DH), and transient gluten intolerance. In these disorders, protein fractions in wheat, rye, oats, and barley set off a chain of events that leads to tissue damage. The brochure describes the symptoms of these disorders, diagnosis, and treatment options, which primarily involve the institution of a gluten-free diet (avoiding wheat, rye, oats, and barley). The author emphasizes that proper substitutions can make the diets of persons with GSE varied and appealing. Combinations of rice, corn, soy, and potato flours are used to make cookies, pasta, cakes, and breads. The brochure lists immune system disorders associated with celiac sprue and DH, including type 1 diabetes, systemic lupus erythematosus, Sjogren's syndrome, scleroderma, autoimmune chronic active hepatitis, Graves' disease, Addisons' disease, and myasthenia gravis. The brochure also describes the Gluten Intolerance Group of North America, an organization that offers assistance to persons with celiac sprue or dermatitis herpetiformis through publications, outreach programs, local chapter support, advocacy, funding of research, and increasing awareness of these diseases. The brochure lists some of the publications and videotapes available from the organization. (AA-M). •

Atopic Dermatitis in Children Source: San Rafael, CA: National Eczema Association for Science and Education. 2003. 8 p. Contact: Available from National Eczema Association for Science and Education. 4460 Redwood Highway, Suite 16-Box D, San Rafael, CA 94903-1953. (415) 499-3474. Fax: (415) 472-5345. Website: www.nationaleczema.org. Email: [email protected]. PRICE: Single copy free. Summary: This brochure provides information to parents of children with atopic dermatitis (AD). AD, or eczema, is caused by too many reactive inflammatory cells in the skin and is triggered by dry skin, irritants, stress, heat and sweating, infections, and allergens. Diagnosis of AD is based on age of onset, presence of itching, location and appearance of the rash, and heredity. AD is often associated with asthma and hay fever. It is difficult to predict if a child will outgrow AD. Strategies for negating trigger factors including keeping the skin cool, avoiding stress, systematically eliminating foods if a food allergy is suspected, and learning to recognize signs of infection so they can be treated early. Medicines used to treat AD include moisturizers, corticosteroids, antibiotics, antihistamines, topical immunomodulators, and tar preparations.

•

Poison Ivy Dermatitis Source: American Osteopathic College of Dermatology. 2001. 2 p. Contact: Available from American Osteopathic College of Dermatology. (800) 449-2623. Fax: (660) 627-2623. Website: www.aocd.org/skin. Email: [email protected]. Summary: This fact sheet discusses poison ivy prevention and treatment. Poison ivy is an allergic reaction to urushiol, the oily coating of the poison ivy plant. Direct contact to the plant is not necessary; contact with objects or items that have been exposed to the rushiol can also cause poison ivy rash. Poison ivy can be contracted through contaminated clothing or by petting exposed animals. This rash can be prevented by applying Ivy Block lotion and if exposed, washing with Tecnu liquid. Jewelweed plant can be rubbed on exposed skin as the tannins in this plant bind with the urushiol, preventing the rash. The rash appears as quickly as a few hours or as long as 10 days after exposure but is not contagious. Mild rashes can clear up without treatment. For

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severe reactions oral cortisone medications are effective and safe to take if the duration is no longer than two to three weeks. Blisters and itching can be improved with moist compresses or applications of Burows solution. •

Seborrheic Dermatitis: What It Is and How to Treat It Source: American Academy of Family Physicians. March 2002. 2 p. Contact: Available from American Academy of Family Physicians. Website: www.familydoctor.org. Summary: This fact sheet discusses the treatment of seborrheic dermatitis, a condition causing flaking of the skin. This condition generally occurs on the scalp and is known as dandruff in adults and cradle cap when it affects babies. Shampoos that contain salicylic acid, selenium sulfide, or pyrithione zinc are used to treat seborrheic dermatitis of the scalp in adults and adolescents. Steroid lotions are used to treat the skin of adolescents and adults with this condition. For babies, a soft brush can be used to help loosen scalp flakes. In addition, a mild shampoo may be helpful. If these methods do not work, the doctor may prescribe a tar shampoo. Gentle steroid lotions are use to treat this condition in the skin creases of babies.

•

Dermatitis, Herpetiformis Source: in Griffith, H.W. Instructions for Patients. 5th ed. Philadelphia, PA: W.B. Saunders Company. 1994. p. 116. Contact: Available from W.B. Saunders Company. Book Order Fulfillment, 6277 Sea Harbor Drive, Orlando, FL 32887-4430. (800) 545-2522. Fax (800) 874-6418. PRICE: $49.95. ISBN: 0721649300 (English); 0721669972 (Spanish). Summary: This fact sheet provides basic information on frequent signs and symptoms, causes, risk factors, preventive measures, etc.; treatment, medication, and diet; and when to contact one's health care provider. The fact sheet is designed to be photocopied and distributed to patients as a reinforcement of oral instructions and as a teaching tool. The book in which the fact sheet appears is available in English or Spanish.

•

Diaper Dermatitis Source: Kirksville, MO: American Osteopathic College of Dermatology (AOCD). 2001. 2 p. Contact: Available online from American Osteopathic College of Dermatology. 1501 East Illinois Street, P.O. Box 7525, Kirksville, MO 63501. (800) 449-2623 or (660) 665-2184. Fax (660) 627-2623. E-mail: [email protected]. Website: www.aocd.org/skin/dermatologic_diseases/ index.html. Summary: This fact sheet provides parents of children who have diaper dermatitis or diaper rash with information on this irritation of the skin covering the groin, lower stomach, upper thighs, and buttocks. Although the condition is most commonly seen in infants and in children younger than 2 years of age, people who are incontinent or paralyzed may develop it. Diaper dermatitis begins when prolonged contact with urine and feces irritates the skin, leading to redness and inflammation. Once this occurs, bacteria and yeast grow on the raw areas, making the diaper rash worse. The best treatment is to prevent diaper dermatitis by using absorbent disposable diapers, which do not allow urine to come in contact with the skin. Reusable cloth diapers must be changed each time after they become wet or every 1 to 2 hours. Powder is not needed to

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keep the skin dry or to prevent diaper rash. Desitin applied at bedtime is often helpful. Other ointments that can be used include triple paste, as well as Lotrimin AF or Micatin creams. 1 figure. •

Allergic Contact Dermatitis Source: Kirksville, MO: American Osteopathic College of Dermatology (AOCD). 2001. 3 p. Contact: Available online from American Osteopathic College of Dermatology. 1501 East Illinois Street, P.O. Box 7525, Kirksville, MO 63501. (800) 449-2623 or (660) 665-2184. Fax (660) 627-2623. E-mail: [email protected]. Website: www.aocd.org/skin/dermatologic_diseases/ index.html. Summary: This fact sheet provides people who have allergic contact dermatitis with information on the substances that cause this skin condition. Skin manifestations include redness, swelling, and formation of water blisters. Common allergens include nickel found in earrings and clothing accessories; rubber products such as gloves; paraphenylenedeamine found in permanent hair dyes; chromates found in cement, leather, some matches, paints, and antirust compounds; and poison ivy, poison oak, and poison sumac. A dermatologist can work with a patient to identify the allergen. In addition, a dermatologist can perform a patch test to diagnose contact allergies. People with allergic contact dermatitis should avoid the allergen that causes the reaction and materials that cross react with it, as well as substitute products made of materials that do not cause reactions. 2 figures.

•

Eczema--Atopic Dermatitis Source: Kirksville, MO: American Osteopathic College of Dermatology (AOCD). 2001. 4 p. Contact: Available online from American Osteopathic College of Dermatology. 1501 East Illinois Street, P.O. Box 7525, Kirksville, MO 63501. (800) 449-2623 or (660) 665-2184. Fax (660) 627-2623. E-mail: [email protected]. Website: www.aocd.org/skin/dermatologic_diseases/ index.html. Summary: This fact sheet provides people with atopic dermatitis, or eczema, with information on this chronic skin condition, which causes red, itchy skin. In people who have this condition, the skin fails to hold moisture, becomes dry, then inflamed, itchy, and often infected. The most common factors causing this condition are allergies leading to an overactive immune system and hereditary dry skin (ichthyosis vulgaris). Treatment involves hydrating the skin by soaking the affected area in lukewarm water for 15 to 20 minutes, blotting or patting the skin dry, and applying a moisturizing cream. Other therapies for eczema include tars and extracts of crude coal tar, topical steroids such as hydrocortisone ointment or cream, ultraviolet light therapy, antibiotics, antipruritics such as antihistamines, zafirlukast, montelukast, cyclosporine, and tacrolimus. Hospitalization may be suggested for acute flares. 3 figures.

•

Patient Education: A Dozen Ways To Treat Atopic Dermatitis Source: Nurse Practitioner. 25(4): 74. April 2000. Summary: This journal article provides people who have atopic dermatitis with suggestions on treating this skin condition. Tips include taking a daily 15 to 20 minute bath, patting away excess water and applying moisturizer or a prescribed skin medication, using only gentle skin cleansers, using sunscreen to avoid sunburn, and

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reapplying moisturizer throughout the day. Other suggestions include washing new clothing before wearing it to remove irritating chemicals; wearing clothing that allows air to pass freely to the skin; working and sleeping in comfortable surroundings; keeping fingernails short, smooth, and clean; considering the use of antihistamines to reduce the urge to itch; and rinsing the skin off and applying a moisturizer after swimming or using a hot tub. •

Seborrheic Dermatitis Source: Schaumburg, IL: American Academy of Dermatology. 1995. 6 p. Contact: American Academy of Dermatology, 930 North Meacham Road, P.O. Box 4014, Schaumburg, IL 60168-4014. Summary: This pamphlet for the general public uses a question-and-answer format to discuss seborrheic dermatitis, which is a common inflammation of areas of the skin having the greatest number of sebaceous glands. The pamphlet explains the differences between dandruff, seborrhea, and seborrheic dermatitis, and it identifies the individuals who are most susceptible to seborrheic dermatitis and the other diseases associated with this condition. In addition, the pamphlet discusses whether seborrheic dermatitis can be prevented, whether laboratory tests are useful in diagnosing this condition, and how this condition is treated. 3 photographs.

•

Perioral Dermatitis Source: Schaumburg, IL: American Academy of Dermatology (AAD). 2000. 4 p. Contact: Available from American Academy of Dermatology, Marketing Department. P.O. Box 2289, Carol Stream, IL 60132-2289. (847) 240-1280. Fax (847) 240-1859. E-mail: [email protected]. Website: www.aad.org. PRICE: Single copy free; bulk prices available. Summary: This pamphlet uses a question and answer format to provide people who have perioral dermatitis with information on the etiology, diagnosis, treatment, and prevention of this common skin problem that affects the area around the mouth. Although the problem mostly affects young women, occasionally men or children are affected. Features of this condition include redness of the skin around the mouth, small red bumps or pus bumps, and mild peeling. Although the cause of perioral dermatitis is unknown, some dermatologists believe it is a form of rosacea or seborrheic dermatitis worsened by sunlight. Use of strong corticosteroid creams can cause the condition, as can the use of some types of makeup, moisturizers, and dental products. Diagnosis is usually based on an examination of the skin. The most common treatment is an oral antibiotic such as tetracycline. Topical antibiotic creams may be used for milder cases or for pregnant women. Most patients improve after using oral antibiotics for 2 months, but stopping treatment too soon can cause a recurrence. There is no definitive way to prevent the condition. 2 figures.

•

Living With Eczema: Seborrheic Dermatitis Source: Portland, OR: National Eczema Association for Science and Education (NEASE). 1999. 8 p. Contact: Available from National Eczema Association for Science and Education (NEASE). 1220 SW Morrison, Suite 433, Portland, OR 97205. (800) 818-7546 or (503) 2284430. Fax (503) 224-3363. E-mail: [email protected]. Website: www.eczema-assn.org. PRICE: $25.00 per 100, plus shipping and handling; contact for other quantities.

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Summary: This patient education pamphlet, one of a series of educational pamphlets developed by the National Eczema Association for Science and Education (NEASE), uses a question and answer format to provide people who have seborrheic dermatitis (SD) and their families with information on the etiology, symptoms, and treatment of this common skin disorder. This noncontagious condition, which causes flaking and redness of the skin, usually occurs when there is inflammation in areas of the skin where sebaceous glands are concentrated. Although the exact cause of SD is unknown, a yeast called Pityrosporum ovale may be a factor in its development. SD that occurs in infants is known as cradle cap. This condition is very common and usually responds well to simple treatment or clears up with no treatment within a few months after birth. In adults, SD is more common among the elderly, people who are immunocompromised, or people who have chronic neurological conditions. In addition, people who have had a traumatic medical crisis can also develop SD. There are differences between SD and other skin conditions such as dandruff, psoriasis, and eczema. Although SD cannot be prevented or cured, it can be treated and controlled. Treatment varies depending on the affected areas and the severity of the condition. Mild cases can be treated with medicated shampoos and nonprescription hydrocortisone cream. In more severe cases, prescription medications such as topical steroids may be needed. •

Atopic Dermatitis Source: American Family Physician. 66(10): 1906. November 15, 2002. Summary: This patient education sheet discusses atopic dermatitis, a chronic skin condition characterized by an itchy rash. To keep this rash from getting worse, patients should keep their skin moist by using mild soaps and lukewarm water when bathing, keeping baths and showers short, and using moisturizing lotions after bathing. Patients should be aware that certain foods may make atopic dermatitis worse. Cortisone creams and ointments may be prescribed for the rash. If the rash is very bad or on the face, tacrolimus or pimecrolinus ointments may be prescribed. Antihistamines can help control itching. 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 “dermatitis” (or synonyms). The following was recently posted: •

Seborrhoeic dermatitis Source: Finnish Medical Society Duodecim - Professional Association; 2001 April 21; Various pagings http://www.guideline.gov/summary/summary.aspx?doc_id=3392&nbr=2618&a mp;string=dermatitis 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

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located at http://www.healthfinder.gov. Again, keyword searches can be used to find guidelines. The following was recently found in this database: •

Atopic Dermatitis Summary: Information about atopic dermatitis (or eczema) -- a chronic disease that causes extremely itchy, inflamed skin. Symptoms and treatments are discussed. Source: Federal Citizen Information Center, U.S. General Services Administration http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=5978

•

Dermatitis Herpetiformis Summary: An online definition of this disorder, a known complication of celiac disease that is characterized as an itchy skin eruption distinguished by the formation of small papules or vesicles. Source: Celiac Sprue Association/United States of America, Inc. http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=2571

•

Handout on Health: Atopic Dermatitis Summary: This booklet is for people who have atopic dermatitis (often called “eczema”), parents and caregivers of children with atopic dermatitis, and others interested in learning more about the disease. Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6706

•

Self-Care Flow Charts: Skin Rashes and Other Changes Summary: An online chart of self-care suggestions for common skin rashes and skin changes. These include contact dermatitis, seborrhea, cradle cap, hives, insect bites, and cellulitis. Source: American Academy of Family Physicians http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=4800 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 dermatitis. 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.

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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

•

Family Village: http://www.familyvillage.wisc.edu/specific.htm

•

Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/

•

Med Help International: http://www.medhelp.org/HealthTopics/A.html

•

Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/

•

Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/

•

WebMDHealth: http://my.webmd.com/health_topics

Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to dermatitis. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with dermatitis. 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 dermatitis. 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 “dermatitis” (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

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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 “dermatitis”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop 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 “dermatitis” (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 “dermatitis” (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/

•

Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)

•

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)

•

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/

•

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.

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•

Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml

•

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

•

Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/

•

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

•

Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/

•

Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm

•

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/

•

Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/

•

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

•

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/

•

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

•

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/

•

Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html

•

Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm

•

Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp

•

Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/

•

Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html

•

Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/

•

Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm

•

Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/

•

Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html

•

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

•

Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)

•

National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html

•

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/

•

National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/

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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/

•

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/

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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

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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/

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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

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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

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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).

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

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MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html

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Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/

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Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine

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DERMATITIS DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 1-phosphate: A drug that halts cell suicide in human white blood cells. [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] Abrasion: 1. The wearing away of a substance or structure (such as the skin or the teeth) through some unusual or abnormal mechanical process. 2. An area of body surface denuded of skin or mucous membrane by some unusual or abnormal mechanical 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] 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] 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] Acetylcholinesterase: An enzyme that catalyzes the hydrolysis of acetylcholine to choline and acetate. In the CNS, this enzyme plays a role in the function of peripheral neuromuscular junctions. EC 3.1.1.7. [NIH] Acne: A disorder of the skin marked by inflammation of oil glands and hair glands. [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] Acrylamide: A colorless, odorless, highly water soluble vinyl monomer formed from the hydration of acrylonitrile. It is primarily used in research laboratories for electrophoresis, chromatography, and electron microscopy and in the sewage and wastewater treatment industries. [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] Action Potentials: The electric response of a nerve or muscle to its stimulation. [NIH] Acyl: Chemical signal used by bacteria to communicate. [NIH]

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Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adenine: A purine base and a fundamental unit of adenine nucleotides. [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 Monophosphate: Adenylic acid. Adenine nucleotide containing one phosphate group esterified to the sugar moiety in the 2'-, 3'-, or 5'-position. [NIH] Adhesives: Substances that cause the adherence of two surfaces. They include glues (properly collagen-derived adhesives), mucilages, sticky pastes, gums, resins, or latex. [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] Adoptive Transfer: Form of passive immunization where previously sensitized immunologic agents (cells or serum) are transferred to non-immune recipients. When transfer of cells is used as a therapy for the treatment of neoplasms, it is called adoptive immunotherapy (immunotherapy, adoptive). [NIH] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Adrenal Glands: Paired glands situated in the retroperitoneal tissues at the superior pole of each kidney. [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]

Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] 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] 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

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emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]

Age of Onset: The age or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual. [NIH] Ageing: A physiological or morphological change in the life of an organism or its parts, generally irreversible and typically associated with a decline in growth and reproductive vigor. [NIH] Aggravation: An increasing in seriousness or severity; an act or circumstance that intensifies, or makes worse. [EU] 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] Air Pollutants: Substances which pollute the air. [NIH] Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] Akathisia: 1. A condition of motor restlessness in which there is a feeling of muscular quivering, an urge to move about constantly, and an inability to sit still, a common extrapyramidal side effect of neuroleptic drugs. 2. An inability to sit down because of intense anxiety at the thought of doing so. [EU] 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] 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] Allergy and Immunology: A medical specialty concerned with the hypersensitivity of the individual to foreign substances and protection from the resultant infection or disorder. [NIH]

Allo: A female hormone. [NIH]

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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] Allografts: A graft of tissue obtained from the body of another animal of the same species but with genotype differing from that of the recipient; tissue graft from a donor of one genotype to a host of another genotype with host and donor being members of the same species. [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] Aloe: A genus of the family Liliaceae containing anthraquinone glycosides such as aloinemodin or aloe-emodin (emodin). [NIH] Alopecia: Absence of hair from areas where it is normally present. [NIH] Alpha 1-Antichymotrypsin: Glycoprotein found in alpha(1)-globulin region in human serum. It inhibits chymotrypsin-like proteinases in vivo and has cytotoxic killer-cell activity in vitro. The protein also has a role as an acute-phase protein and is active in the control of immunologic and inflammatory processes, and as a tumor marker. It is a member of the serpin superfamily. [NIH] Alpha 1-Antitrypsin: Plasma glycoprotein member of the serpin superfamily which inhibits trypsin, neutrophil elastase, and other proteolytic enzymes. Commonly referred to as alpha 1-proteinase inhibitor (A1PI), it exists in over 30 different biochemical variant forms known collectively as the PI (protease inhibitor) system. Hereditary A1PI deficiency is associated with pulmonary emphysema. [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-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] 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] 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 Motifs: Commonly observed structural components of proteins formed by simple combinations of adjacent secondary structures. A commonly observed structure may be composed of a conserved sequence which can be represented by a consensus sequence. [NIH]

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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] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Aminophylline: A drug combination that contains theophylline and ethylenediamine. It is more soluble in water than theophylline but has similar pharmacologic actions. It's most common use is in bronchial asthma, but it has been investigated for several other applications. [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] Amnestic: Nominal aphasia; a difficulty in finding the right name for an object. [NIH] Amplification: The production of additional copies of a chromosomal DNA sequence, found as either intrachromosomal or extrachromosomal DNA. [NIH] Amyloidosis: A group of diseases in which protein is deposited in specific organs (localized amyloidosis) or throughout the body (systemic amyloidosis). Amyloidosis may be either primary (with no known cause) or secondary (caused by another disease, including some types of cancer). Generally, primary amyloidosis affects the nerves, skin, tongue, joints, heart, and liver; secondary amyloidosis often affects the spleen, kidneys, liver, and adrenal glands. [NIH] 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] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] Analytes: A component of a test sample the presence of which has to be demonstrated. The term "analyte" includes where appropriate formed from the analyte during the analyses. [NIH]

Anaphylactic: Pertaining to anaphylaxis. [EU] 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] Anaphylaxis: An acute hypersensitivity reaction due to exposure to a previously encountered antigen. The reaction may include rapidly progressing urticaria, respiratory distress, vascular collapse, systemic shock, and death. [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

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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] 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] Aneurysm: A sac formed by the dilatation of the wall of an artery, a vein, or the heart. [NIH] Angina: Chest pain that originates in the heart. [NIH] Angina Pectoris: The symptom of paroxysmal pain consequent to myocardial ischemia usually of distinctive character, location and radiation, and provoked by a transient stressful situation during which the oxygen requirements of the myocardium exceed the capacity of the coronary circulation to supply it. [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] Angioplasty: Endovascular reconstruction of an artery, which may include the removal of atheromatous plaque and/or the endothelial lining as well as simple dilatation. These are procedures performed by catheterization. When reconstruction of an artery is performed surgically, it is called endarterectomy. [NIH] Angiotensinogen: An alpha-globulin of which a fragment of 14 amino acids is converted by renin to angiotensin I, the inactive precursor of angiotensin II. It is a member of the serpin superfamily. [NIH] 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] Animal Welfare: The protection of animals in laboratories or other specific environments and the promotion of their health through better nutrition, housing, and care. This may be carried out through legislation or regulation. [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] Anogenital: Pertaining to the anus and external genitals. [EU] 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] Antecedent: Existing or occurring before in time or order often with consequential effects. [EU]

Anthropogenic: Of human origin or influence. [NIH] Antiallergic: Counteracting allergy or allergic conditions. [EU] Antibacterial: A substance that destroys bacteria or suppresses their growth or

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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] Anticholinergic: An agent that blocks the parasympathetic nerves. Called also parasympatholytic. [EU] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Antidepressant: A drug used to treat depression. [NIH] Antiemetic: An agent that prevents or alleviates nausea and vomiting. Also antinauseant. [EU]

Antifungal: Destructive to fungi, or suppressing their reproduction or growth; effective against fungal infections. [EU] Antifungal Agents: Substances that destroy fungi by suppressing their ability to grow or reproduce. They differ from fungicides, industrial because they defend against fungi present in human or animal tissues. [NIH] 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-Infective Agents: Substances that prevent infectious agents or organisms from spreading or kill infectious agents in order to prevent the spread of infection. [NIH] 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]

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Antineoplastic Agents: Substances that inhibit or prevent the proliferation of neoplasms. [NIH]

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] Antiplasmin: A member of the serpin superfamily found in human plasma that inhibits the lysis of fibrin clots which are induced by plasminogen activator. It is a glycoprotein, molecular weight approximately 70,000 that migrates in the alpha 2 region in immunoelectrophoresis. It is the principal plasmin inactivator in blood, rapidly forming a very stable complex with plasmin. [NIH] Antipruritic: Relieving or preventing itching. [EU] Antipsychotic: Effective in the treatment of psychosis. Antipsychotic drugs (called also neuroleptic drugs and major tranquilizers) are a chemically diverse (including phenothiazines, thioxanthenes, butyrophenones, dibenzoxazepines, dibenzodiazepines, and diphenylbutylpiperidines) but pharmacologically similar class of drugs used to treat schizophrenic, paranoid, schizoaffective, and other psychotic disorders; acute delirium and dementia, and manic episodes (during induction of lithium therapy); to control the movement disorders associated with Huntington's chorea, Gilles de la Tourette's syndrome, and ballismus; and to treat intractable hiccups and severe nausea and vomiting. Antipsychotic agents bind to dopamine, histamine, muscarinic cholinergic, a-adrenergic, and serotonin receptors. Blockade of dopaminergic transmission in various areas is thought to be responsible for their major effects : antipsychotic action by blockade in the mesolimbic and mesocortical areas; extrapyramidal side effects (dystonia, akathisia, parkinsonism, and tardive dyskinesia) by blockade in the basal ganglia; and antiemetic effects by blockade in the chemoreceptor trigger zone of the medulla. Sedation and autonomic side effects (orthostatic hypotension, blurred vision, dry mouth, nasal congestion and constipation) are caused by blockade of histamine, cholinergic, and adrenergic receptors. [EU] Antipyretic: An agent that relieves or reduces fever. Called also antifebrile, antithermic and febrifuge. [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] Antiviral: Destroying viruses or suppressing their replication. [EU] Anus: The opening of the rectum to the outside of the body. [NIH] Anxiety: Persistent feeling of dread, apprehension, and impending disaster. [NIH] Anxiety Disorders: Disorders in which anxiety (persistent feelings of apprehension, tension, or uneasiness) is the predominant disturbance. [NIH] Aphakia: Absence of crystalline lens totally or partially from field of vision, from any cause except after cataract extraction. Aphakia is mainly congenital or as result of lens dislocation and subluxation. [NIH] Apocrine Glands: Large, branched, specialized sweat glands that empty into the upper portion of a hair follicle instead of directly onto the skin. [NIH] 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

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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] Aqueous: Having to do with water. [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] Arcuate Nucleus: A nucleus located in the middle hypothalamus in the most ventral part of the third ventricle near the entrance of the infundibular recess. Its small cells are in close contact with the ependyma. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] 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] Arthritis, Rheumatoid: A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated. [NIH] Arthrosis: A disease of a joint. [EU] 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] Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant. [NIH] Aseptic: Free from infection or septic material; sterile. [EU]

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Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Astringent: Causing contraction, usually locally after topical application. [EU] 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] Attenuated: Strain with weakened or reduced virulence. [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] Autologous bone marrow transplantation: A procedure in which bone marrow is removed from a person, stored, and then given back to the person after intensive treatment. [NIH] Autolysis: The spontaneous disintegration of tissues or cells by the action of their own autogenous enzymes. [NIH]

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Autonomic: Self-controlling; functionally independent. [EU] Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body. [NIH] Bacillus: A genus of Bacillaceae that are spore-forming, rod-shaped cells. Most species are saprophytic soil forms with only a few species being pathogenic. [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 Infections: Infections by bacteria, general or unspecified. [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] Bactericide: An agent that destroys bacteria. [EU] 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] 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] 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] Basophil: A type of white blood cell. Basophils are granulocytes. [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] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]

Benzaldehyde: A colorless oily liquid used as a flavoring agent and to make dyes, perfumes,

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and pharmaceuticals. Benzaldehyde is chemically related to benzene. [NIH] Benzoin: A white crystalline compound prepared by condensation of benzaldehyde in potassium cyanide and used in organic syntheses. [NIH] Benzoyl Peroxide: A peroxide derivative that has been used topically for burns and as a dermatologic agent in the treatment of acne and poison ivy. It is used also as a bleach in the food industry. [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. 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] 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] 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] Biological Transport: The movement of materials (including biochemical substances and drugs) across cell membranes and epithelial layers, usually by passive diffusion. [NIH] Biomarkers: Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Biosynthesis: The building up of a chemical compound in the physiologic processes of a living organism. [EU] 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]

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Bioterrorism: The use of biological agents in terrorism. This includes the malevolent use of bacteria, viruses, or toxins against people, animals, or plants. [NIH] Biotin: Hexahydro-2-oxo-1H-thieno(3,4-d)imidazole-4-pentanoic acid. Growth factor present in minute amounts in every living cell. It occurs mainly bound to proteins or polypeptides and is abundant in liver, kidney, pancreas, yeast, and milk.The biotin content of cancerous tissue is higher than that of normal tissue. [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] Bipolar Disorder: A major affective disorder marked by severe mood swings (manic or major depressive episodes) and a tendency to remission and recurrence. [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] Bleeding Time: Duration of blood flow after skin puncture. This test is used as a measure of capillary and platelet function. [NIH] Blister: Visible accumulations of fluid within or beneath the epidermis. [NIH] Bloating: Fullness or swelling in the abdomen that often occurs after meals. [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 vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blood-Brain Barrier: Specialized non-fenestrated tightly-joined endothelial cells (tight junctions) that form a transport barrier for certain substances between the cerebral capillaries and the brain tissue. [NIH] Body Burden: The total amount of a chemical, metal or radioactive substance present at any time after absorption in the body of man or animal. [NIH] Body Constitution: The physical characteristics of the body, including the mode of performance of functions, the activity of metabolic processes, the manner and degree of reactions to stimuli, and power of resistance to the attack of pathogenic organisms. [NIH] Body Fluids: Liquid components of living organisms. [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

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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 Transplantation: The transference of bone marrow from one human or animal to another. [NIH] Botulinum Toxins: Toxins produced by Clostridium botulinum. There are at least seven different substances, most being proteins. They have neuro-, entero-, and hemotoxic properties, are immunogenic, and include the most potent poisons known. The most commonly used apparently blocks release of acetylcholine at cholinergic synapses. [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] 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 Injuries: Acute and chronic injuries to the brain, including the cerebral hemispheres, cerebellum, and brain stem. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with diffuse axonal injury or coma, posttraumatic. Localized injuries may be associated with neurobehavioral manifestations; hemiparesis, or other focal neurologic deficits. [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] Breast Feeding: The nursing of an infant at the mother's breast. [NIH] Breeding: The science or art of changing the constitution of a population of plants or animals through sexual reproduction. [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] Bronchial Spasm: Spasmodic contraction of the smooth muscle of the bronchi. [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] Bronchodilator: A drug that relaxes the smooth muscles in the constricted airway. [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] Bulimia: Episodic binge eating. The episodes may be associated with the fear of not being

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able to stop eating, depressed mood, or self-deprecating thoughts (binge-eating disorder) and may frequently be terminated by self-induced vomiting (bulimia nervosa). [NIH] Bullous: Pertaining to or characterized by bullae. [EU] 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] Cachexia: General ill health, malnutrition, and weight loss, usually associated with chronic disease. [NIH] Cadmium: An element with atomic symbol Cd, atomic number 48, and atomic weight 114. It is a metal and ingestion will lead to cadmium poisoning. [NIH] Cadmium Poisoning: Poisoning occurring after exposure to cadmium compounds or fumes. It may cause gastrointestinal syndromes, anemia, or pneumonitis. [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] 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 Dobesilate: A drug used to reduce hemorrhage in diabetic retinopathy. [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] Capecitabine: An anticancer drug that belongs to the family of drugs called antimetabolites. [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] Capillary Permeability: Property of blood capillary walls that allows for the selective exchange of substances. Small lipid-soluble molecules such as carbon dioxide and oxygen move freely by diffusion. Water and water-soluble molecules cannot pass through the endothelial walls and are dependent on microscopic pores. These pores show narrow areas (tight junctions) which may limit large molecule movement. [NIH] Capsaicin: Cytotoxic alkaloid from various species of Capsicum (pepper, paprika), of the

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Solanaceae. [NIH] Captopril: A potent and specific inhibitor of peptidyl-dipeptidase A. It blocks the conversion of angiotensin I to angiotensin II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the renin-angiotensin system and inhibits pressure responses to exogenous angiotensin. [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] Carcinogenesis: The process by which normal cells are transformed into cancer cells. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinogens: Substances that increase the risk of neoplasms in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included. [NIH] 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] Cardiotoxicity: Toxicity that affects the heart. [NIH] Cardiovascular: Having to do with the heart and blood vessels. [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] Carnitine: Constituent of striated muscle and liver. It is used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias. [NIH] Carotene: The general name for a group of pigments found in green, yellow, and leafy 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] Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes. [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] Caspase: Enzyme released by the cell at a crucial stage in apoptosis in order to shred all cellular proteins. [NIH] Caspase 1: A member of the caspase family that is highly specific for interleukin-1beta (interleukin-1). It plays a role in inflammation and mammalian apoptosis. Interleukin-1beta converting enzyme is frequently abbreviated ICE. EC 3.4.22.36 [NIH] Catalyse: To speed up a chemical reaction. [EU] Cataract: An opacity, partial or complete, of one or both eyes, on or in the lens or capsule, especially an opacity impairing vision or causing blindness. The many kinds of cataract are classified by their morphology (size, shape, location) or etiology (cause and time of

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occurrence). [EU] Catecholamine: A group of chemical substances manufactured by the adrenal medulla and secreted during physiological stress. [NIH] Catheterization: Use or insertion of a tubular device into a duct, blood vessel, hollow organ, or body cavity for injecting or withdrawing fluids for diagnostic or therapeutic purposes. It differs from intubation in that the tube here is used to restore or maintain patency in obstructions. [NIH] Cations: Postively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis. [NIH] Caudal: Denoting a position more toward the cauda, or tail, than some specified point of reference; same as inferior, in human anatomy. [EU] 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] 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 Adhesion Molecules: Surface ligands, usually glycoproteins, that mediate cell-to-cell adhesion. Their functions include the assembly and interconnection of various vertebrate systems, as well as maintenance of tissue integration, wound healing, morphogenic movements, cellular migrations, and metastasis. [NIH] Cell Cycle: The complex series of phenomena, occurring between the end of one cell division and the end of the next, by which cellular material is divided between daughter cells. [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 Degranulation: The process of losing secretory granules (secretory vesicles). This occurs, for example, in mast cells, basophils, neutrophils, eosinophils, and platelets when secretory products are released from the granules by exocytosis. [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 proliferation: An increase in the number of cells as a result of cell growth and cell division. [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

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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] Cellulitis: An acute, diffuse, and suppurative inflammation of loose connective tissue, particularly the deep subcutaneous tissues, and sometimes muscle, which is most commonly seen as a result of infection of a wound, ulcer, or other skin lesions. [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] Ceramide: A type of fat produced in the body. It may cause some types of cells to die, and is being studied in cancer treatment. [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 hemispheres: The two halves of the cerebrum, the part of the brain that controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. The right hemisphere controls muscle movement on the left side of the body, and the left hemisphere controls muscle movement on the right side of the body. [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] Cetirizine: A potent second-generation histamine H1 antagonist that is effective in the treatment of allergic rhinitis, chronic urticaria, and pollen-induced asthma. Unlike many traditional antihistamines, it does not cause drowsiness or anticholinergic side effects. [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] Cheilitis: Inflammation of the lips. It is of various etiologies and degrees of pathology. [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] Chemoprotective: A quality of some drugs used in cancer treatment. Chemoprotective

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agents protect healthy tissue from the toxic effects of anticancer drugs. [NIH] Chemoreceptor: A receptor adapted for excitation by chemical substances, e.g., olfactory and gustatory receptors, or a sense organ, as the carotid body or the aortic (supracardial) bodies, which is sensitive to chemical changes in the blood stream, especially reduced oxygen content, and reflexly increases both respiration and blood pressure. [EU] 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] Chemotherapy: Treatment with anticancer drugs. [NIH] Chimeras: Organism that contains a mixture of genetically different cells. [NIH] Chlorides: Inorganic compounds derived from hydrochloric acid that contain the Cl- ion. [NIH]

Chlorophyll: Porphyrin derivatives containing magnesium that act to convert light energy in photosynthetic organisms. [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] Choline: A basic constituent of lecithin that is found in many plants and animal organs. It is important as a precursor of acetylcholine, as a methyl donor in various metabolic processes, and in lipid metabolism. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] Cholinesterase Inhibitors: Drugs that inhibit cholinesterases. The neurotransmitter acetylcholine is rapidly hydrolyzed, and thereby inactivated, by cholinesterases. When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. Cholinesterase inhibitors are widely used clinically for their potentiation of cholinergic inputs to the gastrointestinal tract and urinary bladder, the eye, and skeletal muscles; they are also used for their effects on the heart and the central nervous system. [NIH] Chorea: Involuntary, forcible, rapid, jerky movements that may be subtle or become confluent, markedly altering normal patterns of movement. Hypotonia and pendular reflexes are often associated. Conditions which feature recurrent or persistent episodes of chorea as a primary manifestation of disease are referred to as choreatic disorders. Chorea is also a frequent manifestation of basal ganglia diseases. [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] Chromates: Salts of chromic acid containing the CrO(2-)4 radical. [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] Chromic: Catgut sterilized and impregnated with chromium trioxide. [NIH] Chromium: A trace element that plays a role in glucose metabolism. It has the atomic

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symbol Cr, atomic number 24, and atomic weight 52. According to the Fourth Annual Report on Carcinogens (NTP85-002,1985), chromium and some of its compounds have been listed as known carcinogens. [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] 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 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] Cicatricial: Ectropion due to scar tissue on the margins or the surrounding surfaces of the eyelids. [NIH] Ciliary: Inflammation or infection of the glands of the margins of the eyelids. [NIH] Ciliary Body: A ring of tissue extending from the scleral spur to the ora serrata of the retina. It consists of the uveal portion and the epithelial portion. The ciliary muscle is in the uveal portion and the ciliary processes are in the epithelial portion. [NIH] Ciprofloxacin: A carboxyfluoroquinoline antimicrobial agent that is effective against a wide range of microorganisms. It has been successfully and safely used in the treatment of resistant respiratory, skin, bone, joint, gastrointestinal, urinary, and genital infections. [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] 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] Citrus: Any tree or shrub of the Rue family or the fruit of these plants. [NIH] Claviceps: A genus of ascomycetous fungi, family Clavicipitaceae, order Hypocreales, parasitic on various grasses. The sclerotia contain several toxic alkaloids. Claviceps purpurea on rye causes ergotism. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [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] 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]

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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] Clostridium: A genus of motile or nonmotile gram-positive bacteria of the family Bacillaceae. Many species have been identified with some being pathogenic. They occur in water, soil, and in the intestinal tract of humans and lower animals. [NIH] Clostridium botulinum: The etiologic agent of botulism in man, wild ducks, and other waterfowl. It is also responsible for certain forms of forage poisoning in horses and cattle. The bacterium produces a powerful exotoxin that is resistant to proteolytic digestion. [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 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] Cobalt: A trace element that is a component of vitamin B12. It has the atomic symbol Co, atomic number 27, and atomic weight 58.93. It is used in nuclear weapons, alloys, and pigments. Deficiency in animals leads to anemia; its excess in humans can lead to erythrocytosis. [NIH] Cochlea: The part of the internal ear that is concerned with hearing. It forms the anterior part of the labyrinth, is conical, and is placed almost horizontally anterior to the vestibule. [NIH]

Cochlear: Of or pertaining to the cochlea. [EU] Cod Liver Oil: Oil obtained from fresh livers of the cod family, Gadidae. It is a source of vitamins A and D. [NIH] Coenzyme: An organic nonprotein molecule, frequently a phosphorylated derivative of a water-soluble vitamin, that binds with the protein molecule (apoenzyme) to form the active enzyme (holoenzyme). [EU] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [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

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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] Combination chemotherapy: Treatment using more than one anticancer drug. [NIH] Comorbidity: The presence of co-existing or additional diseases with reference to an initial diagnosis or with reference to the index condition that is the subject of study. Comorbidity may affect the ability of affected individuals to function and also their survival; it may be used as a prognostic indicator for length of hospital stay, cost factors, and outcome or survival. [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 1: The first complement component to act in the cytolysis reaction. It is a trimolecular complex held together with Ca ions and, when activated, has esterase activity which initiates the next step in the sequence. [NIH] Complement 1 Inactivators: Compounds which inhibit, antagonize, or inactivate complement 1. A well-known inhibitor is a serum glycoprotein believed to be alpha-2neuroaminoglycoprotein. It inhibits the activated (esterase) form of complement 1 as well as kinin-forming, coagulation, and fibrinolytic systems. Deficiency of this inactivator has been found in patients with hereditary angioneurotic edema. These compounds are members of the serpin superfamily. [NIH] 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]

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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] 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 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] Cones: One type of specialized light-sensitive cells (photoreceptors) in the retina that provide sharp central vision and color vision. [NIH] Congestion: Excessive or abnormal accumulation of blood in a part. [EU] Conjugated: Acting or operating as if joined; simultaneous. [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] Conjunctivitis, Allergic: Conjunctivitis due to hypersensitivity to various allergens. [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: 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] Consensus Sequence: A theoretical representative nucleotide or amino acid sequence in which each nucleotide or amino acid is the one which occurs most frequently at that site in the different sequences which occur in nature. The phrase also refers to an actual sequence which approximates the theoretical consensus. A known conserved sequence set is represented by a consensus sequence. Commonly observed supersecondary protein structures (amino acid motifs) are often formed by conserved sequences. [NIH] Conserved Sequence: A sequence of amino acids in a polypeptide or of nucleotides in DNA or RNA that is similar across multiple species. A known set of conserved sequences is represented by a consensus sequence. Amino acid motifs are often composed of conserved sequences. [NIH]

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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]

Continuum: An area over which the vegetation or animal population is of constantly changing composition so that homogeneous, separate communities cannot be distinguished. [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] Control group: In a clinical trial, the group that does not receive the new treatment being studied. This group is compared to the group that receives the new treatment, to see if the new treatment works. [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

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hypertrophy of the right ventricle. [EU] 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 Circulation: The circulation of blood through the coronary vessels of the heart. [NIH]

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] 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] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [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] Cortisol: A steroid hormone secreted by the adrenal cortex as part of the body's response to stress. [NIH] 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]

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Creatine: An amino acid that occurs in vertebrate tissues and in urine. In muscle tissue, creatine generally occurs as phosphocreatine. Creatine is excreted as creatinine in the urine. [NIH]

Creatinine: A compound that is excreted from the body in urine. Creatinine levels are measured to monitor kidney function. [NIH] Criterion: A standard by which something may be judged. [EU] Cromolyn Sodium: A chromone complex that acts by inhibiting the release of chemical mediators from sensitized mast cells. It is used in the prophylactic treatment of both allergic and exercise-induced asthma, but does not affect an established asthmatic attack. [NIH] Crossing-over: The exchange of corresponding segments between chromatids of homologous chromosomes during meiosia, forming a chiasma. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] 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] Cyclophosphamide: Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the liver to form the active aldophosphamide. It is used in the treatment of lymphomas, leukemias, etc. Its side effect, alopecia, has been made use of in defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer. [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] Cysteine: A thiol-containing non-essential amino acid that is oxidized to form cystine. [NIH] Cystine: A covalently linked dimeric nonessential amino acid formed by the oxidation of cysteine. Two molecules of cysteine are joined together by a disulfide bridge to form cystine. [NIH]

Cystitis: Inflammation of the urinary bladder. [EU] 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] Cytochrome b: Cytochromes (electron-transporting proteins) with protoheme or a related heme as the prosthetic group. The prosthetic group is not covalently bound to the protein moiety. [NIH] Cytogenetics: A branch of genetics which deals with the cytological and molecular behavior of genes and chromosomes during cell division. [NIH] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytomegalovirus: A genus of the family Herpesviridae, subfamily Betaherpesvirinae,

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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] Cytopenia: A reduction in the number of blood cells. [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] Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytotoxic: Cell-killing. [NIH] Databases, Bibliographic: Extensive collections, reputedly complete, of references and citations to books, articles, publications, etc., generally on a single subject or specialized subject area. Databases can operate through automated files, libraries, or computer disks. The concept should be differentiated from factual databases which is used for collections of data and facts apart from bibliographic references to them. [NIH] Day Care: Institutional health care of patients during the day. The patients return home at night. [NIH] 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] Decubitus: An act of lying down; also the position assumed in lying down. [EU] Decubitus Ulcer: An ulceration caused by prolonged pressure in patients permitted to lie too still for a long period of time. The bony prominences of the body are the most frequently affected sites. The ulcer is caused by ischemia of the underlying structures of the skin, fat, and muscles as a result of the sustained and constant pressure. [NIH] Defecation: The normal process of elimination of fecal material from the rectum. [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] Dehydration: The condition that results from excessive loss of body water. [NIH] Dehydroepiandrosterone: DHEA. A substance that is being studied as a cancer prevention drug. It belongs to the family of drugs called steroids. [NIH] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Delirium: (DSM III-R) an acute, reversible organic mental disorder characterized by reduced ability to maintain attention to external stimuli and disorganized thinking as manifested by rambling, irrelevant, or incoherent speech; there are also a reduced level of consciousness, sensory misperceptions, disturbance of the sleep-wakefulness cycle and level of psychomotor activity, disorientation to time, place, or person, and memory impairment. Delirium may be caused by a large number of conditions resulting in derangement of cerebral metabolism, including systemic infection, poisoning, drug intoxication or withdrawal, seizures or head trauma, and metabolic disturbances such as hypoxia, hypoglycaemia, fluid, electrolyte, or acid-base imbalances, or hepatic or renal failure. Called also acute confusional state and acute brain syndrome. [EU]

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Delivery of Health Care: The concept concerned with all aspects of providing and distributing health services to a patient population. [NIH] Delusions: A false belief regarding the self or persons or objects outside the self that persists despite the facts, and is not considered tenable by one's associates. [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] Demethylation: Process that releases substantial amounts of carbon dioxide in the liver. [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]

Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Dental Care: The total of dental diagnostic, preventive, and restorative services provided to meet the needs of a patient (from Illustrated Dictionary of Dentistry, 1982). [NIH] Dental Hygienists: Persons trained in an accredited school or dental college and licensed by the state in which they reside to provide dental prophylaxis under the direction of a licensed dentist. [NIH] Dental Materials: Materials used in the production of dental bases, restorations, impressions, prostheses, etc. [NIH] Dentists: Individuals licensed to practice dentistry. [NIH] Dentition: The teeth in the dental arch; ordinarily used to designate the natural teeth in position in their alveoli. [EU] 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] Dermal: Pertaining to or coming from the skin. [NIH] Dermatitis: Any inflammation of the skin. [NIH] Dermatitis Herpetiformis: Rare, chronic, papulo-vesicular disease characterized by an intensely pruritic eruption consisting of various combinations of symmetrical, erythematous, papular, vesicular, or bullous lesions. The disease is strongly associated with the presence of HLA-B8 and HLA-DR3 antigens. A variety of different autoantibodies has been detected in small numbers in patients with dermatitis herpetiformis. [NIH] Dermatitis, Contact: A type of acute or chronic skin reaction in which sensitivity is 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]

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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] 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] 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] Developed Countries: Countries that have reached a level of economic achievement through an increase of production, per capita income and consumption, and utilization of natural and human resources. [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] Diaper Rash: A type of irritant dermatitis localized to the area in contact with a diaper and occurring most often as a reaction to prolonged contact with urine, feces, or retained soap or detergent. [NIH] Diarrhea: Passage of excessively liquid or excessively frequent stools. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Diclofenac: A non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt, diclofenac sodium. [NIH] Diclofenac Sodium: The sodium form of diclofenac. It is used for its analgesic and antiinflammatory properties. [NIH] Diencephalon: The paired caudal parts of the prosencephalon from which the thalamus, hypothalamus, epithalamus, and subthalamus are derived. [NIH] Dietary Fats: Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados. [NIH]

Dietary Fiber: The remnants of plant cell walls that are resistant to digestion by the alimentary enzymes of man. It comprises various polysaccharides and lignins. [NIH] Dietary Proteins: Proteins obtained from foods. They are the main source of the essential amino acids. [NIH]

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Diethylcarbamazine: An anthelmintic used primarily as the citrate in the treatment of filariasis, particularly infestations with Wucheria bancrofti or Loa loa. [NIH] Diffuse Axonal Injury: A relatively common sequela of blunt head injury, characterized by a global disruption of axons throughout the brain. Associated clinical features may include neurobehavioral manifestations; persistent vegetative state; dementia; and other disorders. [NIH]

Diffusion: The tendency of a gas or solute to pass from a point of higher pressure or concentration to a point of lower pressure or concentration and to distribute itself throughout the available space; a major mechanism of biological transport. [NIH] 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] Dilatation: The act of dilating. [NIH] Dilatation, Pathologic: The condition of an anatomical structure's being dilated beyond normal dimensions. [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] Dimerization: The process by which two molecules of the same chemical composition form a condensation product or polymer. [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] Disease Outbreaks: Sudden increase in the incidence of a disease. The concept includes epidemics. [NIH] Disinfectant: An agent that disinfects; applied particularly to agents used on inanimate objects. [EU] Disorientation: The loss of proper bearings, or a state of mental confusion as to time, place, or identity. [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]

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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] Diuretic: A drug that increases the production of urine. [NIH] Dizziness: An imprecise term which may refer to a sense of spatial disorientation, motion of the environment, or lightheadedness. [NIH] Docetaxel: An anticancer drug that belongs to the family of drugs called mitotic inhibitors. [NIH]

Domesticated: Species in which the evolutionary process has been influenced by humans to meet their needs. [NIH] Donepezil: A drug used in the treatment of Alzheimer's disease. It belongs to the family of drugs called cholinesterase inhibitors. It is being studied as a treatment for side effects caused by radiation therapy to the brain. [NIH] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate 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] Dorsum: A plate of bone which forms the posterior boundary of the sella turcica. [NIH] Doxepin: A dibenzoxepin tricyclic compound. It displays a range of pharmacological actions including maintaining adrenergic innervation. Its mechanism of action is not fully understood, but it appears to block reuptake of monoaminergic neurotransmitters into presynaptic terminals. It also possesses anticholinergic activity and modulates antagonism of histamine H(1)- and H(2)-receptors. [NIH] Dross: Residue remaining in an opium pipe which has been smoked; contains 50 % of the morphine present in the original drug. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [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] Dura mater: The outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain and spinal cord; called also pachymeninx. [EU] Dyes: Chemical substances that are used to stain and color other materials. The coloring may or may not be permanent. Dyes can also be used as therapeutic agents and test reagents in medicine and scientific research. [NIH] Dyscrasia: A term formerly used to indicate an abnormal mixture of the four humours; in surviving usages it now is roughly synonymous with 'disease' or 'pathologic condition'. [EU]

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Dysentery: Any of various disorders marked by inflammation of the intestines, especially of the colon, and attended by pain in the abdomen, tenesmus, and frequent stools containing blood and mucus. Causes include chemical irritants, bacteria, protozoa, or parasitic worms. [EU]

Dyskinesia: Impairment of the power of voluntary movement, resulting in fragmentary or incomplete movements. [EU] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [NIH] Dystonia: Disordered tonicity of muscle. [EU] Dystrophy: Any disorder arising from defective or faulty nutrition, especially the muscular dystrophies. [EU] Eating Disorders: A group of disorders characterized by physiological and psychological disturbances in appetite or food intake. [NIH] Echinostomiasis: Infection by flukes of the genus Echinostoma. [NIH] Eclampsia: Onset of convulsions or coma in a previously diagnosed pre-eclamptic patient. [NIH]

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] Egg Proteins: Proteins which are found in eggs or ova from any species. [NIH] Elasticity: Resistance and recovery from distortion of shape. [NIH] Elastin: The protein that gives flexibility to tissues. [NIH] Electrocardiograph: Apparatus which, by means of currents produced by contractions of the cardiac muscle, records heart movements as electro-cardiograms. [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] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electrons: Stable elementary particles having the smallest known negative charge, present in all elements; also called negatrons. Positively charged electrons are called positrons. The numbers, energies and arrangement of electrons around atomic nuclei determine the chemical identities of elements. Beams of electrons are called cathode rays or beta rays, the latter being a high-energy biproduct of nuclear decay. [NIH] 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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Electroplating: Coating with a metal or alloy by electrolysis. [NIH] Ellagic Acid: A fused four ring compound occurring free or combined in galls. Isolated from the kino of Eucalyptus maculata Hook and E. Hemipholia F. Muell. Activates Factor XII of the blood clotting system which also causes kinin release; used in research and as a dye. [NIH]

Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Emodin: Purgative anthraquinone found in several plants, especially Rhamnus frangula. It was formerly used as a laxative, but is now used mainly as tool in toxicity studies. [NIH] Emollient: Softening or soothing; called also malactic. [EU] Emphysema: A pathological accumulation of air in tissues or organs. [NIH] Empirical: A treatment based on an assumed diagnosis, prior to receiving confirmatory laboratory test results. [NIH] 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] Endarterectomy: Surgical excision, performed under general anesthesia, of the atheromatous tunica intima of an artery. When reconstruction of an artery is performed as an endovascular procedure through a catheter, it is called atherectomy. [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 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] 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] Endorphins: One of the three major groups of endogenous opioid peptides. They are large peptides derived from the pro-opiomelanocortin precursor. The known members of this group are alpha-, beta-, and gamma-endorphin. The term endorphin is also sometimes used to refer to all opioid peptides, but the narrower sense is used here; opioid peptides is used for the broader group. [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,

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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] Endotoxemia: A condition characterized by the presence of endotoxins in the blood. If endotoxemia is the result of gram-negative rod-shaped bacteria, shock may occur. [NIH] Endotoxic: Of, relating to, or acting as an endotoxin (= a heat-stable toxin, associated with the outer membranes of certain gram-negative bacteria. Endotoxins are not secreted and are released only when the cells are disrupted). [EU] 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] Enkephalin: A natural opiate painkiller, in the hypothalamus. [NIH] Enteritis: Inflammation of the intestine, applied chiefly to inflammation of the small intestine; see also enterocolitis. [EU] Enterocolitis: Inflammation of the intestinal mucosa of the small and large bowel. [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]

Environmental Pollutants: Substances which pollute the environment. Use environmental pollutants in general or for which there is no specific heading. [NIH]

for

Environmental tobacco smoke: ETS. Smoke that comes from the burning of a tobacco product and smoke that is exhaled by smokers (second-hand smoke). Inhaling ETS is called involuntary or passive smoking. [NIH] Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. [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] Ependyma: A thin membrane that lines the ventricles of the brain and the central canal of the spinal cord. [NIH] Epidemic: Occurring suddenly in numbers clearly in excess of normal expectancy; said

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especially of infectious diseases but applied also to any disease, injury, or other healthrelated event occurring in such outbreaks. [EU] Epidemiologic Studies: Studies designed to examine associations, commonly, hypothesized causal relations. They are usually concerned with identifying or measuring the effects of risk factors or exposures. The common types of analytic study are case-control studies, cohort studies, and cross-sectional studies. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU] 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] 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] Episcleritis: Inflammation of the episclera and/or the outer layers of the sclera itself. [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]

Erectile: The inability to get or maintain an erection for satisfactory sexual intercourse. Also called impotence. [NIH] Erection: The condition of being made rigid and elevated; as erectile tissue when filled with blood. [EU] Ergot: Cataract due to ergot poisoning caused by eating of rye cereals contaminated by a fungus. [NIH] Erythema: Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes. [NIH] Erythema Multiforme: A skin and mucous membrane disease characterized by an eruption of macules, papules, nodules, vesicles, and/or bullae with characteristic "bull's-eye" lesions usually occurring on the dorsal aspect of the hands and forearms. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Esophagitis: Inflammation, acute or chronic, of the esophagus caused by bacteria, chemicals, or trauma. [NIH] Esophagitis, Peptic: Inflammation of the esophagus caused by reflux of gastric juice and/or stomach and duodenal contents. [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

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from the alternate contraction and relaxation of opposing groups of muscles. [NIH] Estradiol: The most potent mammalian estrogenic hormone. It is produced in the ovary, placenta, testis, and possibly the adrenal cortex. [NIH] Estrogen: One of the two female sex hormones. [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] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Evacuation: An emptying, as of the bowels. [EU] Evoke: The electric response recorded from the cerebral cortex after stimulation of a peripheral sense organ. [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] Exfoliation: A falling off in scales or layers. [EU] Exhaustion: The feeling of weariness of mind and body. [NIH] Exocytosis: Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the cell membrane. [NIH] 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 of the protein. In many eucaryotic genes, the coding sequences consist of a series of exons alternating with intron sequences. [NIH] Exotoxin: Toxic substance excreted by living bacterial cells. [NIH] Expiration: The act of breathing out, or expelling air from the lungs. [EU] Expiratory: The volume of air which leaves the breathing organs in each expiration. [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]

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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] Extracorporeal: Situated or occurring outside the body. [EU] Extraction: The process or act of pulling or drawing out. [EU] Extrapyramidal: Outside of the pyramidal tracts. [EU] Extravasation: A discharge or escape, as of blood, from a vessel into the tissues. [EU] Extremity: A limb; an arm or leg (membrum); sometimes applied specifically to a hand or foot. [EU] Eye socket: One of the two cavities in the skull which contains an eyeball. Each eye is located in a bony socket or orbit. [NIH] Facial: Of or pertaining to the face. [EU] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [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. [NIH]

Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Febrile: Pertaining to or characterized by fever. [EU] Feces: The excrement discharged from the intestines, consisting of bacteria, cells exfoliated from the intestines, secretions, chiefly of the liver, and a small amount of food residue. [EU] Fermentation: An enzyme-induced chemical change in organic compounds that takes place in the absence of oxygen. The change usually results in the production of ethanol or lactic acid, and the production of energy. [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] Fibrinolysis: The natural enzymatic dissolution of fibrin. [NIH]

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Fibrinolytic: Pertaining to, characterized by, or causing the dissolution of fibrin by enzymatic action [EU] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibronectin: An adhesive glycoprotein. One form circulates in plasma, acting as an opsonin; another is a cell-surface protein which mediates cellular adhesive interactions. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Fish Products: Food products manufactured from fish (e.g., fish flour, fish meal). [NIH] Fissure: Any cleft or groove, normal or otherwise; especially a deep fold in the cerebral cortex which involves the entire thickness of the brain wall. [EU] Fistulas: An abnormal passage from one hollow structure of the body to another, or from a hollow structure to the surface, formed by an abscess, disease process, incomplete closure of a wound, or by a congenital anomaly. [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 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] Flatus: Gas passed through the rectum. [NIH] Flavoring Agents: Substances added to foods and medicine to improve the quality of taste. [NIH]

Fleas: Parasitic, blood-sucking, wingless insects comprising the order Siphonaptera. [NIH] 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] 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]

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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] Fluvoxamine: A selective serotonin reuptake inhibitor. It is effective in the treatment of depression, obsessive-compulsive disorders, anxiety, panic disorders, and alcohol amnestic disorders. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Follicles: Shafts through which hair grows. [NIH] Folliculitis: Inflammation of follicles, primarily hair follicles. [NIH] Food Additives: Substances which are of little or no nutritive value, but are used in the processing or storage of foods or animal feed, especially in the developed countries; includes antioxidants, food preservatives, food coloring agents, flavoring agents, anti-infective agents (both plain and local), vehicles, excipients and other similarly used substances. Many of the same substances are pharmaceutic aids when added to pharmaceuticals rather than to foods. [NIH]

Food Coloring Agents: Natural or synthetic dyes used as coloring agents in processed foods. [NIH] Food Hypersensitivity: Gastrointestinal disturbances, skin eruptions, or shock due to allergic reactions to allergens ingested in food. [NIH] Food Preservatives: Substances capable of inhibiting, retarding or arresting the process of fermentation, acidification or other deterioration of foods. [NIH] Forearm: The part between the elbow and the wrist. [NIH] Friction: Surface resistance to the relative motion of one body against the rubbing, sliding, rolling, or flowing of another with which it is in contact. [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] Fumigation: The application of smoke, vapor, or gas for the purpose of disinfecting or destroying pests or microorganisms. [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] 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] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH]

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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] Gap Junctions: Connections between cells which allow passage of small molecules and electric current. Gap junctions were first described anatomically as regions of close apposition between cells with a narrow (1-2 nm) gap between cell membranes. The variety in the properties of gap junctions is reflected in the number of connexins, the family of proteins which form the junctions. [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] Gastric: Having to do with the stomach. [NIH] Gastric Acid: Hydrochloric acid present in gastric juice. [NIH] Gastric Juices: Liquids produced in the stomach to help break down food and kill bacteria. [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]

Gastroenterologist: A doctor who specializes in diagnosing and treating disorders of the digestive system. [NIH] Gastrointestinal: Refers to the stomach and intestines. [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] 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 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,

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transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genetics, Biochemical: A branch of genetics which deals with the chemical structure of the genes and with the mechanisms by which the genes control and regulate the structure and synthesis of proteins. [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] Geographic Locations: All of the continents and every country situated within, the United States and each of the constituent states arranged by region, Canada and each of its provinces, Australia and each of its states, the major bodies of water and major islands on both hemispheres, and selected major cities. Although the geographic locations are not printed in index medicus as main headings, in indexing they are significant in epidemiologic studies and historical articles and for locating administrative units in education and the delivery of health care. [NIH] Germinal Center: The activated center of a lymphoid follicle in secondary lymphoid tissue where B-lymphocytes are stimulated by antigens and helper T cells (T-lymphocytes, helperinducer) are stimulated to generate memory cells. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Giant Cells: Multinucleated masses produced by the fusion of many cells; often associated with viral infections. In AIDS, they are induced when the envelope glycoprotein of the HIV virus binds to the CD4 antigen of uninfected neighboring T4 cells. The resulting syncytium leads to cell death and thus may account for the cytopathic effect of the virus. [NIH] 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]

Glomeruli: Plural of glomerulus. [NIH] Glomerulonephritis: Glomerular disease characterized by an inflammatory reaction, with leukocyte infiltration and cellular proliferation of the glomeruli, or that appears to be the result of immune glomerular injury. [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

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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] Glucose tolerance: The power of the normal liver to absorb and store large quantities of glucose and the effectiveness of intestinal absorption of glucose. The glucose tolerance test is a metabolic test of carbohydrate tolerance that measures active insulin, a hepatic function based on the ability of the liver to absorb glucose. The test consists of ingesting 100 grams of glucose into a fasting stomach; blood sugar should return to normal in 2 to 21 hours after ingestion. [NIH] Glucose Tolerance Test: Determination of whole blood or plasma sugar in a fasting state before and at prescribed intervals (usually 1/2 hr, 1 hr, 3 hr, 4 hr) after taking a specified amount (usually 100 gm orally) of glucose. [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] 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]

Glutamine: A non-essential amino acid present abundantly throught the body and is involved in many metabolic processes. It is synthesized from glutamic acid and ammonia. It is the principal carrier of nitrogen in the body and is an important energy source for many cells. [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] 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] Glycosaminoglycan: A type of long, unbranched polysaccharide molecule. Glycosaminoglycans are major structural components of cartilage and are also found in the cornea of the eye. [NIH] Gonad: A sex organ, such as an ovary or a testicle, which produces the gametes in most multicellular animals. [NIH] Gonadal: Pertaining to a gonad. [EU] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [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-versus-host disease: GVHD. A reaction of donated bone marrow or peripheral stem cells against a person's tissue. [NIH]

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Gram-negative: Losing the stain or decolorized by alcohol in Gram's method of staining, a primary characteristic of bacteria having a cell wall composed of a thin layer of peptidoglycan covered by an outer membrane of lipoprotein and lipopolysaccharide. [EU] Gram-positive: Retaining the stain or resisting decolorization by alcohol in Gram's method of staining, a primary characteristic of bacteria whose cell wall is composed of a thick layer of peptidologlycan with attached teichoic acids. [EU] Gram-Positive Bacteria: Bacteria which retain the crystal violet stain when treated by Gram's method. [NIH] Granule: A small pill made from sucrose. [EU] Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [NIH] Granulomatous Disease, Chronic: A recessive X-linked defect of leukocyte function in which phagocytic cells ingest but fail to digest bacteria, resulting in recurring bacterial infections with granuloma formation. [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] 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] Guinea Pigs: A common name used for the family Caviidae. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research. [NIH]

Habitat: An area considered in terms of its environment, particularly as this determines the type and quality of the vegetation the area can carry. [NIH] Habitual: Of the nature of a habit; according to habit; established by or repeated by force of habit, customary. [EU] Hair Color: Color of hair or fur. [NIH] Hair Dyes: Dyes used as cosmetics to change hair color either permanently or temporarily. [NIH]

Hair follicles: Shafts or openings on the surface of the skin through which hair grows. [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] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or

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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] 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] Health Promotion: Encouraging consumer behaviors most likely to optimize health potentials (physical and psychosocial) through health information, preventive programs, and access to medical care. [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] Hematologic malignancies: Cancers of the blood or bone marrow, including leukemia and lymphoma. Also called hematologic cancers. [NIH] Hematopoietic Stem Cell Transplantation: The transference of stem cells from one animal or human to another (allogeneic), or within the same individual (autologous). The source for the stem cells may be the bone marrow or peripheral blood. Stem cell transplantation has been used as an alternative to autologous bone marrow transplantation in the treatment of a variety of neoplasms. [NIH] Hemiparesis: The weakness or paralysis affecting one side of 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] 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 failure. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH]

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Hemorrhoids: Varicosities of the hemorrhoidal venous plexuses. [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] Hepatic: Refers to the liver. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatocytes: The main structural component of the liver. They are specialized epithelial cells that are organized into interconnected plates called lobules. [NIH] Hepatotoxicity: How much damage a medicine or other substance does to the liver. [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 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]

Heterogenic: Derived from a different source or species. Also called heterogenous. [NIH] Heterogenous: Derived from a different source or species. Also called heterogenic. [NIH] Hidradenitis: The inflammation of a sweat gland (usually of the apocrine type). The condition can be idiopathic or occur as a result of or in association with another underlying condition. Neutrophilic eccrine hidradenitis is a relatively rare variant that has been reported in patients undergoing chemotherapy, usually for non-Hodgkin lymphomas or leukemic conditions. [NIH] Hidradenitis Suppurativa: A chronic suppurative and cicatricial disease of the apocrine glands occurring chiefly in the axillae in women and in the groin and anal regions in men. It is characterized by poral occlusion with secondary bacterial infection, evolving into abscesses which eventually rupture. As the disease becomes chronic, ulcers appear, sinus tracts enlarge, fistulas develop, and fibrosis and scarring become evident. Hormonal mechanisms are expected in its pathogenesis. [NIH]

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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] Histology: The study of tissues and cells under a microscope. [NIH] Homogenate: A suspension of animal tissue that is ground in the all-glass "homogenizer" described by Potter and Elvehjem in 1936. [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] 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 Development: Continuous sequential changes which occur in the physiological and psychological functions during the individual's life. [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 also crossing. [NIH] Hybridoma: A hybrid cell resulting from the fusion of a specific antibody-producing spleen cell with a myeloma cell. [NIH] Hydration: Combining with water. [NIH] Hydrochloric Acid: A strong corrosive acid that is commonly used as a laboratory reagent. It is formed by dissolving hydrogen chloride in water. Gastric acid is the hydrochloric acid component of gastric juice. [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]

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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] 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] Hydroxylamine: A colorless inorganic compound (HONH2) used in organic synthesis and as a reducing agent, due to its ability to donate nitric oxide. [NIH] 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] Hygienic: Pertaining to hygiene, or conducive to health. [EU] Hyperaemia: An excess of blood in a part; engorgement. [EU] Hyperhidrosis: Excessive sweating. In the localized type, the most frequent sites are the palms, soles, axillae, inguinal folds, and the perineal area. Its chief cause is thought to be emotional. Generalized hyperhidrosis may be induced by a hot, humid environment, by fever, or by vigorous exercise. [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] Hypersecretion: Excessive secretion. [EU] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [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] Hypesthesia: Absent or reduced sensitivity to cutaneous stimulation. [NIH] Hypoglycaemia: An abnormally diminished concentration of glucose in the blood, which may lead to tremulousness, cold sweat, piloerection, hypothermia, and headache, accompanied by irritability, confusion, hallucinations, bizarre behaviour, and ultimately, convulsions and coma. [EU] Hypotension: Abnormally low blood pressure. [NIH] 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] Ichthyosis: Any of several generalized skin disorders characterized by dryness, roughness,

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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 and strivings of the individual. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH] Idiotype: The unique antigenic determinant in the variable region. [NIH] Ifosfamide: Positional isomer of cyclophosphamide which is active as an alkylating agent and an immunosuppressive agent. [NIH] Ileitis: Inflammation of the ileum. [EU] Ileostomy: Surgical creation of an external opening into the ileum for fecal diversion or drainage. Loop or tube procedures are most often employed. [NIH] Ileum: The lower end of the small intestine. [NIH] Imidazole: C3H4N2. The ring is present in polybenzimidazoles. [NIH] Immaturity: The state or quality of being unripe or not fully developed. [EU] 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] Immunochemistry: Field of chemistry that pertains to immunological phenomena and the study of chemical reactions related to antigen stimulation of tissues. It includes physicochemical interactions between antigens and antibodies. [NIH] Immunocompromised: Having a weakened immune system caused by certain diseases or treatments. [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunogenic: Producing immunity; evoking an immune response. [EU]

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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] Immunophenotyping: Process of classifying cells of the immune system based on structural and functional differences. The process is commonly used to analyze and sort Tlymphocytes into subsets based on CD antigens by the technique of flow cytometry. [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 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] 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] Impotence: The inability to perform sexual intercourse. [NIH] 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] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] Incubated: Grown in the laboratory under controlled conditions. (For instance, white blood

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cells can be grown in special conditions so that they attack specific cancer cells when returned to the body.) [NIH] Incubation: The development of an infectious disease from the entrance of the pathogen to the appearance of clinical symptoms. [EU] Incubation period: The period of time likely to elapse between exposure to the agent of the disease and the onset of clinical symptoms. [NIH] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU] 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] Infancy: The period of complete dependency prior to the acquisition of competence in walking, talking, and self-feeding. [NIH] Infantile: Pertaining to an infant or to infancy. [EU] 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, 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] 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]

Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH] Ingestion: Taking into the body by mouth [NIH] Inguinal: Pertaining to the inguen, or groin. [EU] 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] Innervation: 1. The distribution or supply of nerves to a part. 2. The supply of nervous energy or of nerve stimulus sent to a part. [EU] Inorganic: Pertaining to substances not of organic origin. [EU] Inositol: An isomer of glucose that has traditionally been considered to be a B vitamin

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although it has an uncertain status as a vitamin and a deficiency syndrome has not been identified in man. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1379) Inositol phospholipids are important in signal transduction. [NIH] Inositol 1,4,5-Trisphosphate: Intracellular messenger formed by the action of phospholipase C on phosphatidylinositol 4,5-bisphosphate, which is one of the phospholipids that make up the cell membrane. Inositol 1,4,5-trisphosphate is released into the cytoplasm where it releases calcium ions from internal stores within the cell's endoplasmic reticulum. These calcium ions stimulate the activity of B kinase or calmodulin. [NIH] Inotropic: Affecting the force or energy of muscular contractions. [EU] 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 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] 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-11: Lymphohematopoietic cytokine that has the ability to modulate antigen-

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specific antibody responses, potentiate megakaryocytes, and regulate bone marrow adipogenesis. [NIH] Interleukin-13: T-lymphocyte-derived cytokine that produces proliferation, immunoglobulin isotype switching, and immunoglobulin production by immature Blymphocytes. It appears to play a role in regulating inflammatory and immune responses. [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-4: Soluble factor produced by activated T-lymphocytes that causes proliferation and differentiation of B-cells. Interleukin-4 induces the expression of class II major histocompatibility complex and Fc receptors on B-cells. It also acts on T-lymphocytes, mast cell lines, and several other hematopoietic lineage cells including granulocyte, megakaryocyte, and erythroid precursors, as well as macrophages. [NIH] Interleukin-8: A cytokine that activates neutrophils and attracts neutrophils and Tlymphocytes. It is released by several cell types including monocytes, macrophages, Tlymphocytes, 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] 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] Interstitial Collagenase: A member of the metalloproteinase family of enzymes that is principally responsible for cleaving fibrillar collagen. It can degrade interstitial collagens, types I, II and III. EC 3.4.24.7. [NIH] Intervertebral: Situated between two contiguous vertebrae. [EU] Intestinal: Having to do with the intestines. [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] Intracranial Pressure: Pressure within the cranial cavity. It is influenced by brain mass, the circulatory system, CSF dynamics, and skull rigidity. [NIH] Intraepithelial: Within the layer of cells that form the surface or lining of an organ. [NIH] Intramuscular: IM. Within or into muscle. [NIH] Intravenous: IV. Into a vein. [NIH] Intravesical: Within the bladder. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Intubation: Introduction of a tube into a hollow organ to restore or maintain patency if obstructed. It is differentiated from catheterization in that the insertion of a catheter is

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usually performed for the introducing or withdrawing of fluids from the body. [NIH] 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] Iodoacetamide: An alkylating sulfhydryl reagent. Its actions are similar to those of iodoacetate. [NIH] Ion Channels: Gated, ion-selective glycoproteins that traverse membranes. The stimulus for 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] Irritable Bowel Syndrome: A disorder that comes and goes. Nerves that control the muscles in the GI tract are too active. The GI tract becomes sensitive to food, stool, gas, and stress. Causes abdominal pain, bloating, and constipation or diarrhea. Also called spastic colon or mucous colitis. [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] Isocyanates: Organic compounds that contain the -NCO radical. [NIH] Isoelectric: Separation of amphoteric substances, dissolved in water, based on their isoelectric behavior. The amphoteric substances are a mixture of proteins to be separated and of auxiliary "carrier ampholytes". [NIH] Isoelectric Point: The pH in solutions of proteins and related compounds at which the dipolar ions are at a maximum. [NIH] Isoenzyme: Different forms of an enzyme, usually occurring in different tissues. The isoenzymes of a particular enzyme catalyze the same reaction but they differ in some of their properties. [NIH]

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Isotonic: A biological term denoting a solution in which body cells can be bathed without a net flow of water across the semipermeable cell membrane. Also, denoting a solution having the same tonicity as some other solution with which it is compared, such as physiologic salt solution and the blood serum. [EU] Isozymes: The multiple forms of a single enzyme. [NIH] Jejunum: That portion of the small intestine which extends from the duodenum to the ileum; called also intestinum jejunum. [EU] Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [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] Keratolytic: An agent that promotes keratolysis. [EU] Keratosis: Any horny growth such as a wart or callus. [NIH] Keto: It consists of 8 carbon atoms and within the endotoxins, it connects poysaccharide and lipid A. [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] Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Laceration: 1. The act of tearing. 2. A torn, ragged, mangled wound. [EU] Lacrimal: Pertaining to the tears. [EU] Laminin: Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement membrane. Evidence suggests that the protein plays a role in tumor invasion. [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]

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Lavage: A cleaning of the stomach and colon. Uses a special drink and enemas. [NIH] Laxative: An agent that acts to promote evacuation of the bowel; a cathartic or purgative. [EU]

Lead Poisoning: Disease caused by the gradual accumulation of a significant body burden of lead. [NIH] Lectins: Protein or glycoprotein substances, usually of plant origin, that bind to sugar moieties in cell walls or membranes and thereby change the physiology of the membrane to cause agglutination, mitosis, or other biochemical changes in the cell. [NIH] Leishmaniasis: A disease caused by any of a number of species of protozoa in the genus Leishmania. There are four major clinical types of this infection: cutaneous (Old and New World), diffuse cutaneous, mucocutaneous, and visceral leishmaniasis. [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] Leprosy: A chronic granulomatous infection caused by Mycobacterium leprae. The granulomatous lesions are manifested in the skin, the mucous membranes, and the peripheral nerves. Two polar or principal types are lepromatous and tuberculoid. [NIH] Leptospirosis: Infections with bacteria of the genus Leptospira. [NIH] Lesion: An area of abnormal tissue change. [NIH] Lethal: Deadly, fatal. [EU] Leucine: An essential branched-chain amino acid important for hemoglobin formation. [NIH] 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] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [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] 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] 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] Ligation: Application of a ligature to tie a vessel or strangulate a part. [NIH] Lincomycin: (2S-trans)-Methyl 6,8-dideoxy-6-(((1-methyl-4-propyl-2pyrrolidinyl)carbonyl)amino)-1-thio-D-erythro-alpha-D-galacto-octopyranoside. An antibiotic produced by Streptomyces lincolnensis var. lincolnensis. It has been used in the treatment of staphylococcal, streptococcal, and Bacteroides fragilis infections. [NIH]

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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] Lip: Either of the two fleshy, full-blooded margins of the mouth. [NIH] Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3. [NIH] Lipid: Fat. [NIH] Lipid A: Lipid A is the biologically active component of lipopolysaccharides. It shows strong endotoxic activity and exhibits immunogenic properties. [NIH] Lipopolysaccharides: Substance consisting of polysaccaride and lipid. [NIH] Liposome: A spherical particle in an aqueous medium, formed by a lipid bilayer enclosing an aqueous compartment. [EU] 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] 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]

Livedo: A discoloured spot or patch on the skin, commonly due to passive congestion; commonly used alone to refer to l. reticularis. [EU] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Lobe: A portion of an organ such as the liver, lung, breast, or brain. [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] Longitudinal study: Also referred to as a "cohort study" or "prospective study"; the analytic method of epidemiologic study in which subsets of a defined population can be identified who are, have been, or in the future may be exposed or not exposed, or exposed in different degrees, to a factor or factors hypothesized to influence the probability of occurrence of a given disease or other outcome. The main feature of this type of study is to observe large numbers of subjects over an extended time, with comparisons of incidence rates in groups that differ in exposure levels. [NIH] Loss of Heterozygosity: The loss of one allele at a specific locus, caused by a deletion mutation; or loss of a chromosome from a chromosome pair. It is detected when heterozygous markers for a locus appear monomorphic because one of the alleles was deleted. When this occurs at a tumor suppressor gene locus where one of the alleles is already abnormal, it can result in neoplastic transformation. [NIH] Lovastatin: A fungal metabolite isolated from cultures of Aspergillus terreus. The

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compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (hydroxymethylglutaryl CoA reductases), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver. [NIH] Lubricants: Oily or slippery substances. [NIH] Lucida: An instrument, invented by Wollaton, consisting essentially of a prism or a mirror through which an object can be viewed so as to appear on a plane surface seen in direct view and on which the outline of the object may be traced. [NIH] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [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]

Lymphadenopathy: Disease or swelling of the lymph nodes. [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] 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] 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] Lymphokine: A soluble protein produced by some types of white blood cell that stimulates other white blood cells to kill foreign invaders. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Lymphoproliferative: Disorders characterized by proliferation of lymphoid tissue, general or unspecified. [NIH] Lymphotoxin: Soluble substance released by lymphocytes activated by antigens or T-cell mitogens, that is cytotoxic to other cells. It is involved in allergies and chronic inflammatory diseases. Lymphotoxin is antigenically distinct from tumor necrosis factor-alpha (tumor necrosis factor), though they both share a common receptor, biological activities, and significant amino acid sequences. [NIH] Maceration: The softening of a solid by soaking. In histology, the softening of a tissue by soaking, especially in acids, until the connective tissue fibres are so dissolved that the tissue components can be teased apart. In obstetrics, the degenerative changes with discoloration and softening of tissues, and eventual disintegration, of a fetus retained in the uterus after its death. [EU] Macrolides: A group of organic compounds that contain a macrocyclic lactone ring linked glycosidically to one or more sugar moieties. [NIH]

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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] 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] Malaria: A protozoan disease caused in humans by four species of the genus Plasmodium (P. falciparum (malaria, falciparum), P. vivax (malaria, vivax), P. ovale, and P. malariae) and transmitted by the bite of an infected female mosquito of the genus Anopheles. Malaria is endemic in parts of Asia, Africa, Central and South America, Oceania, and certain Caribbean islands. It is characterized by extreme exhaustion associated with paroxysms of high fever, sweating, shaking chills, and anemia. Malaria in animals is caused by other species of plasmodia. [NIH] Malaria, Falciparum: Malaria caused by Plasmodium falciparum. This is the severest form of malaria and is associated with the highest levels of parasites in the blood. This disease is characterized by irregularly recurring febrile paroxysms that in extreme cases occur with acute cerebral, renal, or gastrointestinal manifestations. [NIH] Malaria, Vivax: Malaria caused by Plasmodium vivax. This form of malaria is less severe than malaria, falciparum, but there is a higher probability for relapses to occur. Febrile paroxysms often occur every other day. [NIH] 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]

Mania: Excitement of psychotic proportions manifested by mental and physical hyperactivity, disorganization of behaviour, and elevation of mood. [EU] Manic: Affected with mania. [EU] Manic-depressive psychosis: One of a group of psychotic reactions, fundamentally marked by severe mood swings and a tendency to remission and recurrence. [NIH] 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] Mastocyte: A mast cell. [EU] Mastocytosis: A group of diseases resulting from proliferation of mast cells. [NIH] Matrilysin: The smallest member of the matrix metalloproteinases. It plays a role in tumor progression. EC 3.4.24.23. [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

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properly, they are called metalloproteinases. Matrix metalloproteinases are involved in wound healing, angiogenesis, and tumor cell metastasis. [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 Records: Recording of pertinent information concerning patient's illness or illnesses. [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] Meibomian: A series of simple, branched, alveolar, sebaceous glands, located in the tarso of the eyelids, whose ducts empty into the eyelid margins in line with and lateral to the lacrimal puncta. [NIH] 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] Membrane: A very thin layer of tissue that covers a surface. [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] Meningioma: A type of tumor that occurs in the meninges, the membranes that cover and protect the brain and spinal cord. Meningiomas usually grow slowly. [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] 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] 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] Mental Health: The state wherein the person is well adjusted. [NIH] Mental Retardation: Refers to sub-average general intellectual functioning which originated

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during the developmental period and is associated with impairment in adaptive behavior. [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] Mesna: A sulfhydryl compound used to prevent urothelial toxicity by inactivating metabolites from antineoplastic agents, such as ifosfamide or cyclophosphamide. [NIH] Mesolimbic: Inner brain region governing emotion and drives. [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] 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] Methacrylates: Acrylic acids or acrylates which are substituted in the C-2 position with a methyl group. [NIH] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [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] 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] 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

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cannot be properly seen by the unaided eye. [NIH] Microscopy, Fluorescence: Microscopy of specimens stained with fluorescent dye (usually fluorescein isothiocyanate) or of naturally fluorescent materials, which emit light when exposed to ultraviolet or blue light. Immunofluorescence microscopy utilizes antibodies that are labeled with fluorescent dye. [NIH] Microspheres: Small uniformly-sized spherical particles frequently radioisotopes or various reagents acting as tags or markers. [NIH]

labeled

with

Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Mineral Oil: A mixture of liquid hydrocarbons obtained from petroleum. It is used as laxative, lubricant, ointment base, and emollient. [NIH] 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] Minocycline: A semisynthetic staphylococcus infections. [NIH]

antibiotic

effective

against

tetracycline-resistant

Miscible: Susceptible of being mixed. [EU] 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] Mitotic inhibitors: Drugs that kill cancer cells by interfering with cell division (mitostis). [NIH]

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] 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] Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecular Structure: The location of the atoms, groups or ions relative to one another in a molecule, as well as the number, type and location of covalent bonds. [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, 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

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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] Monophosphate: So called second messenger for neurotransmitters and hormones. [NIH] Morphine: The principal alkaloid in opium and the prototype opiate analgesic and narcotic. Morphine has widespread effects in the central nervous system and on smooth muscle. [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] Movement Disorders: Syndromes which feature dyskinesias as a cardinal manifestation of the disease process. Included in this category are degenerative, hereditary, post-infectious, medication-induced, post-inflammatory, and post-traumatic conditions. [NIH] Mucins: A secretion containing mucopolysaccharides and protein that is the chief constituent of mucus. [NIH] Mucociliary: Pertaining to or affecting the mucus membrane and hairs (including eyelashes, nose hair, .): mucociliary clearing: the clearance of mucus by ciliary movement ( particularly in the respiratory system). [EU] Mucocutaneous: Pertaining to or affecting the mucous membrane and the skin. [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] Multiple Organ Failure: A progressive condition usually characterized by combined failure of several organs such as the lungs, liver, kidney, along with some clotting mechanisms, usually postinjury or postoperative. [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] 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, 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] Musculoskeletal System: Themuscles, bones, and cartilage of the body. [NIH]

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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] Mutagenesis: Process of generating genetic mutations. It may occur spontaneously or be induced by mutagens. [NIH] 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] Mutate: To change the genetic material of a cell. Then changes (mutations) can be harmful, beneficial, or have no effect. [NIH] Myasthenia: Muscular debility; any constitutional anomaly of muscle. [EU] Mydriatic: 1. Dilating the pupil. 2. Any drug that dilates the pupil. [EU] Myelin: The fatty substance that covers and protects nerves. [NIH] Myeloid Cells: Cells which include the monocytes and the granulocytes. [NIH] Myeloma: Cancer that arises in plasma cells, a type of white blood cell. [NIH] Myelosuppression: A condition in which bone marrow activity is decreased, resulting in fewer red blood cells, white blood cells, and platelets. Myelosuppression is a side effect of some cancer treatments. [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 Ischemia: A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (coronary arteriosclerosis), to obstruction by a thrombus (coronary thrombosis), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (myocardial infarction). [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]

Myocarditis: Inflammation of the myocardium; inflammation of the muscular walls of the heart. [EU]

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Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myopia: That error of refraction in which rays of light entering the eye parallel to the optic axis are brought to a focus in front of the retina, as a result of the eyeball being too long from front to back (axial m.) or of an increased strength in refractive power of the media of the eye (index m.). Called also nearsightedness, because the near point is less distant than it is in emmetropia with an equal amplitude of accommodation. [EU] 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] Myotonic Dystrophy: A condition presenting muscle weakness and wasting which may be progressive. [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] Naloxone: A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors. [NIH] Narcosis: A general and nonspecific reversible depression of neuronal excitability, produced by a number of physical and chemical aspects, usually resulting in stupor. [NIH] Narcotic: 1. Pertaining to or producing narcosis. 2. An agent that produces insensibility or stupor, applied especially to the opioids, i.e. to any natural or synthetic drug that has morphine-like actions. [EU] Narcotic Antagonists: Agents inhibiting the effect of narcotics on the central nervous system. [NIH] Nasal Cavity: The proximal portion of the respiratory passages on either side of the nasal septum, lined with ciliated mucosa, extending from the nares to the pharynx. [NIH] Nasal Mucosa: The mucous membrane lining the nasal cavity. [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] Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Necrotizing Enterocolitis: A condition in which part of the tissue in the intestines is destroyed. Occurs mainly in under-weight newborn babies. A temporary ileostomy may be necessary. [NIH] 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] 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]

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Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] 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] Nerve Fibers: Slender processes of neurons, especially the prolonged axons that conduct nerve impulses. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Nervousness: Excessive excitability and irritability, with mental and physical unrest. [EU] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neuritis: A general term indicating inflammation of a peripheral or cranial nerve. Clinical manifestation may include pain; paresthesias; paresis; or hypesthesia. [NIH] Neurobehavioral Manifestations: Signs and symptoms of higher cortical dysfunction caused by organic conditions. These include certain behavioral alterations and impairments of skills involved in the acquisition, processing, and utilization of knowledge or information. [NIH]

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] Neuroendocrine: Having to do with the interactions between the nervous system and the endocrine system. Describes certain cells that release hormones into the blood in response to stimulation of the nervous system. [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] Neuroleptic: A term coined to refer to the effects on cognition and behaviour of antipsychotic drugs, which produce a state of apathy, lack of initiative, and limited range of emotion and in psychotic patients cause a reduction in confusion and agitation and normalization of psychomotor activity. [EU] Neurologic: Having to do with nerves or the nervous system. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU] Neuromuscular Junction: The synapse between a neuron and a muscle. [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] Neuropeptides: Peptides released by neurons as intercellular messengers. Many neuropeptides are also hormones released by non-neuronal cells. [NIH] Neuroretinitis: Inflammation of the optic nerve head and adjacent retina. [NIH]

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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] Neurotoxic: Poisonous or destructive to nerve tissue. [EU] Neurotoxins: Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept. [NIH] Neurotransmitters: Endogenous signaling molecules that alter the behavior of neurons or effector cells. Neurotransmitter is used here in its most general sense, including not only messengers that act directly to regulate ion channels, but also those that act through second messenger systems, and those that act at a distance from their site of release. Included are neuromodulators, neuroregulators, neuromediators, and neurohumors, whether or not acting at synapses. [NIH] Neutralization: An act or process of neutralizing. [EU] 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] Neutropenia: An abnormal decrease in the number of neutrophils, a type of white blood cell. [NIH] Neutrophil: A type of white blood cell. [NIH] Neutrophil Collagenase: A member of the matrix metalloproteinases that cleaves triplehelical collagens types I, II, and III. EC 3.4.24.34. [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] Niacin: Water-soluble vitamin of the B complex occurring in various animal and plant tissues. Required by the body for the formation of coenzymes NAD and NADP. Has pellagra-curative, vasodilating, and antilipemic properties. [NIH] Niche: The ultimate unit of the habitat, i. e. the specific spot occupied by an individual organism; by extension, the more or less specialized relationships existing between an organism, individual or synusia(e), and its environment. [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] Nitrates: Inorganic or organic salts and esters of nitric acid. These compounds contain the NO3- radical. [NIH] Nitric acid: A toxic, corrosive, colorless liquid used to make fertilizers, dyes, explosives, and other chemicals. [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.

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[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] 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] 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] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nummular: Coin-sized and coin-shaped. [EU] Nurse Practitioners: Nurses who are specially trained to assume an expanded role in providing medical care under the supervision of a physician. [NIH] Nutritive Value: An indication of the contribution of a food to the nutrient content of the diet. This value depends on the quantity of a food which is digested and absorbed and the amounts of the essential nutrients (protein, fat, carbohydrate, minerals, vitamins) which it contains. This value can be affected by soil and growing conditions, handling and storage, and processing. [NIH] Obstetrics: A medical-surgical specialty concerned with management and care of women during pregnancy, parturition, and the puerperium. [NIH] Occupational Exposure: The exposure to potentially harmful chemical, physical, or biological agents that occurs as a result of one's occupation. [NIH] Occupational Health: The promotion and maintenance of physical and mental health in the work environment. [NIH] Ocular: 1. Of, pertaining to, or affecting the eye. 2. Eyepiece. [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] Oligopeptides: Peptides composed of between two and twelve amino acids. [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] Onychomycosis: Mycosis of the nails, possibly due to some extent to humidity. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Opium: The air-dried exudate from the unripe seed capsule of the opium poppy, Papaver somniferum, or its variant, P. album. It contains a number of alkaloids, but only a few morphine, codeine, and papaverine - have clinical significance. Opium has been used as an

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analgesic, antitussive, antidiarrheal, and antispasmodic. [NIH] Opportunistic Infections: An infection caused by an organism which becomes pathogenic under certain conditions, e.g., during immunosuppression. [NIH] Opsin: A visual pigment protein found in the retinal rods. It combines with retinaldehyde to form rhodopsin. [NIH] Optic Chiasm: The X-shaped structure formed by the meeting of the two optic nerves. At the optic chiasm the fibers from the medial part of each retina cross to project to the other side of the brain while the lateral retinal fibers continue on the same side. As a result each half of the brain receives information about the contralateral visual field from both eyes. [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. [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] Orbit: One of the two cavities in the skull which contains an eyeball. Each eye is located in a bony socket or orbit. [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] Orthodontic Brackets: Small metal or ceramic attachments used to fasten an arch wire. These attachments are soldered or welded to an orthodontic band or cemented directly onto the teeth. Bowles brackets, edgewise brackets, multiphase brackets, ribbon arch brackets, twin-wire brackets, and universal brackets are all types of orthodontic brackets. [NIH] Orthopaedic: Pertaining to the correction of deformities of the musculoskeletal system; pertaining to orthopaedics. [EU] Orthostatic: Pertaining to or caused by standing erect. [EU] Osmotic: Pertaining to or of the nature of osmosis (= the passage of pure solvent from a solution of lesser to one of greater solute concentration when the two solutions are separated by a membrane which selectively prevents the passage of solute molecules, but is permeable to the solvent). [EU] Osteoarthritis: Degeneration of articular cartilage. Primary osteoarthritis is very common in older persons, especially affecting weight-bearing joints. Articular cartilage becomes soft, frayed and thinned. [NIH] 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] Otitis: Inflammation of the ear, which may be marked by pain, fever, abnormalities of hearing, hearing loss, tinnitus, and vertigo. [EU] Otitis Media: Inflammation of the middle ear. [NIH]

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Otitis Media with Effusion: Inflammation of the middle ear with a clear pale yellowcolored transudate. [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] Ovalbumin: An albumin obtained from the white of eggs. It is a member of the serpin superfamily. [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] Overdose: An accidental or deliberate dose of a medication or street drug that is in excess of what is normally used. [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] Oxazolone: Immunologic adjuvant and sensitizing agent. [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] 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] Pacemaker: An object or substance that influences the rate at which a certain phenomenon occurs; often used alone to indicate the natural cardiac pacemaker or an artificial cardiac pacemaker. In biochemistry, a substance whose rate of reaction sets the pace for a series of interrelated reactions. [EU] Pachymeningitis: Inflammation of the dura mater of the brain, the spinal cord or the optic nerve. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] 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 gland that secretes digestive enzymes. [NIH]

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Pancreatic: Having to do with the pancreas. [NIH] Pancreatic cancer: Cancer of the pancreas, a salivary gland of the abdomen. [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] Panic: A state of extreme acute, intense anxiety and unreasoning fear accompanied by disorganization of personality function. [NIH] Panic Disorder: A type of anxiety disorder characterized by unexpected panic attacks that last minutes or, rarely, hours. Panic attacks begin with intense apprehension, fear or terror and, often, a feeling of impending doom. Symptoms experienced during a panic attack include dyspnea or sensations of being smothered; dizziness, loss of balance or faintness; choking sensations; palpitations or accelerated heart rate; shakiness; sweating; nausea or other form of abdominal distress; depersonalization or derealization; paresthesias; hot flashes or chills; chest discomfort or pain; fear of dying and fear of not being in control of oneself or going crazy. Agoraphobia may also develop. Similar to other anxiety disorders, it may be inherited as an autosomal dominant trait. [NIH] 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] Paraffin: A mixture of solid hydrocarbons obtained from petroleum. It has a wide range of uses including as a stiffening agent in ointments, as a lubricant, and as a topical antiinflammatory. It is also commonly used as an embedding material in histology. [NIH] Paranasal Sinuses: Air-filled extensions of the respiratory part of the nasal cavity into the frontal, ethmoid, sphenoid, and maxillary cranial bones. They vary in size and form in different individuals and are lined by the ciliated mucous membranes of the nasal cavity. [NIH]

Parasite: An animal or a plant that lives on or in an organism of another species and gets at least some of its nutrition from that other organism. [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] Parenteral: Not through the alimentary canal but rather by injection through some other route, as subcutaneous, intramuscular, intraorbital, intracapsular, intraspinal, intrasternal, intravenous, etc. [EU] Paresis: A general term referring to a mild to moderate degree of muscular weakness, occasionally used as a synonym for paralysis (severe or complete loss of motor function). In the older literature, paresis often referred specifically to paretic neurosyphilis. "General paresis" and "general paralysis" may still carry that connotation. Bilateral lower extremity paresis is referred to as paraparesis. [NIH] Paresthesias: Abnormal touch sensations, such as burning or prickling, that occur without an outside stimulus. [NIH] 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] Parkinsonism: A group of neurological disorders characterized by hypokinesia, tremor, and

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muscular rigidity. [EU] Parotid: The space that contains the parotid gland, the facial nerve, the external carotid artery, and the retromandibular vein. [NIH] Paroxetine: A serotonin uptake inhibitor that is effective in the treatment of depression. [NIH]

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] Particle: A tiny mass of material. [EU] Patch: A piece of material used to cover or protect a wound, an injured part, etc.: a patch over the eye. [NIH] Patch Tests: Skin tests in which the sensitizer is applied to a patch of cotton cloth or gauze held in place for approximately 48-72 hours. It is used for the elicitation of a contact hypersensitivity reaction. [NIH] 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 Education: The teaching or training of patients concerning their own health needs. [NIH]

Patient Satisfaction: The degree to which the individual regards the health care service or product or the manner in which it is delivered by the provider as useful, effective, or beneficial. [NIH] Pelvic: Pertaining to the pelvis. [EU] Pemphigus: Group of chronic blistering diseases characterized histologically by acantholysis and blister formation within the epidermis. [NIH] Penicillin: An antibiotic drug used to treat infection. [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 Fragments: Partial proteins formed by partial hydrolysis of complete proteins. [NIH]

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Perception: The ability quickly and accurately to recognize similarities and differences 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] Perennial: Lasting through the year of for several years. [EU] Perianal: Located around the anus. [EU] Pericardium: The fibroserous sac surrounding the heart and the roots of the great vessels. [NIH]

Perinatal: Pertaining to or occurring in the period shortly before and after birth; variously defined as beginning with completion of the twentieth to twenty-eighth week of gestation and ending 7 to 28 days after birth. [EU] Perineal: Pertaining to the perineum. [EU] Perineum: The area between the anus and the sex organs. [NIH] Periodontal disease: Disease involving the supporting structures of the teeth (as the gums and periodontal membranes). [NIH] Periodontitis: Inflammation of the periodontal membrane; also called periodontitis simplex. [NIH]

Perioral: Situated or occurring around the mouth. [EU] Periorbital: Situated around the orbit, or eye socket. [EU] Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral Nerves: The nerves outside of the brain and spinal cord, including the autonomic, cranial, and spinal nerves. Peripheral nerves contain non-neuronal cells and connective tissue as well as axons. The connective tissue layers include, from the outside to the inside, the epineurium, the perineurium, and the endoneurium. [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] Peritoneal: Having to do with the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [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] Peroxide: Chemical compound which contains an atom group with two oxygen atoms tied to each other. [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]

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Phagocyte: An immune system cell that can surround and kill microorganisms and remove dead cells. Phagocytes include macrophages. [NIH] Pharmaceutic Aids: Substances which are of little or no therapeutic value, but are necessary in the manufacture, compounding, storage, etc., of pharmaceutical preparations or drug dosage forms. They include solvents, diluting agents, and suspending agents, and emulsifying agents. Also, antioxidants; preservatives, pharmaceutical; dyes (coloring agents); flavoring agents; vehicles; excipients; ointment bases. [NIH] 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] 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] Pharyngitis: Inflammation of the throat. [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] Phosphodiesterase: Effector enzyme that regulates the levels of a second messenger, the cyclic GMP. [NIH] Phosphodiesterase Inhibitors: Compounds which inhibit or antagonize the biosynthesis or actions of phosphodiesterases. [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] 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] 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

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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] Photopheresis: A process in which peripheral blood is exposed in an extracorporeal flow system to photoactivated 8-methoxypsoralen (methoxsalen) and ultraviolet light - a procedure known as PUVA therapy. Photopheresis is at present a standard therapy for advanced cutaneous T-cell lymphoma; it shows promise in the treatment of autoimmune diseases. [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] 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 cells, tissues, and organs. [NIH] Pigment: A substance that gives color to tissue. Pigments are responsible for the color of skin, eyes, and hair. [NIH] Pigmentation: Coloration or discoloration of a part by a pigment. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH] Piperidines: A family of hexahydropyridines. Piperidine itself is found in the pepper plant as the alkaloid piperine. [NIH] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [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] Plana: The radiographic term applied to a vertebral body crushed to a thin plate. [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]

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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] Plasma protein: One of the hundreds of different proteins present in blood plasma, including carrier proteins ( such albumin, transferrin, and haptoglobin), fibrinogen and other coagulation factors, complement components, immunoglobulins, enzyme inhibitors, precursors of substances such as angiotension and bradykinin, and many other types of proteins. [EU] 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] 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] Plasminogen Inactivators: Important modulators of the activity of plasminogen activators. Four inhibitors, all belonging to the serpin family of proteins, have been implicated in plasminogen activation inhibition. They are PAI-1, PAI-2, protease-nexin, and protein C inhibitor (PAI-3). All inhibit both the tissue-type and urokinase-type plasminogen activators. [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] Platelet Factor 4: A high-molecular-weight proteoglycan-platelet factor complex which is released from blood platelets by thrombin. It acts as a mediator in the heparin-neutralizing capacity of the blood and plays a role in platelet aggregation. At high ionic strength (I=0.75), the complex dissociates into the active component (molecular weight 29,000) and the proteoglycan carrier (chondroitin 4-sulfate, molecular weight 350,000). The molecule exists in the form of a dimer consisting of 8 moles of platelet factor 4 and 2 moles of proteoglycan. [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] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH]

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Pollen: The male fertilizing element of flowering plants analogous to sperm in animals. It is released from the anthers as yellow dust, to be carried by insect or other vectors, including wind, to the ovary (stigma) of other flowers to produce the embryo enclosed by the seed. The pollens of many plants are allergenic. [NIH] Polyarteritis Nodosa: A form of necrotizing vasculitis involving small- and medium-sized arteries. The signs and symptoms result from infarction and scarring of the affected organ system. [NIH] 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]

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] Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called tripeptides, tetrapeptides, etc. according to the number of amino acids contained. [EU] 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] Port: An implanted device through which blood may be withdrawn and drugs may be infused without repeated needle sticks. Also called a port-a-cath. [NIH] Port-a-cath: An implanted device through which blood may be withdrawn and drugs may be infused without repeated needle sticks. Also called a port. [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] Postoperative: After surgery. [NIH] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Post-translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [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 Cyanide: Potassium cyanide (K(CN)). A highly poisonous compound that is an inhibitor of many metabolic processes, but has been shown to be an especially potent

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inhibitor of heme enzymes and hemeproteins. It is used in many industrial processes. [NIH] Potentiate: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiating: 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] 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] Preeclampsia: A toxaemia of late pregnancy characterized by hypertension, edema, and proteinuria, when convulsions and coma are associated, it is called eclampsia. [EU] Presynaptic: Situated proximal to a synapse, or occurring before the synapse is crossed. [EU] Presynaptic Terminals: The distal terminations of axons which are specialized for the release of neurotransmitters. Also included are varicosities along the course of axons which have similar specializations and also release transmitters. Presynaptic terminals in both the central and peripheral nervous systems are included. [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] Private Sector: That distinct portion of the institutional, industrial, or economic structure of a country that is controlled or owned by non-governmental, private interests. [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] Prodrug: A substance that gives rise to a pharmacologically active metabolite, although not itself active (i. e. an inactive precursor). [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

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severity. [EU] Projection: A defense mechanism, operating unconsciously, whereby that which is emotionally unacceptable in the self is rejected and attributed (projected) to others. [NIH] Prolapse: The protrusion of an organ or part of an organ into a natural or artificial orifice. [NIH]

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] Prone: Having the front portion of the body downwards. [NIH] Prone Position: The posture of an individual lying face down. [NIH] Pro-Opiomelanocortin: A precursor protein, MW 30,000, synthesized mainly in the anterior pituitary gland but also found in the hypothalamus, brain, and several peripheral tissues. It incorporates the amino acid sequences of ACTH and beta-lipotropin. These two hormones, in turn, contain the biologically active peptides MSH, corticotropin-like intermediate lobe peptide, alpha-lipotropin, endorphins, and methionine enkephalin. [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] Propylene Glycol: A clear, colorless, viscous organic solvent and diluent used in pharmaceutical preparations. [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

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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] 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 Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. Quaternary protein structure describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain). [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] 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] 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] Protozoa: A subkingdom consisting of unicellular organisms that are the simplest in the

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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] Psychogenic: Produced or caused by psychic or mental factors rather than organic factors. [EU]

Psychomotor: Pertaining to motor effects of cerebral or psychic activity. [EU] Psychosis: A mental disorder characterized by gross impairment in reality testing as evidenced by delusions, hallucinations, markedly incoherent speech, or disorganized and agitated behaviour without apparent awareness on the part of the patient of the incomprehensibility of his behaviour; the term is also used in a more general sense to refer to mental disorders in which mental functioning is sufficiently impaired as to interfere grossly with the patient's capacity to meet the ordinary demands of life. Historically, the term has been applied to many conditions, e.g. manic-depressive psychosis, that were first described in psychotic patients, although many patients with the disorder are not judged psychotic. [EU] Psyllium: Dried, ripe seeds of Plantago psyllium, P. indica, and P. ovata (Plantaginaceae). Plantain seeds swell in water and are used as demulcents and bulk laxatives. [NIH] Puberty: The period during which the secondary sex characteristics begin to develop and the capability of sexual reproduction is attained. [EU] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] 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] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]

Pulmonary: Relating to the lungs. [NIH] Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs. [NIH]

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Pulmonary Circulation: The circulation of blood through the lungs. [NIH] Pulmonary hypertension: Abnormally high blood pressure in the arteries of the lungs. [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] Purpura: Purplish or brownish red discoloration, easily visible through the epidermis, caused by hemorrhage into the tissues. [NIH] Pustular: Pertaining to or of the nature of a pustule; consisting of pustules (= a visible collection of pus within or beneath the epidermis). [EU] Pyridones: Pyridine derivatives with one or more keto groups on the ring. [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] Quercetin: Aglucon of quercetrin, rutin, and other glycosides. It is widely distributed in the plant kingdom, especially in rinds and barks, clover blossoms, and ragweed pollen. [NIH] Quiescent: Marked by a state of inactivity or repose. [EU] 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 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] Radioallergosorbent Test: An in vitro allergen radioimmunoassay in which allergens are coupled to an immunosorbent. The coupled allergens bind the IgE in the sera of patients which in turn binds radioisotope-labeled anti-IgE antibodies. [NIH] Radiodermatitis: A cutaneous inflammatory reaction occurring as a result of exposure to ionizing radiation. [NIH] Radioimmunoassay: Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Nonimmunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation. [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,

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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] Radioisotope: An unstable element that releases radiation as it breaks down. Radioisotopes can be used in imaging tests or as a treatment for cancer. [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] Rarefaction: The reduction of the density of a substance; the attenuation of a gas. [NIH] Reagent: A substance employed to produce a chemical reaction so as to detect, measure, produce, etc., other substances. [EU] Reality Testing: The individual's objective evaluation of the external world and the ability to differentiate adequately between it and the internal world; considered to be a primary ego function. [NIH] Receptivity: The condition of the reproductive organs of a female flower that permits effective pollination. [NIH] 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] Receptors, Serotonin: Cell-surface proteins that bind serotonin and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action. [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] Recombinant Proteins: Proteins prepared by recombinant DNA technology. [NIH] 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] Rectal: By or having to do with the rectum. The rectum is the last 8 to 10 inches of the large intestine and ends at the anus. [NIH] Rectum: The last 8 to 10 inches of the large intestine. [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

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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] Reflex: An involuntary movement or exercise of function in a part, excited in response to a stimulus applied to the periphery and transmitted to the brain or spinal cord. [NIH] Reflux: The term used when liquid backs up into the esophagus from the stomach. [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 progressive renal glomerular tubular or interstitial 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] Renin-Angiotensin System: A system consisting of renin, angiotensin-converting enzyme, and angiotensin II. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming angiotensin I. The converting enzyme contained in the lung acts on angiotensin I in the plasma converting it to angiotensin II, the most powerful directly pressor substance known. It causes contraction of the arteriolar smooth muscle and has other indirect actions mediated through the adrenal cortex. [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] Respiratory Burst: A large increase in oxygen uptake by neutrophils and most types of tissue macrophages through activation of an NADPH-cytochrome b-dependent oxidase that reduces oxygen to a superoxide. Individuals with an inherited defect in which the oxidase that reduces oxygen to superoxide is decreased or absent (granulomatous disease, chronic)

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often die as a result of recurrent bacterial infections. [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] Respiratory syncytial virus: RSV. A virus that causes respiratory infections with cold-like symptoms. [NIH] Respiratory System: The tubular and cavernous organs and structures, by means of which pulmonary ventilation and gas exchange between ambient air and the blood are brought about. [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]

Response rate: The percentage of patients whose cancer shrinks or disappears after treatment. [NIH] Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH] Reticular: Coarse-fibered, netlike dermis layer. [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] 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] Retinal Detachment: Separation of the inner layers of the retina (neural retina) from the pigment epithelium. Retinal detachment occurs more commonly in men than in women, in eyes with degenerative myopia, in aging and in aphakia. It may occur after an uncomplicated cataract extraction, but it is seen more often if vitreous humor has been lost during surgery. (Dorland, 27th ed; Newell, Ophthalmology: Principles and Concepts, 7th ed, p310-12). [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] 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] Retroperitoneal: Having to do with the area outside or behind the peritoneum (the tissue

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that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Retrospective: Looking back at events that have already taken place. [NIH] Retrospective study: A study that looks backward in time, usually using medical records and interviews with patients who already have or had a disease. [NIH] Retroviral vector: RNA from a virus that is used to insert genetic material into cells. [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 as possible causes. [NIH] Rhinitis: Inflammation of the mucous membrane of the nose. [NIH] Ribavirin: 1-beta-D-Ribofuranosyl-1H-1,2,4-triazole-3-carboxamide. A nucleoside antimetabolite antiviral agent that blocks nucleic acid synthesis and is used against both RNA and DNA viruses. [NIH] Riboflavin: Nutritional factor found in milk, eggs, malted barley, liver, kidney, heart, and leafy vegetables. The richest natural source is yeast. It occurs in the free form only in the retina of the eye, in whey, and in urine; its principal forms in tissues and cells are as FMN and FAD. [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] 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] Risk patient: Patient who is at risk, because of his/her behaviour or because of the type of person he/she is. [EU] Rod: A reception for vision, located in the retina. [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] Rutin: 3-((6-O-(6-Deoxy-alpha-L-mannopyranosyl)-beta-D-glucopyranosyl)oxy)-2-(3,4dihydroxyphenyl)-5,7-dihydroxy-4H-1-benzopyran-4-one. Found in many plants, including buckwheat, tobacco, forsythia, hydrangea, pansies, etc. It has been used therapeutically to decrease capillary fragility. [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]

Salicylamides: Amides of salicylic acid. [NIH] Salicylanilides: 2-Hydroxy-N-phenylbenzamides. N-phenyl substituted salicylamides.

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Derivatives have been used as fungicides, anti-mildew agents and topical antifungal agents. In concentrated form may cause irritation of skin and mucous membranes. [NIH] Salicylic: A tuberculosis drug. [NIH] Saline: A solution of salt and water. [NIH] Saliva: The clear, viscous fluid secreted by the salivary glands and mucous glands of the mouth. It contains mucins, water, organic salts, and ptylin. [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 when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] Sarcoidosis: An idiopathic systemic inflammatory granulomatous disorder comprised of epithelioid and multinucleated giant cells with little necrosis. It usually invades the lungs with fibrosis and may also involve lymph nodes, skin, liver, spleen, eyes, phalangeal bones, and parotid glands. [NIH] Sarcoma: A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant. [NIH] Satellite: Applied to a vein which closely accompanies an artery for some distance; in cytogenetics, a chromosomal agent separated by a secondary constriction from the main body of the chromosome. [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] 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] Scleral Buckling: An operation for retinal detachment which reduces the size of the globe by indenting the sclera so that it approximates the retina. [NIH] Scleritis: Refers to any inflammation of the sclera including episcleritis, a benign condition affecting only the episclera, which is generally short-lived and easily treated. Classic scleritis, on the other hand, affects deeper tissue and is characterized by higher rates of visual acuity loss and even mortality, particularly in necrotizing form. Its characteristic symptom is severe and general head pain. Scleritis has also been associated with systemic collagen disease. Etiology is unknown but is thought to involve a local immune response. Treatment is difficult and includes administration of anti-inflammatory and immunosuppressive agents such as corticosteroids. Inflammation of the sclera may also be secondary to inflammation of adjacent tissues, such as the conjunctiva. [NIH]

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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] 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] Seafood: Marine fish and shellfish used as food or suitable for food. (Webster, 3d ed) shellfish and fish products are more specific types of seafood. [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] 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] Secretory Vesicles: Vesicles derived from the golgi apparatus containing material to be released at the cell surface. [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] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Senescence: The bodily and mental state associated with advancing age. [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] Sensor: A device designed to respond to physical stimuli such as temperature, light, magnetism or movement and transmit resulting impulses for interpretation, recording, movement, or operating control. [NIH]

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Sepsis: The presence of bacteria in the bloodstream. [NIH] Septic: Produced by or due to decomposition by microorganisms; putrefactive. [EU] Septicemia: Systemic disease associated with the presence and persistence of pathogenic microorganisms or their toxins in the blood. Called also blood poisoning. [EU] 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] Serine Endopeptidases: Any member of the group of endopeptidases containing at the active site a serine residue involved in catalysis. EC 3.4.21. [NIH] Serine Proteinase Inhibitors: Exogenous or endogenous compounds which inhibit serine endopeptidases. [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 broad physiological actions and distribution of this biochemical mediator. [NIH] Serotonin Agonists: Agents that have an affinity for serotonin receptors and are able to mimic the effects of serotonin by stimulating the physiologic activity at the cell receptors. These compounds are used as antidepressants, anxiolytics, and in the treatment of migraine. [NIH]

Serotonin Antagonists: Drugs that bind to but do not activate serotonin receptors, thereby blocking the actions of serotonin or serotonin agonists. [NIH] Serous: Having to do with serum, the clear liquid part of blood. [NIH] Serpins: A family of serine proteinase inhibitors which are similar in amino acid sequence and mechanism of inhibition, but differ in their specificity toward proteolytic enzymes. This family includes alpha 1-antitrypsin, angiotensinogen, ovalbumin, antiplasmin, alpha 1antichymotrypsin, thyroxine-binding protein, complement 1 inactivators, antithrombin III, heparin cofactor II, plasminogen inactivators, gene Y protein, placental plasminogen activator inhibitor, and barley Z protein. Some members of the serpin family may be substrates rather than inhibitors of serine endopeptidases, and some serpins occur in plants where their function is not known. [NIH] Serrata: The serrated anterior border of the retina located approximately 8.5 mm from the limbus and adjacent to the pars plana of the ciliary body. [NIH] Serrated: Having notches or teeth on the edge as a saw has. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [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]

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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] Simvastatin: A derivative of lovastatin and potent competitive inhibitor of 3-hydroxy-3methylglutaryl coenzyme A reductase (hydroxymethylglutaryl CoA reductases), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL receptors, it increases breakdown of LDL-cholesterol (lipoproteins, LDL cholesterol). [NIH] Sinusitis: An inflammatory process of the mucous membranes of the paranasal sinuses that occurs in three stages: acute, subacute, and chronic. Sinusitis results from any condition causing ostial obstruction or from pathophysiologic changes in the mucociliary transport mechanism. [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 many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skin Care: Maintenance of the hygienic state of the skin under optimal conditions of cleanliness and comfort. Effective in skin care are proper washing, bathing, cleansing, and the use of soaps, detergents, oils, etc. In various disease states, therapeutic and protective solutions and ointments are useful. The care of the skin is particularly important in various occupations, in exposure to sunlight, in neonates, and in decubitus ulcer. [NIH] Skin Manifestations: Dermatologic disorders attendant upon non-dermatologic disease or injury. [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]

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Smallpox: A generalized virus infection with a vesicular rash. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]

Snails: Marine, freshwater, or terrestrial mollusks of the class Gastropoda. Most have an enclosing spiral shell, and several genera harbor parasites pathogenic to man. [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] 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] 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] Soma: The body as distinct from the mind; all the body tissue except the germ cells; all the axial body. [NIH] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Somatic mutations: Alterations in DNA that occur after conception. Somatic mutations can occur in any of the cells of the body except the germ cells (sperm and egg) and therefore are not passed on to children. These alterations can (but do not always) cause cancer or other diseases. [NIH] Soybean Oil: Oil from soybean or soybean plant. [NIH] Spasmogenic: Capable of producing convulsions. [NIH] Spastic: 1. Of the nature of or characterized by spasms. 2. Hypertonic, so that the muscles are stiff and the movements awkward. 3. A person exhibiting spasticity, such as occurs in spastic paralysis or in cerebral palsy. [EU] 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]

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Species Specificity: Restriction of a characteristic or response to the members of one species; it usually refers to that property of the immune response which differentiates one species from another on the basis of antigen recognition, but the concept is not limited to immunology and is used loosely at levels higher than the species. [NIH] 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] 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] 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] Spinous: Like a spine or thorn in shape; having spines. [NIH] Spirochete: Lyme disease. [NIH] Spirometry: Measurement of volume of air inhaled or exhaled by the lung. [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] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Sprue: A non febrile tropical disease of uncertain origin. [NIH] Stabilizer: A device for maintaining constant X-ray tube voltage or current. [NIH] Standard therapy: A currently accepted and widely used treatment for a certain type of cancer, based on the results of past research. [NIH] Staphylococcal Infections: Infections with bacteria of the genus Staphylococcus. [NIH] Staphylococcal Scalded Skin Syndrome: A disease of infants due to group 2 phage type 17 staphylococci that produce an epidermolytic exotoxin. Superficial fine vesicles and bullae form and rupture easily, resulting in loss of large sheets of epidermis. [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] Stasis: A word termination indicating the maintenance of (or maintaining) a constant level; preventing increase or multiplication. [EU] Statistically significant: Describes a mathematical measure of difference between groups. The difference is said to be statistically significant if it is greater than what might be expected to happen by chance alone. [NIH] Steady state: Dynamic equilibrium. [EU] Stem Cells: Relatively undifferentiated cells of the same lineage (family type) that retain the

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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] 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] 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] 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] Streptavidin: A 60kD extracellular protein of Streptomyces avidinii with four high-affinity biotin binding sites. Unlike AVIDIN, streptavidin has a near neutral isoelectric point and is free of carbohydrate side chains. [NIH] Streptococcal: Caused by infection due to any species of 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] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] 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] Stromelysin 1: An extracellular endopeptidase of vertebrate tissues similar to interstitial collagenase. It digests proteoglycan, fibronectin, collagen types III, IV, V, and IX, and activates procollagenase. (Enzyme Nomenclature, 1992) EC 3.4.24.17. [NIH] Stupor: Partial or nearly complete unconsciousness, manifested by the subject's responding only to vigorous stimulation. Also, in psychiatry, a disorder marked by reduced responsiveness. [EU] 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]

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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 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] Suction: The removal of secretions, gas or fluid from hollow or tubular organs or cavities by means of a tube and a device that acts on negative pressure. [NIH] Sulfapyridine: Antibacterial, potentially toxic, used to treat certain skin diseases. [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] Superoxide: Derivative of molecular oxygen that can damage cells. [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] Suppurative: Consisting of, containing, associated with, or identified by the formation of pus. [NIH] Suramin: A polyanionic compound with an unknown mechanism of action. It is used parenterally in the treatment of African trypanosomiasis and it has been used clinically with diethylcarbamazine to kill the adult Onchocerca. (From AMA Drug Evaluations Annual, 1992, p1643) It has also been shown to have potent antineoplastic properties. [NIH] 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]

Survival Rate: The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods. [NIH] Suspensions: Colloids with liquid continuous phase and solid dispersed phase; the term is used loosely also for solid-in-gas (aerosol) and other colloidal systems; water-insoluble drugs may be given as suspensions. [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]

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Sympathomimetic: 1. Mimicking the effects of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. 2. An agent that produces effects similar to those of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. Called also adrenergic. [EU] Symphysis: A secondary cartilaginous joint. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Symptomatic treatment: Therapy that eases symptoms without addressing the cause of disease. [NIH] Synapses: Specialized junctions at which a neuron communicates with a target cell. At classical synapses, a neuron's presynaptic terminal releases a chemical transmitter stored in synaptic vesicles which diffuses across a narrow synaptic cleft and activates receptors on the postsynaptic membrane of the target cell. The target may be a dendrite, cell body, or axon of another neuron, or a specialized region of a muscle or secretory cell. Neurons may also communicate through direct electrical connections which are sometimes called electrical synapses; these are not included here but rather in gap junctions. [NIH] Synapsis: The pairing between homologous chromosomes of maternal and paternal origin during the prophase of meiosis, leading to the formation of gametes. [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 meiosis). [EU] Synaptic Transmission: The communication from a neuron to a target (neuron, muscle, or secretory cell) across a synapse. In chemical synaptic transmission, the presynaptic neuron releases a neurotransmitter that diffuses across the synaptic cleft and binds to specific synaptic receptors. These activated receptors modulate ion channels and/or secondmessenger systems to influence the postsynaptic cell. Electrical transmission is less common in the nervous system, and, as in other tissues, is mediated by gap junctions. [NIH] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Synovial: Of pertaining to, or secreting synovia. [EU] 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] 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] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Tachycardia: Excessive rapidity in the action of the heart, usually with a heart rate above 100 beats per minute. [NIH] Tacrine: A cholinesterase inhibitor that crosses the blood-brain barrier. Tacrine has been used to counter the effects of muscle relaxants, as a respiratory stimulant, and in the

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treatment of Alzheimer's disease and other central nervous system disorders. [NIH] 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] Talcum: A native magnesium silicate. [NIH] Talcum powder: A native magnesium silicate. [NIH] Tardive: Marked by lateness, late; said of a disease in which the characteristic lesion is late in appearing. [EU] Tea Tree Oil: Essential oil extracted from Melaleuca alternifolia (tea tree). It is used as a topical antimicrobial due to the presence of terpineol. [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] Tenesmus: Straining, especially ineffectual and painful straining at stool or in urination. [EU] Testicular: Pertaining to a testis. [EU] 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] Tetani: Causal agent of tetanus. [NIH] Tetanic: Having the characteristics of, or relating to tetanus. [NIH] Tetanus: A disease caused by tetanospasmin, a powerful protein toxin produced by Clostridium tetani. Tetanus usually occurs after an acute injury, such as a puncture wound or laceration. Generalized tetanus, the most common form, is characterized by tetanic muscular contractions and hyperreflexia. Localized tetanus presents itself as a mild condition with manifestations restricted to muscles near the wound. It may progress to the generalized form. [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] 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]

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Thermoregulation: Heat regulation. [EU] Thigh: A leg; in anatomy, any elongated process or part of a structure more or less comparable to a leg. [NIH] Third Ventricle: A narrow cleft inferior to the corpus callosum, within the diencephalon, between the paired thalami. Its floor is formed by the hypothalamus, its anterior wall by the lamina terminalis, and its roof by ependyma. It communicates with the fourth ventricle by the cerebral aqueduct, and with the lateral ventricles by the interventricular foramina. [NIH] Thorax: A part of the trunk between the neck and the abdomen; the chest. [NIH] 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] 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] Thyroxine: An amino acid of the thyroid gland which exerts a stimulating effect on thyroid metabolism. [NIH] Tic: An involuntary compulsive, repetitive, stereotyped movement, resembling a purposeful movement because it is coordinated and involves muscles in their normal synergistic relationships; tics usually involve the face and shoulders. [EU] 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] Tinea Pedis: Dermatological pruritic lesion in the feet, caused by Trichophyton rubrum, T. mentagrophytes, or Epidermophyton floccosum. [NIH] Tinnitus: Sounds that are perceived in the absence of any external noise source which may take the form of buzzing, ringing, clicking, pulsations, and other noises. Objective tinnitus refers to noises generated from within the ear or adjacent structures that can be heard by other individuals. The term subjective tinnitus is used when the sound is audible only to the

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affected individual. Tinnitus may occur as a manifestation of cochlear diseases; vestibulocochlear nerve diseases; intracranial hypertension; craniocerebral trauma; and other conditions. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Plasminogen Activator: A proteolytic enzyme in the serine protease family found in many tissues which converts plasminogen to plasmin. It has fibrin-binding activity and is immunologically different from urinary plasminogen activator. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases. EC 3.4.21.68. [NIH] 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] Tonicity: The normal state of muscular tension. [NIH] Topical: On the surface of the body. [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] Toxicokinetics: Study of the absorption, distribution, metabolism, and excretion of test substances. [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] Toxins: Specific, characterizable, poisonous chemicals, often proteins, with specific biological properties, including immunogenicity, produced by microbes, higher plants, or animals. [NIH] 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] Tractus: A part of some structure, usually that part along which something passes. [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] 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]

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Transgenes: Genes that are introduced into an organism using gene transfer techniques. [NIH]

Translating: Conversion from one language to another language. [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] Translocate: 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] Triamcinolone Acetonide: An esterified form of triamcinolone. It is an anti-inflammatory glucocorticoid used topically in the treatment of various skin disorders. Intralesional, intramuscular, and intra-articular injections are also administered under certain conditions. [NIH]

Trichloroethylene: A highly volatile inhalation anesthetic used mainly in short surgical procedures where light anesthesia with good analgesia is required. It is also used as an industrial solvent. Prolonged exposure to high concentrations of the vapor can lead to cardiotoxicity and neurological impairment. [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] Tricyclic: Containing three fused rings or closed chains in the molecular structure. [EU] Trigger zone: Dolorogenic zone (= producing or causing pain). [EU] Tropical Sprue: A condition of unknown cause. Abnormalities in the lining of the small intestine prevent the body from absorbing food normally. [NIH] Tropism: Directed movements and orientations found in plants, such as the turning of the sunflower to face the sun. [NIH] Trypanosomiasis: Infection with protozoa of the genus Trypanosoma. [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] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [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]

Dictionary 375

Tumor marker: A substance sometimes found in an increased amount in the blood, other body fluids, or tissues and which may mean that a certain type of cancer is in the body. Examples of tumor markers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and gastrointestinal tract cancers), and PSA (prostate cancer). Also called biomarker. [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] Tumor suppressor gene: Genes in the body that can suppress or block the development of cancer. [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] 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] Ubiquitin: A highly conserved 76 amino acid-protein found in all eukaryotic cells. [NIH] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH] Ulceration: 1. The formation or development of an ulcer. 2. An ulcer. [EU] Ulcerative colitis: Chronic inflammation of the colon that produces ulcers in its lining. This condition is marked by abdominal pain, cramps, and loose discharges of pus, blood, and mucus from the bowel. [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] Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [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]

Urbanization: The process whereby a society changes from a rural to an urban way of life. It refers also to the gradual increase in the proportion of people living in urban 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] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]

Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary Plasminogen Activator: A proteolytic enzyme that converts plasminogen to plasmin where the preferential cleavage is between arginine and valine. It was isolated originally from human urine, but is found in most tissues of most vertebrates. EC 3.4.21.73.

376 Dermatitis

[NIH]

Urinary Retention: Inability to urinate. The etiology of this disorder includes obstructive, neurogenic, pharmacologic, and psychogenic causes. [NIH] Urinate: To release urine from the bladder to the outside. [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] Urogenital: Pertaining to the urinary and genital apparatus; genitourinary. [EU] 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] Vaccine adjuvant: A substance added to a vaccine to improve the immune response so that less vaccine is needed. [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] Vaginal: Of or having to do with the vagina, the birth canal. [NIH] Variola: A generalized virus infection with a vesicular rash. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasculitis: Inflammation of a blood vessel. [NIH] Vasoactive: Exerting an effect upon the calibre of blood vessels. [EU] Vasoactive Intestinal Peptide: A highly basic, single-chain polypeptide isolated from the intestinal mucosa. It has a wide range of biological actions affecting the cardiovascular, gastrointestinal, and respiratory systems. It is also found in several parts of the central and peripheral nervous systems and is a neurotransmitter. [NIH] Vasoconstriction: Narrowing of the blood vessels without anatomic change, for which constriction, pathologic is used. [NIH] Vasodilatation: A state of increased calibre of the blood vessels. [EU] Vasodilation: Physiological dilation of the blood vessels without anatomic change. For dilation with anatomic change, dilatation, pathologic or aneurysm (or specific aneurysm) is

Dictionary 377

used. [NIH] Vasodilator: An agent that widens blood vessels. [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] Venoms: Poisonous animal secretions forming fluid mixtures of many different enzymes, toxins, and other substances. These substances are produced in specialized glands and secreted through specialized delivery systems (nematocysts, spines, fangs, etc.) for disabling prey or predator. [NIH] Venous: Of or pertaining to the veins. [EU] Ventral: 1. Pertaining to the belly or to any venter. 2. Denoting a position more toward the belly surface than some other object of reference; same as anterior in human anatomy. [EU] 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] Vertigo: An illusion of movement; a sensation as if the external world were revolving around the patient (objective vertigo) or as if he himself were revolving in space (subjective vertigo). The term is sometimes erroneously used to mean any form of dizziness. [EU] 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] Villi: The tiny, fingerlike projections on the surface of the small intestine. Villi help absorb nutrients. [NIH] Villous: Of a surface, covered with villi. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] 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] Viscera: Any of the large interior organs in any one of the three great cavities of the body, especially in the abdomen. [NIH] Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Visual Acuity: Acuteness or clearness of vision, especially of form vision, which is dependent mainly on the sharpness of the retinal focus. [NIH] Vitamin A: A substance used in cancer prevention; it belongs to the family of drugs called

378 Dermatitis

retinoids. [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] Vitreous Hemorrhage: Hemorrhage into the vitreous body. [NIH] Vitreous Humor: The transparent, colorless mass of gel that lies behind the lens and in front of the retina and fills the center of the eyeball. [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] Wakefulness: A state in which there is an enhanced potential for sensitivity and an efficient responsiveness to external stimuli. [NIH] War: Hostile conflict between organized groups of people. [NIH] Wart: A raised growth on the surface of the skin or other organ. [NIH] Weight-Bearing: The physical state of supporting an applied load. This often refers to the weight-bearing bones or joints that support the body's weight, especially those in the spine, hip, knee, and foot. [NIH] Wheezing: Breathing with a rasp or whistling sound; a sign of airway constriction or obstruction. [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] Wound Healing: Restoration of integrity to traumatized tissue. [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'

Dictionary 379

and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] Zinc Oxide: A mild astringent and topical protectant with some antiseptic action. It is also used in bandages, pastes, ointments, dental cements, and as a sunblock. [NIH] Zygosaccharomyces: A genus of ascomycetous fungi of the family Saccharomycetaceae, order Saccharomycetales. [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]

381

INDEX 1 1-phosphate, 51, 277 A Abdomen, 193, 277, 289, 290, 308, 319, 328, 332, 346, 348, 361, 367, 368, 372, 377 Abdominal, 26, 39, 194, 236, 277, 329, 336, 345, 346, 348, 361, 375 Abdominal Pain, 26, 39, 236, 277, 329, 348, 375 Aberrant, 15, 71, 277 Abrasion, 54, 277 Acantholysis, 277, 347 Acceptor, 277, 315, 345 Acetylcholine, 91, 277, 290, 295, 342 Acetylcholinesterase, 190, 277 Acne, 141, 167, 168, 190, 195, 205, 215, 217, 228, 277, 288 Acrodermatitis, 69, 94, 97, 111, 122, 141, 251, 277 Acrylamide, 74, 277 Acrylonitrile, 277, 361 Actin, 58, 277, 340 Actinic keratosis, 208, 277 Action Potentials, 166, 277 Acyl, 212, 277 Adaptability, 49, 278, 293, 294 Adenine, 202, 278, 357 Adenosine, 144, 164, 278, 349, 371 Adenosine Monophosphate, 144, 164, 278 Adhesives, 184, 277, 278 Adjustment, 198, 278 Adjuvant, 48, 278, 316, 345 Adoptive Transfer, 14, 20, 31, 35, 56, 278 Adrenal Cortex, 278, 301, 312, 322, 353, 359 Adrenal Glands, 191, 278, 281 Adrenergic, 240, 278, 284, 307, 311, 370 Adverse Effect, 16, 76, 236, 278, 365 Aerobic, 188, 278, 345 Aerosol, 278, 369 Afferent, 20, 278 Affinity, 29, 51, 278, 279, 286, 364, 366, 368 Agar, 278, 350 Age of Onset, 7, 261, 279 Ageing, 191, 279 Aggravation, 105, 167, 279 Agonist, 201, 279, 307, 340 Agranulocytosis, 195, 279

Air Pollutants, 188, 279 Airway, 20, 30, 63, 279, 290, 378 Akathisia, 279, 284 Albumin, 34, 279, 345, 351, 357 Algorithms, 279, 288 Alimentary, 279, 305, 346, 347 Alkaline, 165, 210, 279, 281, 291, 345, 349 Alkaloid, 279, 291, 338, 350, 371 Alleles, 4, 31, 279, 332 Allergy and Immunology, 11, 29, 38, 71, 82, 83, 84, 86, 87, 89, 90, 94, 108, 132, 279 Allo, 14, 279 Allogeneic, 62, 280, 318, 320 Allogeneic bone marrow transplantation, 62, 280 Allografts, 280, 322 Allylamine, 280 Aloe, 121, 145, 280 Alopecia, 5, 210, 280, 302 Alpha 1-Antichymotrypsin, 280, 364 Alpha 1-Antitrypsin, 280, 364 Alpha Particles, 280, 357 Alpha-helix, 280, 330 Alternative medicine, 234, 280 Alveoli, 280, 304 Amber, 280, 325 Amine, 208, 280, 322 Amino Acid Motifs, 280, 299 Amino Acid Sequence, 165, 181, 281, 283, 299, 312, 316, 333, 354, 364 Aminophylline, 108, 281 Ammonia, 174, 193, 280, 281, 318, 369, 375 Amnestic, 281, 315 Amplification, 52, 281 Amyloidosis, 94, 281 Anaesthesia, 281, 326 Anal, 281, 311, 314, 321, 332 Analgesic, 163, 281, 305, 338, 344 Analogous, 281, 352, 373 Analytes, 50, 281 Anaphylactic, 33, 182, 198, 281 Anaphylatoxins, 17, 281, 298 Anaphylaxis, 12, 27, 33, 73, 259, 281 Anatomical, 35, 227, 281, 286, 300, 306, 309, 325, 363 Androgens, 278, 281, 301 Anemia, 26, 194, 202, 224, 252, 282, 291, 297, 334

382 Dermatitis

Anesthesia, 93, 279, 282, 309, 374 Aneurysm, 282, 376 Angina, 162, 202, 282 Angina Pectoris, 202, 282 Angiogenesis, 22, 44, 282, 335 Angioplasty, 162, 282, 339 Angiotensinogen, 282, 359, 364 Animal model, 14, 16, 24, 28, 35, 42, 55, 65, 71, 163, 189, 282 Animal Welfare, 12, 282 Anionic, 121, 282 Anions, 279, 282, 329 Anogenital, 208, 228, 282 Anorexia, 195, 202, 282, 375 Antagonism, 58, 171, 282, 307, 371 Antecedent, 24, 41, 282 Anthropogenic, 66, 282 Antiallergic, 187, 199, 200, 213, 282, 301 Antibacterial, 117, 125, 139, 203, 282, 367, 369 Antibiotic, 140, 179, 217, 264, 282, 283, 331, 337, 347, 367, 371 Anticholinergic, 283, 294, 307 Anticoagulant, 283, 355 Antidepressant, 283, 291 Antiemetic, 283, 284 Antifungal, 206, 283, 330, 362 Antifungal Agents, 283, 362 Antigen-Antibody Complex, 283, 298 Antigen-presenting cell, 12, 48, 232, 283, 304 Anti-infective, 283, 315, 329, 366 Anti-Infective Agents, 283, 315 Anti-inflammatory, 16, 23, 56, 64, 116, 169, 187, 189, 190, 283, 301, 305, 317, 346, 362, 374 Anti-Inflammatory Agents, 283, 301 Antimetabolite, 283, 361 Antimicrobial, 84, 126, 127, 203, 283, 296, 305, 354, 371 Antimycotic, 283, 354 Antineoplastic, 283, 284, 301, 302, 316, 336, 369 Antineoplastic Agents, 284, 336 Antioxidant, 99, 188, 203, 284, 285, 345 Antiplasmin, 284, 364 Antipruritic, 126, 284, 297 Antipsychotic, 171, 284, 341 Antipyretic, 284, 305 Antiseptic, 182, 284, 379 Antiserum, 61, 284 Antiviral, 208, 284, 316, 327, 361

Anus, 227, 281, 282, 284, 290, 348, 358 Anxiety, 9, 65, 171, 202, 279, 284, 315, 346 Anxiety Disorders, 171, 284, 346 Aphakia, 284, 360 Apocrine Glands, 284, 321 Apoptosis, 13, 69, 81, 115, 284, 292 Aqueous, 166, 173, 183, 184, 197, 207, 285, 287, 303, 309, 331, 332 Arachidonic Acid, 198, 285, 331, 354 Arcuate Nucleus, 205, 285 Arginine, 64, 281, 285, 342, 375 Arterial, 162, 209, 280, 285, 292, 300, 323, 355, 370 Arteries, 285, 289, 301, 336, 339, 352, 357, 372, 375 Arterioles, 178, 285, 289, 291, 336, 339 Arteriolosclerosis, 285 Arteriosclerosis, 178, 285, 339 Arthritis, Rheumatoid, 197, 285 Arthrosis, 205, 285 Articular, 285, 344, 374 Artifacts, 18, 285 Ascorbic Acid, 216, 285, 323 Aseptic, 285, 344, 368 Assay, 14, 26, 50, 56, 60, 286, 324, 357 Astringent, 286, 379 Astrocytes, 286, 321 Asymptomatic, 22, 194, 286, 346 Ataxia, 175, 199, 252, 286, 371 Atopic Eczema, 7, 75, 80, 84, 85, 89, 91, 96, 109, 110, 116, 173, 185, 220, 225, 257, 286 Atrial, 286, 300, 374 Atrioventricular, 286, 300 Atrium, 286, 300, 374, 377 Atrophy, 6, 191, 252, 277, 285, 286 Attenuated, 47, 286 Autoantibodies, 33, 40, 50, 62, 80, 286, 304 Autoantigens, 14, 286 Autodigestion, 286, 346 Autoimmune disease, 15, 26, 29, 40, 168, 175, 176, 180, 192, 197, 199, 205, 210, 286, 338, 350 Autoimmunity, 15, 18, 50, 80, 202, 286 Autologous, 38, 103, 286, 320 Autologous bone marrow transplantation, 286, 320 Autolysis, 209, 286 Autonomic, 277, 284, 287, 343, 348 Axons, 287, 306, 341, 344, 348, 353 B Bacillus, 33, 287 Bacterial Infections, 287, 294, 319, 360

Index 383

Bacterial toxin, 218, 287 Bactericidal, 168, 287, 312 Bactericide, 190, 287 Bacteriophage, 287, 350, 373 Bacterium, 287, 297, 320 Basal cell carcinoma, 126, 208, 287 Basal cells, 287 Basal Ganglia, 284, 286, 287, 295 Basal Ganglia Diseases, 286, 287, 295 Base, 26, 85, 174, 278, 287, 303, 304, 316, 330, 337, 348, 349, 375 Basement Membrane, 287, 312, 330 Basophil, 27, 287, 322 Baths, 126, 226, 237, 259, 265, 287 Benign, 141, 202, 285, 287, 319, 340, 342, 358, 362 Benzaldehyde, 287, 288 Benzoin, 174, 288 Benzoyl Peroxide, 188, 288 Beta-Thromboglobulin, 288, 328 Bilateral, 73, 288, 346, 360 Bile, 288, 315, 322, 332, 368 Biliary, 288, 346 Biliary Tract, 288, 346 Bilirubin, 279, 288 Binding Sites, 30, 181, 288, 368 Bioavailability, 195, 288 Biochemical, 19, 51, 58, 177, 279, 280, 283, 288, 314, 331, 364 Biological response modifier, 288, 327 Biological therapy, 288, 319 Biological Transport, 288, 306 Biomarkers, 21, 49, 288 Biopsy, 8, 39, 158, 288, 312, 348 Biosynthesis, 285, 288, 333, 349, 355, 364, 365 Biotechnology, 66, 68, 117, 133, 223, 234, 247, 250, 251, 252, 253, 288 Bioterrorism, 48, 289 Biotin, 46, 119, 289, 368 Biotransformation, 289 Bipolar Disorder, 171, 289 Bismuth, 116, 289 Bladder, 33, 214, 289, 295, 302, 325, 328, 338, 341, 355, 375, 376 Bleeding Time, 31, 289 Blister, 8, 40, 157, 158, 289, 347 Bloating, 224, 289, 329 Blood Coagulation, 31, 289, 291, 372 Blood Coagulation Factors, 289 Blood Glucose, 205, 289, 320 Blood Platelets, 289, 335, 351, 364

Blood pressure, 203, 289, 292, 295, 323, 337, 357, 366 Blood-Brain Barrier, 289, 370 Body Burden, 289, 331 Body Constitution, 213, 289 Body Fluids, 174, 184, 288, 289, 307, 366, 375 Bone Marrow, 20, 38, 58, 62, 202, 286, 289, 290, 302, 318, 320, 324, 328, 333, 335, 339, 366 Bone Marrow Transplantation, 290 Botulinum Toxins, 217, 290 Bowel, 9, 23, 142, 171, 197, 202, 209, 281, 290, 306, 310, 326, 328, 331, 348, 368, 375 Bowel Movement, 290, 306, 368 Brachytherapy, 290, 328, 329, 357, 378 Bradykinin, 290, 342, 351 Brain Injuries, 49, 290 Brain Stem, 290, 294 Branch, 169, 273, 290, 302, 317, 333, 347, 356, 366, 371 Breakdown, 16, 184, 290, 306, 316, 365 Breast Feeding, 7, 290 Breeding, 19, 31, 290 Bronchi, 290, 311, 371, 373 Bronchial, 17, 35, 82, 169, 173, 182, 198, 204, 213, 281, 290, 322, 371 Bronchial Spasm, 169, 290 Bronchitis, 176, 290, 296 Bronchoconstriction, 198, 290 Bronchodilator, 17, 169, 290 Bronchus, 290 Buccal, 290, 333 Bulimia, 202, 290 Bullous, 18, 40, 74, 77, 114, 127, 291, 304 Bupropion, 110, 291 Burns, 49, 82, 170, 183, 203, 288, 291 Burns, Electric, 291 C Cachexia, 176, 187, 202, 291 Cadmium, 174, 291 Cadmium Poisoning, 291 Calcification, 285, 291 Calcium, 71, 291, 298, 327, 334, 339, 365 Calcium Dobesilate, 71, 291 Callus, 291, 330 Calmodulin, 165, 291, 327 Capecitabine, 86, 132, 291 Capillary, 10, 173, 289, 290, 291, 361, 377 Capillary Permeability, 173, 290, 291 Capsaicin, 61, 291 Captopril, 115, 292

384 Dermatitis

Carbohydrate, 30, 64, 193, 292, 301, 315, 318, 343, 352, 368 Carbon Dioxide, 291, 292, 303, 304, 314, 350 Carcinogenesis, 19, 292 Carcinogenic, 292, 297, 326, 343, 354, 368 Carcinogens, 292, 296, 297, 339, 343, 345 Carcinoma, 86, 132, 194, 292, 305 Cardiac, 14, 74, 280, 292, 300, 308, 311, 312, 316, 339, 340, 345, 368 Cardiotoxicity, 292, 374 Cardiovascular, 202, 292, 331, 364, 376 Cardiovascular disease, 202, 292 Carnitine, 119, 292 Carotene, 292, 360 Carrier Proteins, 292, 351, 357 Case report, 73, 74, 122, 135, 292, 296 Caspase, 188, 292 Caspase 1, 188, 292 Catalyse, 166, 292 Cataract, 198, 284, 292, 311, 360 Catecholamine, 293, 307, 349 Catheterization, 74, 282, 293, 328, 339 Cations, 293, 329 Caudal, 293, 305, 323, 352 Causal, 293, 311, 320, 371 Cause of Death, 162, 293 Caustic, 293, 366 Celiac Disease, 4, 5, 8, 26, 39, 142, 224, 235, 248, 258, 266, 293, 317 Cell, 10, 12, 13, 14, 15, 19, 22, 23, 24, 27, 28, 29, 30, 32, 33, 34, 35, 37, 39, 41, 42, 43, 44, 48, 49, 51, 53, 55, 56, 58, 59, 60, 61, 62, 64, 69, 84, 86, 91, 96, 108, 114, 157, 162, 165, 166, 168, 169, 176, 177, 185, 188, 189, 192, 197, 200, 202, 203, 206, 209, 214, 215, 225, 237, 251, 252, 277, 279, 280, 281, 283, 284, 285, 286, 287, 288, 289, 292, 293, 294, 295, 296, 298, 302, 303, 304, 305, 308, 309, 310, 312, 314, 315, 316, 317, 319, 320, 322, 324, 325, 326, 327, 328, 330, 331, 333, 334, 335, 337, 338, 339, 340, 343, 344, 345, 349, 350, 351, 352, 353, 354, 358, 363, 364, 365, 370, 371, 372, 373, 374, 375, 378 Cell Adhesion, 10, 42, 44, 60, 162, 176, 197, 293, 327 Cell Adhesion Molecules, 10, 42, 60, 176, 293 Cell Cycle, 55, 293 Cell Death, 41, 215, 284, 293, 317, 340 Cell Degranulation, 13, 225, 293

Cell Differentiation, 189, 203, 293, 365 Cell Division, 215, 251, 287, 293, 302, 319, 335, 337, 350, 354, 363 Cell membrane, 166, 288, 292, 293, 304, 312, 316, 327, 330, 349 Cell proliferation, 162, 165, 177, 189, 203, 215, 285, 293, 328, 365 Cell Size, 293, 314 Cell Survival, 293, 319 Cell Transplantation, 294, 320 Cellulitis, 142, 266, 294 Cellulose, 294, 315, 350 Central Nervous System Infections, 294, 320 Centrifugation, 210, 294 Ceramide, 67, 165, 212, 294 Cerebellar, 286, 294, 359 Cerebellum, 290, 294, 359 Cerebral hemispheres, 287, 290, 294 Cerebrovascular, 198, 287, 292, 294, 371 Cerebrum, 294, 374 Cetirizine, 94, 294 Character, 282, 294, 303, 318 Cheilitis, 260, 294 Chemokines, 30, 31, 33, 35, 61, 169, 294 Chemoprotective, 55, 211, 294 Chemoreceptor, 284, 295 Chemotactic Factors, 169, 295, 298 Chemotaxis, 69, 169, 295 Chemotherapy, 126, 189, 210, 295, 321 Chimeras, 35, 38, 58, 295 Chlorides, 174, 295 Chlorophyll, 295, 315 Cholesterol, 210, 288, 295, 301, 333, 365, 368 Choline, 277, 295 Cholinergic, 191, 284, 290, 295 Cholinesterase Inhibitors, 190, 295, 307 Chorea, 284, 295 Chorioretinitis, 295, 360 Choroid, 295, 360, 376 Chromates, 263, 295 Chromatin, 285, 295 Chromic, 295 Chromium, 74, 105, 295 Chromosomal, 281, 295, 296, 362 Chromosome, 4, 296, 319, 332, 362, 363, 374 Chronic Disease, 25, 30, 45, 169, 202, 266, 291, 296, 298 Chronic Obstructive Pulmonary Disease, 162, 186, 187, 197, 198, 296

Index 385

Chronic renal, 296, 352, 375 Cicatricial, 296, 321 Ciliary, 296, 338, 364, 376 Ciliary Body, 296, 364, 376 Ciprofloxacin, 171, 296 Circulatory system, 296, 309, 328 CIS, 107, 174, 296, 360 Citrus, 285, 296 Claviceps, 296, 361 Clinical Medicine, 296, 353 Clinical study, 296, 300 Clinical trial, 9, 34, 53, 157, 159, 247, 296, 300, 302, 355, 358 Clone, 13, 296 Cloning, 20, 30, 205, 288, 297 Clostridium, 217, 290, 297, 371 Clostridium botulinum, 217, 290, 297 Clot Retraction, 297, 351 Coagulation, 32, 289, 297, 298, 321, 351, 372 Coal, 240, 241, 263, 297 Coal Tar, 240, 241, 263, 297 Cobalt, 174, 297 Cochlea, 297 Cochlear, 36, 297, 373 Cod Liver Oil, 297, 309 Coenzyme, 285, 297, 333, 365 Cofactor, 297, 342, 355, 364, 372 Colitis, 143, 166, 178, 179, 192, 209, 217, 297, 329 Collagen, 191, 201, 278, 285, 287, 297, 298, 313, 314, 316, 322, 328, 334, 351, 354, 362, 368 Collagen disease, 298, 322, 362 Collapse, 281, 290, 298 Colloidal, 147, 279, 298, 308, 348, 369 Combination chemotherapy, 86, 132, 298 Comorbidity, 9, 298 Complement, 17, 44, 281, 298, 299, 316, 327, 334, 351, 363, 364 Complement 1, 298, 364 Complement 1 Inactivators, 298, 364 Complement Activation, 17, 44, 281, 298 Complementary and alternative medicine, 121, 153, 299 Complementary medicine, 10, 121, 139, 299 Complete remission, 299, 359 Computational Biology, 247, 250, 299 Conception, 299, 313, 366, 368 Concomitant, 5, 107, 110, 299 Cones, 299, 360

Congestion, 173, 284, 299, 311, 332 Conjugated, 64, 299, 302 Conjunctiva, 299, 362 Conjunctivitis, 46, 162, 169, 173, 178, 179, 182, 198, 201, 211, 213, 217, 299 Conjunctivitis, Allergic, 169, 173, 182, 299 Connective Tissue Cells, 299 Consciousness, 281, 299, 303, 304, 306 Consensus Sequence, 34, 280, 299 Conserved Sequence, 280, 299 Constipation, 164, 186, 209, 227, 284, 300, 329, 348 Constitutional, 300, 339, 360 Constriction, 300, 329, 362, 376, 378 Constriction, Pathologic, 300, 376 Consultation, 43, 300 Consumption, 300, 305 Continuum, 47, 300 Contraindications, ii, 257, 300 Control group, 5, 300 Controlled clinical trial, 95, 300 Controlled study, 116, 131, 140, 300 Conventional therapy, 300 Conventional treatment, 200, 300 Convulsions, 300, 308, 323, 353, 366 Coordination, 294, 300, 338 Cor, 61, 300, 354 Cornea, 301, 318, 362, 376 Corneum, 36, 52, 64, 95, 102, 107, 179, 188, 212, 301, 311, 324 Coronary, 48, 75, 162, 282, 292, 301, 336, 339 Coronary Circulation, 282, 301 Coronary heart disease, 162, 292, 301 Coronary Thrombosis, 301, 336, 339 Corpus, 301, 353, 372 Corpus Luteum, 301, 353 Cortex, 181, 182, 286, 301, 312, 314, 359 Corticosteroid, 17, 69, 117, 126, 167, 215, 226, 264, 301 Cortisol, 279, 301 Cortisone, 262, 265, 301 Cowpox, 301, 376 Cowpox Virus, 301, 376 Cranial, 294, 301, 319, 328, 341, 344, 346, 348 Craniocerebral Trauma, 287, 301, 320, 371, 373 Creatine, 34, 302 Creatinine, 302, 375 Criterion, 7, 302 Cromolyn Sodium, 185, 302

386 Dermatitis

Crossing-over, 302, 358 Curative, 302, 342, 371 Cyclic, 164, 291, 302, 319, 342, 349, 354, 371 Cyclophosphamide, 302, 324, 336 Cyclosporine, 7, 94, 225, 233, 263, 302 Cysteine, 169, 294, 302, 309, 369 Cystine, 302 Cystitis, 33, 214, 302 Cytochrome, 302, 359 Cytochrome b, 302, 359 Cytogenetics, 302, 362 Cytomegalovirus, 108, 302 Cytopenia, 202, 303 Cytoplasm, 10, 199, 285, 293, 303, 310, 319, 327, 361 Cytoskeleton, 303, 327 Cytotoxic, 13, 14, 80, 215, 280, 291, 303, 325, 333, 357, 358, 365 D Databases, Bibliographic, 247, 303 Day Care, 25, 303 Deamination, 303, 375 Decarboxylation, 303, 322 Decubitus, 172, 303, 365 Decubitus Ulcer, 172, 303, 365 Defecation, 228, 303 Defense Mechanisms, 42, 303, 327 Degenerative, 303, 321, 333, 338, 360 Dehydration, 224, 303 Dehydroepiandrosterone, 191, 303 Deletion, 31, 165, 285, 303, 332 Delirium, 202, 284, 303 Delivery of Health Care, 304, 317, 320 Delusions, 304, 356 Dementia, 187, 190, 202, 284, 304, 306 Demethylation, 171, 304 Dendrites, 304, 341 Dendritic, 29, 35, 37, 40, 48, 56, 71, 72, 96, 304, 335 Dendritic cell, 29, 35, 37, 40, 48, 71, 96, 304 Density, 36, 55, 77, 89, 294, 304, 314, 333, 343, 352, 358 Dental Care, 16, 304 Dental Hygienists, 88, 304 Dental Materials, 16, 304 Dentists, 16, 304 Dentition, 48, 304 Depigmentation, 304, 378 Depolarization, 304, 365 Dermal, 20, 21, 22, 36, 49, 64, 171, 191, 207, 208, 304

Dermatitis, Contact, 207, 304 Dermatitis, Irritant, 24, 304 Dermatologist, 158, 263, 304 Dermatosis, 18, 175, 190, 195, 199, 305 DES, 281, 305 Desensitization, 13, 53, 305 Detergents, 93, 232, 305, 365 Detoxification, 40, 305 Deuterium, 305, 323 Developed Countries, 182, 305, 315 Diabetes Mellitus, 176, 305, 318, 320, 327 Diabetic Retinopathy, 162, 205, 291, 305, 350 Diagnostic procedure, 161, 235, 305 Diaper Rash, 174, 184, 193, 257, 262, 305 Diarrhea, 26, 39, 194, 224, 305, 329 Diastolic, 305, 323 Diclofenac, 101, 305 Diclofenac Sodium, 305 Diencephalon, 305, 323, 372 Dietary Fats, 305, 332 Dietary Fiber, 209, 228, 305 Dietary Proteins, 23, 305 Diethylcarbamazine, 306, 369 Diffuse Axonal Injury, 290, 306 Diffusion, 24, 36, 288, 291, 306, 326 Digestion, 194, 210, 279, 288, 290, 297, 305, 306, 328, 332, 347, 368 Digestive system, 160, 306, 316, 338 Digestive tract, 306, 365 Digital photography, 158, 306 Dihydrotestosterone, 306, 359 Dilatation, 282, 306, 353, 376 Dilatation, Pathologic, 306, 376 Dilation, 178, 191, 290, 306, 376 Dimerization, 199, 306 Diploid, 306, 350 Disease Outbreaks, 66, 306 Disinfectant, 306, 312 Disorientation, 303, 306 Disposition, 21, 306 Dissection, 88, 306 Dissociation, 278, 306 Distal, 42, 307, 308, 353, 356 Diuretic, 210, 307 Dizziness, 195, 307, 346, 377 Docetaxel, 86, 103, 130, 132, 133, 138, 307 Domesticated, 177, 307, 319 Donepezil, 190, 307 Dopamine, 171, 284, 291, 307, 349 Dorsal, 61, 307, 311, 352 Dorsum, 307

Index 387

Doxepin, 108, 307 Dross, 307, 354 Drug Interactions, 170, 241, 307 Drug Tolerance, 307, 373 Duct, 293, 307, 362, 369 Duodenum, 81, 288, 307, 330, 342, 368 Dura mater, 307, 335, 345 Dyes, 138, 287, 307, 315, 319, 342, 349, 369 Dyscrasia, 82, 307 Dysentery, 31, 308 Dyskinesia, 284, 308 Dysplasia, 252, 308 Dystonia, 284, 308 Dystrophy, 252, 308 E Eating Disorders, 163, 186, 308 Echinostomiasis, 66, 308 Eclampsia, 288, 308, 353 Edema, 22, 167, 298, 300, 305, 308, 339, 353, 375 Effector, 14, 17, 27, 33, 48, 49, 56, 61, 277, 298, 308, 342, 349 Effector cell, 14, 27, 33, 308, 342 Efficacy, 14, 17, 47, 49, 64, 78, 83, 84, 106, 116, 122, 127, 129, 130, 131, 163, 195, 212, 308 Egg Proteins, 89, 308 Elasticity, 285, 308 Elastin, 297, 308, 313 Electrocardiograph, 77, 308 Electrocoagulation, 297, 308 Electrode, 36, 129, 308 Electrolyte, 301, 303, 308, 337, 352, 366, 375 Electrons, 284, 287, 308, 329, 345, 357, 358 Electrophoresis, 277, 308 Electroplating, 309, 369 Ellagic Acid, 35, 309 Embryo, 293, 309, 326, 352, 375 Emodin, 280, 309 Emollient, 68, 70, 85, 111, 122, 124, 184, 231, 309, 330, 337, 343 Emphysema, 280, 296, 309 Empirical, 9, 309 Emulsion, 84, 131, 172, 193, 309, 314 Enamel, 249, 309, 330 Endarterectomy, 282, 309 Endemic, 42, 309, 334, 367 Endocrine System, 309, 341 Endopeptidases, 309, 355, 364 Endorphins, 309, 354

Endothelial cell, 10, 22, 30, 44, 162, 197, 289, 309, 328, 372 Endothelium, 22, 31, 162, 309, 310, 342, 351 Endothelium, Lymphatic, 309 Endothelium, Vascular, 309, 310 Endothelium-derived, 310, 342 Endotoxemia, 58, 310 Endotoxic, 310, 332 Endotoxin, 57, 310, 375 End-stage renal, 296, 310, 352 Enhancer, 176, 310, 360 Enkephalin, 310, 354 Enteritis, 62, 166, 310 Enterocolitis, 310 Environmental Exposure, 30, 46, 172, 310, 343 Environmental Health, 46, 70, 246, 248, 310 Environmental Pollutants, 7, 310 Environmental tobacco smoke, 25, 310 Enzymatic, 58, 193, 291, 292, 298, 310, 313, 314, 322, 360 Enzyme Inhibitors, 175, 199, 310, 351 Eosinophil, 35, 63, 115, 169, 202, 310 Eosinophilia, 63, 310 Eosinophilic, 310 Ependyma, 285, 310, 372 Epidemic, 16, 71, 310, 367 Epidemiologic Studies, 311, 317 Epidemiological, 10, 54, 187, 249, 311 Epinephrine, 278, 307, 311, 343, 375 Episcleritis, 311, 362 Epithelial, 10, 165, 194, 211, 288, 296, 311, 321, 330 Epithelial Cells, 311, 321, 330 Epithelium, 165, 287, 309, 311, 316, 346, 360 Epitope, 13, 50, 60, 181, 311 Erectile, 205, 311 Erection, 311 Ergot, 311, 361 Erythema, 8, 85, 104, 125, 128, 167, 300, 311, 369, 376 Erythema Multiforme, 125, 128, 311 Erythrocytes, 282, 290, 311, 320, 358, 363 Esophagitis, 178, 179, 217, 311 Esophagitis, Peptic, 178, 179, 217, 311 Esophagus, 306, 311, 359, 368 Essential Tremor, 252, 311 Estradiol, 58, 312 Estrogen, 74, 312

388 Dermatitis

Ethanol, 210, 312, 313 Ether, 193, 312 Eukaryotic Cells, 312, 325, 344, 375 Evacuation, 300, 312, 331 Evoke, 312, 368 Excipient, 183, 312 Excisional, 31, 312 Excitability, 312, 340, 341 Excitation, 295, 312, 314 Exfoliation, 42, 312 Exhaustion, 282, 312, 334 Exocytosis, 58, 293, 312, 322 Exogenous, 11, 33, 188, 191, 221, 289, 292, 308, 312, 355, 364 Exon, 85, 312 Exotoxin, 297, 312, 367 Expiration, 312 Expiratory, 17, 312 Extensor, 7, 23, 312, 356, 378 External-beam radiation, 312, 329, 357, 378 Extracellular, 30, 55, 163, 202, 206, 286, 299, 312, 313, 314, 327, 334, 366, 368 Extracellular Matrix, 30, 55, 163, 206, 299, 312, 313, 314, 327, 334 Extracellular Matrix Proteins, 30, 313, 334 Extracellular Space, 312, 313 Extracorporeal, 225, 313, 350 Extraction, 173, 210, 284, 313, 360 Extrapyramidal, 279, 284, 307, 313 Extravasation, 60, 61, 313 Extremity, 49, 313, 346 Eye socket, 313, 348 F Facial, 103, 104, 110, 125, 313, 347 Family Planning, 247, 313 Fat, 25, 285, 289, 292, 294, 300, 301, 303, 313, 330, 332, 338, 343, 352, 361, 363, 366, 369 Fatigue, 9, 194, 196, 224, 313, 320 Fatty acids, 25, 279, 313, 332, 354, 366 Febrile, 313, 334, 367 Feces, 172, 192, 193, 262, 300, 305, 313, 368 Fermentation, 212, 313, 315 Fertilizers, 313, 342, 369 Fetus, 30, 313, 333, 350, 375, 376 Fibrin, 32, 284, 289, 297, 313, 314, 348, 351, 372, 373 Fibrinogen, 32, 313, 351, 372 Fibrinolysis, 31, 313 Fibrinolytic, 32, 298, 314 Fibroblasts, 22, 299, 314, 328

Fibronectin, 206, 314, 368 Fibrosis, 142, 162, 183, 187, 192, 252, 280, 314, 321, 362, 363 Fish Products, 314, 363 Fissure, 16, 314 Fistulas, 314, 321 Fixation, 314, 363 Flatus, 314, 316 Flavoring Agents, 314, 315, 349 Fleas, 172, 314 Flexor, 312, 314 Flow Cytometry, 15, 26, 38, 56, 60, 314, 325 Fluorescence, 45, 314, 315 Fluorescent Dyes, 314, 315 Fluvoxamine, 171, 315 Fold, 13, 50, 59, 314, 315 Follicles, 315 Folliculitis, 179, 257, 315 Food Additives, 7, 187, 315 Food Coloring Agents, 315 Food Hypersensitivity, 181, 234, 315 Food Preservatives, 315 Forearm, 158, 289, 315 Friction, 73, 184, 315 Fucose, 315 Fucosyltransferases, 45, 315 Fumigation, 315 Fungi, 67, 283, 296, 315, 336, 378, 379 Fungus, 42, 311, 315, 361 G Gallbladder, 277, 288, 306, 315 Gamma Rays, 316, 357, 358 Gamma-interferon, 139, 316, 327 Ganglia, 61, 277, 287, 316, 341, 348 Gap Junctions, 316, 370 Gas, 36, 224, 281, 292, 306, 314, 315, 316, 323, 329, 339, 342, 343, 358, 360, 369 Gastric, 249, 286, 292, 311, 316, 322, 347 Gastric Acid, 249, 316 Gastric Juices, 316, 347 Gastric Mucosa, 316, 347 Gastrin, 316, 322 Gastroenterologist, 227, 316 Gastrointestinal tract, 295, 312, 316, 331, 364, 375 Gelatin, 316, 318, 372 Gels, 24, 183, 316 Gene Expression, 29, 56, 60, 71, 253, 316 Genetic Code, 316, 343 Genetic Engineering, 288, 297, 316

Index 389

Genetics, 19, 37, 38, 49, 88, 225, 258, 260, 302, 317 Genetics, Biochemical, 260, 317 Genital, 54, 88, 167, 296, 317, 376 Genitourinary, 56, 317, 376 Genotype, 30, 280, 317, 349 Geographic Locations, 31, 317 Germinal Center, 62, 317 Gestation, 317, 348, 350 Giant Cells, 317, 362 Gland, 168, 205, 278, 301, 317, 321, 333, 345, 346, 347, 350, 355, 363, 368, 369, 372 Gliadin, 23, 258, 317 Glomerular, 317, 359 Glomeruli, 317 Glomerulonephritis, 162, 201, 317 Glucocorticoid, 225, 317, 322, 374 Glucose, 205, 252, 285, 289, 294, 295, 305, 317, 318, 320, 323, 326, 327, 362 Glucose Intolerance, 305, 317 Glucose tolerance, 205, 318 Glucose Tolerance Test, 318 Glucuronic Acid, 318, 321 Glutamic Acid, 318, 354 Glutamine, 194, 318 Glutathione Peroxidase, 318, 363 Gluten, 4, 5, 8, 22, 39, 79, 120, 155, 194, 222, 224, 235, 248, 258, 260, 261, 293, 317, 318 Glycine, 318, 364 Glycogen, 198, 318 Glycoprotein, 280, 284, 298, 313, 314, 315, 317, 318, 330, 331, 372, 375 Glycosaminoglycan, 31, 318 Gonad, 318 Gonadal, 47, 318, 368 Governing Board, 318, 353 Graft, 14, 59, 62, 192, 280, 318, 322, 325, 339, 356 Graft Rejection, 14, 318, 325 Graft-versus-host disease, 318, 356 Gram-negative, 310, 319 Gram-positive, 297, 319, 367, 368 Gram-Positive Bacteria, 297, 319 Granule, 27, 58, 115, 319, 361 Granulocytes, 279, 287, 319, 331, 339, 365, 378 Granulomatous Disease, Chronic, 319, 359 Gravis, 261, 319 Groin, 262, 319, 321, 326 Growth factors, 163, 203, 214, 319 Guanylate Cyclase, 319, 342

Guinea Pigs, 16, 201, 319 H Habitat, 319, 342 Habitual, 65, 294, 319 Hair Color, 319 Hair Dyes, 263, 319 Hair follicles, 36, 315, 319, 367, 378 Haploid, 319, 350 Haplotypes, 30, 39, 319 Haptens, 14, 33, 278, 319, 357 Headache, 9, 195, 196, 319, 320, 323 Headache Disorders, 320 Health Care Costs, 45, 320 Health Expenditures, 320 Health Promotion, 227, 320 Heart attack, 292, 320 Heart failure, 202, 320 Hematologic malignancies, 14, 320 Hematopoietic Stem Cell Transplantation, 14, 320 Hemiparesis, 290, 320 Hemoglobin, 282, 311, 320, 331 Hemoglobinuria, 252, 320 Hemolysis, 195, 320 Hemolytic, 320, 325 Hemorrhage, 291, 301, 308, 320, 339, 357, 368, 378 Hemorrhoids, 227, 321 Hemostasis, 30, 32, 321, 327, 364 Heparan Sulfate Proteoglycan, 30, 321 Heparin, 31, 321, 351, 364 Hepatic, 40, 279, 303, 318, 321, 365 Hepatitis, 62, 261, 321 Hepatocytes, 321 Hepatotoxicity, 191, 321 Hereditary, 8, 20, 39, 260, 261, 263, 277, 280, 298, 321, 338, 360 Heredity, 6, 261, 316, 317, 321 Herpes, 69, 104, 321 Herpes Zoster, 321 Herpetiformis, 4, 5, 8, 22, 26, 39, 79, 80, 81, 88, 91, 96, 142, 155, 166, 190, 194, 195, 221, 224, 229, 235, 248, 251, 258, 260, 261, 262, 266, 304, 321 Heterodimers, 321, 327 Heterogeneity, 278, 321 Heterogenic, 321 Heterogenous, 26, 321 Hidradenitis, 205, 321 Hidradenitis Suppurativa, 205, 321 Histamine, 35, 61, 140, 173, 189, 200, 201, 202, 204, 211, 281, 284, 294, 307, 322

390 Dermatitis

Histamine Release, 200, 202, 281, 322 Histidine, 322 Histocompatibility, 4, 322 Histology, 18, 322, 333, 346 Homogenate, 19, 322 Homogeneous, 56, 285, 300, 322 Homologous, 53, 199, 279, 302, 322, 363, 370, 374 Hormonal, 47, 58, 191, 286, 301, 321, 322 Horny layer, 201, 311, 322 Human Development, 66, 246, 322 Human papillomavirus, 208, 322 Humoral, 49, 188, 215, 318, 322 Humour, 322 Hybrid, 296, 322, 361 Hybridoma, 62, 322 Hydration, 6, 8, 36, 76, 225, 277, 322 Hydrochloric Acid, 295, 322 Hydrocortisone, 85, 263, 265, 322 Hydrogen, 164, 169, 192, 277, 280, 287, 292, 305, 313, 318, 322, 323, 337, 342, 345, 355 Hydrolysis, 165, 277, 289, 323, 347, 349, 352, 355 Hydrophilic, 193, 305, 323 Hydrophobic, 208, 305, 323 Hydroxylamine, 41, 323 Hydroxylysine, 297, 323 Hydroxyproline, 212, 297, 323 Hygienic, 323, 365 Hyperaemia, 299, 323 Hyperhidrosis, 155, 217, 220, 323 Hyperplasia, 33, 141, 323 Hypersecretion, 63, 323, 363 Hypertension, 102, 202, 285, 292, 320, 323, 353, 373, 375 Hypertrophy, 202, 301, 323, 324, 331, 374 Hypesthesia, 323, 341 Hypoglycaemia, 303, 323 Hypotension, 202, 284, 300, 323, 342 Hypothalamus, 205, 285, 305, 310, 323, 342, 350, 354, 372 Hypoxia, 303, 323, 371 I Ichthyosis, 260, 263, 323, 324 Ichthyosis Vulgaris, 263, 324 Id, 5, 118, 125, 141, 256, 257, 265, 267, 272, 274, 324 Idiopathic, 164, 277, 321, 324, 362 Idiotype, 13, 324 Ifosfamide, 324, 336 Ileitis, 166, 324

Ileostomy, 324, 340 Ileum, 324, 330, 342 Imidazole, 166, 289, 322, 324 Immaturity, 24, 324 Immersion, 18, 108, 287, 324 Immune function, 11, 25, 47, 60, 324, 325 Immune Sera, 324 Immunity, 14, 17, 33, 44, 49, 60, 84, 189, 215, 324, 373 Immunization, 13, 14, 35, 38, 278, 324, 325, 363 Immunoassay, 27, 324 Immunochemistry, 38, 324 Immunocompromised, 42, 265, 324 Immunodeficiency, 91, 202, 251, 324 Immunogenic, 43, 290, 324, 332, 357 Immunoglobulin, 82, 116, 131, 173, 225, 260, 283, 325, 328, 337 Immunohistochemistry, 27, 58, 60, 61, 325 Immunomodulator, 206, 224, 325 Immunophenotyping, 80, 325 Immunosuppressant, 206, 325 Immunosuppressive, 14, 180, 302, 317, 324, 325, 362, 371 Immunosuppressive Agents, 180, 325, 362 Immunosuppressive therapy, 14, 325 Immunotherapy, 225, 278, 288, 305, 325 Impairment, 39, 65, 112, 286, 303, 308, 325, 335, 336, 356, 374 Impetigo, 40, 42, 77, 256, 325 Implant radiation, 325, 328, 329, 357, 378 Impotence, 311, 325 In situ, 48, 60, 61, 79, 206, 325 In Situ Hybridization, 60, 325 Incision, 325, 329 Incontinence, 193, 325 Incubated, 41, 325 Incubation, 114, 326 Incubation period, 114, 326 Indicative, 220, 326, 347, 376 Induction, 11, 12, 13, 38, 52, 157, 163, 189, 194, 197, 282, 284, 326, 365 Infancy, 20, 99, 185, 207, 225, 233, 260, 326 Infantile, 260, 277, 326 Infarction, 326, 352, 359 Infertility, 179, 217, 326 Infiltration, 10, 35, 58, 61, 200, 214, 317, 326 Inflammatory bowel disease, 162, 166, 168, 175, 178, 179, 199, 201, 209, 216, 217, 228, 326 Infusion, 121, 326, 339

Index 391

Ingestion, 46, 127, 194, 209, 291, 318, 326, 351 Inguinal, 323, 326 Inhalation, 35, 42, 46, 278, 326, 351, 374 Initiation, 15, 44, 169, 326, 354, 373 Innervation, 307, 326 Inorganic, 166, 177, 200, 201, 295, 323, 326, 338, 342 Inositol, 51, 326, 327 Inositol 1,4,5-Trisphosphate, 51, 327 Inotropic, 307, 327 Insight, 35, 40, 42, 50, 327 Insomnia, 195, 327 Insulator, 327, 338 Insulin, 318, 327 Integrins, 58, 327 Intercellular Adhesion Molecule-1, 162, 327 Intercellular Junctions, 22, 327 Interferon, 14, 20, 25, 215, 316, 327 Interferon-alpha, 215, 327 Interleukin-1, 80, 92, 178, 216, 217, 292, 327, 328 Interleukin-11, 178, 216, 217, 327 Interleukin-13, 80, 92, 328 Interleukin-2, 33, 177, 327, 328 Interleukin-4, 80, 199, 200, 328 Interleukin-8, 44, 328 Interleukins, 325, 328 Internal radiation, 328, 329, 357, 378 Interstitial, 33, 92, 93, 206, 214, 290, 313, 328, 329, 359, 368, 378 Interstitial Collagenase, 206, 328, 368 Intervertebral, 93, 328 Intestinal, 23, 82, 192, 194, 202, 258, 292, 293, 297, 310, 318, 328, 334, 376 Intestine, 8, 290, 310, 328, 330, 368 Intoxication, 303, 328, 378 Intracellular, 42, 51, 58, 79, 91, 164, 165, 203, 206, 326, 327, 328, 342, 352, 354, 358, 363, 365 Intracranial Pressure, 36, 328 Intraepithelial, 56, 328 Intramuscular, 328, 346, 374 Intravenous, 24, 82, 133, 326, 328, 346 Intravesical, 33, 328 Intrinsic, 52, 70, 72, 76, 80, 105, 109, 216, 278, 287, 328 Intubation, 293, 328 Invasive, 18, 324, 329 Involuntary, 287, 295, 310, 311, 329, 340, 359, 366, 372

Iodine, 8, 329 Iodoacetamide, 74, 329 Ion Channels, 166, 286, 329, 342, 370 Ionizing, 280, 310, 329, 357, 358 Ions, 166, 206, 287, 291, 298, 306, 308, 323, 327, 329, 337 Irradiation, 55, 329, 336, 378 Irritable Bowel Syndrome, 9, 164, 186, 329 Irritants, 6, 8, 10, 21, 26, 28, 37, 167, 185, 219, 226, 259, 260, 261, 304, 308, 329 Ischemia, 162, 286, 303, 329, 339, 359 Isocyanates, 97, 329 Isoelectric, 329, 368 Isoelectric Point, 329, 368 Isoenzyme, 164, 171, 329 Isotonic, 185, 330 Isozymes, 30, 330 J Jejunum, 39, 330 Joint, 285, 296, 314, 330, 370 K Kb, 246, 330 Keratin, 191, 330, 363 Keratinocytes, 35, 37, 40, 53, 62, 69, 140, 164, 174, 175, 221, 328, 330 Keratolytic, 197, 330 Keratosis, 260, 277, 330 Keto, 330, 357 Ketoconazole, 94, 103, 330 Kidney Disease, 160, 228, 246, 252, 330 Kinetic, 18, 329, 330 L Labile, 298, 330 Laceration, 330, 371 Lacrimal, 330, 335 Laminin, 206, 287, 313, 330 Lanolin, 163, 193, 330 Large Intestine, 306, 328, 330, 358, 365 Latent, 108, 330, 353 Lavage, 54, 331 Laxative, 278, 309, 331, 337 Lead Poisoning, 49, 331 Lectins, 34, 331 Leishmaniasis, 214, 331 Lens, 284, 292, 331, 378 Leprosy, 190, 195, 331 Leptospirosis, 31, 331 Lesion, 67, 125, 138, 207, 331, 332, 365, 371, 372, 375 Lethal, 287, 331, 339 Leucine, 331, 347 Leucocyte, 310, 331

392 Dermatitis

Leukemia, 96, 180, 192, 251, 320, 331 Leukocytes, 31, 58, 60, 64, 162, 164, 178, 202, 290, 294, 295, 319, 327, 328, 331, 375 Leukotrienes, 131, 204, 285, 331 Library Services, 272, 331 Lichenification, 260, 331 Ligament, 331, 355 Ligands, 30, 64, 203, 293, 327, 331 Ligation, 29, 228, 331 Lincomycin, 115, 331 Linkage, 20, 33, 39, 332 Lip, 107, 236, 332 Lipase, 171, 332 Lipid, 25, 58, 107, 121, 165, 201, 212, 285, 291, 295, 327, 330, 332, 338 Lipid A, 201, 332 Lipopolysaccharides, 332 Liposome, 183, 332 Lipoxygenase, 197, 331, 332 Lithium, 94, 284, 332 Livedo, 116, 332 Lobe, 332, 346, 354 Localization, 40, 42, 62, 176, 205, 325, 332 Locomotion, 332, 350 Longitudinal study, 21, 332 Loss of Heterozygosity, 20, 332 Lovastatin, 332, 365 Lubricants, 333, 348 Lucida, 330, 333 Lupus, 5, 50, 142, 143, 162, 180, 197, 333, 370 Lymph, 26, 28, 35, 38, 138, 296, 309, 322, 333, 362 Lymph node, 28, 35, 38, 333, 362 Lymphadenopathy, 138, 333 Lymphatic, 192, 309, 326, 333, 336, 366, 367, 372 Lymphatic system, 333, 366, 367, 372 Lymphocyte, 25, 37, 38, 58, 59, 115, 283, 328, 333, 334, 335 Lymphocytic, 28, 333 Lymphoid, 15, 38, 45, 82, 283, 317, 331, 333 Lymphokine, 214, 333 Lymphoma, 4, 5, 59, 84, 194, 249, 251, 320, 333, 350 Lymphoproliferative, 14, 25, 28, 64, 89, 333 Lymphotoxin, 38, 333 M Maceration, 184, 333 Macrolides, 6, 206, 333 Macrophage, 42, 44, 327, 334

Maintenance therapy, 232, 334 Major Histocompatibility Complex, 15, 319, 328, 334 Malabsorption, 39, 142, 194, 224, 252, 293, 334 Malaria, 190, 195, 334 Malaria, Falciparum, 334 Malaria, Vivax, 334 Malignancy, 5, 315, 334, 346 Malignant, 5, 251, 283, 285, 334, 340, 358, 362 Malnutrition, 224, 279, 286, 291, 334, 338 Mania, 171, 334 Manic, 202, 284, 289, 332, 334, 356 Manic-depressive psychosis, 334, 356 Manifest, 58, 194, 334 Mannans, 315, 334 Mastocyte, 198, 334 Mastocytosis, 19, 158, 198, 334 Matrilysin, 206, 334 Matrix metalloproteinase, 205, 206, 334, 342 Medial, 285, 335, 344 Mediate, 17, 44, 47, 60, 203, 293, 307, 335 Mediator, 33, 44, 53, 189, 203, 328, 335, 351, 364 Medical Records, 9, 27, 335, 361 MEDLINE, 247, 250, 252, 335 Megakaryocytes, 328, 335 Meibomian, 205, 335 Meiosis, 335, 370 Melanin, 304, 335, 349, 375 Melanocytes, 335, 342 Melanoma, 91, 251, 335 Memory, 14, 49, 56, 59, 82, 176, 190, 195, 282, 303, 304, 317, 335 Meninges, 294, 301, 307, 335 Meningioma, 192, 335 Meningitis, 178, 335 Menstrual Cycle, 335, 353 Mental Disorders, 160, 335, 356 Mental Health, iv, 9, 160, 246, 249, 335, 343, 356 Mental Retardation, 202, 253, 335 Mercury, 174, 182, 314, 336 Mesenchymal, 285, 336 Mesentery, 336, 348 Mesna, 97, 336 Mesolimbic, 284, 336 Metabolic disorder, 225, 336 Metabolite, 171, 198, 203, 289, 332, 336, 350, 353

Index 393

Metastasis, 293, 335, 336 Metastatic, 86, 132, 336 Methacrylates, 3, 70, 336 Methionine, 336, 354, 369 Methoxsalen, 240, 336, 350 MI, 275, 336 Microbe, 336, 373 Microbiological, 21, 54, 95, 336 Microbiology, 38, 106, 111, 336 Microcirculation, 336, 351 Microorganism, 81, 189, 297, 336, 347, 378 Microscopy, 37, 277, 287, 336, 337 Microscopy, Fluorescence, 37, 337 Microspheres, 50, 337 Migration, 22, 23, 49, 56, 58, 63, 64, 69, 169, 176, 178, 327, 337 Mineral Oil, 174, 297, 337 Mineralocorticoids, 278, 301, 337 Minocycline, 69, 337 Miscible, 208, 337 Mitosis, 285, 331, 337 Mitotic, 307, 337 Mitotic inhibitors, 307, 337 Mobilization, 51, 337 Modeling, 36, 46, 337 Modification, 30, 60, 179, 192, 316, 337, 357 Molecular, 12, 14, 16, 19, 22, 25, 37, 38, 40, 42, 49, 57, 58, 60, 63, 67, 72, 114, 117, 181, 192, 205, 247, 250, 280, 284, 288, 291, 299, 302, 313, 321, 337, 351, 358, 361, 369, 374, 375 Molecular Structure, 337, 374 Monitor, 302, 337, 343 Monoclonal, 16, 45, 59, 62, 163, 181, 329, 337, 357, 378 Monoclonal antibodies, 181, 337 Monocyte, 71, 75, 80, 338 Mononuclear, 42, 107, 163, 169, 214, 338, 375 Monophosphate, 164, 338 Morphine, 47, 57, 307, 338, 340, 343 Morphological, 19, 28, 53, 279, 309, 315, 335, 338 Morphology, 292, 338 Motility, 338, 364 Motion Sickness, 338, 340 Movement Disorders, 284, 338, 371 Mucins, 338, 362 Mucociliary, 338, 365 Mucocutaneous, 331, 338

Mucosa, 169, 202, 293, 310, 316, 333, 338, 340, 376 Mucositis, 178, 179, 210, 217, 338 Mucus, 30, 63, 308, 338, 375 Multiple Organ Failure, 178, 338 Multiple sclerosis, 162, 168, 169, 176, 179, 180, 192, 197, 217, 338 Muscle Fibers, 338, 340 Muscular Atrophy, 252, 338 Muscular Dystrophies, 308, 338 Musculoskeletal System, 338, 344 Mustard Gas, 329, 339 Mutagenesis, 176, 339 Mutagens, 339 Mutate, 49, 339 Myasthenia, 261, 339 Mydriatic, 306, 339 Myelin, 338, 339 Myeloid Cells, 58, 339 Myeloma, 322, 339 Myelosuppression, 202, 339 Myocardial infarction, 162, 179, 202, 217, 288, 301, 336, 339 Myocardial Ischemia, 282, 339 Myocardial Reperfusion, 339, 359 Myocardial Reperfusion Injury, 339, 359 Myocarditis, 14, 339 Myocardium, 282, 336, 339, 340 Myopia, 340, 359, 360 Myosin, 14, 340 Myotonic Dystrophy, 252, 340 N Naive, 14, 48, 56, 60, 340 Naloxone, 11, 340 Narcosis, 340 Narcotic, 163, 338, 340 Narcotic Antagonists, 163, 340 Nasal Cavity, 340, 346 Nasal Mucosa, 27, 340 Nausea, 186, 195, 283, 284, 340, 346, 375 NCI, 1, 157, 158, 159, 245, 296, 340 Necrosis, 284, 326, 333, 336, 339, 340, 359, 362 Necrotizing Enterocolitis, 178, 179, 217, 340 Neonatal, 50, 340 Neoplasia, 178, 251, 340, 341 Neoplasm, 157, 340, 341, 362, 375 Neoplastic, 157, 322, 332, 333, 341 Nephropathy, 68, 330, 341

394 Dermatitis

Nerve, 61, 78, 205, 277, 278, 282, 286, 287, 304, 326, 335, 338, 341, 342, 344, 347, 352, 363, 368, 373, 374 Nerve Fibers, 61, 78, 341 Nervous System, 75, 186, 187, 224, 252, 277, 278, 294, 295, 316, 318, 331, 335, 338, 340, 341, 342, 344, 348, 364, 370, 371 Nervousness, 195, 341 Neural, 177, 251, 278, 322, 341, 360 Neuritis, 195, 341 Neurobehavioral Manifestations, 290, 306, 341 Neurodermatitis, 131, 185, 257, 341 Neuroendocrine, 60, 341 Neurogenic, 23, 341, 376 Neurogenic Inflammation, 23, 341 Neuroleptic, 279, 284, 341 Neurologic, 290, 341 Neuromuscular, 277, 341, 375 Neuromuscular Junction, 277, 341 Neuronal, 340, 341, 348 Neurons, 304, 316, 341, 342, 370 Neuropeptides, 23, 61, 205, 341 Neuroretinitis, 341, 360 Neurotensin, 61, 201, 342 Neurotoxic, 342 Neurotoxins, 218, 342 Neurotransmitters, 307, 338, 342, 353 Neutralization, 15, 49, 342 Neutrons, 280, 329, 342, 357 Neutropenia, 202, 342 Neutrophil, 23, 31, 96, 206, 280, 327, 342 Neutrophil Collagenase, 206, 342 Nevus, 158, 217, 342 Niacin, 118, 179, 342, 374 Niche, 43, 342 Nickel, 21, 74, 85, 96, 104, 109, 114, 116, 126, 129, 130, 174, 177, 182, 263, 342 Nitrates, 174, 342 Nitric acid, 342 Nitric Oxide, 47, 323, 342 Nitrogen, 204, 279, 280, 282, 302, 313, 314, 318, 343, 374 Norepinephrine, 278, 307, 343 Nuclear, 10, 176, 199, 214, 287, 297, 308, 312, 316, 340, 343 Nucleic acid, 172, 316, 325, 339, 343, 357, 361 Nummular, 226, 343 Nurse Practitioners, 7, 343 Nutritive Value, 315, 343

O Obstetrics, 333, 343 Occupational Exposure, 46, 343 Occupational Health, 43, 223, 343 Ocular, 178, 179, 198, 205, 217, 343 Ointments, 53, 172, 183, 184, 226, 259, 260, 263, 265, 343, 346, 365, 366, 379 Oligopeptides, 194, 343 Oncogene, 175, 251, 343 Oncogenic, 327, 343 Onychomycosis, 69, 343 Opacity, 292, 304, 343 Opium, 307, 338, 343 Opportunistic Infections, 11, 344 Opsin, 344, 360 Optic Chiasm, 323, 344 Optic Disk, 305, 344 Optic Nerve, 341, 344, 345, 360, 362 Orbit, 313, 344, 348 Organ Culture, 23, 344 Organelles, 294, 303, 335, 344 Orthodontic Brackets, 16, 344 Orthopaedic, 73, 344 Orthostatic, 284, 344 Osmotic, 279, 344 Osteoarthritis, 143, 175, 179, 199, 202, 217, 344 Osteoporosis, 26, 175, 176, 179, 194, 199, 202, 217, 224, 344 Otitis, 182, 344, 345 Otitis Media, 182, 344, 345 Otitis Media with Effusion, 182, 345 Outpatient, 78, 129, 345 Ovalbumin, 13, 35, 345, 364 Ovary, 301, 312, 318, 345, 352 Overdose, 163, 345 Overexpress, 28, 345 Ovum, 301, 317, 345, 353 Oxazolone, 31, 345 Oxidants, 102, 188, 215, 345 Oxidation, 188, 277, 284, 289, 302, 318, 345 Oxidation-Reduction, 289, 345 Oxidative metabolism, 331, 345 Oxides, 174, 345 P Pacemaker, 85, 345 Pachymeningitis, 335, 345 Palliative, 345, 371 Pancreas, 277, 288, 289, 306, 327, 332, 345, 346, 375 Pancreatic, 192, 251, 292, 346 Pancreatic cancer, 192, 251, 346

Index 395

Pancreatitis, 179, 217, 346 Panic, 315, 346 Panic Disorder, 315, 346 Papilla, 346 Papillary, 179, 346 Papillomavirus, 346 Paraffin, 163, 346 Paranasal Sinuses, 346, 365 Parasite, 33, 346 Parasitic, 202, 256, 257, 296, 308, 314, 346 Parenteral, 121, 224, 346 Paresis, 341, 346 Paresthesias, 341, 346 Parietal, 346, 348 Parkinsonism, 284, 346 Parotid, 347, 362 Paroxetine, 65, 347 Paroxysmal, 252, 282, 320, 347 Partial remission, 347, 359 Particle, 332, 347, 373 Patch Tests, 7, 87, 105, 347 Pathogen, 48, 67, 326, 347 Pathogenesis, 7, 12, 17, 18, 23, 30, 31, 32, 35, 37, 42, 43, 63, 178, 321, 347 Pathologic, 285, 288, 301, 307, 323, 347, 356 Pathologic Processes, 285, 347 Pathologies, 22, 64, 347 Pathophysiology, 10, 18, 40, 48, 62, 100, 347 Patient Education, 6, 8, 258, 263, 265, 270, 272, 275, 347 Patient Satisfaction, 52, 347 Pelvic, 347, 355 Pemphigus, 40, 77, 277, 347 Penicillin, 282, 347 Pepsin, 209, 347 Pepsin A, 209, 347 Peptic, 179, 217, 347 Peptic Ulcer, 179, 217, 347 Peptide, 13, 15, 23, 34, 50, 62, 209, 309, 330, 347, 352, 354, 355 Peptide Fragments, 34, 347 Perception, 95, 180, 348, 362 Percutaneous, 21, 36, 75, 200, 348 Perennial, 7, 202, 348, 374 Perianal, 228, 348 Pericardium, 348, 370 Perinatal, 25, 348 Perineal, 54, 323, 348 Perineum, 193, 348, 367 Periodontal disease, 31, 348 Periodontitis, 48, 178, 179, 217, 348

Perioral, 81, 228, 257, 264, 348 Periorbital, 167, 348 Peripheral blood, 18, 30, 38, 71, 89, 90, 225, 320, 327, 348, 350 Peripheral Nerves, 331, 348 Peripheral Nervous System, 348, 353, 369, 376 Peritoneal, 202, 348 Peritoneum, 18, 336, 348, 360 Peritonitis, 18, 31, 32, 348 Peroxide, 73, 288, 318, 348 Petrolatum, 122, 174, 309, 348 Petroleum, 6, 226, 228, 337, 346, 348 Phagocyte, 345, 349 Pharmaceutic Aids, 315, 349 Pharmaceutical Preparations, 183, 211, 294, 312, 316, 349, 354 Pharmacokinetic, 349 Pharmacologic, 281, 282, 349, 373, 376 Pharmacotherapy, 131, 349 Pharyngitis, 178, 179, 217, 349 Phenolphthalein, 309, 349 Phenotype, 20, 29, 37, 44, 52, 55, 58, 59, 108, 175, 349 Phenyl, 162, 169, 183, 349, 361 Phenylalanine, 347, 349, 375 Phosphodiesterase, 164, 176, 187, 197, 225, 349 Phosphodiesterase Inhibitors, 225, 349 Phospholipases, 349, 365 Phospholipids, 313, 327, 349 Phosphorus, 291, 349 Phosphorylated, 20, 176, 216, 297, 349 Phosphorylation, 10, 19, 175, 199, 203, 349, 355 Photochemotherapy, 237, 349 Photocoagulation, 297, 349 Photodermatitis, 24, 101, 143, 224, 350 Photopheresis, 225, 233, 350 Photosensitivity, 128, 134, 137, 143, 224, 350 Photosensitizing Agents, 349, 350 Phototherapy, 8, 67, 84, 96, 101, 137, 236, 260, 350 Physical Examination, 7, 46, 350 Physiologic, 223, 279, 288, 330, 335, 350, 354, 358, 364 Physiology, 21, 30, 31, 61, 101, 107, 139, 331, 350 Pigment, 288, 304, 335, 344, 350, 360 Pigmentation, 69, 191, 350 Pilot study, 12, 71, 109, 110, 131, 350

396 Dermatitis

Piperidines, 164, 350 Pituitary Gland, 301, 350, 354 Placenta, 312, 350, 353, 375 Plana, 350, 364 Plaque, 162, 197, 282, 350 Plasma cells, 13, 214, 283, 339, 351 Plasma protein, 178, 279, 310, 351 Plasmin, 32, 284, 351, 373, 375 Plasminogen, 31, 32, 200, 284, 351, 364, 373, 375 Plasminogen Activators, 32, 351 Plasminogen Inactivators, 351, 364 Platelet Activation, 351, 365 Platelet Aggregation, 198, 281, 342, 351, 372 Platelet Factor 4, 328, 351 Platelets, 288, 293, 339, 342, 351, 372 Platinum, 182, 351 Pleated, 330, 351 Poisoning, 218, 291, 297, 303, 311, 328, 336, 340, 351, 364 Pollen, 144, 163, 181, 186, 187, 211, 294, 352, 357 Polyarteritis Nodosa, 75, 352 Polycystic, 252, 352 Polyethylene, 182, 352 Polymers, 64, 352, 355, 368 Polymorphism, 92, 352 Polypeptide, 82, 165, 203, 205, 281, 297, 299, 313, 347, 351, 352, 355, 376, 379 Polysaccharide, 201, 209, 283, 294, 318, 352, 355 Polyunsaturated fat, 25, 131, 352, 372 Port, 196, 352 Port-a-cath, 352 Posterior, 281, 286, 294, 295, 307, 345, 352, 362 Postmenopausal, 344, 352 Postnatal, 352, 368 Postoperative, 338, 352 Postsynaptic, 352, 365, 370 Post-translational, 60, 352 Post-traumatic, 290, 320, 338, 352 Potassium, 116, 130, 166, 177, 288, 337, 352, 366 Potassium Cyanide, 288, 352 Potentiate, 328, 353 Potentiating, 207, 353 Potentiation, 295, 353, 365 Practice Guidelines, 249, 265, 353 Precancerous, 277, 353 Preclinical, 64, 353

Precursor, 50, 52, 282, 285, 295, 302, 307, 308, 309, 310, 343, 349, 351, 353, 354, 374, 375 Predisposition, 40, 353 Preeclampsia, 179, 217, 353 Presynaptic, 307, 353, 370 Presynaptic Terminals, 307, 353 Prickle, 277, 330, 353 Private Sector, 37, 353 Probe, 21, 165, 353 Prodrug, 353 Progesterone, 73, 353, 368 Progression, 11, 15, 50, 64, 102, 190, 282, 334, 353 Progressive, 285, 293, 296, 304, 307, 319, 338, 340, 351, 353, 359, 375 Projection, 303, 343, 344, 354, 359 Prolapse, 228, 354 Proline, 194, 297, 323, 354 Promoter, 57, 85, 354 Promotor, 354, 360 Prone, 63, 93, 354 Prone Position, 93, 354 Pro-Opiomelanocortin, 205, 309, 354 Prophase, 354, 370 Prophylaxis, 88, 132, 171, 207, 304, 354, 376 Propolis, 125, 135, 138, 354 Propylene Glycol, 184, 193, 194, 354 Prospective study, 4, 89, 132, 332, 354 Prostaglandin, 21, 35, 114, 198, 202, 354, 372 Prostaglandins A, 354, 355 Prostate, 141, 183, 192, 251, 288, 355, 375 Protease, 40, 42, 61, 171, 210, 280, 351, 355, 373 Protease Inhibitors, 171, 355 Protein Binding, 37, 355 Protein C, 17, 20, 31, 58, 59, 60, 99, 169, 279, 281, 287, 330, 355, 375 Protein Conformation, 281, 330, 355 Protein S, 35, 203, 223, 252, 253, 288, 299, 316, 355, 361, 371 Proteins, 10, 15, 20, 22, 27, 32, 34, 43, 49, 52, 64, 115, 166, 169, 172, 176, 188, 194, 199, 280, 281, 283, 289, 290, 292, 293, 295, 297, 298, 302, 305, 308, 313, 316, 317, 321, 327, 329, 330, 334, 337, 343, 347, 351, 352, 355, 358, 363, 364, 372, 373 Protein-Tyrosine Kinase, 63, 355 Proteinuria, 353, 355 Proteoglycan, 31, 351, 355, 368

Index 397

Proteolytic, 117, 280, 297, 298, 313, 351, 355, 364, 373, 375 Protocol, 17, 130, 355 Protons, 280, 323, 329, 355, 357 Protozoa, 308, 331, 336, 355, 374 Proximal, 57, 307, 340, 353, 356 Pruritic, 7, 77, 163, 186, 194, 207, 213, 304, 308, 331, 356, 372 Pruritus, 6, 8, 65, 69, 95, 116, 137, 163, 167, 186, 200, 225, 341, 356, 375 Psoralen, 7, 8, 237, 356 Psychiatric, 65, 335, 356 Psychiatry, 11, 314, 356, 368 Psychogenic, 341, 356, 376 Psychomotor, 303, 341, 356 Psychosis, 170, 171, 195, 284, 356 Psyllium, 151, 356 Puberty, 185, 356 Public Health, 47, 50, 249, 356 Public Policy, 247, 356 Publishing, 3, 11, 67, 172, 356 Pulmonary, 18, 25, 42, 78, 187, 204, 280, 289, 300, 310, 331, 356, 357, 360, 369, 377 Pulmonary Artery, 289, 356, 377 Pulmonary Circulation, 204, 357 Pulmonary hypertension, 300, 357 Pupil, 301, 306, 339, 357 Purines, 357, 364 Purpura, 166, 357 Pustular, 6, 190, 195, 197, 321, 325, 357 Pyridones, 183, 357 Q Quality of Life, 26, 65, 110, 140, 260, 357 Quaternary, 193, 355, 357 Quercetin, 35, 357 Quiescent, 357, 378 R Race, 25, 216, 337, 357 Radiation therapy, 189, 210, 307, 312, 328, 329, 357, 378 Radioactive, 26, 289, 323, 325, 328, 329, 338, 343, 357, 358, 378 Radioallergosorbent Test, 89, 357 Radiodermatitis, 75, 357 Radioimmunoassay, 288, 357 Radioimmunotherapy, 357, 358 Radioisotope, 357, 358 Radiolabeled, 329, 357, 358, 378 Radiological, 348, 358 Radiotherapy, 55, 211, 290, 329, 357, 358, 378

Randomized, 17, 65, 69, 88, 94, 95, 103, 110, 121, 122, 132, 139, 308, 358 Rarefaction, 285, 358 Reagent, 165, 322, 329, 358 Reality Testing, 356, 358 Receptivity, 63, 358 Receptors, Serotonin, 358, 364 Recombinant, 15, 16, 34, 41, 49, 178, 202, 217, 358, 377 Recombinant Proteins, 15, 358 Recombination, 31, 358 Reconstitution, 56, 358 Rectal, 228, 358 Rectum, 284, 290, 303, 306, 314, 316, 325, 326, 330, 355, 358 Recurrence, 130, 197, 264, 289, 334, 358 Red blood cells, 39, 311, 320, 339, 358, 362 Red Nucleus, 286, 358 Reductase, 179, 333, 359, 365 Refer, 1, 290, 298, 307, 309, 314, 315, 321, 332, 340, 341, 342, 356, 358, 359 Reflex, 90, 359 Reflux, 311, 359 Refraction, 340, 359, 367 Refractory, 107, 308, 359 Regeneration, 168, 358, 359 Regimen, 170, 197, 308, 349, 359 Relapse, 68, 111, 197, 231, 359 Reliability, 45, 359 Remission, 177, 289, 334, 358, 359 Renal failure, 303, 320, 359 Renin, 282, 292, 359 Renin-Angiotensin System, 292, 359 Reperfusion, 162, 178, 179, 198, 217, 339, 359 Reperfusion Injury, 162, 178, 179, 217, 359 Respiratory Burst, 58, 359 Respiratory distress syndrome, 17, 360 Respiratory syncytial virus, 20, 360 Respiratory System, 338, 360, 376 Response Elements, 10, 360 Response rate, 33, 54, 360 Restoration, 339, 358, 359, 360, 378 Reticular, 179, 360 Retina, 86, 295, 296, 299, 305, 331, 340, 341, 344, 360, 361, 362, 364, 376, 378 Retinal, 36, 86, 198, 305, 344, 360, 362, 377 Retinal Detachment, 86, 198, 305, 360, 362 Retinitis, 178, 179, 217, 360 Retinoblastoma, 251, 360 Retinol, 360 Retroperitoneal, 278, 360

398 Dermatitis

Retrospective, 4, 114, 361 Retrospective study, 4, 114, 361 Retroviral vector, 58, 361 Rheumatic Diseases, 50, 178, 361 Rheumatism, 361 Rhinitis, 7, 12, 17, 21, 25, 27, 30, 45, 102, 108, 115, 141, 162, 169, 173, 179, 182, 187, 189, 192, 198, 201, 204, 211, 213, 214, 217, 225, 236, 279, 294, 361 Ribavirin, 214, 361 Riboflavin, 119, 361 Ribose, 278, 361 Ribosome, 361, 374 Rigidity, 328, 347, 350, 361 Risk factor, 21, 24, 46, 54, 82, 93, 228, 262, 311, 354, 361 Risk patient, 15, 49, 361 Rod, 287, 310, 361 Rubber, 3, 6, 128, 182, 228, 263, 277, 361 Rutin, 357, 361 Rye, 194, 224, 261, 296, 311, 317, 361 S Salicylamides, 361 Salicylanilides, 224, 361 Salicylic, 166, 193, 194, 240, 241, 262, 361, 362 Saline, 185, 209, 362 Saliva, 172, 362 Salivary, 303, 306, 346, 362 Salivary glands, 303, 306, 362 Saponins, 362, 368 Sarcoidosis, 5, 168, 201, 362 Sarcoma, 190, 192, 195, 362 Satellite, 28, 362 Schizoid, 362, 378 Schizophrenia, 143, 171, 202, 362, 378 Schizotypal Personality Disorder, 362, 378 Sclera, 295, 299, 311, 362, 376 Scleral Buckling, 86, 362 Scleritis, 166, 362 Scleroderma, 166, 197, 261, 285, 363 Scleroproteins, 330, 363 Sclerosis, 183, 209, 252, 285, 298, 338, 363 Screening, 19, 24, 26, 41, 54, 63, 166, 168, 205, 206, 213, 214, 296, 363 Seafood, 46, 363 Sebaceous, 264, 265, 329, 335, 363, 378 Sebaceous gland, 264, 265, 329, 335, 363, 378 Seborrhea, 177, 215, 222, 264, 266, 363 Sebum, 191, 363

Secretion, 33, 62, 65, 166, 180, 191, 198, 214, 249, 301, 322, 323, 328, 337, 338, 363 Secretory, 27, 293, 363, 370 Secretory Vesicles, 293, 363 Segregation, 4, 358, 363 Seizures, 303, 347, 363 Selenium, 119, 241, 262, 363 Semen, 144, 355, 363 Semisynthetic, 337, 363 Senescence, 174, 175, 363 Senile, 190, 277, 344, 363 Sensitization, 12, 13, 24, 28, 30, 35, 46, 48, 53, 57, 60, 63, 70, 82, 96, 111, 124, 132, 167, 363 Sensor, 93, 363 Sepsis, 176, 192, 364 Septic, 17, 106, 178, 202, 285, 364 Septicemia, 122, 364 Sequencing, 31, 181, 364 Serine, 40, 42, 203, 309, 364, 373 Serine Endopeptidases, 309, 364 Serine Proteinase Inhibitors, 364 Serologic, 324, 364 Serology, 50, 364 Serotonin, 65, 284, 315, 347, 349, 358, 364, 374 Serotonin Agonists, 364 Serotonin Antagonists, 65, 364 Serous, 309, 364 Serpins, 31, 364 Serrata, 145, 296, 364 Serrated, 364 Sex Characteristics, 282, 356, 364, 371 Sex Determination, 252, 364 Shedding, 177, 365 Shock, 17, 163, 178, 186, 187, 198, 202, 281, 310, 315, 322, 365, 374 Signal Transduction, 28, 165, 176, 203, 327, 365 Signs and Symptoms, 171, 262, 352, 359, 365, 375 Simvastatin, 75, 365 Sinusitis, 45, 182, 201, 365 Skeletal, 218, 282, 295, 338, 365 Skeleton, 277, 330, 354, 365 Skin Care, 6, 164, 170, 174, 192, 193, 194, 260, 365 Skin Manifestations, 42, 365 Skull, 301, 313, 328, 344, 365 Small intestine, 194, 224, 307, 310, 322, 324, 328, 330, 365, 374, 377 Smallpox, 14, 48, 257, 366, 376

Index 399

Smooth muscle, 162, 173, 204, 280, 281, 290, 299, 322, 338, 359, 366, 369 Snails, 66, 366 Sneezing, 173, 211, 365, 366 Soaps, 265, 365, 366 Social Environment, 357, 366 Sodium, 79, 116, 124, 130, 305, 337, 366, 369 Soft tissue, 289, 365, 366 Solid tumor, 282, 366 Solvent, 21, 166, 207, 312, 344, 354, 366, 374 Soma, 366 Somatic, 17, 19, 322, 335, 337, 348, 366 Somatic mutations, 19, 366 Soybean Oil, 352, 366 Spasmogenic, 281, 366 Spastic, 329, 366 Spatial disorientation, 307, 366 Specialist, 83, 267, 306, 366 Species Specificity, 42, 367 Specificity, 13, 14, 23, 26, 42, 50, 52, 62, 181, 278, 309, 364, 367 Spectrum, 31, 54, 183, 203, 330, 367 Sperm, 282, 296, 352, 366, 367 Spinal cord, 61, 205, 286, 290, 294, 295, 307, 310, 335, 341, 345, 348, 359, 367 Spinous, 311, 330, 367 Spirochete, 31, 367, 370 Spirometry, 46, 367 Spleen, 28, 165, 281, 303, 322, 333, 362, 367 Sporadic, 20, 360, 367 Sprue, 194, 224, 248, 258, 259, 260, 261, 266, 367 Stabilizer, 61, 367 Standard therapy, 350, 367 Staphylococcal Infections, 103, 367 Staphylococcal Scalded Skin Syndrome, 40, 367 Staphylococcus, 40, 42, 77, 83, 86, 117, 126, 139, 325, 337, 367 Staphylococcus aureus, 40, 42, 77, 83, 86, 117, 126, 139, 325, 367 Stasis, 71, 96, 226, 367 Statistically significant, 21, 367 Steady state, 10, 367 Stem Cells, 55, 59, 280, 318, 320, 367 Sterility, 302, 326, 368 Steroid, 17, 117, 191, 259, 262, 301, 362, 365, 368 Stimulant, 322, 368, 370

Stimulus, 177, 308, 312, 326, 328, 329, 341, 346, 359, 368, 372 Stomach, 262, 277, 286, 306, 311, 316, 318, 322, 331, 340, 347, 359, 365, 367, 368 Stool, 228, 325, 329, 330, 368, 371 Strand, 23, 166, 368 Streptavidin, 46, 368 Streptococcal, 331, 368 Streptococci, 325, 368 Stress, 8, 60, 61, 84, 99, 176, 213, 219, 225, 233, 259, 261, 293, 301, 329, 340, 353, 361, 368, 376 Stroke, 160, 163, 175, 186, 199, 246, 292, 368 Stromelysin 1, 206, 368 Stupor, 340, 368 Styrene, 361, 368 Subacute, 50, 326, 365, 368 Subarachnoid, 320, 368 Subclinical, 21, 108, 326, 363, 368 Subcutaneous, 17, 180, 294, 308, 346, 368 Subspecies, 366, 369, 376 Substance P, 200, 209, 289, 336, 358, 363, 369 Substrate, 55, 171, 310, 369 Suction, 157, 158, 369 Sulfapyridine, 195, 242, 369 Sulfur, 119, 209, 240, 241, 313, 336, 369 Sulfuric acid, 209, 369 Sunburn, 143, 263, 369 Superoxide, 359, 369 Supplementation, 88, 132, 369 Support group, 248, 369 Suppression, 20, 24, 301, 369 Suppurative, 294, 321, 369 Suramin, 202, 369 Surfactant, 166, 369 Survival Rate, 5, 369 Suspensions, 19, 183, 369 Sweat, 36, 90, 284, 321, 323, 363, 369 Sweat Glands, 36, 284, 363, 369 Sympathomimetic, 307, 311, 343, 370 Symphysis, 355, 370 Symptomatic, 23, 47, 190, 234, 346, 370 Symptomatic treatment, 190, 370 Synapses, 290, 295, 342, 370 Synapsis, 370 Synaptic, 166, 365, 370 Synaptic Transmission, 166, 370 Synergistic, 190, 191, 206, 207, 216, 370, 372 Synovial, 45, 285, 370

400 Dermatitis

Synovial Membrane, 285, 370 Syphilis, 31, 370 Systemic disease, 285, 324, 364, 370 Systemic lupus erythematosus, 50, 62, 178, 192, 261, 298, 370 Systolic, 323, 370 T Tachycardia, 195, 370 Tacrine, 190, 370 Tacrolimus, 5, 6, 7, 53, 69, 71, 78, 83, 93, 104, 107, 109, 111, 224, 232, 234, 241, 263, 265, 371 Talcum, 54, 371 Talcum powder, 54, 371 Tardive, 284, 371 Tea Tree Oil, 116, 125, 137, 150, 371 Tear Gases, 329, 371 Telangiectasia, 252, 371 Tenesmus, 308, 371 Testicular, 202, 371 Testis, 312, 371 Testosterone, 359, 371 Tetani, 371 Tetanic, 371 Tetanus, 218, 371 Tetracycline, 152, 264, 337, 371 Thalamic, 286, 371 Thalamic Diseases, 286, 371 Theophylline, 281, 357, 371 Therapeutics, 12, 59, 61, 78, 167, 175, 199, 242, 371 Thermoregulation, 180, 372 Thigh, 319, 372 Third Ventricle, 285, 323, 372 Thorax, 277, 372 Threonine, 203, 364, 372 Threshold, 95, 312, 323, 372 Thrombin, 313, 351, 355, 372 Thrombolytic, 351, 372 Thrombomodulin, 355, 372 Thrombosis, 162, 288, 327, 355, 368, 372 Thromboxanes, 285, 372 Thrombus, 31, 301, 326, 339, 351, 372 Thymus, 15, 45, 101, 152, 324, 333, 372 Thyroid, 5, 180, 249, 329, 372, 375 Thyroxine, 279, 349, 364, 372 Tic, 171, 372 Ticks, 211, 372 Tin, 174, 351, 372 Tinea Pedis, 104, 372 Tinnitus, 344, 372 Tissue Plasminogen Activator, 31, 373

Tolerance, 28, 278, 318, 373 Tonicity, 308, 320, 330, 373 Toxaemia, 353, 373 Toxicity, 21, 65, 168, 195, 224, 292, 307, 309, 336, 373 Toxicokinetics, 373 Toxicology, 53, 79, 123, 223, 248, 373 Toxins, 42, 178, 218, 283, 289, 290, 318, 326, 338, 357, 364, 373, 377 Trace element, 295, 297, 342, 372, 373 Trachea, 290, 372, 373 Tractus, 205, 373 Transcription Factors, 10, 360, 373 Transdermal, 174, 200, 217, 373 Transduction, 203, 365, 373 Transfection, 288, 373 Transfer Factor, 324, 373 Transgenes, 62, 374 Translating, 28, 374 Translation, 176, 199, 374 Translational, 28, 374 Translocate, 176, 374 Translocation, 10, 199, 374 Transmitter, 277, 286, 307, 329, 335, 343, 370, 374 Transplantation, 31, 162, 296, 324, 334, 374 Trauma, 54, 69, 164, 175, 178, 186, 228, 290, 303, 311, 340, 346, 374 Trees, 280, 361, 374 Triamcinolone Acetonide, 215, 374 Trichloroethylene, 21, 374 Tricuspid Atresia, 300, 374 Tricyclic, 204, 307, 374 Trigger zone, 284, 374 Tropical Sprue, 248, 374 Tropism, 64, 374 Trypanosomiasis, 369, 374 Tryptophan, 297, 364, 374 Tuberculosis, 300, 333, 362, 374 Tuberous Sclerosis, 252, 374 Tumor marker, 280, 288, 375 Tumor Necrosis Factor, 215, 333, 375 Tumor suppressor gene, 332, 375 Tumour, 176, 375 Tyrosine, 19, 58, 180, 197, 204, 307, 355, 375 U Ubiquitin, 176, 375 Ulcer, 175, 209, 294, 303, 347, 375 Ulceration, 303, 375 Ulcerative colitis, 176, 178, 179, 180, 187, 198, 209, 217, 326, 375

Index 401

Umbilical Arteries, 375 Umbilical Cord, 62, 375 Unconscious, 303, 324, 375 Uraemia, 346, 375 Urbanization, 66, 375 Urea, 188, 369, 375 Urethra, 355, 375, 376 Urinary, 34, 202, 214, 295, 296, 302, 317, 325, 373, 375, 376 Urinary Plasminogen Activator, 373, 375 Urinary Retention, 202, 376 Urinate, 376 Urine, 33, 165, 192, 193, 262, 289, 302, 305, 307, 320, 325, 355, 361, 375, 376 Urogenital, 317, 376 Urticaria, 27, 46, 157, 158, 169, 179, 192, 194, 198, 204, 211, 217, 223, 260, 281, 294, 376 Uterus, 301, 333, 342, 353, 376 Uvea, 376 Uveitis, 178, 179, 192, 217, 376 V Vaccination, 13, 15, 48, 61, 257, 376 Vaccine, 13, 43, 48, 208, 257, 278, 355, 376 Vaccine adjuvant, 208, 376 Vaccinia, 14, 49, 376 Vaccinia Virus, 49, 376 Vagina, 305, 376 Vaginal, 54, 376 Variola, 49, 376 Vasculitis, 346, 352, 376 Vasoactive, 61, 82, 201, 376 Vasoactive Intestinal Peptide, 201, 376 Vasoconstriction, 198, 311, 376 Vasodilatation, 198, 376 Vasodilation, 173, 376 Vasodilator, 290, 307, 322, 339, 377 Vector, 66, 373, 376, 377 Vein, 282, 328, 343, 347, 362, 375, 377 Venereal, 370, 377 Venoms, 342, 377 Venous, 71, 288, 321, 355, 374, 377 Ventral, 285, 323, 377 Ventricle, 286, 300, 356, 370, 372, 374, 377 Ventricular, 300, 339, 374, 377 Venules, 60, 178, 289, 291, 309, 336, 377 Vertebrae, 328, 367, 377 Vertigo, 344, 377

Vesicular, 104, 286, 304, 321, 366, 376, 377 Veterinary Medicine, 114, 247, 377 Villi, 224, 377 Villous, 293, 377 Viral, 20, 30, 49, 112, 162, 175, 199, 202, 214, 317, 343, 373, 377 Virulence, 11, 32, 49, 286, 373, 377 Virus, 11, 20, 48, 90, 287, 294, 301, 310, 316, 317, 322, 327, 350, 360, 361, 366, 373, 376, 377 Viscera, 336, 366, 377 Visceral, 331, 348, 377 Visual Acuity, 362, 377 Vitamin A, 193, 327, 360, 377 Vitiligo, 5, 356, 378 Vitreous Hemorrhage, 305, 378 Vitreous Humor, 360, 378 Vitro, 10, 13, 22, 29, 31, 33, 38, 41, 44, 45, 48, 53, 56, 60, 65, 84, 174, 175, 197, 221, 280, 321, 325, 357, 364, 371, 378 Vivo, 17, 18, 24, 25, 28, 29, 33, 36, 43, 44, 45, 48, 53, 55, 56, 58, 60, 61, 63, 64, 65, 76, 84, 197, 215, 221, 280, 321, 325, 345, 371, 372, 378 Vulgaris, 91, 92, 101, 110, 126, 130, 135, 277, 378 W Wakefulness, 303, 378 War, 99, 339, 378 Wart, 330, 378 Weight-Bearing, 344, 378 Wheezing, 20, 30, 236, 378 White blood cell, 177, 277, 283, 287, 326, 331, 333, 334, 338, 339, 342, 351, 378 Windpipe, 290, 372, 378 Withdrawal, 11, 17, 39, 303, 378 Wound Healing, 31, 61, 293, 327, 335, 378 X Xenograft, 282, 378 X-ray, 314, 316, 329, 343, 357, 358, 367, 378 X-ray therapy, 329, 378 Y Yeasts, 315, 349, 378 Z Zinc Oxide, 200, 379 Zygosaccharomyces, 203, 379 Zymogen, 355, 379

402 Dermatitis

Index 403

404 Dermatitis