ANTIPHOSPHOLIPID SYNDROME 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 2004 by ICON Group International, Inc. Copyright 2004 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., 1960Antiphospholipid Syndrome: 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: 0-497-00077-6 1. Antiphospholipid Syndrome-Popular works. I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on antiphospholipid syndrome. 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 ANTIPHOSPHOLIPID SYNDROME .............................................................. 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Antiphospholipid Syndrome ......................................................... 4 E-Journals: PubMed Central ....................................................................................................... 18 The National Library of Medicine: PubMed ................................................................................ 19 CHAPTER 2. NUTRITION AND ANTIPHOSPHOLIPID SYNDROME .................................................... 65 Overview...................................................................................................................................... 65 Finding Nutrition Studies on Antiphospholipid Syndrome ........................................................ 65 Federal Resources on Nutrition ................................................................................................... 67 Additional Web Resources ........................................................................................................... 67 CHAPTER 3. ALTERNATIVE MEDICINE AND ANTIPHOSPHOLIPID SYNDROME .............................. 69 Overview...................................................................................................................................... 69 National Center for Complementary and Alternative Medicine.................................................. 69 Additional Web Resources ........................................................................................................... 71 General References ....................................................................................................................... 72 CHAPTER 4. PATENTS ON ANTIPHOSPHOLIPID SYNDROME........................................................... 73 Overview...................................................................................................................................... 73 Patents on Antiphospholipid Syndrome ...................................................................................... 73 Patent Applications on Antiphospholipid Syndrome................................................................... 77 Keeping Current .......................................................................................................................... 78 CHAPTER 5. BOOKS ON ANTIPHOSPHOLIPID SYNDROME .............................................................. 81 Overview...................................................................................................................................... 81 Chapters on Antiphospholipid Syndrome .................................................................................... 81 CHAPTER 6. PERIODICALS AND NEWS ON ANTIPHOSPHOLIPID SYNDROME ................................ 83 Overview...................................................................................................................................... 83 News Services and Press Releases................................................................................................ 83 Newsletter Articles ...................................................................................................................... 85 Academic Periodicals covering Antiphospholipid Syndrome....................................................... 85 CHAPTER 7. RESEARCHING MEDICATIONS .................................................................................... 87 Overview...................................................................................................................................... 87 U.S. Pharmacopeia....................................................................................................................... 87 Commercial Databases ................................................................................................................. 88 APPENDIX A. PHYSICIAN RESOURCES ............................................................................................ 91 Overview...................................................................................................................................... 91 NIH Guidelines............................................................................................................................ 91 NIH Databases............................................................................................................................. 93 Other Commercial Databases....................................................................................................... 95 APPENDIX B. PATIENT RESOURCES ................................................................................................. 97 Overview...................................................................................................................................... 97 Patient Guideline Sources............................................................................................................ 97 Finding Associations.................................................................................................................. 100 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 103 Overview.................................................................................................................................... 103 Preparation................................................................................................................................. 103 Finding a Local Medical Library................................................................................................ 103 Medical Libraries in the U.S. and Canada ................................................................................. 103 ONLINE GLOSSARIES................................................................................................................ 109 Online Dictionary Directories ................................................................................................... 109
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ANTIPHOSPHOLIPID SYNDROME DICTIONARY............................................................ 111 INDEX .............................................................................................................................................. 157
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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 antiphospholipid syndrome 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 antiphospholipid syndrome, 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 antiphospholipid syndrome, 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 antiphospholipid syndrome. Abundant guidance is given on how to obtain free-ofcharge 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 antiphospholipid syndrome, 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 antiphospholipid syndrome. 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 ANTIPHOSPHOLIPID SYNDROME Overview In this chapter, we will show you how to locate peer-reviewed references and studies on antiphospholipid syndrome.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and antiphospholipid syndrome, 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 “antiphospholipid syndrome” (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: •
Pancreaticoportal Fistula in Association with Antiphospholipid Syndrome Presenting as Ascites and Portal System Thrombosis Source: Canadian Journal of Gastroenterology. 16(9): 601-605. September 2002. Contact: Available from Pulsus Group, Inc. 2902 South Sheridan Way, Oakville, Ontario, Canada L6J 7L6. Fax (905) 829-4799. E-mail:
[email protected]. Summary: Fistulous communication (an abnormal opening) between the pancreas and the portal venous system is extremely rare and is usually a complication of chronic pancreatitis or pancreatic pseudocysts. In this article, the authors describe a patient who presented with abdominal pain and ascites (fluid accumulation) secondary to a pancreaticoportal fistula and portal system thrombosis. The diagnosis was made by
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Antiphospholipid Syndrome
endoscopic retrograde cholangiopancreatography (ERCP) and confirmed by immediate postprocedure computed tomographic scanning (CT scan). Laboratory studies identified concomitant antiphospholipid syndrome. The patient responded favorably to supportive medical therapy. 5 figures. 32 references. •
Antiphospholipid Syndrome: Current Diagnostic and Therapeutic Issues Source: Journal of Musculoskeletal Medicine. 19(5): 184-186,188-189, 193-194. May 2002. Summary: This journal article uses a question and answer format to provide health professionals with information on the main clinical, laboratory, and therapeutic aspects of antiphospholipid syndrome (APS). APS is a disorder in which patients have recurrent thrombotic events associated with the persistent presence of anticardiolipin antibodies and lupus anticoagulant. It appears to occur predominantly in women. The disorder should be suspected in patients with recurrent arterial and venous thrombosis, thrombosis at a young age, venous thrombosis in locations other than the deep veins of the legs, arterial thrombosis in the absence of atherosclerosis, a history of stillbirths, unexplained thrombocytopenia, or livedo reticularis. Differential diagnosis involves consideration of various thrombogenic conditions. Assays for anticardiolipin antibodies and lupus anticoagulant are the diagnostic tests of choice according to the Sapporo criteria. Solid phase enzyme linked immunosorbent assay is the method of choice for the detection of all three isotypes of anticardiolipin antibodies. Management includes reduction of other risk factors for thrombosis. Careful monitoring of hypertension, diabetes, and hyperlipidemia should be performed. Patients should be encouraged to quit smoking, avoid oral contraceptives, and increase physical activity. In patients with systemic lupus erythematosus, hydroxychloroquine therapy has been found to reduce glucose and cholesterol levels and to control musculoskeletal and cutaneous manifestations. Long term anticoagulant therapy may be required to maintain pregnancies and to prevent repeated thrombotic events. Although there is a lack of long term data, the overall prognosis for patients with APS appears quite poor. High titers of immunoglobulin G anticardiolipin antibodies have been found to be a significant predictor for subsequent thrombosis in different studies. 4 figures and 48 references. (AA-M).
Federally Funded Research on Antiphospholipid Syndrome The U.S. Government supports a variety of research studies relating to antiphospholipid syndrome. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to antiphospholipid syndrome.
2 Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
Studies
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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 antiphospholipid syndrome. The following is typical of the type of information found when searching the CRISP database for antiphospholipid syndrome: •
Project Title: ANALYSIS OF APOLIPOPROTEIN H IN LUPUS Principal Investigator & Institution: Kamboh, M Ilyas.; Professor; Human Genetics; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2002; Project Start 01-JAN-1997; Project End 31-MAY-2007 Summary: (provided by applicant): The risk of coronary heart disease (CHD) in systemic lupus erythematosus (SLE) women is up to 50 times higher than in the general population. The conventional risk factors are insufficient to explain premature CHD in SLE patients. Compared to about 1-5 percent prevalence of antiphospholipid antibodies (APA) in the general U.S. white population, about 50 percent of the SLE patients are positive for APA. ApoH is a principal autoantigen for the production of APA in patients with autoimmune diseases. ApoH inhibits the in vitro uptake of oxidized low-density lipoprotein (oxLDL) by macrophages, but in the presence of APA it promotes the ihflux of oxLDL into macrophages. As the accumulation of oxLDL in macrophages is believed to initiate the atherosclerotic process, these findings suggest that apoH-mediated immune response in patients with autoimmune diseases, like SLE, may lead to atherosclerosis. In this renewal we propose to examine the joint roles of APA, antibodies to oxLDL (anti-oxLDL) and APOH genetic variation (known and discovered as part of this proposal) in relation to the occurrence of CHD in SUE and non-SLE patients. Our hypothesis is that individuals positive for APA and/or anti-oxLDL are prone to premature CHD and this susceptibility is modified by common genetic variation in the APOH gene. The objectives of the study will be achieved by fulfilling the five aims. Aim 1) identify and characterize naturally occurring common mutations in all exons, introns and the 3' region of the APOH gene by polymerase chain reaction (PCR), denaturing HPLC analysis and DNA sequencing in SLE and non-SLE CHD patients, and African blacks positive for APA. Aim 2) determine the prevalence and correlation between APA (anti-apoH, anticardiolipin, lupus anticoagulant) and anti-oxLDL in plasma samples from SLE patients and controls. Aim 3) determine the relationship between APOH genetic variation (data generated in Aim 1) and the occurrence of APA and anti-oxLDL (data generated in Aim 2). Aim 4) examine the relationship between APOH genetic variation (data generated in Aim 1) and the occurrence of subclinical cardiovascular events in SLE patients and with coronary atherosclerosis in non-SLE patients. Aim 5) perform in vitro mutagenesis and expression studies to express different apoH allelicisoforms to evaluate isoform-specific inhibition of LDL oxidation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ANTICARDIOLIPIN PHOSPHOLIPIDS
ANTIBODIES
AND
OXIDIZED
Principal Investigator & Institution: Witztum, Joseph L.; Professor; Medicine; University of California San Diego La Jolla, Ca 920930934 Timing: Fiscal Year 2002; Project Start 01-JAN-1997; Project End 31-JUL-2005 Summary: Patients with the antiphospholipid antibody syndrome (APS) have autoantibodies to certain phospholipids (aPL) such as cardiolipin and/or the lupus anticoagulant and clinically experience recurrent venous or arterial thrombosis, history
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Antiphospholipid Syndrome
of fetal death and autoimmune thrombocytopenia. Increased aPL also appear to predict increased risk of stroke and myocardial infarction in otherwise healthy men as well. However, controversy exists about the target antigens of aPL, and even university laboratories cannot agree who has elevated aPL titers. In turn, clinical management is hampered by lack of an underlying hypothesis to explain why antibodies should form to such ubiquitous compounds as PL. We have developed the novel hypothesis that many aPL are directed against epitopes of oxidized PL (OxPL) and/or against covalent adducts of OxPL and associated PL binding proteins, such as beta2GPI. Our hypothesis suggests that states of enhanced lipid peroxidation, as occurs in inflammation or atherosclerosis, leads to oxidation of PL (such as in LDL or in membranes of apoptotic or dying cells) which creates neo self-determinants and immunogenic epitopes. The resultant autoantibodies can then target such neoepitopes in many tissues, and may have a variety of biological consequences. Cardiolipin (CL) is the most common PL used to test for aPL. We have shown that APS plasma bind exclusively to OxCL, or to OxCL adducts with beta2GPI, and not to native CL. We propose to further test our hypothesis by determining if antibodies to other OxPL are also present in sera from patients and mice with lupus- like syndromes. We will generate a panel of such aOxPL murine monoclonals from (NZWxBXSB) F1 males. Similar Fab and scFv antibodies will be generated from a human phage-display library. We will determine the epitopes to which they bind and their impact on in vitro and in vivo coagulation, with an emphasis on the Protein C pathway. We will treat lupus-prone mice with potent antioxidants to see if changes in aPL titers and/or other clinical parameters occur. Understanding the etiology of even some of the aPL should lead not only to development of more standardized assays, which should improve our ability to detect high risk individuals, but also to consideration of new therapeutic modalities for patients with aPL and APS (e.g. aggressive anti-inflammatory and/or antioxidant interventions). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SYNDROME
ANTICARDIOLIPIN
ANTIBODIES
IN
ANTIPHOSPHOLIPID
Principal Investigator & Institution: Chen, Pojen P.; Professor; Medicine; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2004; Project Start 25-FEB-1996; Project End 31-MAR-2008 Summary: (provided by applicant): The long-term objectives of this project are to identify and characterize pathogenic anticardiolipin antibodies (aCL) in the antiphospholipid syndrome (APS). Recently, we found 4/5 patient-derived, prothrombotic, monoclonal IgG aCL bind to plasmin, thrombin and activated protein C (APC). Of these 4 plasmin-reactive aCL, CL15 inhibits plasmin-mediated fibrinolysis and anticoagulant activity of APC, and causes fetal loss when injected into pregnant mice. It binds to plasmin with a relative Kd value of 7 x 10/-10 that is 3-4 logs higher than the affinity of IgG anti-beta2GPI antibodies (Ab) toward beta2GPI, the major autoantigen in APS. These data lead us to hypothesize that plasmin is an important autoantigen that drives certain IgG aCL in some APS patients, and that some of the plasmin-driven IgG aCL are prothrombotic (like CL15). To test these hypotheses, the specific aims are: 1. To study the prevalence, characteristics and pathogenic significance of the plasmin-reactive IgG aCL in APS patients. IgG will be purified and analyzed for Ab against CL and plasmin, and by cross inhibition to determine the presence of plasmin-reactive IgG aCL. The plasmin-reactive IgG aCL will be affinity purified and analyzed for binding affinity to plasmin, reactivity with thrombin an APC, and for lupus anticoagulant activity and pathogenicity. 2. To immunize mice with human plasmin and
Studies
7
study the induced Ab and the pregnancy outcomes. Blood samples will be analyzed for IgG Ab against human plasmin and CL, and by cross inhibition to determine the presence of plasmin-reactive IgG aCL. Female mice with high titers of plasmin-reactive IgG aCL will be mated and the pregnancy outcomes will be examined to assess the pathogenicity of the plasmin-reactive IgG aCL. 3. To generate and study monoclonal plasmin-reactive aCL from immunized mice. The monoclonal Ab will be injected (individually or in pairs) into pregnant mice to study their pathogenic potentials, and be analyzed for reactivity with murine plasmin, and human thrombin and APC, and for relevant functional activity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ANTI-PHOSPHOLIPID ANTIBODIES AND THE PROTEIN C SYSTEM Principal Investigator & Institution: Esmon, Naomi L.; Associate Member; Oklahoma Medical Research Foundation Oklahoma City, Ok 731045005 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2007 Summary: (provided by the applicant): Lupus anticoagulants (LAs) and antiphospholipid antibodies (APAs) are associated with an increased risk of thrombosis. It is our hypothesis that APA and/or LA subgroup(s) lead to thrombosis through the selective inhibition of the protein C anticoagulant pathway. We have found that the membrane requirements of the activated protein C (APC) complex are different from those of the procoagulant complexes. Specifically, the APC complex requires phosphatidylethanolamine (PE) for activity. Recently, we have also observed that phospholipid oxidation enhances APC activity specifically. These requirements mimic those of at least a subpopulation of autoantibodies found in lupus patients with thrombosis for the selective inhibition of the APC complex and thus may provide both the specificity and the link between the APC pathway, LA/APAs and thrombosis. It is the goal of this application to determine the relationship between the differential membrane structure requirements of the procoagulant and anticoagulant complexes and the specificity of pathogenic antibodies with emphasis on the role of oxidation. We will determine the mechanism of inhibition of the APC complex by prothrombotic antibodies (Abs) in terms of phospholipid requirements (presence of PE; role of oxidation), the target of the Abs (protein; membrane; protein/membrane) and possible role of other cofactor proteins. The utility of a chimeric form of APC to identify prothrombotic Abs and the prevalence of Abs to other members of the protein C pathway, TM and EPCR will also be investigated. Appreciation of the molecular mechanisms involved in the selective inhibition of the protein C pathway by identifiable subgroup(s) of LA/APAs should lead to better predictive and monitoring tests and potentially more specific and safer therapies in these difficult to manage patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ANTIPHOSPHOLIPID ANTIBODY HETEROGENEITY Principal Investigator & Institution: Rote, Neal S.; Reproductive Biology; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 30-APR-2008 Summary: (provided by applicant): The Antiphospholipid Syndrome is characterized by naturally occurring antiphospholipid antibodies and increased risk of pregnancy loss or a variety of obstetric complications. Antiphospholipid antibodies are directed against phospholipid-dependent antigens, phospholipid-binding proteins, or a combination of
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Antiphospholipid Syndrome
these. There is little information concerning the relevance and relationship of particular antibody specificities to pathophysiology. Considerable data support the proposal that the placental trophoblast is a primary cellular target of antiphospholipid antibodies. The hypothesis is that antiphospholipid antibody-induced pregnancy loss occurs through the binding of a select subgroup of antibodies directly with trophoblast resulting in detrimental effects on placental development. Some of these effects involve thrombosis on the trophoblast surface, but most are non-thrombotic and result in incomplete trophoblast differentiation. A prediction, based on preliminary data, is that the most relevant antibodies will be against phosphatidylserine-dependent antigens. To test this hypothesis, the following Aims will be addressed. Aim 1 will investigate the heterogeneity of antiphospholipid antibodies within individual patients. This Aim is designed to determine within individual pregnancy loss patients the spectrum of reactivities against relevant phospholipids and phospholipid-binding proteins. Individual antiphospholipid antibodies will be purified based on antigenic specificity and characterized. Aim 2 will clone antiphospholipid antibodies from individual patients using single cell PCR techniques. The goal is to clone each relevant antibody present in a minimum of 3 individual patients. The cloned antibodies will be characterized. Aim 3 will investigate the relationship between antibody specificity and biological activity against trophoblast. Reagents prepared in Aims I and 2 will be tested for reactivity against trophoblast. These reactivities will include binding to normal human placental tissue, binding to trophoblast undergoing differentiation in vitro, inhibition of trophoblast invasion, inhibition of intertrophoblast fusion, and induction of apoptosis. This will be the first study to thoroughly investigate the spectrum of antiphospholipid antibodies in individual patients and correlate those data to effects on placental trophoblast. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: AUTOIMMUNE MECHANISMS OF THROMBOSIS Principal Investigator & Institution: Roubey, Robert A.; Associate Professor; Medicine; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 Timing: Fiscal Year 2002; Project Start 30-SEP-2001; Project End 31-JUL-2005 Summary: (provided by applicant): The Antiphospholipid Syndrome (APS) represents an interface between the immune system and blood coagulation. In APS, an abnormal immune response leads to the production of autoantibodies with an apparent specificity for anionic phospholipids. These autoantibodies are strongly associated with both arterial and venous thrombosis. New insights into the pathophysiology of APS have been provided by the discovery that most of the autoantibodies associated with the syndrome are directed against a number of phospholipid-binding plasma proteins, such as beta2-glycoprotein I (beta2GPI), rather than phospholipids alone. A growing body of evidence supports the view that autoantibodies directly contribute to the thrombotic diathesis in APS. Recent data suggest that an important mechanism of autoantibodymediated thrombosis is upregulation of the tissue factor (TF) pathway, the physiological trigger of normal coagulation and an important trigger in thrombosis. These observations lead us to hypothesize that increased TF activity on blood monocytes is an important cause of hypercoagulability in APS. This hypothesis will be tested through the following specific aims. Aim 1 is to identify and characterize the particular autoantibodies that increase TF activity on normal monocytes in vitro, focusing on antibeta2GPI autoantibodies and autoantibodies to tissue factor pathway inhibitor (TFPI), a critical inhibitor of both factor VIIa/TF and factor Xa. Whole blood TF activity in APS
Studies
9
patients will be measured to determine if certain autoantibodies are associated with increased TF on circulating monocytes in vivo. Aims 2 and 3 will determine the general mechanisms by which autoantibodies increase monocyte TF activity. Aim 2 is to determine the effects of antibodies on a) the quantitative expression of TF mRNA and protein and b) the qualitative functional status of TF molecules on the monocyte surface. Experiments in this aim will also examine whether certain pharmacological agents that block monocyte TF expression in response to other stimuli are also capable of inhibiting monocyte TF expression induced by APS autoantibodies. Aim 3 is to determine whether autoantibodies enhance TF activity by blocking the effects of TFPI. Together, the proposed experiments will identify autoantibodies capable of inducing monocyte TF activity and the general mechanisms that are involved. These data will be useful in focusing future research efforts on specific pathways of antibody-mediated monocyte activation and hypercoagulability and in designing new therapeutic strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BRAIN CONNECTIONS Principal Investigator & Institution: Petri, Michelle A.; Associate Professor; Medicine; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 26-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): Neuropsychiatric manifestations of Systemic Lupus Erythematosus (NPSLE) are both common and an important source of morbidity. Of the case definitions for NPSLE syndromes that have recently been developed, cognitive dysfunction appears to be the most prevalent. Little is known about the influence of comorbidities or ethnicity/race on disease outcomes or the underlying biological basis for this important NPSLE syndrome. Perhaps most importantly, no rational therapeutic approach for the treatment of SLE-related cognitive dysfunction currently exists and is unlikely to be developed without a better understanding of disease mechanisms. New brain imaging techniques have great potential to uncover mechanisms underlying NPSLE syndromes, particularly if specific syndromes are targeted. Brain imaging and the evaluation of prospectively measured biomarkers will also help determine factors that are relevant to NPSLE manifestations and may help distinguish reversible from irreversible processes. We propose to study 100 newly diagnosed patients with SLE from 10 sites for the development of cognitive dysfunction, determined using both repeatable computerized and traditional neuropsychological tests. We will prospectively evaluate the relationship of structural and functional brain imaging (using anatomic magnetic resonance imaging and resting FDG-PET), several relevant biomarkers (antiphospholipid antibodies, cytokines and adhesion molecules) and comorbidities (race/ethnicity, depression, fibromyalgia and corticosteroid use) to cognitive dysfunction. We will also determine the impact of cognitive dysfunction on quality of life. Factors distinguishing transient or reversible versus irreversible cognitive dysfunction will be determined using a repeated measures analysis approach. The ability to study the relationship between changes in cognitive functioning and these other variables in a group of newly diagnosed SLE patients is crucial to the successful discovery of early pathologic changes that could be potentially amenable to diseasereversing therapies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: COGNITIVE DYSFUNCTION IN NEUROPSYCHIATRIC-SLE Principal Investigator & Institution: Lockshin, Michael D.; Director; Hospital for Special Surgery New York, Ny 100214872
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Antiphospholipid Syndrome
Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2004 Summary: (provided by applicant): Neuropsychiatric SLE consists of 19 defined neuropsychiatric syndromes, of which cognitive dysfunction is one of the most disabling and least understood. Cognitive dysfunction occurs in more than 25% of SLE patients. In some patients cognitive dysfunction is due to stroke, but in others its cause is unknown. Autoantibody-induced neuronal cytotoxicity is a possible cause for cognitive dysfunction, and autoantibody to the NMDA receptor may play a role in cognitive dysfunction. We propose that cognitive dysfunction is due to both regional (by vascular occlusion) and global (by antibody to the NMDA receptor) brain injury, the latter by glutamate excitotoxicity due to the antibody.This application has the following aims: to characterize cognitive dysfunction in patients in whom lupus disease activity, damage, atherosclerosis, and antiphospholipid antibody are quantified; to determine the association of anti-NMIDA (glutamate) receptor and antiphospholipid antibodies to cognitive dysfunction, to test whether magnetic resonance spectroscopy detects lesions that underlie cognitive dysfunction, and to delineate the relationship of MRS abnormalities to anti-NMDA receptor antibody, lupus disease activity, atherosclerosis, and antiphospholipid antibody. We will do this by carefully assessing, with two independent methods, cognitive function in an already well characterized population of SLE patients who do not have MRI evidence of vascular injury, by obtaining MRS evaluations focusing on the hippocampus, by testing for anti-NMDA and antiphospholipid antibody, and by establishing correlations with measures of SLE activity, damage, and atherosclerosis. We expect to find: that distinguishable forms of cognitive dysfunction are mediated by vascular occlusion (due to atherosclerosis or antiphospholipid antibody) and by NMDA receptor antibody-induced excitotoxic response; that vascular occlusion or stroke causes cognitive dysfunction that correlates with SLE activity and damage, with antiphospholipid antibody, and atherosclerosis risk factors; and that excitotoxic neuron death correlates with anti-NMDA antibody. Successful completion of this research will redefine the pathogenesis of cognitive dysfunction and suggest therapeutic targets for intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: COSTIMULATORY BLOCKADE AND STATINS FOR MURINE SLE Principal Investigator & Institution: Davidson, Anne; Associate Professor; Albert Einstein College of Med Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-AUG-2008 Summary: Statins, inhibitors of HMG CoA reductase, a key enzyme in the cholesterol synthetic pathway, effectively prevent both primary and secondary coronary vascular disease. The beneficial effect of the statins is not all due to their cholesterol lowering function. Recently multiple immunosuppressive effects of statins have been demonstrated both in models of inflammation and of vascular injury. Most of these effects are due to decreased synthesis of mevalonate-derived intermediates that are required for full activation of small GTP binding proteins such as Rho and Ras. Thus there has been increasing interest in possible clinical utility of statins for autoimmune diseases. Our laboratory is interested in developing therapeutic combination regimens of drugs that act on different pathways of immune activation and target organ damage. We have previously focused on the mechanism of action of biologic agents that inhibit costimulatory pathways of B and T cell activation. In this proposal we will ask whether treatment with statins will synergize with costimulatory blockade for the treatment of two different manifestations of SLE; inflammatory renal disease and non-inflammatory vasculopathy. The initiation of both these SLE manifestations is immune mediated but
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the tissue response to autoantibody-mediated damage is different in each case. Both however may be susceptible to the beneficial effects of statins. In aim 1 we will determine the effect of statins in SLE nephritis. We will ask whether statins will synergize with CTLA4Ig in prevention of SLE nephritis and whether they will help maintain remission of nephritis after treatment with a short course of CTLA4Ig and cyclophosphamide. Effects of therapy on immunologic parameters and effector responses in the kidney will be evaluated by a series of assays that are well established in the laboratory. In aim 2 we will utilize a murine model of vasculopathy induced by anti-phospholipid antibodies and ask whether statins, with or without CTLA4Ig, will prevent disease intitiation or progression. In aim 3 we will determine whether monocytes and dendritic cells from patients with inactive SLE are susceptible to the known immunoregulatory effects of statins and determine which statin is most potent. These studies will gather information that may support a clinical trial of statins in SLE patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MECHANISMS OF ANTIPHOSPHOLIPID-INDUCED THROMBOSIS. Principal Investigator & Institution: Pierangeli, Silvia S.; Associate Professor; Morehouse School of Medicine Atlanta, Ga 30310 Timing: Fiscal Year 2002; Project Start 30-SEP-1987; Project End 31-JUL-2006 Summary: (provided by applicant): The association of antiphospholipid (aPL) antibodies with thrombosis in patients with Antiphospholipid Syndrome (APS) is well documented in humans and in animal studies. However, the mechanism(s) by which these antibodies induce thrombosis is the subject of much current study. Previous studies have shown that aPL up regulate endothelial cells (ECs) adhesion molecules (CAMs): intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion-1 (VCAM-1) and E-selectin (E-sel) or induce tissue factor (TF) on monocytes. APL also induced activation of ECs and enhanced thrombus formation in vivo. One study suggested that the anti-hyperchlorestoralemic drug fluvastatin inhibited the enhanced adhesion of monocytes to ECs by aPL in vitro. What is uncertain is the molecular and intracellular events that are induced by aPL interaction with ECs leading to expression of CAM and TF. Other studies also suggest that aPL antibodies may activate platelets as demonstrated by increased expression of GPIIb/ IIIa when platelets are treated with aPL in the presence of an agonist. The intracellular events triggered by aPL interaction with platelets are also unknown. This study proposes to investigate the molecular and intracellular events of two important pathogenic mechanisms mediated by aPL: EC activation (up regulation of CAM and TF), and activation of platelets. First, whether aPL-mediated up-regulation of CAMs on ECs involves de novo protein synthesis, cytoskeleton movements, activation of NF-kappa-B, mitogen-activated protein kinase (MAP- kinase) and protein kinase C (PKC) and transcription of specific genes will be examined. Second, whether TF expression and function is affected by aPL on ECs and the intracellular mechanisms involved will be determined. The effects of the drug fluvastatin on the proadhesive and procoagulant effect of aPL on ECs invitro and in vivo experiments will be also studied. Third, the intracellular events involved in aPLinduced platelet activation and whether aPL effects on thrombosis in vivo are mediated by platelet activation (i.e. increase expression of GPIIb/ IIIa) will be determined. One strategy to examine the importance of aPL-induced platelet activation in thrombosis will be to utilize the anti-platelet drug abciximab, a platelet membrane GPIIb/ IIIa receptor antagonist which inhibits expression of GPIIb/ IIIa. This study will determine whether this agent inhibits aPL-induced thrombosis in mice. In another set of experiments beta-3-
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Antiphospholipid Syndrome
integrin deficient-mice (GPIIb/ IIIa knock-out mice) will be used to establish whether platelet activation is involved in enhanced thrombosis in vivo mediated by aPL/. Understanding the intracellular and molecular events in thrombosis associated with aPL is important and will provide significant information that may help to establish new ways of treatment and prevention of recurrences of thrombosis in APS patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PATHOPHYSIOLOGY OF ANTI-B2GPI ANTIBODIES IN APS Principal Investigator & Institution: Wolberg, Alisa S.; Pathology and Lab Medicine; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 Timing: Fiscal Year 2004; Project Start 01-JUL-2004; Project End 30-JUN-2009 Summary: (provided by applicant): In applying for the Mentored Research Scientist Development Award, the principal investigator is requesting support for an intensive program of training under the supervision of Dr. Susan Lord, Professor of Pathology, and Dr. Robert Roubey, Associate Professor of Medicine, at the University of North Carolina at Chapel Hill. The objectives of this proposal are designed to strengthen the applicant's scientific background in the biochemical basis of coagulation and cell biology. The award, if funded, will facilitate the long-term goals of the applicant in developing an independent scientific research career in the field of hemostasis and thrombosis. The Candidate and her mentors have developed a career development plan which includes: a) assurance of protected research time of 100 %, b) a training program exposing the Candidate to new areas of scientific investigation in biochemistry, biology and medicine, and c) graduate level studies to reinforce the laboratory experience. The studies proposed in this application will extend the applicant's previous work in hemostasis and thrombosis research. The prevalence of venous thrombosis associated with the primary Antiphospholipid Syndrome (APS) may be as high as 0.3 to 1% of the general population, possibly making APS one of the most common autoimmune diseases. It is hypothesized that antibodies against the plasma protein B2GPI are involved in the pathogenesis of this disease. Annexin A2 has recently been identified as the cellular receptor for B2GPI. To study the biological and cellular interactions of antiB2GPI antibodies, the following specific aims will be addressed: 1) Determining whether annexin A2 mediates anti-B2GPI antibody-regulated expression of TF activity, 2) Determining whether annexin A2-mediated fibrinolytic activity is regulated by B2GPI or B2GPI/anti-B2GPI, and 3) Determining whether APS autoantibodies alter the structure and fibrinolytic susceptibility of the fibrin clot. It is expected that these proposed studies will contribute to a fundamental understanding of pathogenic mechanisms for thrombosis in APS and lead to future investigations addressing therapeutic interventions in APS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PATHOPHYSIOLOGY SYNDROMES
OF
ANTIPHOSPHOLIPID
ANTIBODY
Principal Investigator & Institution: Ortel, Thomas L.; Associate Professor; Medicine; Duke University Durham, Nc 27710 Timing: Fiscal Year 2002; Project Start 01-APR-1999; Project End 31-MAR-2004 Summary: Antiphospholipid antibodies are a heterogenous family of antibodies associated with an increased risk for venous and arterial thrombosis, recurrent fetal loss, and thrombocytopenia. Several kindreds have been described with a familial form of the
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antiphospholipid antibody syndrome, confirming an inherited tendency to antibody formation. In these patients, autoantibodies that bind to proteins involved in normal hemostasis (e.g., prothrombin) are associated with an increased thrombotic risk. Antiphospholipid antibodies are also frequently seen in patients with vascular grafts who sustain thrombotic occlusions. Bovine thrombin is commonly used during vascular surgery, and we have shown that most patients exposed to bovine thrombin during cardiovascular surgery develop elevated antibody levels to several bovine and human coagulation proteins, as well as elevated antiphospholipid antibody levels. We hypothesize that different groups of patients with antiphospholipid antibodies and thrombotic complications share a common clinical phenotype that has developed in response to distinct etiologic mechanisms. To probe the pathophysiologic mechanisms of these antibodies, we propose to investigate two prothrombotic antibody subsets frequently identified in patients with autoantibodies by the following aims. First, we will define the molecular interactions of antiprothrombin autoantibodies with prothrombin and determine the functional and clinical significance of these autoantibodies. Epitopes recognized by antiprothrombin autoantibodies will be identified. Functional consequences of antibody binding to prothrombin will be determined and correlated to thrombotic events. Second, we will investigate the mechanisms whereby antiphospholipid autoantibodies interfere with the anticoagulant mechanisms of activated protein C. The functional consequences of antiphospholipid autoantibodies on the inactivation of factor Va by the activated protein C complex will be characterized and correlated to clinical outcome. Third, antiphospholipid antibodies that develop in patients exposed to bovine thrombin will be compared to antiphospholipid autoantibodies for antiprothrombin activity as well as inhibition of the activated protein C complex. These studies will improve our understanding of the role(s) of distinct antibody subsets in producing a hypercoagulable state in different patient subsets with antiphospholipid antibody syndromes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: POLYMORPHISMS OF ANTIPHOSPHOLIPID PROTEIN ANTIGENS Principal Investigator & Institution: Merrill, Joan T.; Member and Head; Oklahoma Medical Research Foundation Oklahoma City, Ok 731045005 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2006 Summary: (provided by applicant): The antiphospholipid syndrome (APS) is a lifethreatening thrombotic disorder characterized by a spectrum of autoantibodies that interfere with blood clotting. Recent evidence suggests that minor genetic variations in coagulation proteins may affect the likelihood for thrombosis in APS patients, either by an indirect, additive risk, or by altering the function of target proteins in a way that affects autoantibody incidence or pathogenicity. This application proposes: Aim 1: To determine if combined, common variants of specific candidate genes associate with APS. A TDT analysis of 1,000 APS patients and their parents will be performed, examining strategic single nucleotide polymorphisms in three interacting coagulation proteins known to be implicated in APS pathology: 1.) the anticoagulant, protein S 2.) its plasma inhibitor, C4b Binding Protein (C4BP) 3.) beta 2-glycoprotein I, a major APS antigen which also may regulate protein S. Aim 2: To produce functional, recombinant protein S, beta 2-glycoprotein I and C4BP domains (both wild-type and polymorphic) in an insect cell system and to compare each in binding interactions with the others, and in their effects on protein S function in vitro. Aim 3: To evaluate individual APS plasma for the decreased free protein S which is known to be prevalent in these patients and to correlate this with presence or absence of candidate polymorphisms and with antibody
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Antiphospholipid Syndrome
specificities for the recombinant wild type or polymorphic domains. Single or combined genetic factors may determine the tertiary structures and strength of interactions between several, key protein targets of APS antibodies. Determining the impact of common polymorphisms on the occurrence and/or pathogenicity of autoantibodies could lead to improved diagnostic tests and/or novel, mechanism-based treatments for APS. Additionally, the study of differences in interactions between these coagulation proteins conferred by common, inherited polymorphisms will have intrinsic value, not limited to the antiphospholipid syndrome. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PREDICTORS OF NEUROPSYCHIATRIC SLE Principal Investigator & Institution: Brey, Robin L.; Professor; Medicine; University of Texas Hlth Sci Ctr San Ant 7703 Floyd Curl Dr San Antonio, Tx 78229 Timing: Fiscal Year 2002; Project Start 15-MAR-1998; Project End 28-FEB-2005 Summary: (Adapted from the Investigator's Abstract) The long-term objectives of this prospective cohort study are to (1) characterize the spectrum of nervous system (NS) involvement in patients with systemic lupus erythematosus (SLE), a significant cause of morbidity in up to 75 percent of patients and (2) define important risk factors which may be unique for specifically targeted NS manifestations including stroke, cognitive dysfunction, and psychiatric manifestations. Our preliminary data suggests that the frequency of stroke and other NS manifestations in our predominately MexicanAmerican (MA) SLE population is high. The specific hypotheses which will be tested in this proposed 5-year project are: (1) the risk of initial thrombo-occlusive events will be higher in SLE patients who have persistently abnormal levels of antiphospholipid (aPL) and antiapolipoprotein H (anti-apoH) antibodies; (2) the development of cognitive dysfunction in SLE patients will be temporally associated with abnormal levels of aPL and anti-apoH antibodies; (3) the development of psychiatric manifestations (psychosis, depression, or anxiety) in SLE patients will be temporally associated with abnormal serum levels of antiribosomal P (anti-P) antibodies for SLE disease activity, cumulative SLE-related organ damage or the presence of cardiovascular risk factors will all contribute to the risk of developing targeted NS manifestations in a way that is independent of aPL, anti-apoH or anti-P antibody status. We will perform serial neurological, cognitive, psychiatric, rheumatological and immunological evaluations every four months and at the time of an endpoint event occurrence over a five year period. Kaplan-Meier curves will be constructed comparing the time between thrombotic events and antibody positive and negative groups. Cox regression will be used to construct multivariate models to control for the effects of the potential confounders. Cognitive dysfunction will be measured as a continuous variable, with fluctuations in functioning about the baseline for each patient compared with antibody levels. Close attention will be paid to problems of multiple comparisons. An approach similar to that described for cognitive dysfunction will be used for psychiatric manifestations. The project will identify risk factors which may account for significant morbidity in and provide crucial natural history data about SLE-related NS manifestations which are currently unavailable. The information gained will bridge important gaps in our knowledge about NS involvement in SLE and will lead to new hypothesis-driven studies of etiopathogenesis and treatment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PREDICTORS OF PREGNANCY OUTCOME IN SLE AND APS Principal Investigator & Institution: Salmon, Jane E.; Professor; Hospital for Special Surgery New York, Ny 100214872 Timing: Fiscal Year 2003; Project Start 25-SEP-2003; Project End 31-AUG-2008 Summary: (provided by applicant): Thrombosis and pregnancy loss are common features of systemic lupus erythematosus (SLE), particularly in the presence of antiphospholipid (aPL) antibodies. The in vivo mechanisms by which aPL antibodies lead to vascular events and, specifically, to recurrent fetal loss are largely unknown. Our studies in a murine model of antiphospholipid antibody syndrome (APS) indicate that in vivo complement activation is necessary for fetal loss caused by aPL antibodies. This proposal represents a first time effort to translate novel research observations on the potential role of complement activation in the pathogenesis of aPL antibody-mediated pregnancy loss to a clinically relevant human study. No study has investigated whether complement is activated in patients with aPL-associated poor pregnancy outcomes (with or without SLE), and whether particular patterns of complement activation characterize and thus can distinguish these patients from SLE patients without aPL antibodies or fetal loss, and from patients with normal pregnancy. Our preliminary data in murine APS, the availability of more accurate tests of complement activation, and the recent development of effective and specific complement inhibitors argue persuasively that the role of complement in aPL associated pregnancy complications shouldnow be examined. Accordingly, the specific aim of the study is: To determine whether elevations of split products generated by activation of the alternative or classical complement pathways predict poor fetal outcome in patients with antiphospholipid antibodies and/or SLE. We propose a prospective observational study of over 400 pregnant patients, enrolled at 6 major clinical centers, and grouped and analyzed according to the presence or absence of aPL and preexisting SLE. We have assembled a core group of investigators with recognized expertise in SLE and aPL pregnancy, highrisk obstetrics, the basic biology of complement, and statistical methods in SLE studies. We will obtain detailed medical and obstetrical information during the course of pregnancy and serial blood specimens for complement and cytokine assays, and analyze these data to identify predictors of poor fetal outcome. We will study placentas to characterize tissue pathology and mediators of injury. RNA, DNA, serum, and urine will be stored for studies to elucidate temporal changes in gene expression during the course of complicated and uncomplicated pregnancies and to investigate genetic polymorphisms. We believe that our study will provide insights into the mechanisms of complement-mediated inflammatory disorders and suggest means to prevent, arrest, or modify these conditions. Characterization of clinically applicable surrogate markers that predict poor pregnancy outcome will enable us to initiate an interventional trial of complement inhibition in patients at risk for aPL antibody-associated fetal loss. The identification of such surrogate markers in aPL and SLE patients may also prove generally applicable to anticipate complications during pregnancy in disease-free women. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: REDUCTION OF ANNEXIN IN ANTIPHOSPHOLIPID PREGNANCY LOSS Principal Investigator & Institution: Rand, Jacob H.; Professor; Medicine; Mount Sinai School of Medicine of Nyu of New York University New York, Ny 10029 Timing: Fiscal Year 2002; Project Start 01-AUG-1999; Project End 31-JAN-2003
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Antiphospholipid Syndrome
Summary: We recently discovered a thrombogenic mechanism for pregnancy loss in the antiphospholipid antibody syndrome that antiphospholipid antibodies displace the placental anticoagulant protein, annexin-V, from the anionic phospholipid surfaces of trophoblasts and accelerate coagulation reactions at that site. The core hypotheses of this grant are: a) Annexin-V serves a thromboregulatory role at the anatomic site where maternal blood and placental villi interface by shielding anionic phospholipids (which markedly accelerate coagulation enzyme reactions) from participation in coagulation reactions and; b) antiphospholipid antibodies competitively displace annexin-V from that phospholipid surface, disrupting the annexin-V "shield", thereby increasing the exposure of the thrombogenic anionic phospholipid. This process leads to thrombosis in the maternal circulation at the sites of interface with fetal trophoblasts and to ultimately to pregnancy complications and losses and determine their clinical efficacy. Our specific aims are: 1) To determine the mechanism(s) by which antiphospholipid antibodies and cofactors reduce the quantity of annexin-V on trophoblast apical membrane and accelerate coagulation reactions and 2) To develop tests for the reduction of annexin-V binding to phospholipids and the inhibition of annexin-V anticoagulant activity. This innovative project opens a new path toward elucidating the mechanism of pregnancy loss in the antiphospholipid syndrome and is likely to lead to improved diagnosis and treatment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SURROGATE MARKERS FOR SEVERE PULMONARY EMBOLISM Principal Investigator & Institution: Kline, Jeffrey A.; Carolinas Medical Center Box 3286, 11000 Blythe Blvd Charlotte, Nc 282322861 Timing: Fiscal Year 2003; Project Start 08-JUL-2003; Project End 30-JUN-2006 Summary: (provided by applicant): Echocardiography can help risk-stratify the severity of pulmonary embolism (PE) diagnosed in normotensive patients. However, because echocardiography is not uniformly available in U.S. hospitals, more accessible surrogate criteria are needed: to facilitate the immediate recognition of disabling PE in hemodynamically stable patients. Prior work by the Pi has led to the hypothesis that cardiopulmonary stress from severe PE can be recognized by abnormalities in vital signs, the 12- lead ECG and the serum troponin measurement. For this project, a screening instrument to rule out severe PE has been defined asthe combination of a shock index (pulse/systolic blood pressure) 91 percent, a Daniel ECG score <8 points, and a troponin I <0.4 ng/mh The hypothesis of this project is that patients with a negative screening instrument will not have right ventricular (RV) strain on echocardiography and are at very low risk of death or cardiopulmonary disability from PE treated with standard: anticoagulation. The first specific aim of the project is to test the diagnostic accuracy of the proposed screening instrument, using RV strain on transthoracic echocardiography as the criterion standard. The second aim will compare the diagnostic accuracy of the screening instrument with echocardiography for the prediction of an adverse outcome from PE. Because the screening instrument may notpredict RV damage from recurrent or unresolved PE, the second hypothesis is that nonmalignant thrombophilic conditions will increase risk of an adverse outcomefrom PE. Accordingly, :the third aim will test if patients with PE complicated by an adverse outcome are more likely to have antiphospholipid antibodies, or factor V Leiden G1691A, prothrombin G20210A, methylenetetrahydrofolate reductase C677T mutations, or low red blood cell methylfolate or high :plasma homocysteine concentrations, compared with patients with PE and no adverse outcome. An adverse clinical outcome will include death or anoxic brain insult :within 30 :days of diagnosis, recurrent PE, or
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cardiopuimonary disability, determined six months after diagnosis. Cardiopulmonary disability will be defined by New York Heart Association functional class II or worse, a repeat transthoracic echocardiogram with persistent RV strain, and a six-minute walk distance less than 330 meters. This study will determine if criteria that are widely and immediately available in most hospitals can be used to risk-stratify severity of PE and to clarify the role of nonmalignant thrombophilias on the prognosis of PE. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SYNDROME
THERAPY
WITH
ANNEXINS
FOR
ANTIPHOSPHOLIPID
Principal Investigator & Institution: Campos-Naciff, Maria-Begona M.; Molecular and Cellular Physio; University of Cincinnati 2624 Clifton Ave Cincinnati, Oh 45221 Timing: Fiscal Year 2002; Project Start 08-MAY-2001; Project End 30-APR-2005 Summary: (Scanned from the applicant's description): APS is a disorder characterized by venous and arterial thrombosis, recurrent fetal loss, thrombocytopenia and by the presence of antiphospholipid antibodies. Recurrent pregnancy loss is produced also in APS patients due to thrombosis in the placental vasculature. Patients with APS also have higher risks of other obstetric and postnatal complications like preeclampsia, fetal distress, fetal growth impairment, premature delivery, maternal postpartum thrombosis and postpartum lung syndrome. In vitro, the annexins, a family of calcium dependent membrane binding proteins, are extremely potent inhibitors of blood coagulation. Annexin V has been proposed to regulate thrombosis and homeostasis on the villous trophoblast surface by shielding the anionic phospholipid membrane that may accelerate the coagulation cascade whereas the antiphospholipid antibodies have been proposed to displace the annexin V shield, causing exposure of phospholipid surfaces that produce activation in the coagulation cascade. Therefore, our initial hypothesis is that annexins could act in vivo as potent anticoagulants and could be beneficial in treating APS. In this study, we will evaluate therapeutic potential of wild type annexin V and mutants annexin V in vivo. Our prediction is that annexin mutants with higher affinity for phospholipid membranes may act as better anticoagulants. To test this hypothesis annexin V mutants will be created. The phospholipid binding affinity of wild type annexin and mutated annexin V will be compared with the antiphospholipid antibodies using three distinct approaches. Using a pregnant mice model, we will evaluate the therapeutic potential of these in vivo against the pathological effects of the antiphospholipid antibodies. Mice will be evaluated for fetal viability and size, fetal loss, placental thrombosis in the fetal and in the maternal side. We predict that annexin V may ameliorate the pathological consequences of the infusion of an antiphospholipid antibody. Transgenic mice will be used to evaluate the potential therapeutic of extracellular annexin V in the context of the whole animal. The results obtained with this work will provide useful treatment strategies to ameliorate the symptoms associated with the antiphospholipid syndrome. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TREATMENT STRATEGIES FOR THE ANTI PHOSPHOLIPID SYNDROME Principal Investigator & Institution: Dedman, John R.; Professor; Molecular and Cellular Physio; University of Cincinnati 2624 Clifton Ave Cincinnati, Oh 45221 Timing: Fiscal Year 2002; Project Start 01-FEB-2000; Project End 31-JAN-2004
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Antiphospholipid Syndrome
Summary: Antiphospholipid Syndrome (APS), also known as Hughes Syndrome, is a multiorgan vascular disease associated with myocardial infarction, stroke thrombosis and recurrent fetal loss. Forty- five percent of the people under the age of fifty who suffer strokes also demonstrate elevated levels of phospholipid antibody. Our hypothesis is that the presence of antiphospholipid antibodies in the circulation leads to vascular disorders, and that the escalating tissue damage can be abated with agents that bind the destructive antibodies. In order to test this hypothesis, it is necessary to create a genetically defined APS mouse that secretes antiphospholipid antibodies into the blood. We have produced and characterized a mouse monoclonal antibody which specifically recognizes phosphatidylserine. Preliminary data demonstrates that our monoclonal antibody binding specificity is similar to antibodies present in APS patients; this monoclonal antibody is therefore appropriate to develop a treatment model. The heavy and light chain of our monoclonal antiphospholipid antibody will be cloned by RT-PCR. These cDNAs will include the endogenous secretory peptide signal sequence. Bigenic mice will be used to direct ligand induced expression in the liver. Each monoclonal immunoglobulin chain will be differentially tagged with HA or FLAG epitopes. The transgenic animals will be characterized and compared with normal animals for the hallmark symptoms of APS, including prolonged in vitro coagulation times, recurrent fetal loss and vascular disease. An additional goal of this proposal is to develop treatment strategies for APS. Our approach is to neutralize the disease-causing antibodies. Peptides which bind and block the monoclonal antiphospholipid antibody in vitro can be selected from a combinatorial phage-display library of random peptides. Isolated peptides will be assessed for the ability to reduce the symptoms of APS displayed by this transgenic mouse. This study will produce a genetically-defined mouse model of APS which will prove useful for developing treatment strategies to ameliorate the symptoms associated with APS. 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 unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “antiphospholipid syndrome” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for antiphospholipid syndrome in the PubMed Central database:
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. 5 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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A Monoclonal IgG Anticardiolipin Antibody from a Patient with the Antiphospholipid Syndrome is Thrombogenic in Mice. by Olee T, Pierangeli SS, Handley HH, Le DT, Wei X, Lai C, En J, Novotny W, Harris EN, Woods VL, Chen PP.; 1996 Aug 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=38720
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Prevention of experimental antiphospholipid syndrome and endothelial cell activation by synthetic peptides. by Blank M, Shoenfeld Y, Cabilly S, Heldman Y, Fridkin M, Katchalski-Katzir E.; 1999 Apr 27; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=21834
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 antiphospholipid syndrome, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “antiphospholipid syndrome” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for antiphospholipid syndrome (hyperlinks lead to article summaries): •
A "primary" antiphospholipid syndrome? Author(s): Asherson RA. Source: The Journal of Rheumatology. 1988 December; 15(12): 1742-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14552307
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A case of antiphospholipid syndrome with cutaneous ulcer and intrauterine fetal growth retardation. Author(s): Nakano J, Nakamura M, Ito T, Murata M, Fujiyama J. Source: The Journal of Dermatology. 2003 July; 30(7): 533-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12928543
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Adrenal involvement in the antiphospholipid syndrome. Author(s): Espinosa G, Cervera R, Font J, Asherson RA. Source: Lupus. 2003; 12(7): 569-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12892401
6 PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.
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Anetoderma associated with antiphospholipid syndrome and systemic lupus erythematosus. Author(s): Bilen N, Bayramgurler D, Sikar A, Ercin C, Yilmaz A. Source: Lupus. 2003; 12(9): 714-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14514137
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Anti-beta 2-glycoprotein I and antiphosphatidylserine antibodies are predictors of arterial thrombosis in patients with antiphospholipid syndrome. Author(s): Lopez LR, Dier KJ, Lopez D, Merrill JT, Fink CA. Source: American Journal of Clinical Pathology. 2004 January; 121(1): 142-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14750252
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Anti-beta(2)-glycoprotein I antibodies and the antiphospholipid syndrome. Author(s): Li Z, Krilis SA. Source: Autoimmunity Reviews. 2003 September; 2(5): 229-34. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12965172
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Antibodies to tissue-type plasminogen activator (tPA) in patients with antiphospholipid syndrome: evidence of interaction between the antibodies and the catalytic domain of tPA in 2 patients. Author(s): Cugno M, Cabibbe M, Galli M, Meroni PL, Caccia S, Russo R, Bottasso B, Mannucci PM. Source: Blood. 2004 March 15; 103(6): 2121-6. Epub 2003 November 20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14630788
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Anticardiolipin, other antiphospholipid antibody tests and diagnosis of the antiphospholipid syndrome. Author(s): Smikle M, Wharfe G, Fletcher H, Reid M, Roye-Green K, Fredrick J, Pierangeli S. Source: Human Antibodies. 2003; 12(3): 63-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14646034
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Antiphospholipid syndrome and endocrine damage: why bilateral adrenal thrombosis? Author(s): Berneis K, Buitrago-Tellez C, Muller B, Keller U, Tsakiris DA. Source: European Journal of Haematology. 2003 October; 71(4): 299-302. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12950241
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Antiphospholipid syndrome presenting as dilated cardiomyopathy in an 11-year-old boy. Author(s): Al-Kiyumi WA, Venugopalan P. Source: Acta Cardiol. 2003 August; 58(4): 359-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12948043
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Antiphospholipid syndrome triggered by thalidomide in a patient with discoid lupus erythematosus. Author(s): Tektonidou MG, Vlachoyiannopoulos PG. Source: Lupus. 2003; 12(9): 723-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14514139
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Antiphospholipid syndrome. Author(s): Gezer S. Source: Disease-A-Month : Dm. 2003 December; 49(12): 696-741. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14679358
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Antiphospholipid syndrome. Author(s): Cuadrado MJ, Lopez-Pedrera C. Source: Clinical and Experimental Medicine. 2003 November; 3(3): 129-39. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14648227
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Antiphospholipid syndrome: a consensus for treatment? Author(s): Khamashta MA, Shoenfeld Y. Source: Lupus. 2003; 12(7): 495. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12892385
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Antiphospholipid syndrome: a survey of clinical characters in ten cases. Author(s): Chen LH, Jiang LL, Li YM, Peng QB. Source: Journal of Zhejiang University. Science. 2003 September-October; 4(5): 616-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12958725
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Antiphospholipid syndrome: genetic review. Author(s): Namjou B. Source: Curr Rheumatol Rep. 2003 October; 5(5): 391-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12967526
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Antiphospholipid syndrome: obstetric diagnosis, management, and controversies. Author(s): Damron DP. Source: Obstetrics and Gynecology. 2003 October; 102(4): 873; Author Reply 873. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14551021
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Antiphospholipid syndrome: pathogenic mechanisms. Author(s): Espinosa G, Cervera R, Font J, Shoenfeld Y. Source: Autoimmunity Reviews. 2003 March; 2(2): 86-93. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12848964
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Aortic valve replacement and perioperative management in hemodialyzed patient wth antiphospholipid syndrome. Author(s): Lango R, Pawlaczyk R, Raszeja-Specht A, Smolenski RT, Rogowski J, Rutkowski B, Szutowicz A. Source: Int J Artif Organs. 2004 January; 27(1): 69-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14984186
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Atherosclerosis in primary antiphospholipid syndrome. Author(s): Ames PR, Sokoll K, Weston M, Margarita A, Brancaccio V. Source: Annals of the Rheumatic Diseases. 2004 May; 63(5): 610-1; Author Reply 610-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15082506
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Bacterial induction of autoantibodies to beta2-glycoprotein-I accounts for the infectious etiology of antiphospholipid syndrome. Author(s): Blank M, Krause I, Fridkin M, Keller N, Kopolovic J, Goldberg I, Tobar A, Shoenfeld Y. Source: The Journal of Clinical Investigation. 2002 March; 109(6): 797-804. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11901188
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Barraquer-Simons lipodystrophy associated with antiphospholipid syndrome. Author(s): Requena Caballero C, Angel Navarro Mira M, Bosch IF, Bauxauli JM, Aliaga Boniche A. Source: Journal of the American Academy of Dermatology. 2003 October; 49(4): 768-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14512940
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Benign intracranial hypertension: a non-thrombotic complication of the primary antiphospholipid syndrome? Author(s): Orefice G, De Joanna G, Coppola M, Brancaccio V, Ames PR. Source: Lupus. 1995 August; 4(4): 324-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8528233
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Beta 2 glycoprotein I and placental anticoagulant protein I in placentae from patients with antiphospholipid syndrome. Author(s): La Rosa L, Meroni PL, Tincani A, Balestrieri G, Faden D, Lojacono A, Morassi L, Brocchi E, Del Papa N, Gharavi A, et al. Source: The Journal of Rheumatology. 1994 September; 21(9): 1684-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7799350
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beta 2 Glycoprotein I--a key player in the antiphospholipid syndrome. Author(s): Lutters BC, de Groot PG, Derksen RH. Source: Isr Med Assoc J. 2002 November; 4(11 Suppl): 958-62. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12455190
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beta 2 glycoprotein-I inhibits factor XII activation on triglyceride rich lipoproteins: the effect of antibodies from plasma of patients with antiphospholipid syndrome. Author(s): McNally T, Mackie IJ, Isenberg DA, Machin SJ. Source: Thrombosis and Haemostasis. 1996 August; 76(2): 220-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8865535
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beta 2-Glycoprotein I reactivity of monoclonal anticardiolipin antibodies from patients with the antiphospholipid syndrome. Author(s): Ichikawa K, Khamashta MA, Koike T, Matsuura E, Hughes GR. Source: Arthritis and Rheumatism. 1994 October; 37(10): 1453-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7945470
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beta2-Glycoprotein 1 as a marker of antiphospholipid syndrome in women with recurrent pregnancy loss. Author(s): Franklin RD, Hollier N, Kutteh WH. Source: Fertility and Sterility. 2000 March; 73(3): 531-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10689008
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Beta2GP-I in the anti phospholipid (Hughes') syndrome--from a cofactor to an autoantigen--from induction to prevention of antiphospholipid syndrome. Author(s): Shoenfeld Y, Gharavi A, Koike T. Source: Lupus. 1998; 7(8): 503-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9863890
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Bilateral adrenal hemorrhage and acute addisonian crisis--a complication of antiphospholipid syndrome. Author(s): Garris GW, Smith BD. Source: J Tenn Med Assoc. 1996 April; 89(4): 120. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8867230
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Bilateral choroidal infarction in a patient with antiphospholipid syndrome: a case report. Author(s): Ang LP, Yap EY, Fam HB. Source: Clinical & Experimental Ophthalmology. 2000 August; 28(4): 326-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11021567
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Binding of complement component C1q to anti-beta2 glycoprotein I antibodies from patients with antiphospholipid syndrome. Author(s): Odorczuk M, Keil LB, DeBari VA. Source: Inflammation Research : Official Journal of the European Histamine Research Society. [et Al.]. 1999 October; 48(10): 524-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10563468
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Bleeding and recurrent thrombosis in definite antiphospholipid syndrome: analysis of a series of 66 patients treated with oral anticoagulation to a target international normalized ratio of 3.5. Author(s): Ruiz-Irastorza G, Khamashta MA, Hunt BJ, Escudero A, Cuadrado MJ, Hughes GR. Source: Archives of Internal Medicine. 2002 May 27; 162(10): 1164-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12020188
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Bleeding tendency and relapsing small vessel thromboses in a patient with secondary antiphospholipid syndrome. Author(s): Sipek-Dolnicar A, Hojnik M, Rozman B. Source: Clin Exp Rheumatol. 2003 May-June; 21(3): 412-3. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12846077
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Brain vascular changes in the case of primary antiphospholipid syndrome. Author(s): Szpak GM, Kuczynska-Zardzewialy A, Popow J. Source: Folia Neuropathol. 1996; 34(2): 92-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8791898
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Budd-Chiari syndrome associated with primary antiphospholipid syndrome. Author(s): Nanke Y, Kotake S, Nakanishi Y, Hara M, Kamatani N. Source: Clin Exp Rheumatol. 2002 May-June; 20(3): 433. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12102488
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Budd-Chiari syndrome complicating severe preeclampsia in a parturient with primary antiphospholipid syndrome. Author(s): Segal S, Shenhav S, Segal O, Zohav E, Gemer O. Source: European Journal of Obstetrics, Gynecology, and Reproductive Biology. 1996 September; 68(1-2): 227-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8886713
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Budd-Chiari syndrome in the context of antiphospholipid syndrome: diagnostic and therapeutic implications. Author(s): Archimandritis A, Christopoulou V, Tsirantonaki M, Vlachoyiannopoulos P, Zavos G, Aroni K. Source: Lupus. 1995 August; 4(4): 329-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8528236
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Budd-Chiari syndrome secondary to antiphospholipid syndrome: clinical and immunologic characteristics of 43 patients. Author(s): Espinosa G, Font J, Garcia-Pagan JC, Tassies D, Reverter JC, Gaig C, Cervantes F, Cervera R, Bosch J, Ingelmo M. Source: Medicine; Analytical Reviews of General Medicine, Neurology, Psychiatry, Dermatology, and Pediatrics. 2001 November; 80(6): 345-54. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11704712
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Buerger's disease and antiphospholipid syndrome. Author(s): Puechal X, Job-Deslandre C, Menkes CJ, Fiessinger JN. Source: Annals of the Rheumatic Diseases. 1993 October; 52(10): 766. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8110267
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Cardiac disease in the antiphospholipid syndrome: recommendations for treatment. Committee consensus report. Author(s): Lockshin M, Tenedios F, Petri M, McCarty G, Forastiero R, Krilis S, Tincani A, Erkan D, Khamashta MA, Shoenfeld Y. Source: Lupus. 2003; 12(7): 518-23. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12892391
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Cardiac valvulopathy in the antiphospholipid syndrome. Author(s): Lev S, Shoenfeld Y. Source: Clinical Reviews in Allergy & Immunology. 2002 December; 23(3): 341-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12402416
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Catastrophic antiphospholipid syndrome complicating orthotopic liver transplantation. Author(s): Villamil A, Sorkin E, Basta MC, Mysler E, Macias S, Pekolj J, Ciardullo M, Eleta F, de Santibanes E, Allievi A, Gadano A. Source: Lupus. 2003; 12(2): 140-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12630760
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Catastrophic antiphospholipid syndrome in the intensive care unit. Author(s): Westney GE, Harris EN. Source: Critical Care Clinics. 2002 October; 18(4): 805-17. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12418442
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Catastrophic antiphospholipid syndrome masquerading as ischaemic colitis. Author(s): Jurgensen JS, Kettritz R, Schneider W, Koop H, Hildebrand TS, Frei U, Eckardt KU. Source: Rheumatology International. 2003 July; 23(4): 204-6. Epub 2003 March 29. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12679877
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Catastrophic antiphospholipid syndrome precipitated by bowel surgery. Author(s): Lee J, Chang JE, Cho YJ, Kim MY, Rheu YJ, Kim YW. Source: Scandinavian Journal of Rheumatology. 2002; 31(2): 110-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12109646
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Catastrophic antiphospholipid syndrome. Author(s): Asherson RA, Cervera R. Source: Curr Rheumatol Rep. 2003 October; 5(5): 395-400. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12967527
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Catastrophic antiphospholipid syndrome: international consensus statement on classification criteria and treatment guidelines. Author(s): Asherson RA, Cervera R, de Groot PG, Erkan D, Boffa MC, Piette JC, Khamashta MA, Shoenfeld Y; Catastrophic Antiphospholipid Syndrome Registry Project Group. Source: Lupus. 2003; 12(7): 530-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12892393
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Catastrophic antiphospholipid syndrome: where do we stand? Author(s): Erkan D, Cervera R, Asherson RA. Source: Arthritis and Rheumatism. 2003 December; 48(12): 3320-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14673983
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Central retinal venous occlusion with co-existent thrombotic thrombocytopenic purpura and antiphospholipid syndrome. Author(s): Murphy PT, Rao P. Source: The British Journal of Ophthalmology. 2003 May; 87(5): 658-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12714426
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Cervico-cranial artery dissection and antiphospholipid syndrome: is there a link? Author(s): Sibilia J, Hercelin D, Gottenberg JE, Goetz J, Dietemann JL, Harle JR, Sanmarco M. Source: The American Journal of Medicine. 2004 January 15; 116(2): 138-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14715332
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Clinical and epidemiological aspects in the antiphospholipid syndrome. Author(s): Cervera R, Asherson RA. Source: Immunobiology. 2003; 207(1): 5-11. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12638896
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Clinical features related to antiphospholipid syndrome in patients with chronic viral infections (hepatitis C virus/HIV infection): description of 82 cases. Author(s): Ramos-Casals M, Cervera R, Lagrutta M, Medina F, Garcia-Carrasco M, de la Red G, Bove A, Ingelmo M, Font J; Hispanoamerican Study Group of Autoimmune Manifestations of Chronic Viral Disease (HISPAMEC). Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 2004 April 1; 38(7): 1009-16. Epub 2004 March 15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15034835
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Clinical spectrum of males with primary antiphospholipid syndrome and systemic lupus erythematosus: a comparative study of 73 patients. Author(s): Medina G, Vera-Lastra O, Barile L, Salas M, Jara LJ. Source: Lupus. 2004; 13(1): 11-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14870912
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CNS dysfunction in the antiphospholipid syndrome. Author(s): Katzav A, Chapman J, Shoenfeld Y. Source: Lupus. 2003; 12(12): 903-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14714909
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Combined plasmapheresis and immunosuppression as rescue treatment of a patient with catastrophic antiphospholipid syndrome occurring despite anticoagulation: a case report. Author(s): Koschmieder S, Miesbach W, Fauth F, Bojunga J, Scharrer I, Brodt HR. Source: Blood Coagulation & Fibrinolysis : an International Journal in Haemostasis and Thrombosis. 2003 June; 14(4): 395-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12945882
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Consecutive central retinal artery and vein occlusions in primary antiphospholipid syndrome. Author(s): Levy J, Baumgarten A, Rosenthal G, Rabinowitz R, Lifshitz T. Source: Retina (Philadelphia, Pa.). 2002 December; 22(6): 784-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12476107
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Contraceptive practices in women with systemic lupus erythematosus and/or antiphospholipid syndrome: what advice should we be giving? Author(s): Lakasing L, Khamashta M. Source: The Journal of Family Planning and Reproductive Health Care / Faculty of Family Planning & Reproductive Health Care, Royal College of Obstetricians & Gynaecologists. 2001 January; 27(1): 7-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12457539
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Cross-reactivity between anti-cardiolipin, anti-high-density lipoprotein and antiapolipoprotein A-I IgG antibodies in patients with systemic lupus erythematosus and primary antiphospholipid syndrome. Author(s): Delgado Alves J, Kumar S, Isenberg DA. Source: Rheumatology (Oxford, England). 2003 July; 42(7): 893-9. Epub 2003 April 16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12730551
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Cytomegalovirus infection and antiphospholipid syndrome in humans. Author(s): Orts J, Colomina J, Zuniga A, Guerrero A. Source: Arthritis and Rheumatism. 2003 November; 48(11): 3296-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14613298
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Definition and classification of the antiphospholipid syndrome. Author(s): Wiedermann FJ, Mayr A, Schobersberger W, Mutz N. Source: The Journal of Cardiovascular Surgery. 1999 December; 40(6): 919-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10776732
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Definitive adrenal insufficiency due to bilateral adrenal hemorrhage and primary antiphospholipid syndrome. Author(s): Caron P, Chabannier MH, Cambus JP, Fortenfant F, Otal P, Suc JM. Source: The Journal of Clinical Endocrinology and Metabolism. 1998 May; 83(5): 1437-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9589635
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Dermatologic aspects of antiphospholipid syndrome. Author(s): Gantcheva M. Source: International Journal of Dermatology. 1998 March; 37(3): 173-80. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9556101
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Dermatomyositis and polymyositis associated with the antiphospholipid syndrome-a novel overlap syndrome. Author(s): Sherer Y, Livneh A, Levy Y, Shoenfeld Y, Langevitz P. Source: Lupus. 2000; 9(1): 42-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10713646
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Detection and clinical significance of Ba2+- and Sr2+-dependent antiprothrombin antibodies in patients with systemic lupus erythematosus and antiphospholipid syndrome. Author(s): Sanaka T, Matsuda J, Teramoto T. Source: Lupus. 2003; 12(2): 117-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12630756
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Detection of anti-annexin IV and V antibodies in patients with antiphospholipid syndrome and systemic lupus erythematosus. Author(s): Satoh A, Suzuki K, Takayama E, Kojima K, Hidaka T, Kawakami M, Matsumoto I, Ohsuzu F. Source: The Journal of Rheumatology. 1999 August; 26(8): 1715-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10451067
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Diagnosis and management of patients with the antiphospholipid syndrome. Author(s): Alving BM. Source: Journal of Thrombosis and Thrombolysis. 2001 September; 12(1): 89-93. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11711694
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Diagnosis of the antiphospholipid syndrome: a proposal for use of laboratory tests. Author(s): Harris EN, Pierangeli SS, Gharavi AE. Source: Lupus. 1998; 7 Suppl 2: S144-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9814693
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Diagnostic usefulness of 3 dimensional gadolinium enhanced magnetic resonance venography in antiphospholipid syndrome. Author(s): Erel H, Erkan D, Lehman TJ, Prince MR. Source: The Journal of Rheumatology. 2002 June; 29(6): 1338-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12064857
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Different types of antiphospholipid antibodies in AIDS: a comparison with syphilis and the antiphospholipid syndrome. Author(s): de Larranaga GF, Forastiero RR, Carreras LO, Alonso BS. Source: Thrombosis Research. 1999 October 1; 96(1): 19-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10554081
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Differential effects of anti-beta2-glycoprotein I antibodies on endothelial cells and on the manifestations of experimental antiphospholipid syndrome. Author(s): George J, Blank M, Levy Y, Meroni P, Damianovich M, Tincani A, Shoenfeld Y. Source: Circulation. 1998 March 10; 97(9): 900-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9521339
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Diffuse alveolar hemorrhage in the antiphospholipid syndrome: spectrum of disease and treatment. Author(s): Gertner E. Source: The Journal of Rheumatology. 1999 April; 26(4): 805-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10229400
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Disseminated thrombosis in primary antiphospholipid syndrome: MR findings. Author(s): Provenzale JM, Spritzer CE, Nelson RC, Ortel TL. Source: European Journal of Radiology. 1998 February; 26(3): 244-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9587749
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Distinguishing features of anti-beta2 glycoprotein I antibodies between patients with leprosy and the antiphospholipid syndrome. Author(s): Arvieux J, Renaudineau Y, Mane I, Perraut R, Krilis SA, Youinou P. Source: Thrombosis and Haemostasis. 2002 April; 87(4): 599-605. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12008941
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Distribution of lupus anticoagulant and anticardiolipin antibody isotypes in a population with antiphospholipid syndrome. Author(s): Guglielmone HA, Fernandez EJ. Source: The Journal of Rheumatology. 1999 January; 26(1): 86-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9918246
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Do antibodies to beta2-glycoprotein 1 contribute to the better characterization of the antiphospholipid syndrome? Author(s): Detkov, Gil-Aguado A, Lavilla P, Cuesta MV, Fontan G, Pascual-Salcedo D. Source: Lupus. 1999; 8(6): 430-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10483010
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Do we know which patients with the antiphospholipid syndrome should receive long-term high dose anti-coagulation? Author(s): Derksen RH, de Groot PG. Source: Journal of Autoimmunity. 2000 September; 15(2): 255-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10968920
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Do we need an international consensus statement on classification criteria for the antiphospholipid syndrome in the paediatric population? Author(s): Avcin T, Cimaz R, Meroni PL. Source: Lupus. 2001; 10(12): 897-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11787885
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Does aspirin have a role in improving pregnancy outcome for women with the antiphospholipid syndrome? A randomized controlled trial. Author(s): Pattison NS, Chamley LW, Birdsall M, Zanderigo AM, Liddell HS, McDougall J. Source: American Journal of Obstetrics and Gynecology. 2000 October; 183(4): 1008-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11035355
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Dual antibody reactivity to beta2-glycoprotein I and protein S: increased association with thrombotic events in the antiphospholipid syndrome. Author(s): Erkan D, Zhang HW, Shriky RC, Merrill JT. Source: Lupus. 2002; 11(4): 215-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12043884
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Echocardiographic evaluation of patients with primary antiphospholipid syndrome. Author(s): Espinola-Zavaleta N, Vargas-Barron J, Colmenares-Galvis T, Cruz-Cruz F, Romero-Cardenas A, Keirns C, Amigo MC. Source: American Heart Journal. 1999 May; 137(5): 973-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10220649
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Effect of anticardiolipin/beta2-glycoprotein I complexes on production of thromboxane A2 by platelets from patients with the antiphospholipid syndrome. Author(s): Robbins DL, Leung S, Miller-Blair DJ, Ziboh V. Source: The Journal of Rheumatology. 1998 January; 25(1): 51-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9458202
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Effect of heat inactivation and sheep erythrocyte adsorption on the titer of anticardiolipin antibodies in primary antiphospholipid syndrome and healthy blood donors' sera. Author(s): Nava A, Banales JL, Reyes PA. Source: Journal of Clinical Laboratory Analysis. 1992; 6(3): 148-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1506982
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Effect of plasma from patients with primary antiphospholipid syndrome on platelet function in a collagen rich perfusion system. Author(s): Reverter JC, Tassies D, Escolar G, Font J, Lopez Soto A, Ingelmo M, Ordinas A. Source: Thrombosis and Haemostasis. 1995 January; 73(1): 132-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7740485
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Effect of sera from women with systemic lupus erythematosus or antiphospholipid syndrome and recurrent abortions on human placental explants in culture. Author(s): Yacobi S, Ornoy A, Blumenfeld Z, Miller RK. Source: Teratology. 2002 December; 66(6): 300-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12486763
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Effects of H1 histones and a monoclonal autoantibody to H1 histones on clot formation in vitro: possible implications in the antiphospholipid syndrome. Author(s): Kheiri SA, Fasy TM, Billett HH. Source: Thrombosis Research. 1996 April 1; 82(1): 43-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8731508
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Effects of inherited thrombophilic mutations in an adolescent with antiphospholipid syndrome and systemic lupus erythematosus. Author(s): Higginbotham EA, Zimmerman SA, Howard TA, Schanberg L, Kredich D, Ware RE. Source: The Journal of Rheumatology. 2001 February; 28(2): 370-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11246680
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Elevated anti-annexin V antibody levels in antiphospholipid syndrome and their involvement in antiphospholipid antibody specificities. Author(s): Ogawa H, Zhao D, Dlott JS, Cameron GS, Yamazaki M, Hata T, Triplett DA. Source: American Journal of Clinical Pathology. 2000 October; 114(4): 619-28. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11026109
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Elevated plasma lipoprotein(a) level and its association with impaired fibrinolysis in patients with antiphospholipid syndrome. Author(s): Atsumi T, Khamashta MA, Andujar C, Leandro MJ, Amengual O, Ames PR, Hughes GR. Source: The Journal of Rheumatology. 1998 January; 25(1): 69-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9458205
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Endothelium-derived haemostatic factors and the antiphospholipid syndrome. Author(s): Mackworth-Young CG, Andreotti F, Harmer I, Loizou S, Pottinger BE, Pearson JD, Davies GJ, Maseri A, Walport MJ. Source: British Journal of Rheumatology. 1995 March; 34(3): 201-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7728392
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Endstage renal failure in primary antiphospholipid syndrome--case report and review of literature. Author(s): Dayal NA, Isenberg DA. Source: Rheumatology (Oxford, England). 2003 September; 42(9): 1128-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12923280
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Epitope specificity of monoclonal anti-beta 2-glycoprotein I antibodies derived from patients with the antiphospholipid syndrome. Author(s): Wang MX, Kandiah DA, Ichikawa K, Khamashta M, Hughes G, Koike T, Roubey R, Krilis SA. Source: Journal of Immunology (Baltimore, Md. : 1950). 1995 August 1; 155(3): 1629-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7543528
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Evaluation of antibodies to beta2-glycoprotein 1 in the causation of coronary atherosclerosis as part of the antiphospholipid syndrome. Author(s): Limaye V, Beltrame J, Cook R, Gillis D, Pile K. Source: Aust N Z J Med. 1999 December; 29(6): 789-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10677123
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Evaluation of cardiac abnormalities and embolic sources in primary antiphospholipid syndrome by transesophageal echocardiography. Author(s): Turiel M, Muzzupappa S, Gottardi B, Crema C, Sarzi-Puttini P, Rossi E. Source: Lupus. 2000; 9(6): 406-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10981643
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Evaluation of clinical and laboratory features of antiphospholipid syndrome: a retrospective study of 637 patients. Author(s): Soltesz P, Veres K, Lakos G, Kiss E, Muszbek L, Szegedi G. Source: Lupus. 2003; 12(4): 302-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12729054
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Evaluation of the obstetrical risks of the antiphospholipid syndrome and therapeutic management. Author(s): Edelman P, Rouquette AM. Source: Clinical Reviews in Allergy & Immunology. 1995 Spring; 13(1): 91-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7648353
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Exclusion criteria for primary antiphospholipid syndrome. Author(s): Piette JC, Wechsler B, Frances C, Papo T, Godeau P. Source: The Journal of Rheumatology. 1993 October; 20(10): 1802-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8295200
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Exposure of anionic phospholipids serves as anti-inflammatory and immunosuppressive signal--implications for antiphospholipid syndrome and systemic lupus erythematosus. Author(s): Gaipl US, Beyer TD, Baumann I, Voll RE, Stach CM, Heyder P, Kalden JR, Manfredi A, Herrmann M. Source: Immunobiology. 2003; 207(1): 73-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12638907
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Exposure of anionic phospholipids upon platelet activation permits binding of beta 2 glycoprotein I and through it that of IgG antiphospholipid antibodies. Studies in platelets from patients with antiphospholipid syndrome and normal subjects. Author(s): Vazquez-Mellado J, Llorente L, Richaud-Patin Y, Alarcon-Segovia D. Source: Journal of Autoimmunity. 1994 June; 7(3): 335-48. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7916907
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Factor XIII Val34Leu polymorphism does not contribute to the prevention of thrombotic complications in patients with antiphospholipid syndrome. Author(s): Diz-Kucukkaya R, Hancer VS, Inanc M, Nalcaci M, Pekcelen Y. Source: Lupus. 2004; 13(1): 32-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14870915
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Factors influencing the prevalence of antiphospholipid syndrome in systemic lupus erythematosus. Author(s): Picillo U, Migliaresi S, Marcialis MR, La Palombara F, Tirri G. Source: The Journal of Rheumatology. 1994 July; 21(7): 1375. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7966094
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Failure of aggressive anticoagulant therapy in catastrophic antiphospholipid syndrome. Author(s): Zoli A, D'Agostino MA, Pompa A, Altomonte L, Mirone L, Magaro A. Source: Clin Exp Rheumatol. 2000 January-February; 18(1): 113. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10728460
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Familial antiphospholipid syndrome and HLA-DRB gene associations. Author(s): Hudson N, Busque L, Rauch J, Kassis J, Fortin PR. Source: Arthritis and Rheumatism. 1997 October; 40(10): 1907-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9336432
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Familial coexistence of primary antiphospholipid syndrome and factor VLeiden. Author(s): Schutt M, Kluter H, Hagedorn-Greiwe M, Fehm HL, Wiedemann GJ. Source: Lupus. 1998; 7(3): 176-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9607641
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Familial Mediterranean fever and primary antiphospholipid syndrome, a rare association. A case report. Author(s): Halabe-Cherem J, Nellen-Hummel H, Flores-Padilla G, Mercado-Atri M, Pizutto-Chavez J. Source: Angiology. 1995 September; 46(9): 859-61. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7661392
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Familial Mediterranean fever is not associated with the antiphospholipid syndrome. Author(s): Rozenbaum M, Rosner I. Source: Clin Exp Rheumatol. 1993 September-October; 11(5): 578-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8275598
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Familial occurrence of primary antiphospholipid syndrome. Author(s): Cantalapiedra A, Avello AG, Navarro JL, Cesar JM. Source: Thrombosis Research. 1999 July 15; 95(2): 127-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10418801
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Familial occurrence of the antiphospholipid syndrome. Author(s): Matthey F, Walshe K, Mackie IJ, Machin SJ. Source: Journal of Clinical Pathology. 1989 May; 42(5): 495-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2499608
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Fatal cerebral infarction in an asymptomatic young patient with primary antiphospholipid syndrome. Author(s): Muneta S, Yokota E, Watanabe S, Matsumoto I, Yamashita Y. Source: Japanese Circulation Journal. 1995 September; 59(9): 641-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7500548
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Fatal cerebral venous thrombosis as the initial manifestation of the antiphospholipid syndrome. Author(s): Agah R, Rice L, Winikates J. Source: Clinical Neurology and Neurosurgery. 1996 May; 98(2): 189-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8836598
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Feasibility of a randomized clinical trial for the prevention of recurrent thrombosis in the antiphospholipid syndrome: the WAPS project. Provisional Steering Committee of the Warfarin in Antiphospholipid Syndrome (WAPS) Study. Author(s): Finazzi G, Barbui T. Source: Annales De Medecine Interne. 1996 September; 147 Suppl 1: 38-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8952760
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Fibrinolytic treatment in primary antiphospholipid syndrome. Author(s): Camps Garcia MT, Guil M, Sanchez-Lora J, Grana MI, Martinez J, de Ramon E. Source: Lupus. 1996 December; 5(6): 627-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9116709
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Fibrosing alveolitis associated with primary antiphospholipid syndrome. Author(s): Savin H, Huberman M, Kott E, Lishner M, Kitai Y, Kidron D, Zissin R, Ravid M. Source: British Journal of Rheumatology. 1994 October; 33(10): 977-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7921762
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Flank ulcer in a patient with primary antiphospholipid syndrome. Author(s): Lee CW, Park MH. Source: Journal of Korean Medical Science. 1999 February; 14(1): 110-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10102536
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Flow cytometric detection of circulating activated platelets in primary antiphospholipid syndrome. Correlation with thrombocytopenia and anticardiolipin antibodies. Author(s): Fanelli A, Bergamini C, Rapi S, Caldini A, Spinelli A, Buggiani A, Emmi L. Source: Lupus. 1997; 6(3): 261-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9104734
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Fluctuations in levels of antiphospholipid antibodies and increased coagulation activation markers in normal and heparin-treated antiphospholipid syndrome pregnancies. Author(s): Donohoe S, Quenby S, Mackie I, Panal G, Farquharson R, Malia R, Kingdom J, Machin S. Source: Lupus. 2002; 11(1): 11-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11898913
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From antiphospholipid syndrome to antibody-mediated thrombosis. Author(s): Roubey RA, Hoffman M. Source: Lancet. 1997 November 22; 350(9090): 1491-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9388393
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Fulminant encephalopathy due to the catastrophic primary antiphospholipid syndrome. Author(s): Chinnery PF, Shaw PJ, Ince PG, Jackson GH, Bishop RI. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1997 March; 62(3): 300-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9069503
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G20210A homozygosity in antiphospholipid syndrome secondary to systemic lupus erythematosus. Author(s): Sivera P, Bosio S, Bertero MT, Demaestri M, Mazza U, Camaschella C. Source: Haematologica. 2000 January; 85(1): 109-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10629608
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Gastroenterological manifestations of antiphospholipid syndrome. Author(s): Gatenby PA. Source: Journal of Gastroenterology and Hepatology. 1997 December; 12(12): 827-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9504893
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Generalized lupus panniculitis and antiphospholipid syndrome in a patient without complement deficiency. Author(s): Nousari HC, Kimyai-Asadi A, Santana HM, Diglio GM, Tausk FA, Cohen BA. Source: Pediatric Dermatology. 1999 July-August; 16(4): 273-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10469410
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Genetics of antiphospholipid syndrome. Author(s): Atsumi T, Bertolaccini ML, Koike T. Source: Rheumatic Diseases Clinics of North America. 2001 August; 27(3): 565-72, Vi. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11534260
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Graft loss and the antiphospholipid syndrome following liver transplantation. Author(s): Collier JD, Sale J, Friend PJ, Jamieson NV, Calne RY, Alexander GJ. Source: Journal of Hepatology. 1998 December; 29(6): 999-1003. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9875649
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Graves' disease associated with the primary antiphospholipid syndrome. Author(s): Hofbauer LC, Spitzweg C, Heufelder AE. Source: The Journal of Rheumatology. 1996 August; 23(8): 1435-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8856626
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Guidelines on the investigation and management of the antiphospholipid syndrome. Author(s): Greaves M, Cohen H, MacHin SJ, Mackie I. Source: British Journal of Haematology. 2000 June; 109(4): 704-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10929019
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Headache and memory loss: rapid response to heparin in the antiphospholipid syndrome. Author(s): Hughes GR, Cuadrado MJ, Khamashta MA, Sanna G. Source: Lupus. 2001; 10(11): 778. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11789486
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Hemolysis, hemorrhage, headache, and hidden abortion: imaging findings in antiphospholipid syndrome. Author(s): Mahnken AH, Brandenburg VM, Frank RD, Haage P, Gunther RW. Source: European Radiology. 2003 December; 13 Suppl 4: L83-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15018171
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Hepatic infarctions during pregnancy are associated with the antiphospholipid syndrome and in addition with complete or incomplete HELLP syndrome. Author(s): Pauzner R, Dulitzky M, Carp H, Mayan H, Kenett R, Farfel Z, Many A. Source: Journal of Thrombosis and Haemostasis : Jth. 2003 August; 1(8): 1758-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12911590
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Hepatic manifestations of the antiphospholipid syndrome. Author(s): Tsutsumi A, Koike T. Source: Intern Med. 2000 January; 39(1): 6-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10674839
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Hereditary hemorrhagic telangiectasia, factor V Leiden and antiphospholipid syndrome: a case report. Author(s): Undas A, Bazan-Socha S, Swadzba J, Musial J. Source: Blood Coagulation & Fibrinolysis : an International Journal in Haemostasis and Thrombosis. 2002 January; 13(1): 53-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11994568
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Heterogeneous recognition of beta 2-glycoprotein I by antibodies from antiphospholipid syndrome patients. Author(s): Guerin J, Sim R, Yu BB, Ferluga J, Feighery C, Jackson J. Source: Thrombosis and Haemostasis. 2000 September; 84(3): 374-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11019958
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High impact of antiphospholipid syndrome on irreversible organ damage and survival of patients with systemic lupus erythematosus. Author(s): Ruiz-Irastorza G, Egurbide MV, Ugalde J, Aguirre C. Source: Archives of Internal Medicine. 2004 January 12; 164(1): 77-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14718326
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High prevalence of thyroid autoantibodies in systemic sclerosis and rheumatoid arthritis but not in the antiphospholipid syndrome. Author(s): Innocencio RM, Romaldini JH, Ward LS. Source: Clinical Rheumatology. 2003 December; 22(6): 494. Epub 2003 October 17. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14677039
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High thrombosis rate after fetal loss in antiphospholipid syndrome: effective prophylaxis with aspirin. Author(s): Erkan D, Merrill JT, Yazici Y, Sammaritano L, Buyon JP, Lockshin MD. Source: Arthritis and Rheumatism. 2001 June; 44(6): 1466-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11407709
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High titers of autoantibodies to tissue factor pathway inhibitor are associated with the antiphospholipid syndrome. Author(s): Forastiero RR, Martinuzzo ME, Broze GJ. Source: Journal of Thrombosis and Haemostasis : Jth. 2003 April; 1(4): 718-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12871406
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Histiocytic necrotizing lymphadenitis (Kikuchi-Fujimoto disease) associated with antiphospholipid syndrome: case report and literature review. Author(s): Papaioannou G, Speletas M, Kaloutsi V, Pavlitou-Tsiontsi A. Source: Annals of Hematology. 2002 December; 81(12): 732-5. Epub 2002 November 14. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12483371
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HLA associations of anti-beta2 glycoprotein I response in a Greek cohort with antiphospholipid syndrome and meta-analysis of four ethnic groups. Author(s): Ioannidis JP, Tektonidou MG, Vlachoyiannopoulos PG, Stavropoulos-Giokas C, Spyropoulou-Vlachou M, Reveille JD, Arnett FC, Moutsopoulos HM. Source: Human Immunology. 1999 December; 60(12): 1274-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10626742
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HLA class II alleles and genetic predisposition to the antiphospholipid syndrome. Author(s): Domenico Sebastiani G, Minisola G, Galeazzi M. Source: Autoimmunity Reviews. 2003 October; 2(6): 387-94. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14550881
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Hormonal contraception and replacement and the use of androgens in the antiphospholipid syndrome. Author(s): Lahita RG. Source: Journal of Autoimmunity. 2000 September; 15(2): 213-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10968912
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Hug(h)e(s') ears: an unusual presentation of antiphospholipid syndrome. Author(s): O'Gradaigh D, Scott DG, Levell N. Source: Annals of the Rheumatic Diseases. 1999 January; 58(1): 65-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10343543
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Hughes syndrome--the syndrome behind the name (otherwise known as antiphospholipid syndrome). Author(s): Hughes GR. Source: Isr Med Assoc J. 1999 October; 1(2): 100-3. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10731307
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Human immunodeficiency virus infection, antiphospholipid antibodies, and the antiphospholipid syndrome. Author(s): Asherson RA, Shoenfeld Y. Source: The Journal of Rheumatology. 2003 February; 30(2): 214-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12563670
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Hyperhomocysteinemia is common in patients with antiphospholipid syndrome and may contribute to expression of major thrombotic events. Author(s): Avivi I, Lanir N, Hoffman R, Brenner B. Source: Blood Coagulation & Fibrinolysis : an International Journal in Haemostasis and Thrombosis. 2002 March; 13(2): 169-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11914660
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Hypertension as the presenting feature of the antiphospholipid syndrome. Author(s): Karim MY, Alba P, Tungekar MF, Abbs IC, Khamashta MA, Hughes GR, Hunt BJ. Source: Lupus. 2002; 11(4): 253-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12043890
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Hypertension due to renal artery occlusion in a patient with antiphospholipid syndrome. Author(s): Riccialdelli L, Arnaldi G, Giacchetti G, Pantanetti P, Mantero F. Source: American Journal of Hypertension : Journal of the American Society of Hypertension. 2001 January; 14(1): 62-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11206681
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Identification and characterization of a peptide mimetic that may detect a species of disease-associated anticardiolipin antibodies in patients with the antiphospholipid syndrome. Author(s): Visvanathan S, Scott JK, Hwang KK, Banares M, Grossman JM, Merrill JT, FitzGerald J, Chukwuocha RU, Tsao BP, Hahn BH, Chen PP. Source: Arthritis and Rheumatism. 2003 March; 48(3): 737-45. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12632428
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Identification of anti-thrombin antibodies in the antiphospholipid syndrome that interfere with the inactivation of thrombin by antithrombin. Author(s): Hwang KK, Grossman JM, Visvanathan S, Chukwuocha RU, Woods VL Jr, Le DT, Hahn BH, Chen PP. Source: Journal of Immunology (Baltimore, Md. : 1950). 2001 December 15; 167(12): 71928. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11739542
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IgG anti-beta(2) glycoprotein I antibodies in Malaysian patients with antiphospholipid syndrome and systemic lupus erythematosus: prevalence and clinical correlations. Author(s): Ong SG, Cheng HM, Soon SC, Goh E, Chow SK, Yeap SS. Source: Clinical Rheumatology. 2002 September; 21(5): 382-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12223986
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Imaging findings in the rare catastrophic variant of the primary antiphospholipid syndrome. Author(s): Thuerl C, Altehoefer C, Spyridonidis A, Laubenberger J. Source: European Radiology. 2002 March; 12(3): 545-8. Epub 2001 September 11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11870468
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Imbalance towards Th2-type response in patients with definite primary antiphospholipid syndrome. Author(s): Forastiero R, Martinuzzo M, Carreras LO. Source: Thrombosis and Haemostasis. 2001 September; 86(3): 934-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11583333
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Immune responses to native beta(2)-glycoprotein I in patients with systemic lupus erythematosus and the antiphospholipid syndrome. Author(s): Davies ML, Young SP, Welsh K, Bunce M, Wordsworth BP, Davies KA, Wagenknecht DR, Taylor E, Gordon C, Jobson S, Briggs D, Bowman SJ. Source: Rheumatology (Oxford, England). 2002 April; 41(4): 395-400. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11961169
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Immune thrombocytopenia in a newborn from a mother with primary antiphospholipid syndrome. Author(s): Darnige L, Boutignon H, Arvieux J, Benhamou E, Kaplan C. Source: American Journal of Hematology. 2004 February; 75(2): 119-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14755386
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Immunoglobulin G from patients with antiphospholipid syndrome impairs the fibrin dissolution with plasmin. Author(s): Kolev K, Gombas J, Varadi B, Skopal J, Mede K, Pitlik E, Nagy Z, Machovich R. Source: Thrombosis and Haemostasis. 2002 March; 87(3): 502-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11916083
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Impact of plasma homocysteine and prothrombin G20210 A on primary antiphospholipid syndrome. Author(s): Ames PR, Margaglione M, Tommasino C, Bossone A, Iannaccone L, Brancaccio V. Source: Blood Coagulation & Fibrinolysis : an International Journal in Haemostasis and Thrombosis. 2001 December; 12(8): 699-704. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11734671
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Importance of planning ovulation induction therapy in systemic lupus erythematosus and antiphospholipid syndrome: a single center retrospective study of 21 cases and 114 cycles. Author(s): Huong du LT, Wechsler B, Vauthier-Brouzes D, Duhaut P, Costedoat N, Lefebvre G, Piette JC. Source: Seminars in Arthritis and Rheumatism. 2002 December; 32(3): 174-88. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12528082
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Increased carotid artery intima-media thickness may be associated with stroke in primary antiphospholipid syndrome. Author(s): Medina G, Casaos D, Jara LJ, Vera-Lastra O, Fuentes M, Barile L, Salas M. Source: Annals of the Rheumatic Diseases. 2003 July; 62(7): 607-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12810420
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Increased circulating platelet-leucocyte complexes and platelet activation in patients with antiphospholipid syndrome, systemic lupus erythematosus and rheumatoid arthritis. Author(s): Joseph JE, Harrison P, Mackie IJ, Isenberg DA, Machin SJ. Source: British Journal of Haematology. 2001 November; 115(2): 451-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11703349
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Increased fibrin polymerization rate in patients with primary antiphospholipid syndrome and systemic lupus erythematosus. Author(s): de Pablo P, Ramirez A, Cortina E, de la Pena A, Zamora J, Izaguirre R, Amigo MC. Source: Clinical and Applied Thrombosis/Hemostasis : Official Journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis. 2003 July; 9(3): 221-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14507110
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Increased morbidity and mortality in patients with antiphospholipid syndrome undergoing valve replacement surgery. Author(s): Berkun Y, Elami A, Meir K, Mevorach D, Naparstek Y. Source: The Journal of Thoracic and Cardiovascular Surgery. 2004 February; 127(2): 41420. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14762349
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Intracardiac thrombus in a patient with autoimmune hemolytic anemia leading to a diagnosis of antiphospholipid syndrome. Author(s): Latagliata R, Celesti F, Bongarzoni V, Di Nucci G, Torromeo C, Morano SG, Cimino G, Alimena G. Source: Acta Haematologica. 2002; 107(3): 170-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11978938
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Intracranial venous thrombosis and pulmonary embolism with antiphospholipid syndrome in systemic lupus erythematosus. Author(s): Yuen SY, Lau KF, Steinberg AW, Grattan-Smith PJ, Hodson EM. Source: Journal of Paediatrics and Child Health. 2001 August; 37(4): 405-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11532066
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Intrapulmonary thrombolytic therapy in a child with acute pulmonary embolism due to primary antiphospholipid syndrome. Author(s): Huang HJ, Wang JN, Tsai YC, Lin CS, Wu JM. Source: Acta Paediatr Taiwan. 2002 November-December; 43(6): 351-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12632791
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Is the determination of anti-beta2 glycoprotein I antibodies useful in patients with venous thromboembolism without the antiphospholipid syndrome? Author(s): Hsieh K, Knobl P, Rintelen C, Kyrle PA, Quehenberger P, Bialonczyk C, Partsch H, Lechner K, Pabinger I. Source: British Journal of Haematology. 2003 November; 123(3): 490-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14617012
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Isolated fascicular oculomotor nerve palsy as the initial presentation of the antiphospholipid syndrome. Author(s): Champion BL, Choy F, Schrieber L, Roche J, Rowe DB. Source: Journal of Clinical Neuroscience : Official Journal of the Neurosurgical Society of Australasia. 2002 November; 9(6): 691-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12604287
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Isolated thrombus producing tricuspid stenosis: an unusual presentation in primary antiphospholipid syndrome. Author(s): Mukhopadhyay S, Suryavanshi S, Yusuf J, Chandrashekhar, Rastogi V, Trehan V, Kaul UA. Source: Indian Heart J. 2004 January-February; 56(1): 61-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15129795
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Kidney involvement in the antiphospholipid syndrome. Author(s): Nochy D, Daugas E, Huong DL, Piette JC, Hill G. Source: Journal of Autoimmunity. 2000 September; 15(2): 127-32. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10968898
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Kingella endocarditis and meningitis in a patient with SLE and associated antiphospholipid syndrome. Author(s): Wolak T, Abu-Shakra M, Flusser D, Liel-Cohen N, Buskila D, Sukenik S. Source: Lupus. 2000; 9(5): 393-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10878736
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Laboratory control of oral anticoagulant treatment by the INR system in patients with the antiphospholipid syndrome and lupus anticoagulant. Results of a collaborative study involving nine commercial thromboplastins. Author(s): Tripodi A, Chantarangkul V, Clerici M, Negri B, Galli M, Mannucci PM. Source: British Journal of Haematology. 2001 December; 115(3): 672-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11736953
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Laboratory diagnosis of the antiphospholipid syndrome. Author(s): Wisloff F, Jacobsen EM, Liestol S. Source: Thrombosis Research. 2002 December 15; 108(5-6): 263-71. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12676184
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Left atrial thrombus caused by the primary antiphospholipid syndrome causing critical functional mitral stenosis. Author(s): Yusuf S, Madden BP, Pumphrey CW. Source: Heart (British Cardiac Society). 2003 March; 89(3): 262. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12591824
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Leptospirosis and the antiphospholipid syndrome. Author(s): Tattevin P, Dupeux S, Hoff J. Source: The American Journal of Medicine. 2003 February 1; 114(2): 164. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12586245
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Link between anti-CD36 antibodies and thrombosis in the antiphospholipid syndrome. Author(s): Pelegri Y, Cerrato G, Martinuzzo ME, Carreras LO, Forastiero RR. Source: Clin Exp Rheumatol. 2003 March-April; 21(2): 221-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12747279
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Livedo reticularis and cerebrovascular accidents (Sneddon's syndrome) as a clinical expression of antiphospholipid syndrome. Author(s): Gantcheva M, Tsankov N. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 1999 March; 12(2): 157-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10343946
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Localized cutaneous necrosis associated with the antiphospholipid syndrome. Author(s): Sharkey MP, Daryanani II, Gillett MB, Jones SK. Source: The Australasian Journal of Dermatology. 2002 August; 43(3): 218-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12121403
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Long term outcome of catastrophic antiphospholipid syndrome survivors. Author(s): Erkan D, Asherson RA, Espinosa G, Cervera R, Font J, Piette JC, Lockshin MD; Catastrophic Antiphospholipid Syndrome Registry Project Group. Source: Annals of the Rheumatic Diseases. 2003 June; 62(6): 530-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12759289
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Longitudinal analysis of serum insulin-like growth factor-I and insulin-like growth factor binding protein-1 in antiphospholipid syndrome and in healthy pregnancy. Author(s): Stone S, Langford K, Seed PT, Khamashta MA, Hunt BJ, Poston L. Source: American Journal of Obstetrics and Gynecology. 2003 July; 189(1): 274-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12861174
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Longitudinal evaluation of markers of endothelial cell dysfunction and hemostasis in treated antiphospholipid syndrome and in healthy pregnancy. Author(s): Stone S, Hunt BJ, Seed PT, Parmar K, Khamashta MA, Poston L. Source: American Journal of Obstetrics and Gynecology. 2003 February; 188(2): 454-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12592255
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Longitudinal study of antinuclear and anticardiolipin antibodies in pregnant women with systemic lupus erythematosus and antiphospholipid syndrome. Author(s): Salazar-Paramo M, Jara LJ, Ramos A, Barile L, Machado G, Garcia-De La Torre I. Source: Rheumatology International. 2002 August; 22(4): 142-7. Epub 2002 June 19. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12172952
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Long-term follow-up of ischaemic retinopathy in the antiphospholipid syndrome with lupus-like disease. Author(s): Kent D, Hickey-Dwyer M, Clark D. Source: Eye (London, England). 2000 June; 14 ( Pt 3A): 313-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11026991
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Long-term prognosis of antiphospholipid syndrome in patients with systemic lupus erythematosus. Author(s): Alarcon-Segovia D, Perez-Ruiz A, Villa AR. Source: Journal of Autoimmunity. 2000 September; 15(2): 157-61. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10968903
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Low dose aspirin after ischemic stroke associated with antiphospholipid syndrome. Author(s): Derksen RH, de Groot PG, Kappelle LJ. Source: Neurology. 2003 July 8; 61(1): 111-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12847169
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Low molecular weight heparin and warfarin in the treatment of patients with antiphospholipid syndrome during pregnancy. Author(s): Pauzner R, Dulitzki M, Langevitz P, Livneh A, Kenett R, Many A. Source: Thrombosis and Haemostasis. 2001 December; 86(6): 1379-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11776303
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Lung cavitation in primary antiphospholipid syndrome. Author(s): Bertoli AM, Tabares AH, Casas JP, Saurit V, Caeiro F, Alvarellos A. Source: Lupus. 2002; 11(1): 57-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11898922
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Lupus anticoagulants are stronger risk factors for thrombosis than anticardiolipin antibodies in the antiphospholipid syndrome: a systematic review of the literature. Author(s): Galli M, Luciani D, Bertolini G, Barbui T. Source: Blood. 2003 March 1; 101(5): 1827-32. Epub 2002 October 03. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12393574
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Lupus band test yields negative results in primary antiphospholipid syndrome. Author(s): Piette JC, Marinho E, Huong DL, Amoura Z, Frances C. Source: Arthritis and Rheumatism. 2001 February; 44(2): 488-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11229484
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Lupus erythematosus with antiphospholipid syndrome and erythema multiformelike lesions. Author(s): Marzano AV, Berti E, Gasparini G, Caputo R. Source: The British Journal of Dermatology. 1999 October; 141(4): 720-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10583125
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Lupus vasculitis: differential diagnosis with antiphospholipid syndrome. Author(s): Golan TD. Source: Curr Rheumatol Rep. 2002 February; 4(1): 18-24. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11798978
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Management of antiphospholipid syndrome during pregnancy. Author(s): Esplin MS. Source: Clinical Obstetrics and Gynecology. 2001 March; 44(1): 20-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11219243
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Management of pregnancy in antiphospholipid syndrome. Author(s): Shehata HA, Nelson-Piercy C, Khamashta MA. Source: Rheumatic Diseases Clinics of North America. 2001 August; 27(3): 643-59. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11534266
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Management of the obstetric antiphospholipid syndrome. Author(s): Derksen RH, Khamashta MA, Branch DW. Source: Arthritis and Rheumatism. 2004 April; 50(4): 1028-39. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15077285
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Management of thrombosis in women with antiphospholipid syndrome. Author(s): Chandramouli NB, Rodgers GM. Source: Clinical Obstetrics and Gynecology. 2001 March; 44(1): 36-47. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11219245
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Massive pulmonary hemorrhage in a Saudi female with primary antiphospholipid syndrome. Author(s): Al-Hajjaj MS. Source: Saudi Med J. 2000 August; 21(8): 777-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11423896
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Maternal antiphospholipid syndrome presenting as neonatal lupus with congenital complete heart block in the fetus. Author(s): Abu-Ras R, Felser K, Rottem M. Source: Isr Med Assoc J. 2001 December; 3(12): 966-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11794929
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Maternal serum human chorionic gonadotrophin levels in systemic lupus erythematosus and antiphospholipid syndrome. Author(s): Maymon R, Cuckle H, Sehmi IK, Herman A, Sherman D. Source: Prenatal Diagnosis. 2001 February; 21(2): 143-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11241544
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Membranous glomerulonephritis, antiphospholipid syndrome, and persistent low C3 levels associated with meningococcal disease. Author(s): Bulucu F, Can C, Oktenli C, Koc B, Polat Z. Source: Nephron. 2002 June; 91(2): 336-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12053076
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Mesenteric vein thrombosis triggered by blunt abdominal trauma in a patient with the primary antiphospholipid syndrome. Author(s): Fried M, Van Ganse W, Van Avermaet S. Source: European Journal of Gastroenterology & Hepatology. 2002 June; 14(6): 697-700. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12072606
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MHC class II and III polymorphisms and the antiphospholipid syndrome. Author(s): Galli M. Source: Thrombosis and Haemostasis. 2001 February; 85(2): 193-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11246530
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Mitral insufficiency associated with primary antiphospholipid syndrome and chronic renal failure. Author(s): Kato Y, Isobe F, Sasaki Y, Kodera K, Kumano H, Nagamachi K. Source: Jpn J Thorac Cardiovasc Surg. 2001 March; 49(3): 171-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11305057
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Mitral valve thrombus mimicking a primary tumor in the antiphospholipid syndrome. Author(s): Mottram PM, Gelman JS. Source: Journal of the American Society of Echocardiography : Official Publication of the American Society of Echocardiography. 2002 July; 15(7): 746-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12094176
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Molecular pathogenesis of the antiphospholipid syndrome. Author(s): Rand JH. Source: Circulation Research. 2002 January 11; 90(1): 29-37. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11786515
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Multiple rib infarcts: a rare form of osteonecrosis in antiphospholipid syndrome. Author(s): Yoo WH. Source: Annals of the Rheumatic Diseases. 2004 April; 63(4): 457-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15020344
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Multiple thromboses in major arteries in a patient with antiphospholipid syndrome associated with excess of a large multimer of von Willebrand factor. Author(s): Mukai M, Ieko M, Atsumi T, Notoya A, Kohno M. Source: Lupus. 2001; 10(12): 895-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11787884
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Myocardial infarction in a young woman with antiphospholipid syndrome. Author(s): Sajeev CG, Vivek Nambiar K, Fasaludeen M, Jayakumar TG, Krishnan MN, Venugopal K. Source: International Journal of Cardiology. 2003 September; 91(1): 99-100. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12957736
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Myocardial infarction with normal coronary arteries in a patient with primary antiphospholipid syndrome--case report and literature review. Author(s): Lagana B, Baratta L, Tubani L, Golluscio V, Delfino M, Rossi Fanelli F. Source: Angiology. 2001 November; 52(11): 785-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11716332
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Myocardial ischaemia with a normal coronary angiogram due to the primary antiphospholipid syndrome. Author(s): de Vries PA, van der Sluis A, van der Horst JC, van Veldhuisen DJ. Source: International Journal of Cardiology. 2002 February; 82(2): 183-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11853907
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Myocardial ischemia during emergency anesthesia in a patient with systemic lupus erythematosus resulting from undiagnosed antiphospholipid syndrome. Author(s): Ozaki M, Minami K, Shigematsu A. Source: Anesthesia and Analgesia. 2002 July; 95(1): 255. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12088987
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Neonatal and pediatric outcome of infants born to mothers with antiphospholipid syndrome. Author(s): Brewster JA, Shaw NJ, Farquharson RG. Source: Journal of Perinatal Medicine. 1999; 27(3): 183-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10503179
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Neonatal antiphospholipid syndrome. Author(s): Navarro F, Dona-Naranjo MA, Villanueva I. Source: The Journal of Rheumatology. 1997 June; 24(6): 1240-1. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9195546
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Neonatal outcome in women treated for the antiphospholipid syndrome during pregnancy. Author(s): Botet F, Romera G, Montagut P, Figueras J, Carmona F, Balasch J. Source: Journal of Perinatal Medicine. 1997; 25(2): 192-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9189840
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Neonatal outcome in women treated for the antiphospholipid syndrome during pregnancy. J Perinat Med 1997;25(2):192-196. Author(s): Cohn GM. Source: Journal of Women's Health / the Official Publication of the Society for the Advancement of Women's Health Research. 1998 March; 7(2): 266-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9555692
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Nephrological and obstetric complications of the antiphospholipid syndrome. Author(s): Isom R, Nickolas TL, Radhakrishnan J. Source: Expert Opinion on Investigational Drugs. 2002 June; 11(6): 819-29. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12036425
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Nephropathy and hypertension as manifestations in a 13-y-old girl with primary antiphospholipid syndrome. Author(s): Ohtomo Y, Matsubara T, Nishizawa K, Unno A, Motohashi T, Yamashiro Y. Source: Acta Paediatrica (Oslo, Norway : 1992). 1998 August; 87(8): 903-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9736241
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Neuroimaging techniques in the diagnostic work-up of patients with the antiphospholipid syndrome. Author(s): Rovaris M, Pedroso C, Filippi M. Source: Curr Rheumatol Rep. 2001 August; 3(4): 301-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11470048
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Neurologic manifestations of the antiphospholipid syndrome. Author(s): Tanne D, Hassin-Baer S. Source: Curr Rheumatol Rep. 2001 August; 3(4): 286-92. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11470046
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Neurological and neuroendocrine-cytokine inter-relationship in the antiphospholipid syndrome. Author(s): Chapman J, Shoenfeld Y. Source: Annals of the New York Academy of Sciences. 2002 June; 966: 415-24. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12114299
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Neurological and obstetric manifestations of the antiphospholipid syndrome. Author(s): Gatenby PA. Source: Lupus. 1996 April; 5(2): 170-2. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8743136
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Neurological involvement as a poor prognostic factor in catastrophic antiphospholipid syndrome: autopsy findings in 12 cases. Author(s): Olguin-Ortega L, Jara LJ, Becerra M, Ariza R, Espinoza L, Wilson W, BarileFabris L. Source: Lupus. 2003; 12(2): 93-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12630752
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Neurological manifestations of polyarteritis nodosa associated with the antiphospholipid syndrome. Author(s): Valeyrie L, Bachot N, Roujeau JC, Authier J, Gherardi R, Hosseini H. Source: Annales De Medecine Interne. 2003 November; 154(7): 479-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14732840
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Neuronal-binding antibodies from patients with antiphospholipid syndrome induce cognitive deficits following intrathecal passive transfer. Author(s): Shoenfeld Y, Nahum A, Korczyn AD, Dano M, Rabinowitz R, Beilin O, Pick CG, Leider-Trejo L, Kalashnikova L, Blank M, Chapman J. Source: Lupus. 2003; 12(6): 436-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12873044
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New approaches to prevention of thrombosis in the antiphospholipid syndrome: hopes, trials, and tribulations. Author(s): Roubey RA. Source: Arthritis and Rheumatism. 2003 November; 48(11): 3004-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14613259
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New basic aspects of the antiphospholipid syndrome. Author(s): Hunt JE, Adelstein S, Krilis SA. Source: Clin Exp Rheumatol. 1994 November-December; 12(6): 661-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7895403
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New registry will benefit patients with antiphospholipid syndrome. Author(s): Franz R. Source: Dermatology Nursing / Dermatology Nurses' Association. 2001 October; 13(5): 393-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11917629
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Non-infective verrucous endocarditis in a patient with 'primary' antiphospholipid syndrome. Author(s): Font J, Cervera R, Pare C, Lopez-Soto A, Pallares L, Azqueta M, Khamashta MA. Source: British Journal of Rheumatology. 1991 August; 30(4): 305-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1863831
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Normal expression of cell adhesion molecules in placentae from women with systemic lupus erythematosus and the antiphospholipid syndrome. Author(s): Lakasing L, Campa JS, Parmar K, Poston R, Hunt BJ, Poston L. Source: Placenta. 2000 March-April; 21(2-3): 142-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10736236
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Normal expression of tissue factor, thrombomodulin, and annexin V in placentas from women with antiphospholipid syndrome. Author(s): Lakasing L, Campa JS, Poston R, Khamashta MA, Poston L. Source: American Journal of Obstetrics and Gynecology. 1999 July; 181(1): 180-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10411817
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Normal fetal growth in women with antiphospholipid syndrome treated with highdose intravenous immunoglobulin (IVIG). Author(s): Valensise H, Vaquero E, De Carolis C, Stipa E, Perricone R, Arduini D, Romanini C. Source: Prenatal Diagnosis. 1995 June; 15(6): 509-17. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7659685
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Obstetric management of antiphospholipid syndrome. Author(s): Rai R. Source: Journal of Autoimmunity. 2000 September; 15(2): 203-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10968910
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Ocular involvement in primary antiphospholipid syndrome. Ocular involvement in primary APS. Author(s): Demirci FY, Kucukkaya R, Akarcay K, Kir N, Atamer T, Demirci H, Ongor E. Source: International Ophthalmology. 1998; 22(6): 323-9. Erratum In: Int Ophthalmol 1999; 23(3): 181. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10937845
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Oculomotor palsy in six patients with systemic lupus erythematosus. A possible role of antiphospholipid syndrome. Author(s): Genevay S, Hayem G, Hamza S, Palazzo E, Meyer O, Kahn MF. Source: Lupus. 2002; 11(5): 313-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12090567
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Ontogeny of beta 2 glycoprotein I and annexin V in villous placenta of normal and antiphospholipid syndrome pregnancies. Author(s): Donohoe S, Kingdom JC, Mackie IJ, Burrell S, Quenby S, Jauniaux E, Machin SJ. Source: Thrombosis and Haemostasis. 2000 July; 84(1): 32-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10928466
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Optic neuropathy in primary antiphospholipid syndrome in childhood. Author(s): Besbas N, Anlar B, Apak A, Kansu T. Source: Journal of Child Neurology. 2001 September; 16(9): 690-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11575613
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Outcome of primary antiphospholipid syndrome in childhood. Author(s): Gattorno M, Falcini F, Ravelli A, Zulian F, Buoncompagni A, Martini G, Resti M, Picco P, Martini A. Source: Lupus. 2003; 12(6): 449-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12873046
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Ovarian vein thrombosis in the antiphospholipid syndrome. Author(s): Andre M, Delevaux I, Amoura Z, Corbi P, Courthaliac C, Aumaitre O, Piette JC. Source: Arthritis and Rheumatism. 2004 January; 50(1): 183-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14730615
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Oxidative stress in systemic lupus erythematosus and antiphospholipid syndrome: a gateway to atherosclerosis. Author(s): Alves JD, Grima B. Source: Curr Rheumatol Rep. 2003 October; 5(5): 383-90. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12967525
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Oxidized low-density lipoprotein and autoimmune antibodies in patients with antiphospholipid syndrome with a history of thrombosis. Author(s): Zhao D, Ogawa H, Wang X, Cameron GS, Baty DE, Dlott JS, Triplett DA. Source: American Journal of Clinical Pathology. 2001 November; 116(5): 760-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11710695
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Oxidized low-density lipoprotein as a risk factor of thrombosis in antiphospholipid syndrome. Author(s): Matsuura E, Kobayashi K, Koike T, Shoenfeld Y, Khamashta MA, Hughes GR. Source: Lupus. 2003; 12(7): 550-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12892397
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Oxidized low-density lipoprotein/beta2-glycoprotein I complexes and autoantibodies to oxLig-1/beta2-glycoprotein I in patients with systemic lupus erythematosus and antiphospholipid syndrome. Author(s): Lopez D, Garcia-Valladares I, Palafox-Sanchez CA, De La Torre IG, Kobayashi K, Matsuura E, Lopez LR. Source: American Journal of Clinical Pathology. 2004 March; 121(3): 426-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15023048
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Platelet and endothelial activation are requisites for the development of antiphospholipid syndrome. Author(s): del Rio Garcia E, Rodriguez C, Rodriguez-Martorell J, Serrano A, GironGonzalez JA. Source: Annals of the Rheumatic Diseases. 2004 May; 63(5): 600-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15082497
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Pregnancy complications of the antiphospholipid syndrome. Author(s): Tincani A, Balestrieri G, Danieli E, Faden D, Lojacono A, Acaia B, Trespidi L, Ventura D, Meroni PL. Source: Autoimmunity. 2003 February; 36(1): 27-32. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12765468
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Pregnancy outcome in women with antiphospholipid syndrome and alloimmunity: a case report. Author(s): Castaneda Ospina SA, Cardona Maya WD, Bueno Sanchez JC, Cadavid Jaramillo AP. Source: Sao Paulo Medical Journal = Revista Paulista De Medicina. 2003 November 6; 121(6): 248-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14989141
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Primary antiphospholipid syndrome as a new cause of autoimmune pancreatitis. Author(s): Spencer HL. Source: Gut. 2004 March; 53(3): 468; Author Reply 468. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14960537
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Primary antiphospholipid syndrome associated with acute adrenal failure. Author(s): Takebayashi K, Aso Y, Tayama K, Takemura Y, Inukai T. Source: The American Journal of the Medical Sciences. 2003 January; 325(1): 41-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12544085
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Primary antiphospholipid syndrome: a cause of fever of unknown origin. Author(s): Ozaras R, Mete B, Hakko E, Mert A, Tabak F, Bilir M, Akman C, Ozturk R. Source: Intern Med. 2003 April; 42(4): 358-61. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12729327
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Prophylaxis of the antiphospholipid syndrome: a consensus report. Author(s): Alarcon-Segovia D, Boffa MC, Branch W, Cervera R, Gharavi A, Khamashta M, Shoenfeld Y, Wilson W, Roubey R. Source: Lupus. 2003; 12(7): 499-503. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12892387
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Prospective observational study of antiphospholipid antibodies in acute lung injury and acute respiratory distress syndrome: comparison with catastrophic antiphospholipid syndrome. Author(s): Wiedermann FJ, Lederer W, Mayr AJ, Sepp N, Herold M, Schobersberger W. Source: Lupus. 2003; 12(6): 462-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12873048
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Purple toes syndrome associated with warfarin therapy in a patient with antiphospholipid syndrome. Author(s): Talmadge DB, Spyropoulos AC. Source: Pharmacotherapy. 2003 May; 23(5): 674-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12741443
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Purpura and leg ulcers in a patient with cryoglobulinaemia, non-Hodgkin's lymphoma, and antiphospholipid syndrome. Author(s): Andrejevic S, Bonaci-Nikolic B, Bukilica M, Milivojevic G, Basanovic J, Nikolic MM. Source: Clinical and Experimental Dermatology. 2003 March; 28(2): 151-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12653701
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Rapid resolution of left ventricular thrombus in antiphospholipid syndrome. Author(s): Willens HJ, Lowery MH, Lopez E, Ewing MH, Myerburg RJ. Source: Echocardiography (Mount Kisco, N.Y.). 2003 January; 20(1): 67-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12848700
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Reactive angioendotheliomatosis in the setting of antiphospholipid syndrome. Author(s): Thai KE, Barrett W, Kossard S. Source: The Australasian Journal of Dermatology. 2003 May; 44(2): 151-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12752193
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Recent advances in the diagnosis of antiphospholipid syndrome. Author(s): Chi HS. Source: International Journal of Hematology. 2002 August; 76 Suppl 2: 47-51. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12430900
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Recurrent thromboembolism, adenocarcinoma and antiphospholipid syndrome. Author(s): Kim JS, Choi EJ. Source: Cerebrovascular Diseases (Basel, Switzerland). 2002; 14(3-4): 266-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12403965
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Reflections on the management of reproductive failure in the antiphospholipid syndrome--the clinician's perspective. Author(s): Balasch J, Cervera R. Source: Lupus. 2002; 11(8): 467-77. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12220100
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Renal cortical perfusion defects caused by antiphospholipid syndrome seen on fusion imaging. Author(s): Calhoun WB, Hartshorne MF, Servilla KS, Tzamaloukas AH. Source: Clinical Nuclear Medicine. 2003 October; 28(10): 853-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14508284
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Renal involvement in primary antiphospholipid syndrome and its response to immunosuppressive therapy. Author(s): Korkmaz C, Kabukcuoglu S, Isiksoy S, Yalcin AU. Source: Lupus. 2003; 12(10): 760-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14596425
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Review of severe vaso-occlusive retinopathy in systemic lupus erythematosus and the antiphospholipid syndrome: associations, visual outcomes, complications and treatment. Author(s): Au A, O'Day J. Source: Clinical & Experimental Ophthalmology. 2004 February; 32(1): 87-100. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14746601
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Role of the Fcgamma receptor IIA polymorphism in the antiphospholipid syndrome: an international meta-analysis. Author(s): Karassa FB, Bijl M, Davies KA, Kallenberg CG, Khamashta MA, Manger K, Michel M, Piette JC, Salmon JE, Song YW, Tsuchiya N, Yoo DH, Ioannidis JP. Source: Arthritis and Rheumatism. 2003 July; 48(7): 1930-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12847687
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Rowell's syndrome and associated antiphospholipid syndrome. Author(s): Pandhi D, Singal A, Agarwal P. Source: Clinical and Experimental Dermatology. 2004 January; 29(1): 22-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14723713
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Seronegative antiphospholipid syndrome. Author(s): Jawad AS. Source: Annals of the Rheumatic Diseases. 2004 May; 63(5): 608; Author Reply 608. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15082504
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Seronegative antiphospholipid syndrome. Author(s): Hughes GR, Khamashta MA. Source: Annals of the Rheumatic Diseases. 2003 December; 62(12): 1127. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14644846
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Severe thrombophilia with antiphospholipid syndrome and hyperhomocysteinemia in a patient with Schnitzler's syndrome. Author(s): Famularo G, Barracchini A, Minisola G. Source: Clin Exp Rheumatol. 2003 May-June; 21(3): 366-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12846060
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Simultaneous pancreas-kidney transplantation in patients with antiphospholipid syndrome. Author(s): Wullstein C, Woeste G, Zapletal C, Dette K, Bechstein WO. Source: Transplantation. 2003 February 27; 75(4): 562-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12605129
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Stroke and the antiphospholipid syndrome: consensus meeting Taormina 2002. Author(s): Brey RL, Chapman J, Levine SR, Ruiz-Irastorza G, Derksen RH, Khamashta M, Shoenfeld Y. Source: Lupus. 2003; 12(7): 508-13. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12892389
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Subclinical, primary antiphospholipid syndrome unmasked by sclerotherapy. Author(s): James MP, Grech H. Source: The British Journal of Dermatology. 2002 March; 146(3): 527-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11952562
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Successful pregnancy outcome in a patient with Gaucher's disease and antiphospholipid syndrome. Author(s): Sherer Y, Dulitzki M, Levy Y, Livneh A, Shoenfeld Y, Langevitz P. Source: Annals of Hematology. 2002 March; 81(3): 161-3. Epub 2002 February 23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11904743
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Superficial thrombophlebitis of the chest wall associated with anticardiolipin antibodies: antiphospholipid syndrome or Mondor's disease? Author(s): Boehlen F, Bader M, de Moerloose P. Source: Lupus. 2004; 13(1): 70-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14870921
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Suppressed intrinsic fibrinolytic activity by monoclonal anti-beta-2 glycoprotein I autoantibodies: possible mechanism for thrombosis in patients with antiphospholipid syndrome. Author(s): Takeuchi R, Atsumi T, Ieko M, Amasaki Y, Ichikawa K, Koike T. Source: British Journal of Haematology. 2002 December; 119(3): 781-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12437660
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Systemic antiphospholipid syndrome. Author(s): Shoenfeld Y. Source: Lupus. 2003; 12(7): 497-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12892386
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T cell epitopes of prothrombin in patients with antiphospholipid syndrome. Author(s): Yoshida K, Tsutsumi A, Ohnishi Y, Akimoto T, Murata H, Sumida T. Source: Annals of the Rheumatic Diseases. 2003 September; 62(9): 905-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12922970
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The antiphospholipid syndrome and atherosclerosis: clue to pathogenesis. Author(s): Merrill JT. Source: Curr Rheumatol Rep. 2003 October; 5(5): 401-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12967528
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The antiphospholipid syndrome. Author(s): Grover R, Kumar A. Source: Natl Med J India. 2003 November-December; 16(6): 311-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14765622
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The antiphospholipid syndrome: multiple faces beyond the classical presentation. Author(s): Asherson RA, Cervera R. Source: Autoimmunity Reviews. 2003 May; 2(3): 140-51. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12848955
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The catastrophic antiphospholipid syndrome--Asherson's syndrome. Author(s): Piette JC, Cervera R, Levy RA, Nasonov EL, Triplett DA, Shoenfeld Y. Source: Annales De Medecine Interne. 2003 September; 154(4): 195-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14593307
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The expanding spectrum of renal diseases associated with antiphospholipid syndrome. Author(s): Fakhouri F, Noel LH, Zuber J, Beaufils H, Martinez F, Lebon P, Papo T, Chauveau D, Bletry O, Grunfeld JP, Piette JC, Lesavre P. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2003 June; 41(6): 1205-11. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12776272
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The role of complement in the antiphospholipid syndrome. Author(s): Salmon JE, Girardi G. Source: Curr Dir Autoimmun. 2004; 7: 133-48. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14719378
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Transient antiphospholipid syndrome in an infant with segmental small bowel infarction. Author(s): Guvenc BH, Sarper N, Tuzlaci A, Gunaltay N. Source: Journal of Pediatric Surgery. 2004 January; 39(1): 124-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14694390
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Treatment of pregnant patients with antiphospholipid syndrome. Author(s): Tincani A, Branch W, Levy RA, Piette JC, Carp H, Rai RS, Khamashta M, Shoenfeld Y. Source: Lupus. 2003; 12(7): 524-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12892392
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Treatment of the antiphospholipid syndrome. Author(s): Lockshin MD, Erkan D. Source: The New England Journal of Medicine. 2003 September 18; 349(12): 1177-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=13679533
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Understanding prostaglandin metabolites and platelet-activating factor in the pathophysiology and treatment of the antiphospholipid syndrome. Author(s): Silver RK, Peaceman AM, Adams DM. Source: Clin Perinatol. 1995 June; 22(2): 357-73. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7671542
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Unusual manifestations of the antiphospholipid syndrome. Author(s): Asherson RA, Cervera R. Source: Clinical Reviews in Allergy & Immunology. 2003 August; 25(1): 61-78. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12794262
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Up-date on the antiphospholipid syndrome. Author(s): Luzzana C, Gerosa M, Riboldi P, Meroni PL. Source: Journal of Nephrology. 2002 July-August; 15(4): 342-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12243362
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Up-regulated tissue factor expression in antiphospholipid syndrome. Author(s): Atsumi T, Khamashta MA, Amengual O, Hughes GR. Source: Thrombosis and Haemostasis. 1997 January; 77(1): 222-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9031483
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Uterine artery Doppler in predicting pregnancy outcome in women with antiphospholipid syndrome. Author(s): Venkat-Raman N, Backos M, Teoh TG, Lo WT, Regan L. Source: Obstetrics and Gynecology. 2001 August; 98(2): 235-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11506839
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Utilization of intravenous immunoglobulin therapy to treat recurrent pregnancy loss in the antiphospholipid syndrome: a review. Author(s): Harris EN, Pierangeli SS. Source: Scand J Rheumatol Suppl. 1998; 107: 97-102. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9759143
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Validation of the Sapporo criteria for antiphospholipid syndrome. Author(s): Lockshin MD, Sammaritano LR, Schwartzman S. Source: Arthritis and Rheumatism. 2000 February; 43(2): 440-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10693886
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Valine/valine genotype at position 247 of the beta2-glycoprotein I gene in Mexican patients with primary antiphospholipid syndrome: association with anti-beta2glycoprotein I antibodies. Author(s): Prieto GA, Cabral AR, Zapata-Zuniga M, Simon AJ, Villa AR, AlarconSegovia D, Cabiedes J. Source: Arthritis and Rheumatism. 2003 February; 48(2): 471-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12571857
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Value of autoantibodies to beta(2)-glycoprotein 1 in the diagnosis of antiphospholipid syndrome. Author(s): Audrain MA, El-Kouri D, Hamidou MA, Mioche L, Ibara A, Langlois ML, Muller JY. Source: Rheumatology (Oxford, England). 2002 May; 41(5): 550-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12011379
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Valvular deposition of antiphospholipid antibodies in the antiphospholipid syndrome: a clue to the origin of the disease. Author(s): Amital H, Langevitz P, Levy Y, Afek A, Goldberg I, Pras M, Livneh A, Shoenfeld Y. Source: Clin Exp Rheumatol. 1999 January-February; 17(1): 99-102. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10084041
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Vascular damage correlates between heparin-induced thrombocytopenia and the antiphospholipid syndrome. Author(s): Walenga JM, Michal K, Hoppensteadt D, Wood JJ, Robinson JA, Bick RL. Source: Clinical and Applied Thrombosis/Hemostasis : Official Journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis. 1999 October; 5 Suppl 1: S76-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10726041
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Vascular endothelial growth factor plasma levels in patients with systemic lupus erythematosus and primary antiphospholipid syndrome. Author(s): Navarro C, Candia-Zuniga L, Silveira LH, Ruiz V, Gaxiola M, Avila MC, Amigo MC. Source: Lupus. 2002; 11(1): 21-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11898914
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Vasculitis and the antiphospholipid syndrome. Author(s): Alarcon-Segovia D, Drenkard C. Source: Rheumatology (Oxford, England). 2000 August; 39(8): 922-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10952752
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Venous thromboembolism in the antiphospholipid syndrome: management guidelines for secondary prophylaxis. Author(s): Meroni PL, Moia M, Derksen RH, Tincani A, McIntyre JA, Arnout JM, Koike T, Piette JC, Khamashta MA, Shoenfeld Y. Source: Lupus. 2003; 12(7): 504-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12892388
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Visual disturbances and pathologic ocular findings in primary antiphospholipid syndrome. Author(s): Gelfand YA, Dori D, Miller B, Brenner B. Source: Ophthalmology. 1999 August; 106(8): 1537-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10442901
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Vitreous hemorrhage as the presenting sign of antiphospholipid syndrome. Author(s): Monshizadeh R, Werner M, Richards H, Tabandeh H, Bhatti MT. Source: Can J Ophthalmol. 2003 December; 38(7): 607-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14740806
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Wegener's granulomatosis associated with antiphospholipid syndrome. Author(s): Castellino G, La Corte R, Santilli D, Trotta F. Source: Lupus. 2000; 9(9): 717-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11199929
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What causes the antiphospholipid syndrome? Author(s): Merrill JT. Source: Curr Rheumatol Rep. 2001 August; 3(4): 293-300. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11470047
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What is going to happen tomorrow regarding the antiphospholipid syndrome? JeanCharles Piette. Author(s): Piette JC. Source: Annales De Medecine Interne. 1995; 146(8): 555-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8734081
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Which antiphospholipid antibodies should be measured in the antiphospholipid syndrome? Author(s): Galli M. Source: Haemostasis. 2000; 30 Suppl 2: 57-62. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11251342
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Which are the best biological markers of the antiphospholipid syndrome? Author(s): Carreras LO, Forastiero RR, Martinuzzo ME. Source: Journal of Autoimmunity. 2000 September; 15(2): 163-72. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10968904
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Widespread cutaneous necrosis associated with antiphospholipid syndrome. Author(s): Jou IM, Liu MF, Chao SC. Source: Clinical Rheumatology. 1996 July; 15(4): 394-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8853176
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Widespread cutaneous necrosis occurring in association with the antiphospholipid syndrome: a report of two cases. Author(s): Creamer D, Hunt BJ, Black MM. Source: The British Journal of Dermatology. 2000 June; 142(6): 1199-203. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10848747
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CHAPTER 2. SYNDROME
NUTRITION
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ANTIPHOSPHOLIPID
Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and antiphospholipid syndrome.
Finding Nutrition Studies on Antiphospholipid Syndrome 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 “antiphospholipid syndrome” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.
7 Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.
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The following information is typical of that found when using the “Full IBIDS Database” to search for “antiphospholipid syndrome” (or a synonym): •
Abnormal regional cerebral blood flow in primary antiphospholipid antibody syndrome patients with normal magnetic resonance imaging findings. A preliminary report. Author(s): Department of Internal Medicine, China Medical College Hospital, Taichung, Taiwan. Source: Chen, J J H Shiau, Y C Wang, J J Ho, S T Kao, A Scand-J-Rheumatol. 2002; 31(2): 89-93 0300-9742
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Autoimmune hepatitis complicated with antiphospholipid syndrome in pregnancy. Author(s): Department of Obstetrics and Gynecology, Mie Prefectural Shima Hospital, Ago, Japan.
[email protected] Source: Tanaka, H Umekawa, T Kikukawa, T Toyoda, N Am-J-Reprod-Immunol. 2002 March; 47(3): 142-5 1046-7408
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Chorea as the presenting clinical feature of primary antiphospholipid syndrome in childhood. Author(s): Department of Paediatrics, University of Innsbruck, Austria. Source: Kiechl Kohlendorfer, U Ellemunter, H Kiechl, S Neuropediatrics. 1999 April; 30(2): 96-8 0174-304X
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Cutaneous necrosis revealing the coexistence of an antiphospholipid syndrome with acquired protein S deficiency, factor V Leiden and hyperhomocysteinemia. Author(s): Department of Dermatology, Instruction Military Hospital Desgenettes, 108, boulevard Pinel, 69003 Lyon, France.
[email protected] Source: Combemale, Patrick Amiral, Jean Estival, Jean Louis Dupin, Michel Chouvet, Brigitte Berruyer, Micheline Eur-J-Dermatol. 2002 May-June; 12(3): 278-82 1167-1122
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Multiple retinal arteriolar occlusions associated with coexisting primary antiphospholipid syndrome and factor V Leiden mutation. Author(s): Department of Ophthalmology, Rambam Medical Center, Haifa, Israel.
[email protected] Source: Dori, D Beiran, I Gelfand, Y Lanir, N Scharf, J Miller, B Brenner, B Am-JOphthalmol. 2000 January; 129(1): 106-8 0002-9394
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Primary antiphospholipid syndrome presented by total infarction of right kidney with nephrotic syndrome. Author(s): Nephrology Department, Hospitais da Universidade de Coimbra, Portugal. Source: Sa, H Freitas, L Mota, A Cunha, F Marques, A Clin-Nephrol. 1999 July; 52(1): 5660 0301-0430
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Successful pregnancies in patients with antiphospholipid syndrome treated with lowdose aspirin. Author(s): Department of Obstetrics & Gynaecology, U.W.I., Jamaica. Source: Fletcher, H M Wharfe, G H Thomas, E West-Indian-Med-J. 1993 December; 42(4): 167-9 0043-3144
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Total occlusion of inferior vena cava in a patient with antiphospholipid antibody syndrome associated with behcet's disease. Author(s): Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Source: Mukai, Y Tsutsui, H Todaka, K Mohri, M Hirai, N Arai, H Takeshita, A Jpn-CircJ. 2001 September; 65(9): 837-8 0047-1828
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Treatment of antiphospholipid syndrome in pregnancy. Author(s): Department of Obstetrics and Gynecology, New York University Medical Center, New York 10016, USA. Source: Cowchock, S Lupus. 1998; 7 Suppl 2S95-7 0961-2033
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Treatment of the antiphospholipid syndrome in pregnancy. Author(s): Lupus Unit. St. Thomas' Hospital, London, UK. Source: Ruiz Irastorza, G Khamashta, M Hughes, G Scand-J-Rheumatol-Suppl. 1998; 10744-7 0301-3847
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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WebMDHealth: http://my.webmd.com/nutrition
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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CHAPTER 3. ALTERNATIVE ANTIPHOSPHOLIPID SYNDROME
MEDICINE
AND
Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to antiphospholipid syndrome. 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 antiphospholipid syndrome 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 “antiphospholipid syndrome” (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 antiphospholipid syndrome: •
A case of primary antiphospholipid syndrome who developed acute myocardial infarction followed by early-onset pre-eclampsia. Author(s): Kurum T, Soy M, Karahasanoglu E, Ozbay G, Sayin NC. Source: Clinical Rheumatology. 2003 May; 22(2): 160-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12740688
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Antiphospholipid antibodies, ischemic stroke in young adults, and calcium supplementation: a hypothesis. Author(s): Newmark J, Newmark HL, Marden LA. Source: Military Medicine. 2000 June; 165(6): 489-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10870370
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Antiphospholipid syndrome associated with progressive systemic sclerosis. Author(s): Chun WH, Bang D, Lee SK. Source: The Journal of Dermatology. 1996 May; 23(5): 347-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8675827
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Current concepts for the management of systemic lupus erythematosus in adults: a therapeutic challenge. Author(s): Ioannou Y, Isenberg DA. Source: Postgraduate Medical Journal. 2002 October; 78(924): 599-606. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12415083
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Delayed cutaneous reactions to heparin in antiphospholipid syndrome during pregnancy. Author(s): Kim J, Smith KJ, Toner C, Skelton H. Source: International Journal of Dermatology. 2004 April; 43(4): 252-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15090006
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Diet and lupus. Author(s): Leiba A, Amital H, Gershwin ME, Shoenfeld Y. Source: Lupus. 2001; 10(3): 246-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11315362
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Effect of Salvia miltiorrhiza Bunge injection on anticardiolipin antibody production induced by beta2 glycoprotein. Author(s): Chen G, Liu RX, Zhang WG, Wang B, Fu J, Feng YG, Zhang XB, Wu F, Ma X. Source: Acta Pharmacologica Sinica. 2001 December; 22(12): 1125-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11749813
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Fish oil derivatives as a prophylaxis of recurrent miscarriage associated with antiphospholipid antibodies (APL): a pilot study. Author(s): Rossi E, Costa M. Source: Lupus. 1993 October; 2(5): 319-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8305926
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Immunosuppression and immunomodulation of experimental models of systemic lupus erythematosus and antiphospholipid syndrome. Author(s): Shoenfeld Y, Krause I. Source: Transplantation Proceedings. 1996 December; 28(6): 3096-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8962199
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Immunosuppression due to MACOP-B does not seem to cure the antiphospholipid syndrome. Author(s): Stefani PM, Pietrogrande F, Sartori R, Girolami A.
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Source: Haematologica. 1999 August; 84(8): 751-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10457414 •
Implications of modifying cardiolipin acyl composition by diet. 1. Cardiolipin acyl chain is an important determinant in the binding to antiphospholipid antibodies in SLE sera. Author(s): Berger A, German JB, Gershwin ME. Source: Journal of Autoimmunity. 1992 April; 5(2): 229-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1627234
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Linseed oil suppresses the anti-beta-2-glycoprotein-I in experimental antiphospholipid syndrome. Author(s): Reifen R, Amital H, Blank M, Sklan D, Berkovich Z, Gershwin E, Shoenfeld Y. Source: Journal of Autoimmunity. 2000 November; 15(3): 381-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11040078
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Mitral valve vegetation and cerebral emboli in a primary antiphospholipid syndrome patient who had hepatitis C virus infection: report of a case and review of the literature. Author(s): Pamuk ON, Cakir N, Soy M, Aktoz M, Celik Y, Akdemir O. Source: Clinical Rheumatology. 2003 May; 22(2): 136-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12740679
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Progressive thrombosis after treatment of diffuse large cell non-Hodgkin's lymphoma and concomitant lupus anticoagulant. Author(s): Keung YK, Cobos E, Meyerrose GE, Roberson GH. Source: Leukemia & Lymphoma. 1996 January; 20(3-4): 341-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8624478
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Thromboagglutination by anticardiolipin antibody complex in the antiphospholipid syndrome: a possible mechanism of immune-mediated thrombosis. Author(s): Wiener MH, Burke M, Fried M, Yust I. Source: Thrombosis Research. 2001 August 1; 103(3): 193-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11672581
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
•
Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMDHealth: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
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. PATENTS ON ANTIPHOSPHOLIPID SYNDROME 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.8 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 “antiphospholipid syndrome” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on antiphospholipid syndrome, we have not necessarily excluded non-medical patents in this bibliography.
Patents on Antiphospholipid Syndrome By performing a patent search focusing on antiphospholipid syndrome, 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. 8Adapted from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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The following is an example of the type of information that you can expect to obtain from a patent search on antiphospholipid syndrome: •
Carrier for binding of anti-phospholipid antibodies, and immunoassay method using the same and a kit therefor Inventor(s): Igarashi; Yoshiko (Choshi, JP), Matsuura; Eiji (Choshi, JP), Nagae; Hisato (Choshi, JP) Assignee(s): Yamasa Shoyu Kabushiki Kaisha (JP) Patent Number: 5,506,110 Date filed: June 14, 1993 Abstract: As a carrier for binding of the antiphospholipid antibodies used for immunological diagnosis of antiphospholipid syndrome, a phospholipid-bound carrier treated with purified serum albumin and a surfactant is used. Thus, immunological diagnosis of antiphospholipid syndrome can be made with high accuracy. By using the fraction or protein obtained from animal serum or plasma, having the activity of enhancing the binding ability of the antibodies specifically present in the antiphospholipid syndrome to the phospholipid, immunological diagnosis of antiphospholipid syndrome can also be made more accurately, as compared to known diagnosis. Excerpt(s): The present invention relates to a carrier for binding of antiphospholipid antibodies, an immunoassay method using the same, a kit therefor, and a fraction and a protein obtained from serum or plasma which can be used in the method for immunoassay. In particular, the present invention relates to determination of autoantibodies specifically appeared in patients with antiphospholipid syndrome. A living body causes immune response against exogenous foreign matters such as pathogenic viruses, bacteria, fungi, parasites, etc. invaded into a living body, which functions to expel the foreign matters. The phenomenon is generally classified into the following two groups: humoral immunity in which antibodies participate and cellular immunity in which immunocompetent cells directly participate, thereby to expel the foreign matters. In diseases collectively referred to as autoimmune diseases, however, recognition mechanism of self or non-self does not work correctly but humoral or cellular immune response occurs against their own cells or tissues. As a representative clinical case in which antibodies reactive with self components (autoantibodies) appear, there is systemic lupus erythematosus (SLE). It is noted that anti-single stranded DNA antibody (anti-ssDNA), anti-double stranded DNA antibody (anti-dsDNA), anti-Sm antibody, anti-cardiolipin antibody, etc. appeaer in blood of SLE patients. Also rheumatoid factors are found to be noted in those with rheumatoid arthritis (RA); antiSS-A antibody, anti-SS-B antibody and anti-mitochondrial antibody in those with Sjogren's syndrome (SjS); anti-scl antibody and anti-single stranded DNA antibody in progressive systemic sclerosis (PSS); and anti-RNP antibody in those with mixed connective tissue diseases (MCTD). At this point of time, there are many unclear points regarding relationship between the induction of these antibodies and significance in occurrence of the diseases. However, it is an important means for diagnosis of the diseases and knowledge of change in prognosis to determine the antibodies. In order to detect these various autoantibodies, immunodiffusion test, counter immunoelectrophoresis, hemagglutination test, radioimmunoassay (RIA), enzyme immunoassay (EIA) and latex agglutination test, etc. have been developed depending on antigenic specificities of antibodies, and biochemical properties and physicochemical properties of antigens.
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Web site: http://www.delphion.com/details?pn=US05506110__ •
Method of assaying autoimmune anticardiolipin antibody and kit therefor Inventor(s): Igarashi; Makoto (Choshi, JP), Igarashi; Yoshiko (Choshi, JP), Koike; Takao (Sapporo, JP), Matsuura; Eiji (Choshi, JP), Nagae; Hisato (Choshi, JP) Assignee(s): Yamasa Corporation (Chiba-ken, JP) Patent Number: 5,998,223 Date filed: May 9, 1996 Abstract: In a method for assaying an anticardiolipin antibody in a sample utilizing.beta.2-glycoprotein I, a polypeptide having the same amino acid sequence as domain IV of.beta.2-glycoprotein I or a polypeptide partially different therefrom but functionally equivalent thereto is used in place of.beta.2-glycoprotein I itself. According to this method, an autoantibody from patients with antiphospholipid syndrome can be accurately assayed in a simple manner. Excerpt(s): The present invention relates to a method for assaying an antiphospholipid antibody and a kit for use in the method. More particularly, the present invention relates to a method for assaying an antiphospholipid antibody and a kit therefor characterized by using, in place of.beta.2-glycoprotein I, a polypeptide containing the same amino acid sequence as a specific domain of.beta.2-glycoprotein I, or a polypeptide different in the amino acid sequence from the specific domain but functionally equivalent thereto. Various assay methods including radioimmunoassay (RIA) and enzyme-linked immunosorbent assay (ELISA) for an anticardiolipin antibody, which is part of the antiphospholipid family, have been reported by Harris et al., Lancet, iii: 1211, 1983; Koike et al., Clin. Exp. Immunl., 56: 193, 1984; and the like. However, those methods are not necessarily satisfactory, since they involve problems that an anticardiolipin antibody cannot be quantitatively assayed with a high accuracy, or that an anticardiolipin antibody from patients with infectious diseases cannot be assayed differentially from these patients with antiphospholipid syndrome. Web site: http://www.delphion.com/details?pn=US05998223__
•
Snake venom lupus anticoagulant protein Inventor(s): Lian; Eric Chun-Yet (Coral Gables, FL) Assignee(s): Eric Chun-Tet Lian (Coral Gables, FL) Patent Number: 5,763,403 Date filed: October 31, 1995 Abstract: A lupus anticoagulant like protein obtained from Agkistrodon halys brevicaudus venom, methods and tests for detecting the presence of lupus anticoagulant in blood and methods of treating antiphospholipid syndrome and thrombotic disorders using the protein are disclosed. Excerpt(s): This invention relates to a lupus anticoagulant like protein, particularly a lupus anticoagulant like protein from Agkistrodon halys brevicaudus venom, to methods and tests for detecting the presence of lupus anticoagulant and methods of treating antiphospholipid syndrome and thrombosis using the protein. Lupus anticoagulants (LA) are immunoglobulins that interfere with blood coagulation. Lupus
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anticoagulants are found in the blood of many people. This includes healthy people and those not suffering from lupus erythematosus. They may also be found in people having other immune system disorders such as viral infections including AIDS, tumors such as lymphoma and prostatic carcinoma, rheumatoid arthritis and the like. Such persons having lupus anticoagulants in their blood system may or may not display symptoms. However, they may suffer from disorders such as antiphospholipid syndrome, thrombosis, spontaneous abortion, thrombocytopenia, pulmonary hypertension and the like. Accordingly, there is a great need to accurately determine the presence of lupus anticoagulants in the blood stream and develop methods of treating adverse consequences of the presence of lupus anticoagulants, such as antiphospholipid syndrome, thrombotic disorders such as venous thrombosis, coronary arterial disease such as myocardial infarction (MI), cerebral vascular disease such as stroke, peripheral arterial disease, disseminated intravascular coagulation (DIC) and the like. Not only has it been a longstanding problem in the art to provide a reliable and consistent means for testing for the presence of lupus anticoagulants, it has further been a longstanding problem to provide effective methods of treatment of adverse symptoms exhibited in the presence of lupus anticoagulants, such as antiphospholipid syndrome, thrombosis and the like. These maladies can be highly dangerous to humans and can result in death. It is therefore quite important that treatments overcome such potentially fatal afflictions. Web site: http://www.delphion.com/details?pn=US05763403__ •
Solid phase reagent and assay method for measuring antibodies specific to antiphospholipid syndrome Inventor(s): Igarashi; Yoshiko (Minami-go-jo Maruyama City House 401, 1-1, Minamigo-jo Nishi 22-chome, Choshi, JP), Koike; Takao (Minami-go-jo Maruyama City House 401, 1-1, Minami-go-jo Nishi 22-chome, Sapporo-shi, Hokkaido 064, JP), Matsuura; Eiji (Minami-go-jo Maruyama City House 401, 1-1, Minami-go-jo Nishi 22-chome, Choshi, JP), Nagae; Hisato (Minami-go-jo Maruyama City House 401, 1-1, Minami-go-jo Nishi 22-chome, Choshi, JP) Assignee(s): Koike; Takao (Hokkaido, JP), Yamasa Corporation (Chiba, JP) Patent Number: 5,472,883 Date filed: October 5, 1993 Abstract: A solid phase reagent is provided which comprises a carrier having a surface onto which functional groups containing a negative charge or a lone pair of electrons and/or free radicals containing a negative charge or a lone pair of electrons have been introduced and having.beta.2-glycoprotein I coated on the surface. Using this reagent, antibodies specific to antiphospholipid syndrome can be specifically assayed. Moreover, antibodies specific to antiphospholipid syndrome can be assayed differentially from antibodies specific to infectious diseases by using the solid phase reagent described above or a further modified solid phase reagent. Excerpt(s): The present invention relates to a solid phase reagent obtained by binding.beta.2-glycoprotein I (.beta.2-GPI) to a specific carrier, an assay method for antibodies specific to antiphospholipid syndrome using the solid phase reagent, a method for detecting antibodies specific to antiphospholipid syndrome and antibodies specific to infectious diseases differentially from each other, and a kit for use in the method. Various assay methods including RIA and ELISA for anticardiolipin antibodies which are antibodies of the antiphospholipid family had been reported by Harris et al. (Lancet, iii: 1211, 1983), by Koike et al. (Clin. Exp. Immunol., 56: 193, 1984), etc.
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However, those methods described above are not necessarily satisfactory since they involve problems in that the anticardiolipin antibodies cannot be assayed quantitatively or they involve problems in that the antibodies associated with infectious diseases cannot be assayed differentially from antibodies found in patients with antiphospholipid syndrome. Web site: http://www.delphion.com/details?pn=US05472883__
Patent Applications on Antiphospholipid Syndrome As of December 2000, U.S. patent applications are open to public viewing.9 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 antiphospholipid syndrome: •
Method for predicting an increased likelihood of antiphospholipid syndrome in a patient Inventor(s): Braun, Paul J.; (Durham, NC), Ortel, Thomas L.; (Durham, NC), Su, Zuowei; (Durham, NC), Tejidor, Liliana; (Raleigh, NC) Correspondence: Judith Roesler; Biomerieux, INC.; 100 Rodolphe Street; Durham; NC; 27712; US Patent Application Number: 20030104493 Date filed: June 28, 2002 Abstract: A method for predicting that an individual has antiphospholipid syndrome or an increased likelihood of having antiphospholipid syndrome, includes: a) providing a test sample from an individual; b) combining the test sample with phospholipids; c) directing a light beam at the test sample and monitoring light scattering or transmittance over time so as to provide a time-dependent measurement profile; d) determining if a value or a slope at or over a particular time in the timedependent measurement profile is beyond a corresponding predetermined value or slope threshold; and if the value or slope in the time-dependent measurement profile is beyond the predetermined threshold, then determining that the individual has antiphospholipid syndrome or an increased risk of antiphospholipid syndrome. The phospholipids can be provided as part of a coagulation reagent, or as part of a reagent where coagulation is not activated. Confirmatory assays for particular antibodies to phospholipid binding proteins can be performed. Excerpt(s): This application claims priority from U.S. Provisional Application No. 60/302,261 to Ortel, et al. filed Jun. 29, 2001 and to U.S. Provisional Application No. 60/318,755 to Ortel, et al. filed Sep. 11, 2001, each incorporated herein by reference. Transmittance waveforms (TW) have been shown to provide useful information for various clinical situations, such as disclosed in U.S. Pat. No. 6,101,449 to Givens et al. issued Aug. 8, 2000, and U.S. Pat. No. 6,321,164 to Braun et al. issued Nov. 20, 2001, the subject matter of each being incorporated herein by reference. As disclosed therein, waveform parameters can be used to predict the presence of heparin or specific factor deficiencies using a neural network model. The magnitude of the waveform signal has also been used to estimate fibrinogen concentrations in plasma samples. These
9
This has been a common practice outside the United States prior to December 2000.
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waveform analysis methods can be used in the present invention for screening patients or predicting an increased likelihood that the patient has antiphospholipid syndrome. In another example (disclosed in WO 01/96864 to Fischer et al. published Dec. 20, 2001, incorporated herein by reference), a "biphasic" change involving the precoagulation phase of the APTT test has been associated with disseminated intravascular coagulation (DIC). This "biphasic" change is characterized by the appearance of a negative slope 1 in the precoagulation phase of the APTT, and is the result of the formation of a precipitate between C-reactive protein (CRP) and a very low density lipoprotein (VLDL). This complex has been named LC-CRP for Lipoprotein Complexed C-Reactive Protein. This negative slope 1 in the APTT was shown to precede the development of abnormalities in standard laboratory tests for DIC (e.g., elevated D-dimer levels), and waveform changes correlated closely with clinical outcomes. As will be seen below, biphasic waveforms for PT (and for APTT) can be useful for predicting that a patient has APLA, and prompting further testing. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Remedies and preventives for antiphospholipid antibody syndrome Inventor(s): Kobayashi, Seiichi; (Belmont, MA), Seto, Toshio; (Ushiku-shi, JP), Yamauchi, Toshihiko; (Ibaraki, JP), Yokohama, Hiromitsu; (Ibaraki, JP) Correspondence: Knobbe Martens Olson & Bear Llp; 2040 Main Street; Fourteenth Floor; Irvine; CA; 92614; US Patent Application Number: 20030170231 Date filed: March 3, 2003 Abstract: Agents for treating and preventing antiphospholipid antibody syndrome (APS) comprising, as an active ingredient, a substance inhibiting interaction between gp39 on a T cell surface, which is a receptor mediating contact-dependent helper effector function, and CD40 on an antigen-presenting cell surface. Excerpt(s): The present invention relates to agents for treating antiphospholipid antibody syndrome (APS) for administrating to APS patients, and agents for preventing afflication of APS for prophylactic administration to patients of autoimmune diseases such as systemic lupus erythematosus (SLE) who are expected to be afflicted by APS. APS is a generic name of diseases in which antibodies for phospholipid such as cardiolipin are positive. APS is often observed in SLE but underlying diseases are recognized to be various. In some cases, no underlying disease is recognized and the case is named as primary antiphospholipid antibody syndrome. It is known that APS causes arterial thrombosis in a brain, a heart and extremities, thrombocytopenia and habitual abortion. Concerning the treatment of APS, antithrombotic treatment using antithrombotic drugs such as heparin and warfarin is the major treatment method. 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 antiphospholipid syndrome, 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
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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 “antiphospholipid syndrome” (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 antiphospholipid syndrome. You can also use this procedure to view pending patent applications concerning antiphospholipid syndrome. 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 5. BOOKS ON ANTIPHOSPHOLIPID SYNDROME Overview This chapter provides bibliographic book references relating to antiphospholipid syndrome. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on antiphospholipid syndrome include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.
Chapters on Antiphospholipid Syndrome In order to find chapters that specifically relate to antiphospholipid syndrome, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and antiphospholipid syndrome 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 “antiphospholipid syndrome” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on antiphospholipid syndrome: •
Immunologically Mediated Disease Source: in Scully, C. and Cawson, R.A. Medical Problems in Dentistry. 4th ed. Woburn, MA: Butterworth-Heinemann. 1998. p. 438-453. Contact: Available from Butterworth-Heinemann. 225 Wildwood Avenue, Woburn, MA 01801-2041. (800) 366-2665 or (781) 904-2500. Fax (800) 446-6520 or (781) 933-6333. E-mail:
[email protected]. Website: www.bh.com. PRICE: $110.00. ISBN: 0723610568. Summary: Immunologically mediated diseases may be allergic, autoimmune, immune complex-mediated or due to a type IV hypersensitivity or other reaction. This chapter on immunologically mediated disease is from a text that covers the general medical and surgical conditions relevant to the oral health care sciences. Topics include atopic disease, food intolerance, acute allergic angioedema, oral allergy syndrome, non-allergic immunologically mediated disease, hereditary angioedema, autoimmune disease,
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connective tissue diseases, Raynaud's disease, systemic lupus erythematosus (SLE), discoid lupus erythematosus, antiphospholipid syndrome, systemic sclerosis (scleroderma), autoimmune thrombocytopenia, Behcet's syndrome, Sweet's syndrome, polyarteritis nodosa, midline granuloma syndrome, and Wegener's granulomatosis. For each condition, the authors discuss general aspects, diagnosis and management issues, dental aspects, and patient care strategies. The chapter includes a summary of the points covered. 3 figures. 10 tables. 29 references. •
Neurological Complications of Rheumatic Diseases Source: in Maddison, P.J.; et al., Eds. Oxford Textbook of Rheumatology. Volume 1. New York, NY: Oxford University Press, Inc. 1993. p. 107-116. Contact: Available from Oxford University Press, Inc., New York, NY. Summary: This chapter for health professionals explores the neurological complications of rheumatic diseases. Neurologic symptoms are discussed, including muscle weakness, muscle pain, muscle twitching, contractures, absent or exaggerated reflexes, sensory loss, and pain. Central nervous system disorders that present to the rheumatologist are described, including neuropsychiatric systemic lupus erythematosus, antiphospholipid syndrome, various connective tissue diseases, brain stem syndromes, and cranial nerve palsies. Spinal cord complications seen in rheumatic diseases are highlighted, including cervical myelopathy, myelopathy, and transverse myelitis. Peripheral nervous involvement in rheumatic diseases is discussed in terms of radicular pain, peripheral neuropathies, entrapment neuropathies, and peripheral neuropathies. 37 references, 1 figure, and 12 tables.
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CHAPTER 6. PERIODICALS ANTIPHOSPHOLIPID SYNDROME
AND
NEWS
ON
Overview In this chapter, we suggest a number of news sources and present various periodicals that cover antiphospholipid syndrome.
News Services and Press Releases One of the simplest ways of tracking press releases on antiphospholipid syndrome 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 “antiphospholipid syndrome” (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 antiphospholipid syndrome. 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 “antiphospholipid syndrome” (or synonyms).
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The NIH Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine. Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name. Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “antiphospholipid syndrome” (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 “antiphospholipid syndrome” (or synonyms). If you know the name of a company that is relevant to antiphospholipid syndrome, 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 “antiphospholipid syndrome” (or synonyms).
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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 “antiphospholipid syndrome” (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 antiphospholipid syndrome: •
Antiphospholipid Syndrome: What We Know Today and What the Future Holds Source: Lupus News. 20(5): 14-16. Winter 2000. Contact: Available from Lupus Foundation of America. 1300 Piccard Drive, Suite 200, Rockville, MD 20850-4303. (800) 558-0121 or (301) 670-9292. Fax (301) 670-9486. Website: www.lupus.org/lupus. Summary: This newsletter article provides people who have lupus with information on the antiphospholipid syndrome (APLS). This blood clotting disorder affects many people who have lupus. People who have APLS develop antibodies to structures in the membranes of cells that line the bloodstream, and these antibodies, known as antiphospholipid (APL) antibodies, interfere with important blood clotting proteins. The article reviews some historical findings that may help explain APLS, including the finding in the 1940s that women with lupus were testing positive for syphilis, the finding in 1948 that some patients with lupus with blood clotting problems had a particular antibody in their blood that increased clotting time in a test tube, and the identification in the 1980s of several antiphospholipid antibodies. There are several tests available to help diagnose APLS, including several versions of the lupus anticoagulant test, tests that directly measure antibodies to phospholipids or associated blood clotting proteins, and a test that measures antibodies to beta-2 glucoprotein 1. Several kinds of therapies are used to prevent future clots once a person has been diagnosed with the APLS, including avoiding the use of medications that may increase blood clotting risk and taking extra precautions in situations that may provoke blood clotting. People who have tested positive for lupus anticoagulant or anticardiolipin antibody but have never had a blood clot may be prescribed one aspirin per day. People who have experienced a blood clot traditionally have been prescribed warfarin, but use of this medication can be problematic because of its drug and food interactions. Although new drugs are in development for APLS and alternative therapies are available, there are significant impediments to research on the disorder. 1 table.
Academic Periodicals covering Antiphospholipid Syndrome Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to antiphospholipid syndrome. In addition to these sources, you can search for articles covering antiphospholipid syndrome 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.”
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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 7. 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 antiphospholipid syndrome. 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 non-profit 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 antiphospholipid syndrome. 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,
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etc.). The following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to antiphospholipid syndrome: Heparin •
Systemic - U.S. Brands: Calciparine; Liquaemin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202280.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, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee. 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 Institute10: •
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/
10
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.11 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:12 •
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
11 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). 12 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 NLM Gateway13 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.14 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “antiphospholipid syndrome” (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 3875 9 518 4 8 4414
HSTAT15 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.16 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.17 Simply search by “antiphospholipid syndrome” (or synonyms) at the following Web site: http://text.nlm.nih.gov.
13
Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.
14
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). 15 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 16 17
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 Biologists18 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.19 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.20 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.
Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •
CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.
•
Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.
18 Adapted 19
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. 20 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.
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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 antiphospholipid syndrome 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 antiphospholipid syndrome. 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 antiphospholipid syndrome. 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 “antiphospholipid syndrome”:
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Autoimmune Diseases http://www.nlm.nih.gov/medlineplus/autoimmunediseases.html Bone Marrow Diseases http://www.nlm.nih.gov/medlineplus/bonemarrowdiseases.html Hormones http://www.nlm.nih.gov/medlineplus/hormones.html Immune System and Disorders http://www.nlm.nih.gov/medlineplus/immunesystemanddisorders.html Laboratory Tests http://www.nlm.nih.gov/medlineplus/laboratorytests.html Liver Diseases http://www.nlm.nih.gov/medlineplus/liverdiseases.html Lupus http://www.nlm.nih.gov/medlineplus/lupus.html Preventing Disease and Staying Healthy http://www.nlm.nih.gov/medlineplus/preventingdiseaseandstayinghealthy.html Scleroderma http://www.nlm.nih.gov/medlineplus/scleroderma.html Sjogren's Syndrome http://www.nlm.nih.gov/medlineplus/sjogrenssyndrome.html You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the 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 antiphospholipid syndrome. 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: •
Antiphospholipid Syndrome (APL) Source: Detroit, MI: American Autoimmune Related Diseases Association, Inc. 199x. 2 p. Contact: Available from American Autoimmune Related Diseases Association, Inc. (AARDA). Michigan National Bank Building, 15475 Gratiot Avenue, Detroit, MI 48205. (313) 371-8600. Website: www.aarda.org. PRICE: Single copy free; send self-addressed, stamped envelope.
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Summary: This fact sheet for people with antiphospholipid (APL) syndrome discusses the affected population, complications, and treatment of this autoimmune syndrome. Although APL antibodies were thought to occur only in patients with lupus, it is now known that they can also constitute a primary syndrome. There is most likely a genetic predisposition , and people most at risk are those with high-titer immunoglobulin G APL antibodies. Patients with these antibodies tend to form blood clots in the legs, brain, and other parts of the body, and they may experience other cardiovascular problems as well. In addition, patients may have false positive test results for syphilis. About 33 percent of patients with lupus have APL antibodies, up to 20 percent of patients with rheumatic arthritis also have them, and 10 to 20 percent of patients with other forms of vasculitis have them as well. The goal of treatment is to prevent problems. Patients with APL antibodies are frequently told to take one baby aspirin a day as a preventive measure. Treatment may also consist of using medications such as antimalarials, blood thinners, or anticoagulants. The fact sheet explains what autoimmunity is, lists other common autoimmune diseases, and outlines the activities of the American Autoimmune Related Diseases Association. 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 antiphospholipid syndrome. 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. 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/
•
WebMDHealth: http://my.webmd.com/health_topics
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Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to antiphospholipid syndrome. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with antiphospholipid syndrome. 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 antiphospholipid syndrome. 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 “antiphospholipid syndrome” (or a synonym), and you will receive information on all relevant organizations listed in the database. Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given the option to search by keyword or by browsing the subject list. When you have received your search results, click on the name of the organization for its description and contact information. The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “antiphospholipid syndrome”. 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 “antiphospholipid syndrome” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months.
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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 “antiphospholipid syndrome” (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.21
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
21
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)22: •
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
•
California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
•
California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
•
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
•
California: Gateway Health Library (Sutter Gould Medical Foundation)
•
California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
•
California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
•
California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
•
California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
•
California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
•
California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
•
California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
•
California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
•
Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
•
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/
22
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
•
Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
•
Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm
•
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
•
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/
•
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
•
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
•
Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
•
Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
•
Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
•
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
•
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
•
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
•
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
•
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
•
New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
•
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
•
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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ANTIPHOSPHOLIPID SYNDROME DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 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] 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] Accommodation: Adjustment, especially that of the eye for various distances. [EU] Actin: Essential component of the cell skeleton. [NIH] Acute renal: A condition in which the kidneys suddenly stop working. In most cases, kidneys can recover from almost complete loss of function. [NIH] Acyl: Chemical signal used by bacteria to communicate. [NIH] Adenocarcinoma: A malignant epithelial tumor with a glandular organization. [NIH] Adipose Tissue: Connective tissue composed of fat cells lodged in the meshes of areolar tissue. [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] Adrenal insufficiency: The reduced secretion of adrenal glands. [NIH] Adsorption: The condensation of gases, liquids, or dissolved substances on the surfaces of solids. It includes adsorptive phenomena of bacteria and viruses as well as of tissues treated with exogenous drugs and chemicals. [NIH] Adsorptive: It captures volatile compounds by binding them to agents such as activated carbon or adsorptive resins. [NIH] Adverse Effect: An unwanted side effect of treatment. [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
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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 emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]
Agarose: A polysaccharide complex, free of nitrogen and prepared from agar-agar which is produced by certain seaweeds (red algae). It dissolves in warm water to form a viscid solution. [NIH] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] 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] Alkaline: Having the reactions of an alkali. [EU] Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Alopecia: Absence of hair from areas where it is normally present. [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] Alveolitis: Inflammation of an alveolus. Called also odontobothritis. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] 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] Ampulla: A sac-like enlargement of a canal or duct. [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] Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in
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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] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Androgens: A class of sex hormones associated with the development and maintenance of the secondary male sex characteristics, sperm induction, and sexual differentiation. In addition to increasing virility and libido, they also increase nitrogen and water retention and stimulate skeletal growth. [NIH] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] 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] Angioedema: A vascular reaction involving the deep dermis or subcutaneous or submucal tissues, representing localized edema caused by dilatation and increased permeability of the capillaries, and characterized by development of giant wheals. [EU] Angiogram: An x-ray of blood vessels; the person receives an injection of dye to outline the vessels on the x-ray. [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] Annealing: The spontaneous alignment of two single DNA strands to form a double helix. [NIH]
Annexins: Family of calcium- and phospholipid-binding proteins which are structurally related and exhibit immunological cross-reactivity. Each member contains four homologous 70 kD repeats. The annexins are differentially distributed in vertebrate tissues (and lower eukaryotes) and appear to be involved in membrane fusion and signal transduction. [NIH] Anterior Cerebral Artery: Artery formed by the bifurcation of the internal carotid artery. Branches of the anterior cerebral artery supply the caudate nucleus, internal capsule, putamen, septal nuclei, gyrus cinguli, and surfaces of the frontal lobe and parietal lobe. [NIH] Antiallergic: Counteracting allergy or allergic conditions. [EU] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]
Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibodies, Anticardiolipin: Antiphospholipid antibodies found in association with systemic lupus erythematosus (lupus erythematosus, systemic), antiphospholipid syndrome, and in a variety of other diseases as well as in healthy individuals. The antibodies are detected by solid-phase immunoassay employing the purified phospholipid antigen cardiolipin. [NIH] Antibodies, Antiphospholipid: Autoantibodies directed against phospholipids. These antibodies are characteristically found in patients with systemic lupus erythematosus,
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antiphospholipid syndrome, related autoimmune diseases, some non-autoimmune diseases, and also in healthy individuals. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Antibody Specificity: The property of antibodies which enables them to react with some antigenic determinants and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site. [NIH] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [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-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antiphospholipid Syndrome: The presence of antibodies directed against phospholipids (antibodies, antiphospholipid). The condition is associated with a variety of diseases, notably systemic lupus erythematosus and other connective tissue diseases, thrombopenia, and arterial or venous thromboses. In pregnancy it can cause abortion. Of the phospholipids, the cardiolipins show markedly elevated levels of anticardiolipin antibodies (antibodies, anticardiolipin). Present also are high levels of lupus anticoagulant (lupus coagulation inhibitor). [NIH] Antithrombotic: Preventing or interfering with the formation of thrombi; an agent that so acts. [EU] Anxiety: Persistent feeling of dread, apprehension, and impending disaster. [NIH] Aorta: The main trunk of the systemic arteries. [NIH] Apolipoproteins: The protein components of lipoproteins which remain after the lipids to which the proteins are bound have been removed. They play an important role in lipid transport and metabolism. [NIH] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the
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pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arteriolar: Pertaining to or resembling arterioles. [EU] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Ascites: Accumulation or retention of free fluid within the peritoneal cavity. [NIH] Aspirin: A drug that reduces pain, fever, inflammation, and blood clotting. Aspirin belongs to the family of drugs called nonsteroidal anti-inflammatory agents. It is also being studied in cancer prevention. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Asymptomatic: Having no signs or symptoms of disease. [NIH] Atopic: Pertaining to an atopen or to atopy; allergic. [EU] Atrial: Pertaining to an atrium. [EU] Atrial Fibrillation: Disorder of cardiac rhythm characterized by rapid, irregular atrial impulses and ineffective atrial contractions. [NIH] 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] 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]
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Autopsy: Postmortem examination of the body. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Barbiturate: A drug with sedative and hypnotic effects. Barbiturates have been used as sedatives and anesthetics, and they have been used to treat the convulsions associated with epilepsy. [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] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]
Beta Rays: A stream of positive or negative electrons ejected with high energy from a disintegrating atomic nucleus; most biomedically used isotopes emit negative particles (electrons or negatrons, rather than positrons). Cathode rays are low-energy negative electrons produced in cathode ray tubes, also called television tubes or oscilloscopes. [NIH] Bilateral: Affecting both the right and left side of body. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile duct: A tube through which bile passes in and out of the liver. [NIH] Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [NIH] Biliary Tract: The gallbladder and its ducts. [NIH] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biological Markers: Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc. [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] 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] Biphasic: Having two phases; having both a sporophytic and a gametophytic phase in the life cycle. [EU]
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Bladder: The organ that stores urine. [NIH] Blastocyst: The mammalian embryo in the post-morula stage in which a fluid-filled cavity, enclosed primarily by trophoblast, contains an inner cell mass which becomes the embryonic disc. [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 Coagulation Tests: Laboratory tests for evaluating the individual's clotting mechanism. [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] Body Fluids: Liquid components of living organisms. [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] Bradycardia: Excessive slowness in the action of the heart, usually with a heart rate below 60 beats per minute. [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 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] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] Bypass: A surgical procedure in which the doctor creates a new pathway for the flow of body fluids. [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] 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] 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
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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] Carcinogenic: Producing carcinoma. [EU] Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]
Cardiac: Having to do with the heart. [NIH] Cardiolipins: Acidic phospholipids composed of two molecules of phosphatidic acid covalently linked to a molecule of glycerol. They occur primarily in mitochondrial inner membranes and in bacterial plasma membranes. They are the main antigenic components of the Wassermann-type antigen that is used in nontreponemal syphilis serodiagnosis. [NIH] Cardiomyopathy: A general diagnostic term designating primary myocardial disease, often of obscure or unknown etiology. [EU] Cardiopulmonary: Having to do with the heart and lungs. [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] 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] Catalytic Domain: The region of an enzyme that interacts with its substrate to cause the enzymatic reaction. [NIH] Catheter: A flexible tube used to deliver fluids into or withdraw fluids from the body. [NIH] Cathode: An electrode, usually an incandescent filament of tungsten, which emits electrons in an X-ray tube. [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 Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Division: The fission of a cell. [NIH]
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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] 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] Central retinal artery: The blood vessel that carries blood into eye; supplies nutrition to the retina. [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] Cerebral Infarction: The formation of an area of necrosis in the cerebrum caused by an insufficiency of arterial or venous blood flow. Infarcts of the cerebrum are generally classified by hemisphere (i.e., left vs. right), lobe (e.g., frontal lobe infarction), arterial distribution (e.g., infarction, anterior cerebral artery), and etiology (e.g., embolic infarction). [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] Cervical: Relating to the neck, or to the neck of any organ or structure. Cervical lymph nodes are located in the neck; cervical cancer refers to cancer of the uterine cervix, which is the lower, narrow end (the "neck") of the uterus. [NIH] Cervix: The lower, narrow end of the uterus that forms a canal between the uterus and vagina. [NIH] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chest wall: The ribs and muscles, bones, and joints that make up the area of the body between the neck and the abdomen. [NIH] Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Cholesterol Esters: Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromosomal: Pertaining to chromosomes. [EU]
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Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic renal: Slow and progressive loss of kidney function over several years, often resulting in end-stage renal disease. People with end-stage renal disease need dialysis or transplantation to replace the work of the kidneys. [NIH] Chylomicrons: A class of lipoproteins that carry dietary cholesterol and triglycerides from the small intestines to the tissues. [NIH] Ciliary: Inflammation or infection of the glands of the margins of the eyelids. [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] 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] Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA molecules. [NIH] Clot Retraction: Retraction of a clot resulting from contraction of platelet pseudopods attached to fibrin strands that is dependent on the contractile protein thrombosthenin. Used as a measure of platelet function. [NIH] Coagulation: 1. The process of clot formation. 2. In colloid chemistry, the solidification of a sol into a gelatinous mass; an alteration of a disperse phase or of a dissolved solid which 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] 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 high content of polar groups which are responsible for its swelling properties. [NIH] Colloidal: Of the nature of a colloid. [EU] Colon: The long, coiled, tubelike organ that removes water from digested food. The remaining material, solid waste called stool, moves through the colon to the rectum and leaves the body through the anus. [NIH] Combinatorial: A cut-and-paste process that churns out thousands of potentially valuable compounds at once. [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
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classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complement Activation: The sequential activation of serum components C1 through C9, initiated by an erythrocyte-antibody complex or by microbial polysaccharides and properdin, and producing an inflammatory response. [NIH] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complete remission: The disappearance of all signs of cancer. Also called a complete response. [NIH] 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] 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,
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adipocytes, smooth muscle cells, and bone cells. [NIH] Connective Tissue Diseases: A heterogeneous group of disorders, some hereditary, others acquired, characterized by abnormal structure or function of one or more of the elements of connective tissue, i.e., collagen, elastin, or the mucopolysaccharides. [NIH] Constriction: The act of constricting. [NIH] Contraception: Use of agents, devices, methods, or procedures which diminish the likelihood of or prevent conception. [NIH] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] 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] Coronary: Encircling in the manner of a crown; a term applied to vessels; nerves, ligaments, etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Corticosteroid: Any of the steroids elaborated by the adrenal cortex (excluding the sex hormones of adrenal origin) in response to the release of corticotrophin (adrenocorticotropic hormone) by the pituitary gland, to any of the synthetic equivalents of these steroids, or to angiotensin II. They are divided, according to their predominant biological activity, into three major groups: glucocorticoids, chiefly influencing carbohydrate, fat, and protein metabolism; mineralocorticoids, affecting the regulation of electrolyte and water balance; and C19 androgens. Some corticosteroids exhibit both types of activity in varying degrees, and others exert only one type of effect. The corticosteroids are used clinically for hormonal replacement therapy, for suppression of ACTH secretion by the anterior pituitary, as antineoplastic, antiallergic, and anti-inflammatory agents, and to suppress the immune response. Called also adrenocortical hormone and corticoid. [EU] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Craniocerebral Trauma: Traumatic injuries involving the cranium and intracranial structures (i.e., brain; cranial nerves; meninges; and other structures). Injuries may be classified by whether or not the skull is penetrated (i.e., penetrating vs. nonpenetrating) or whether there is an associated hemorrhage. [NIH] Criterion: A standard by which something may be judged. [EU] 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
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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] Cystathionine beta-Synthase: A multifunctional pyridoxal phosphate enzyme. In the second stage of cysteine biosynthesis it catalyzes the reaction of homocysteine with serine to form cystathionine with the elimination of water. Deficiency of this enzyme leads to hyperhomocysteinemia and homocystinuria. EC 4.2.1.22. [NIH] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B 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] Cytotoxicity: Quality of being capable of producing a specific toxic action upon cells of special organs. [NIH] De novo: In cancer, the first occurrence of cancer in the body. [NIH] Decidua: The epithelial lining of the endometrium that is formed before the fertilized ovum reaches the uterus. The fertilized ovum embeds in the decidua. If the ovum is not fertilized, the decidua is shed during menstruation. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] 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] Denaturation: Rupture of the hydrogen bonds by heating a DNA solution and then cooling it rapidly causes the two complementary strands to separate. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Dendritic: 1. Branched like a tree. 2. Pertaining to or possessing dendrites. [EU] Dendritic cell: A special type of antigen-presenting cell (APC) that activates T lymphocytes. [NIH]
Dentate Gyrus: Gray matter situated above the gyrus hippocampi. It is composed of three layers. The molecular layer is continuous with the hippocampus in the hippocampal fissure. The granular layer consists of closely arranged spherical or oval neurons, called granule cells, whose axons pass through the polymorphic layer ending on the dendrites of pyramidal cells in the hippocampus. [NIH] Dermis: A layer of vascular connective tissue underneath the epidermis. The surface of the dermis contains sensitive papillae. Embedded in or beneath the dermis are sweat glands, hair follicles, and sebaceous glands. [NIH] Desensitization: The prevention or reduction of immediate hypersensitivity reactions by administration of graded doses of allergen; called also hyposensitization and
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immunotherapy. [EU] Diagnostic procedure: A method used to identify a disease. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Diathesis: A constitution or condition of the body which makes the tissues react in special ways to certain extrinsic stimuli and thus tends to make the person more than usually susceptible to certain diseases. [EU] 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] Dihydrotestosterone: Anabolic agent. [NIH] Dilated cardiomyopathy: Heart muscle disease that leads to enlargement of the heart's chambers, robbing the heart of its pumping ability. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Discoid: Shaped like a disk. [EU] 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] 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] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [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] Echocardiography: Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic. [NIH] Eclampsia: Onset of convulsions or coma in a previously diagnosed pre-eclamptic patient. [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] 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
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based on the results of a randomized control trial. [NIH] Elastic: Susceptible of resisting and recovering from stretching, compression or distortion applied by a force. [EU] Elastin: The protein that gives flexibility to tissues. [NIH] Electrocoagulation: Electrosurgical procedures used to treat hemorrhage (e.g., bleeding ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. [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]
Elementary Particles: Individual components of atoms, usually subatomic; subnuclear particles are usually detected only when the atomic nucleus decays and then only transiently, as most of them are unstable, often yielding pure energy without substance, i.e., radiation. [NIH] Emboli: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embolism: Blocking of a blood vessel by a blood clot or foreign matter that has been transported from a distant site by the blood stream. [NIH] Embolization: The blocking of an artery by a clot or foreign material. Embolization can be done as treatment to block the flow of blood to a tumor. [NIH] Embolus: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Embryo Transfer: Removal of a mammalian embryo from one environment and replacement in the same or a new environment. The embryo is usually in the pre-nidation phase, i.e., a blastocyst. The process includes embryo or blastocyst transplantation or transfer after in vitro fertilization and transfer of the inner cell mass of the blastocyst. It is not used for transfer of differentiated embryonic tissue, e.g., germ layer cells. [NIH] Encephalopathy: A disorder of the brain that can be caused by disease, injury, drugs, or chemicals. [NIH] Endocarditis: Exudative and proliferative inflammatory alterations of the endocardium, characterized by the presence of vegetations on the surface of the endocardium or in the endocardium itself, and most commonly involving a heart valve, but sometimes affecting the inner lining of the cardiac chambers or the endocardium elsewhere. It may occur as a primary disorder or as a complication of or in association with another disease. [EU] Endocardium: The innermost layer of the heart, comprised of endothelial cells. [NIH] Endocrine Glands: Ductless glands that secrete substances which are released directly into
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the circulation and which influence metabolism and other body functions. [NIH] Endocrine System: The system of glands that release their secretions (hormones) directly into the circulatory system. In addition to the endocrine glands, included are the chromaffin system and the neurosecretory systems. [NIH] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endoscope: A thin, lighted tube used to look at tissues inside the body. [NIH] Endoscopic: A technique where a lateral-view endoscope is passed orally to the duodenum for visualization of the ampulla of Vater. [NIH] Endoscopic retrograde cholangiopancreatography: ERCP. A procedure to x-ray the pancreatic duct, hepatic duct, common bile duct, duodenal papilla, and gallbladder. In this procedure, a thin, lighted tube (endoscope) is passed through the mouth and down into the first part of the small intestine (duodenum). A smaller tube (catheter) is then inserted through the endoscope into the bile and pancreatic ducts. A dye is injected through the catheter into the ducts, and an x-ray is taken. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endotoxins: Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells. [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] Entorhinal Cortex: Cortex where the signals are combined with those from other sensory systems. [NIH] Environmental Exposure: The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]
Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] 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] Enzyme-Linked Immunosorbent Assay: An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed. [NIH] 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]
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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] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epithelial: Refers to the cells that line the internal and external 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] 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] Esophageal: Having to do with the esophagus, the muscular tube through which food passes from the throat to the stomach. [NIH] Esophageal Varices: Stretched veins in the esophagus that occur when the liver is not working properly. If the veins burst, the bleeding can cause death. [NIH] Ethnic Groups: A group of people with a common cultural heritage that sets them apart from others in a variety of social relationships. [NIH] Excitotoxicity: Excessive exposure to glutamate or related compounds can kill brain neurons, presumably by overstimulating them. [NIH] Exocrine: Secreting outwardly, via a duct. [EU] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Exons: Coding regions of messenger RNA included in the genetic transcript which survive the processing of RNA in cell nuclei to become part of a spliced messenger of structural RNA in the cytoplasm. They include joining and diversity exons of immunoglobulin genes. [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] Extremity: A limb; an arm or leg (membrum); sometimes applied specifically to a hand or foot. [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] Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Fertilization in Vitro: Fertilization of an egg outside the body when the egg is normally fertilized in the body. [NIH]
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Fetal Blood: Blood of the fetus. Exchange of nutrients and waste between the fetal and maternal blood occurs via the placenta. The cord blood is blood contained in the umbilical vessels at the time of delivery. [NIH] Fetal Death: Death of the young developing in utero. [NIH] Fetal Distress: Adverse or threatening condition of the fetus identified by fetal bradycardia or tachycardia and passage of meconium in vertex presentation. [NIH] Fetal Growth Retardation: The failure of a fetus to attain its expected growth potential at any gestational stage. [NIH] Fetal Viability: The potential of the fetus-in-utero to survive after birth. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fever of Unknown Origin: Fever in which the etiology cannot be ascertained. [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] Fibrinolytic: Pertaining to, characterized by, or causing the dissolution of fibrin by enzymatic action [EU] Fibrinolytic Agents: Fibrinolysin or agents that convert plasminogen to fibrinolysin (plasmin). [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Fistula: Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body. [NIH] Free Radicals: Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated. [NIH] Frontal Lobe: The anterior part of the cerebral hemisphere. [NIH] Gadolinium: An element of the rare earth family of metals. It has the atomic symbol Gd, atomic number 64, and atomic weight 157.25. Its oxide is used in the control rods of some nuclear reactors. [NIH] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Ganglion: 1. A knot, or knotlike mass. 2. A general term for a group of nerve cell bodies located outside the central nervous system; occasionally applied to certain nuclear groups within the brain or spinal cord, e.g. basal ganglia. 3. A benign cystic tumour occurring on a aponeurosis or tendon, as in the wrist or dorsum of the foot; it consists of a thin fibrous capsule enclosing a clear mucinous fluid. [EU]
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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] 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 testing: Analyzing DNA to look for a genetic alteration that may indicate an increased risk for developing a specific disease or disorder. [NIH] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Gestational: Psychosis attributable to or occurring during pregnancy. [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] 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] Glomerulus: A tiny set of looping blood vessels in the nephron where blood is filtered in the kidney. [NIH] Glucocorticoids: A group of corticosteroids that affect carbohydrate metabolism (gluconeogenesis, liver glycogen deposition, elevation of blood sugar), inhibit corticotropin secretion, and possess pronounced anti-inflammatory activity. They also play a role in fat and protein metabolism, maintenance of arterial blood pressure, alteration of the connective tissue response to injury, reduction in the number of circulating lymphocytes, and functioning of the central nervous system. [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] 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] Glutamate: Excitatory neurotransmitter of the brain. [NIH] Glycerol: A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent. [NIH]
Glycerophospholipids: Derivatives of phosphatidic acid in which the hydrophobic regions are composed of two fatty acids and a polar alcohol is joined to the C-3 position of glycerol through a phosphodiester bond. They are named according to their polar head groups, such as phosphatidylcholine and phosphatidylethanolamine. [NIH]
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Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [NIH] Granuloma: A relatively small nodular inflammatory lesion containing grouped mononuclear phagocytes, caused by infectious and noninfectious agents. [NIH] Habitual: Of the nature of a habit; according to habit; established by or repeated by force of habit, customary. [EU] 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 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] 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] 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] 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]
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] Hepatic Duct, Common: Predominantly extrahepatic bile duct which is formed by the
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junction of the right and left hepatic ducts, which are predominantly intrahepatic, and, in turn, joins the cystic duct to form the common bile duct. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatitis C: A form of hepatitis, similar to type B post-transfusion hepatitis, but caused by a virus which is serologically distinct from the agents of hepatitis A, B, and E, and which may persist in the blood of chronic asymptomatic carriers. Hepatitis C is parenterally transmitted and associated with transfusions and drug abuse. [NIH] Hepatocytes: The main structural component of the liver. They are specialized epithelial cells that are organized into interconnected plates called lobules. [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] 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] Hippocampus: A curved elevation of gray matter extending the entire length of the floor of the temporal horn of the lateral ventricle (Dorland, 28th ed). The hippocampus, subiculum, and dentate gyrus constitute the hippocampal formation. Sometimes authors include the entorhinal cortex in the hippocampal formation. [NIH] Histones: Small chromosomal proteins (approx 12-20 kD) possessing an open, unfolded structure and attached to the DNA in cell nuclei by ionic linkages. Classification into the various types (designated histone I, histone II, etc.) is based on the relative amounts of arginine and lysine in each. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] 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] Horseradish Peroxidase: An enzyme isolated from horseradish which is able to act as an antigen. It is frequently used as a histochemical tracer for light and electron microscopy. Its antigenicity has permitted its use as a combined antigen and marker in experimental immunology. [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] Hydrocephalus: Excessive accumulation of cerebrospinal fluid within the cranium which may be associated with dilation of cerebral ventricles, intracranial hypertension; headache;
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lethargy; urinary incontinence; and ataxia (and in infants macrocephaly). This condition may be caused by obstruction of cerebrospinal fluid pathways due to neurologic abnormalities, intracranial hemorrhages; central nervous system infections; brain neoplasms; craniocerebral trauma; and other conditions. Impaired resorption of cerebrospinal fluid from the arachnoid villi results in a communicating form of hydrocephalus. Hydrocephalus ex-vacuo refers to ventricular dilation that occurs as a result of brain substance loss from cerebral infarction and other conditions. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hyperhomocysteinemia: An inborn error of methionone metabolism which produces an excess of homocysteine in the blood. It is often caused by a deficiency of cystathionine betasynthase and is a risk factor for coronary vascular disease. [NIH] Hyperlipidemia: An excess of lipids in the blood. [NIH] 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] Hypnotic: A drug that acts to induce sleep. [EU] Immune response: The activity of the immune system against foreign substances (antigens). [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
Immunoassay: Immunochemical assay or detection of a substance by serologic or immunologic methods. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance. [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunodiffusion: Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction. [NIH]
Immunoelectrophoresis: A technique that combines protein electrophoresis and double
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immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera. [NIH] Immunofluorescence: A technique for identifying molecules present on the surfaces of cells or in tissues using a highly fluorescent substance coupled to a specific antibody. [NIH] Immunogenic: Producing immunity; evoking an immune response. [EU] Immunoglobulins: Glycoproteins present in the blood (antibodies) and in other tissue. They are classified by structure and activity into five classes (IgA, IgD, IgE, IgG, IgM). [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] Immunosuppression: Deliberate prevention or diminution of the host's immune response. It may be nonspecific as in the administration of immunosuppressive agents (drugs or radiation) or by lymphocyte depletion or may be specific as in desensitization or the simultaneous administration of antigen and immunosuppressive drugs. [NIH] 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] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] 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] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] 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
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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]
Inferior vena cava: A large vein that empties into the heart. It carries blood from the legs and feet, and from organs in the abdomen and pelvis. [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] Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [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] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Insulin-like: Muscular growth factor. [NIH] Intensive Care: Advanced and highly specialized care provided to medical or surgical patients whose conditions are life-threatening and require comprehensive care and constant monitoring. It is usually administered in specially equipped units of a health care facility. [NIH]
International Normalized Ratio: System established by the World Health Organization and the International Committee on Thrombosis and Hemostasis for monitoring and reporting blood coagulation tests. Under this system, results are standardized using the International Sensitivity Index for the particular test reagent/instrument combination used. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] 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] Intracellular: Inside a cell. [NIH] Intracranial Hypertension: Increased pressure within the cranial vault. This may result from several conditions, including hydrocephalus; brain edema; intracranial masses; severe systemic hypertension; pseudotumor cerebri; and other disorders. [NIH] Intrathecal: Describes the fluid-filled space between the thin layers of tissue that cover the brain and spinal cord. Drugs can be injected into the fluid or a sample of the fluid can be removed for testing. [NIH] Intravascular: Within a vessel or vessels. [EU] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Introns: Non-coding, intervening sequences of DNA that are transcribed, but are removed from within the primary gene transcript and rapidly degraded during maturation of messenger RNA. Most genes in the nuclei of eukaryotes contain introns, as do mitochondrial
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and chloroplast genes. [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]
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] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Ischemic stroke: A condition in which the blood supply to part of the brain is cut off. Also called "plug-type" strokes. Blocked arteries starve areas of the brain controlling sight, speech, sensation, and movement so that these functions are partially or completely lost. Ischemic stroke is the most common type of stroke, accounting for 80 percent of all strokes. Most ischemic strokes are caused by a blood clot called a thrombus, which blocks blood flow in the arteries feeding the brain, usually the carotid artery in the neck, the major vessel bringing blood to the brain. When it becomes blocked, the risk of stroke is very high. [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] Kidney Transplantation: The transference of a kidney from one human or animal to another. [NIH] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Leg Ulcer: Ulceration of the skin and underlying structures of the lower extremity. About 90% of the cases are due to venous insufficiency (varicose ulcer), 5% to arterial disease, and the remaining 5% to other causes. [NIH] 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] Lesion: An area of abnormal tissue change. [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]
Libido: The psychic drive or energy associated with sexual instinct in the broad sense (pleasure and love-object seeking). It may also connote the psychic energy associated with instincts in general that motivate behavior. [NIH] Life cycle: The successive stages through which an organism passes from fertilized ovum or spore to the fertilized ovum or spore of the next generation. [NIH] Ligaments: Shiny, flexible bands of fibrous tissue connecting together articular extremities of bones. They are pliant, tough, and inextensile. [NIH] Ligands: A RNA simulation method developed by the MIT. [NIH] Linkages: 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] Lipid: Fat. [NIH]
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Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lipodystrophy: A collection of rare conditions resulting from defective fat metabolism and characterized by atrophy of the subcutaneous fat. They include total, congenital or acquired, partial, abdominal infantile, and localized lipodystrophy. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] Lipoprotein(a): A family of lipoprotein particles varying in density and size depending on the protein-lipid ratio and the protein composition. These particles consist of apolipoprotein B-100 covalently linked to apolipoprotein-a by one or two disulfide bonds. There is a correlation between high plasma levels of this lipoprotein and increased risk for atherosclerotic cardiovascular disease. [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] Liver Transplantation: The transference of a part of or an entire liver from one human or animal to another. [NIH] Lobe: A portion of an organ such as the liver, lung, breast, or brain. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Low-density lipoprotein: Lipoprotein that contains most of the cholesterol in the blood. LDL carries cholesterol to the tissues of the body, including the arteries. A high level of LDL increases the risk of heart disease. LDL typically contains 60 to 70 percent of the total serum cholesterol and both are directly correlated with CHD risk. [NIH] 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]
Lymphadenitis: Inflammation 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] Lymphocyte Depletion: Immunosuppression by reduction of circulating lymphocytes or by T-cell depletion of bone marrow. The former may be accomplished in vivo by thoracic duct drainage or administration of antilymphocyte serum. The latter is performed ex vivo on bone marrow before its transplantation. [NIH] Lymphocytes: White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each); those with characteristics of neither major class are called null cells. [NIH]
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Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Lysine: An essential amino acid. It is often added to animal feed. [NIH] Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques. [NIH] Magnetic Resonance Spectroscopy: Spectroscopic method of measuring the magnetic moment of elementary particles such as atomic nuclei, protons or electrons. It is employed in clinical applications such as NMR Tomography (magnetic resonance imaging). [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] 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] Meconium: The thick green-to-black mucilaginous material found in the intestines of a fullterm fetus. It consists of secretions of the intestinal glands, bile pigments, fatty acids, amniotic fluid, and intrauterine debris. It constitutes the first stools passed by a newborn. [NIH]
Mediate: Indirect; accomplished by the aid of an intervening medium. [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] Membrane: A very thin layer of tissue that covers a surface. [NIH] Membrane Fusion: The adherence of cell membranes, intracellular membranes, or artifical membrane models of either to each other or to viruses, parasites, or interstitial particles through a variety of chemical and physical processes. [NIH] Membrane Lipids: Lipids, predominantly phospholipids, cholesterol and small amounts of glycolipids found in membranes including cellular and intracellular membranes. These lipids may be arranged in bilayers in the membranes with integral proteins between the layers and peripheral proteins attached to the outside. Membrane lipids are required for active transport, several enzymatic activities and membrane formation. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Meningitis: Inflammation of the meninges. When it affects the dura mater, the disease is termed pachymeningitis; when the arachnoid and pia mater are involved, it is called leptomeningitis, or meningitis proper. [EU] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Disorders: Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function. [NIH]
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Mentors: Senior professionals who provide guidance, direction and support to those persons desirous of improvement in academic positions, administrative positions or other career development situations. [NIH] Meta-Analysis: A quantitative method of combining the results of independent studies (usually drawn from the published literature) and synthesizing summaries and conclusions which may be used to evaluate therapeutic effectiveness, plan new studies, etc., with application chiefly in the areas of research and medicine. [NIH] 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] 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] 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] Miscarriage: Spontaneous expulsion of the products of pregnancy before the middle of the second trimester. [NIH] Mitochondrial Swelling: Increase in volume of mitochondria due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria. [NIH] Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Mixed Connective Tissue Disease: A syndrome with overlapping clinical features of systemic lupus erythematosus, scleroderma, polymyositis, and Raynaud's phenomenon. The disease is differentially characterized by high serum titers of antibodies to ribonucleasesensitive extractable (saline soluble) nuclear antigen and a "speckled" epidermal nuclear staining pattern on direct immunofluorescence. [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] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] Monocyte: A type of white blood cell. [NIH] Mononuclear: A cell with one nucleus. [NIH] Motor nerve: An efferent nerve conveying an impulse that excites muscular contraction. [NIH]
Mucosa: A mucous membrane, or tunica mucosa. [EU]
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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] Myelin: The fatty substance that covers and protects nerves. [NIH] Myelitis: Inflammation of the spinal cord. Relatively common etiologies include infections; autoimmune diseases; spinal cord; and ischemia (see also spinal cord vascular diseases). Clinical features generally include weakness, sensory loss, localized pain, incontinence, and other signs of autonomic dysfunction. [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] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] 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] 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] Neonatal: Pertaining to the first four weeks after birth. [EU] Nephritis: Inflammation of the kidney; a focal or diffuse proliferative or destructive process which may involve the glomerulus, tubule, or interstitial renal tissue. [EU] Nephrosis: Descriptive histopathologic term for renal disease without an inflammatory component. [NIH] Nephrotic: Pertaining to, resembling, or caused by nephrosis. [EU] Nephrotic Syndrome: Clinical association of heavy proteinuria, hypoalbuminemia, and generalized edema. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] 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] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropathy: A problem in any part of the nervous system except the brain and spinal cord. Neuropathies can be caused by infection, toxic substances, or disease. [NIH] Neuropsychological Tests: Tests designed to assess neurological function associated with certain behaviors. They are used in diagnosing brain dysfunction or damage and central nervous system disorders or injury. [NIH]
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Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins, endorphins, and serotonin. [EU] 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] Nonmalignant: Not cancerous. [NIH] Normotensive: 1. Characterized by normal tone, tension, or pressure, as by normal blood pressure. 2. A person with normal blood pressure. [EU] 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] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Observational study: An epidemiologic study that does not involve any intervention, experimental or otherwise. Such a study may be one in which nature is allowed to take its course, with changes in one characteristic being studied in relation to changes in other characteristics. Analytical epidemiologic methods, such as case-control and cohort study designs, are properly called observational epidemiology because the investigator is observing without intervention other than to record, classify, count, and statistically analyze results. [NIH] Obstetrics: A medical-surgical specialty concerned with management and care of women during pregnancy, parturition, and the puerperium. [NIH] Ocular: 1. Of, pertaining to, or affecting the eye. 2. Eyepiece. [EU] Oculomotor: Cranial nerve III. It originate from the lower ventral surface of the midbrain and is classified as a motor nerve. [NIH] Oculomotor Nerve: The 3d cranial nerve. The oculomotor nerve sends motor fibers to the levator muscles of the eyelid and to the superior rectus, inferior rectus, and inferior oblique muscles of the eye. It also sends parasympathetic efferents (via the ciliary ganglion) to the muscles controlling pupillary constriction and accommodation. The motor fibers originate in the oculomotor nuclei of the midbrain. [NIH] Opsin: A protein formed, together with retinene, by the chemical breakdown of metarhodopsin. [NIH] Oral Health: The optimal state of the mouth and normal functioning of the organs of the mouth without evidence of disease. [NIH] 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] Osteonecrosis: Death of a bone or part of a bone, either atraumatic or posttraumatic. [NIH] Ovulation: The discharge of a secondary oocyte from a ruptured graafian follicle. [NIH]
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Ovulation Induction: Techniques for the artifical induction of ovulation. [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]
Pachymeningitis: Inflammation of the dura mater of the brain, the spinal cord or the optic nerve. [NIH] Paediatric: Of or relating to the care and medical treatment of children; belonging to or concerned with paediatrics. [EU] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Palsy: Disease of the peripheral nervous system occurring usually after many years of increased lead absorption. [NIH] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Pancreatic: Having to do with the pancreas. [NIH] Pancreatic Ducts: Ducts that collect pancreatic juice from the pancreas and supply it to the duodenum. [NIH] Pancreatic Pseudocyst: Cyst-like space not lined by epithelium and contained within the pancreas. [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] Panniculitis: General term for inflammation of adipose tissue, usually of the skin, characterized by reddened subcutaneous nodules. [NIH] Papilla: A small nipple-shaped elevation. [NIH] Partial remission: The shrinking, but not complete disappearance, of a tumor in response to therapy. Also called partial response. [NIH] Parturition: The act or process of given birth to a child. [EU] Patch: A piece of material used to cover or protect a wound, an injured part, etc.: a patch over the eye. [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] 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]
Pelvis: The lower part of the abdomen, located between the hip bones. [NIH]
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Penicillin: An antibiotic drug used to treat infection. [NIH] Peptic: Pertaining to pepsin or to digestion; related to the action of gastric juices. [EU] Peptic Ulcer: An ulceration of the mucous membrane of the esophagus, stomach or duodenum, caused by the action of the acid gastric juice. [NIH] Peptic Ulcer Hemorrhage: Bleeding from a peptic ulcer. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Perfusion: Bathing an organ or tissue with a fluid. In regional perfusion, a specific area of the body (usually an arm or a leg) receives high doses of anticancer drugs through a blood vessel. Such a procedure is performed to treat cancer that has not spread. [NIH] Pericardium: The fibroserous sac surrounding the heart and the roots of the great vessels. [NIH]
Perioperative: Around the time of surgery; usually lasts from the time of going into the hospital or doctor's office for surgery until the time the patient goes home. [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] Peritoneal Cavity: The space enclosed by the peritoneum. It is divided into two portions, the greater sac and the lesser sac or omental bursa, which lies behind the stomach. The two sacs are connected by the foramen of Winslow, or epiploic foramen. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] 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] 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] Photocoagulation: Using a special strong beam of light (laser) to seal off bleeding blood vessels such as in the eye. The laser can also burn away blood vessels that should not have grown in the eye. This is the main treatment for diabetic retinopathy. [NIH] Physicochemical: Pertaining to physics and chemistry. [EU] 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.
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[NIH]
Physiology: The science that deals with the life processes and functions of organismus, their cells, tissues, and organs. [NIH] Pigments: Any normal or abnormal coloring matter in plants, animals, or micro-organisms. [NIH]
Pilot study: The initial study examining a new method or treatment. [NIH] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [NIH] 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] Placental tissue: The tissue intervening between fetal blood and maternal blood in the placenta; it acts as a selective membrane regulating the passage of substances from the maternal to the fetal blood. [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] 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] Plasmapheresis: Procedure whereby plasma is separated and extracted from anticoagulated whole blood and the red cells retransfused to the donor. Plasmapheresis is also employed for therapeutic use. [NIH] Plasmin: A product of the lysis of plasminogen (profibrinolysin) by plasminogen activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH] Plasminogen Activators: A heterogeneous group of proteolytic enzymes that convert plasminogen to plasmin. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation. EC 3.4.21.-. [NIH] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Pneumonia: Inflammation of the lungs. [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]
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Polymerase: An enzyme which catalyses the synthesis of DNA using a single DNA strand as a template. The polymerase copies the template in the 5'-3'direction provided that sufficient quantities of free nucleotides, dATP and dTTP are present. [NIH] Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships. [NIH] Polymorphic: Occurring in several or many forms; appearing in different forms at different stages of development. [EU] 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] Pons: The part of the central nervous system lying between the medulla oblongata and the mesencephalon, ventral to the cerebellum, and consisting of a pars dorsalis and a pars ventralis. [NIH] Portal System: A system of vessels in which blood, after passing through one capillary bed, is conveyed through a second set of capillaries before it returns to the systemic circulation. It pertains especially to the hepatic portal system. [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] Postnatal: Occurring after birth, with reference to the newborn. [EU] 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] 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] Pre-Eclampsia: Development of hypertension with proteinuria, edema, or both, due to pregnancy or the influence of a recent pregnancy. It occurs after the 20th week of gestation, but it may develop before this time in the presence of trophoblastic disease. [NIH] Pregnancy Complications: The co-occurrence of pregnancy and a disease. The disease may precede or follow conception and it may or may not have a deleterious effect on the pregnant woman or fetus. [NIH]
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Pregnancy Outcome: Results of conception and ensuing pregnancy, including live birth, stillbirth, spontaneous abortion, induced abortion. The outcome may follow natural or artificial insemination or any of the various reproduction techniques, such as embryo transfer or fertilization in vitro. [NIH] Pregnancy, High-Risk: Pregnancy in which the mother and/or fetus are at greater than normal risk of morbidity or mortality. Causes include lack of adequate prenatal care, previous obstetrical history, pre-existing maternal disease or pregnancy-induced disease, and multiple gestation, as well as advanced maternal age. [NIH] Prenatal: Existing or occurring before birth, with reference to the fetus. [EU] Prenatal Care: Care provided the pregnant woman in order to prevent complications, and decrease the incidence of maternal and prenatal mortality. [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] Primary tumor: The original tumor. [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] Prognostic factor: A situation or condition, or a characteristic of a patient, that can be used to estimate the chance of recovery from a disease, or the chance of the disease recurring (coming back). [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Prone: Having the front portion of the body downwards. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Prostaglandin: Any of a group of components derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway that are extremely potent mediators of a diverse group of physiologic processes. The abbreviation for prostaglandin is PG; specific compounds are designated by adding one of the letters A through I to indicate the type of substituents found on the hydrocarbon skeleton and a subscript (1, 2 or 3) to indicate the number of double bonds in the hydrocarbon skeleton e.g., PGE2. The predominant naturally occurring prostaglandins all have two double bonds and are synthesized from arachidonic acid (5,8,11,14-eicosatetraenoic acid) by the pathway shown in the illustration. The 1 series and 3 series are produced by the same pathway with fatty acids having one fewer double bond (8,11,14-eicosatrienoic acid or one more double bond (5,8,11,14,17-eicosapentaenoic acid) than arachidonic acid. The subscript a or ß indicates the configuration at C-9 (a denotes a substituent below the plane of the ring, ß, above the plane). The naturally occurring PGF's have the a configuration, e.g., PGF2a. All of the prostaglandins act by binding to specific cell-surface receptors causing an increase in the level of the intracellular second messenger cyclic AMP (and in some cases cyclic GMP also). The effect produced by the cyclic AMP increase depends on the specific cell type. In some cases there is also a positive feedback effect. Increased cyclic AMP increases prostaglandin synthesis leading to further increases in cyclic AMP. [EU] Prostaglandins
A:
(13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic
acid
(PGA(1));
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(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] 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] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [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] Prothrombin: A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia. [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] Pseudotumor Cerebri: A condition marked by raised intracranial pressure and characterized clinically by headaches; nausea; papilledema, peripheral constriction of the visual fields, transient visual obscurations, and pulsatile tinnitus. Obesity is frequently associated with this condition, which primarily affects women between 20 and 44 years of age. Chronic papilledema may lead to optic nerve injury (optic nerve diseases) and visual loss (blindness). [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] 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
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described in psychotic patients, although many patients with the disorder are not judged psychotic. [EU] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] 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]
Puerperium: Period from delivery of the placenta until return of the reproductive organs to their normal nonpregnant morphologic state. In humans, the puerperium generally lasts for six to eight weeks. [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] Pulmonary Embolism: Embolism in the pulmonary artery or one of its branches. [NIH] Pulmonary hypertension: Abnormally high blood pressure in the arteries of the lungs. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Purpura: Purplish or brownish red discoloration, easily visible through the epidermis, caused by hemorrhage into the tissues. [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] 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] 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] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Randomized clinical trial: A study in which the participants are assigned by chance to separate groups that compare different treatments; neither the researchers nor the participants can choose which group. Using chance to assign people to groups means that the groups will be similar and that the treatments they receive can be compared objectively. At the time of the trial, it is not known which treatment is best. It is the patient's choice to be in a randomized trial. [NIH] 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
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function. [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] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [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 Artery: A branch of the abdominal aorta which supplies the kidneys, adrenal glands and ureters. [NIH] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [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] 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 Artery: Central retinal artery and its branches. It arises from the ophthalmic artery, pierces the optic nerve and runs through its center, enters the eye through the porus opticus and branches to supply the retina. [NIH] Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous membranes. Retinol is being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Retinopathy: 1. Retinitis (= inflammation of the retina). 2. Retinosis (= degenerative, noninflammatory condition of the retina). [EU] Retrograde: 1. Moving backward or against the usual direction of flow. 2. Degenerating, deteriorating, or catabolic. [EU]
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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] Rheumatic Diseases: Disorders of connective tissue, especially the joints and related structures, characterized by inflammation, degeneration, or metabolic derangement. [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] Rhodopsin: A photoreceptor protein found in retinal rods. It is a complex formed by the binding of retinal, the oxidized form of retinol, to the protein opsin and undergoes a series of complex reactions in response to visible light resulting in the transmission of nerve impulses to the brain. [NIH] Ribonuclease: RNA-digesting enzyme. [NIH] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Rods: One type of specialized light-sensitive cells (photoreceptors) in the retina that provide side vision and the ability to see objects in dim light (night vision). [NIH] Saline: A solution of salt and water. [NIH] 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] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve. [NIH] Sclerotherapy: Treatment of varicose veins, hemorrhoids, gastric and esophageal varices, and peptic ulcer hemorrhage by injection or infusion of chemical agents which cause localized thrombosis and eventual fibrosis and obliteration of the vessels. [NIH] Screening: Checking for disease when there are no symptoms. [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] Segmental: Describing or pertaining to a structure which is repeated in similar form in successive segments of an organism, or which is undergoing segmentation. [NIH] Segmentation: The process by which muscles in the intestines move food and wastes through the body. [NIH] Sensory loss: A disease of the nerves whereby the myelin or insulating sheath of myelin on the nerves does not stay intact and the messages from the brain to the muscles through the nerves are not carried properly. [NIH] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [NIH] Serologic: Analysis of a person's serum, especially specific immune or lytic serums. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Serum Albumin: A major plasma protein that serves in maintaining the plasma colloidal osmotic pressure and transporting large organic anions. [NIH]
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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] 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] 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] 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] Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH]
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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] Spinal Cord Vascular Diseases: Hypoxic-ischemic and hemorrhagic disorders of the spinal cord. Arteriosclerosis, emboli, and vascular malformations are potential causes of these conditions. [NIH] Spirochete: Lyme disease. [NIH] Spontaneous Abortion: The non-induced birth of an embryo or of fetus prior to the stage of viability at about 20 weeks of gestation. [NIH] Stenosis: Narrowing or stricture of a duct or canal. [EU] 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] Steroids: Drugs used to relieve swelling and inflammation. [NIH] Stillbirth: The birth of a dead fetus or baby. [NIH] Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU]
Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] 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] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [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] Stricture: The abnormal narrowing of a body opening. Also called stenosis. [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] 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] Subiculum: A region of the hippocampus that projects to other areas of the brain. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substrate: A substance upon which an enzyme acts. [EU]
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Supplementation: Adding nutrients to the diet. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [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]
Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Syphilis: A contagious venereal disease caused by the spirochete Treponema pallidum. [NIH]
Systemic: Affecting the entire 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] Systolic blood pressure: The maximum pressure in the artery produced as the heart contracts and blood begins to flow. [NIH] Tachycardia: Excessive rapidity in the action of the heart, usually with a heart rate above 100 beats per minute. [NIH] Telangiectasia: The permanent enlargement of blood vessels, causing redness in the skin or mucous membranes. [NIH] Temporal: One of the two irregular bones forming part of the lateral surfaces and base of the skull, and containing the organs of hearing. [NIH] Testosterone: A hormone that promotes the development and maintenance of male sex characteristics. [NIH] Thalidomide: A pharmaceutical agent originally introduced as a non-barbiturate hypnotic, but withdrawn from the market because of its known tetratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppresive and anti-angiogenic activity. It inhibits release of tumor necrosis factor alpha from monocytes, and modulates other cytokine action. [NIH] Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thermal: Pertaining to or characterized by heat. [EU] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] Thrombocytes: Blood cells that help prevent bleeding by causing blood clots to form. Also called platelets. [NIH] Thrombocytopenia: A decrease in the number of blood platelets. [NIH] Thromboembolism: Obstruction of a vessel by a blood clot that has been transported from a distant site by the blood stream. [NIH] Thrombolytic: 1. Dissolving or splitting up a thrombus. 2. A thrombolytic agent. [EU]
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Thrombolytic Therapy: Use of infusions of fibrinolytic agents to destroy or dissolve thrombi in blood vessels or bypass grafts. [NIH] 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]
Thrombopenia: Reduction in the number of platelets in the blood. [NIH] Thrombophilia: A disorder of hemostasis in which there is a tendency for the occurrence of thrombosis. [NIH] Thrombophlebitis: Inflammation of a vein associated with thrombus formation. [NIH] Thromboses: The formation or presence of a blood clot within a blood vessel during life. [NIH]
Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tone: 1. The normal degree of vigour and tension; in muscle, the resistance to passive elongation or stretch; tonus. 2. A particular quality of sound or of voice. 3. To make permanent, or to change, the colour of silver stain by chemical treatment, usually with a heavy metal. [EU] Torsion: A twisting or rotation of a bodily part or member on its axis. [NIH] Toxaemia: 1. The condition resulting from the spread of bacterial products (toxins) by the bloodstream. 2. A condition resulting from metabolic disturbances, e.g. toxaemia of pregnancy. [EU] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] 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] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transfusion: The infusion of components of blood or whole blood into the bloodstream. The blood may be donated from another person, or it may have been taken from the person earlier and stored until needed. [NIH] 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]
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Triglyceride: A lipid carried through the blood stream to tissues. Most of the body's fat tissue is in the form of triglycerides, stored for use as energy. Triglycerides are obtained primarily from fat in foods. [NIH] Tropomyosin: A protein found in the thin filaments of muscle fibers. It inhibits contraction of the muscle unless its position is modified by troponin. [NIH] Troponin: One of the minor protein components of skeletal muscle. Its function is to serve as the calcium-binding component in the troponin-tropomyosin B-actin-myosin complex by conferring calcium sensitivity to the cross-linked actin and myosin filaments. [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] 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] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [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]
Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [NIH] Ureters: Tubes that carry urine from the kidneys to the bladder. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [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] 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] Vaccines: Suspensions of killed or attenuated microorganisms (bacteria, viruses, fungi, protozoa, or rickettsiae), antigenic proteins derived from them, or synthetic constructs, administered for the prevention, amelioration, or treatment of infectious and other diseases. [NIH]
Valine: A branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway. [NIH]
Varicose: The common ulcer in the lower third of the leg or near the ankle. [NIH]
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Varicose Ulcer: Ulcer due to varicose veins. Chronic venous insufficiency in the deep veins of the legs leads to shunting the venous return into the superficial veins, in which pressure and flow rate, as well as oxygen content, are increased. [NIH] Varicose vein: An abnormal swelling and tortuosity especially of the superficial veins of the legs. [EU] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasculitis: Inflammation of a blood vessel. [NIH] VE: The total volume of gas either inspired or expired in one minute. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Vena: A vessel conducting blood from the capillary bed to the heart. [NIH] Venereal: Pertaining or related to or transmitted by sexual contact. [EU] Venom: That produced by the poison glands of the mouth and injected by the fangs of poisonous snakes. [NIH] Venous: Of or pertaining to the veins. [EU] Venous blood: Blood that has given up its oxygen to the tissues and carries carbon dioxide back for gas exchange. [NIH] Venous Thrombosis: The formation or presence of a thrombus within a vein. [NIH] 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] 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] 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] 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] Warfarin: An anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent coagulation factors. Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, pulmonary embolism, and atrial fibrillation with embolization. It is also used as an adjunct in the prophylaxis of systemic embolism after myocardial infarction. Warfarin is also used as a rodenticide. [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.
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[NIH]
Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH]
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INDEX A Abdomen, 111, 117, 119, 127, 134, 136, 141, 142, 151 Abdominal, 3, 48, 111, 136, 141, 142, 148 Abdominal Pain, 3, 111 Acceptor, 111, 136, 141 Accommodation, 111, 140 Actin, 111, 139, 154 Acute renal, 111, 130 Acyl, 71, 111 Adenocarcinoma, 56, 111 Adipose Tissue, 111, 141 Adrenal Cortex, 111, 122 Adrenal Glands, 111, 148 Adrenal insufficiency, 28, 111 Adsorption, 31, 111 Adsorptive, 111 Adverse Effect, 111, 150 Affinity, 6, 17, 111, 112 Agar, 112, 132 Agarose, 112, 132, 133 Agonist, 11, 112 Albumin, 112, 143 Algorithms, 112, 116 Alkaline, 112, 117 Alleles, 39, 112 Alopecia, 112, 123 Alternative medicine, 84, 112 Alveolitis, 36, 112 Amino Acid Sequence, 75, 112, 113 Amino Acids, 112, 142, 144, 146, 154 Ampulla, 112, 126 Anaesthesia, 112, 133 Anaphylatoxins, 112, 121 Anatomical, 113, 115, 133, 149 Androgens, 39, 111, 113, 122 Anemia, 43, 113 Anesthesia, 49, 113 Angioedema, 81, 113 Angiogram, 49, 113 Anionic, 8, 16, 17, 34, 113 Anions, 112, 113, 135, 149 Annealing, 113, 144 Annexins, 17, 113 Anterior Cerebral Artery, 113, 119 Antiallergic, 113, 122 Antibacterial, 113, 151 Antibiotic, 113, 142, 151
Antibodies, Anticardiolipin, 113, 114 Antibodies, Antiphospholipid, 113, 114 Antibody Specificity, 8, 114 Anticoagulant, 4, 5, 6, 7, 13, 16, 22, 30, 34, 44, 71, 75, 85, 114, 146, 155 Antigen, 13, 78, 111, 113, 114, 118, 121, 123, 126, 131, 132, 133, 138, 147 Antigen-Antibody Complex, 114, 121 Antigen-presenting cell, 78, 114, 123 Anti-inflammatory, 6, 34, 114, 115, 122, 129 Anti-Inflammatory Agents, 114, 115, 122 Antineoplastic, 114, 122, 123 Antioxidant, 6, 114 Antithrombotic, 78, 114 Anxiety, 14, 114 Aorta, 114, 148, 155 Apolipoproteins, 114, 136 Apoptosis, 8, 114 Arachidonic Acid, 115, 145 Arginine, 112, 115, 131 Arterial, 4, 5, 8, 12, 17, 20, 76, 78, 114, 115, 119, 129, 132, 135, 146, 152 Arteries, 49, 114, 115, 117, 122, 135, 136, 139, 143, 147 Arteriolar, 66, 115, 117 Arterioles, 115, 117 Artery, 27, 42, 60, 113, 115, 122, 125, 135, 147, 148, 152 Ascites, 3, 115 Aspirin, 31, 39, 46, 66, 85, 99, 115 Assay, 4, 75, 76, 115, 132, 147 Asymptomatic, 35, 115, 131, 141 Atopic, 81, 115 Atrial, 44, 115, 155 Atrial Fibrillation, 115, 155 Atrium, 115, 155 Atrophy, 115, 136 Autoantibodies, 5, 7, 8, 12, 13, 22, 39, 54, 58, 61, 74, 113, 115 Autoantigens, 115 Autodigestion, 115, 141 Autoimmune disease, 5, 10, 12, 74, 78, 81, 99, 114, 115, 139 Autoimmunity, 20, 22, 30, 34, 39, 44, 46, 52, 54, 59, 63, 71, 99, 115 Autopsy, 51, 116
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B Bacteria, 74, 111, 113, 114, 116, 125, 138, 151, 154 Bacterium, 116, 130 Barbiturate, 116, 152 Base, 116, 135, 152, 154 Benign, 22, 116, 128, 130 Beta Rays, 116, 125 Bilateral, 20, 23, 28, 116 Bile, 116, 126, 128, 130, 131, 136, 137 Bile duct, 116, 126, 130 Biliary, 116, 141 Biliary Tract, 116, 141 Biochemical, 12, 74, 112, 116 Biological Markers, 63, 116 Biomarkers, 9, 116 Biotechnology, 18, 19, 84, 93, 116 Biphasic, 78, 116 Bladder, 117, 133, 146, 154 Blastocyst, 117, 121, 125, 143 Blood Coagulation, 8, 17, 27, 38, 40, 42, 75, 117, 134, 153 Blood Coagulation Factors, 117 Blood Coagulation Tests, 117, 134 Blood Platelets, 117, 152 Blood pressure, 117, 118, 129, 132, 140, 147 Blood vessel, 113, 117, 118, 119, 125, 126, 129, 130, 135, 142, 151, 152, 153, 155 Body Fluids, 116, 117, 124, 154 Bowel, 26, 59, 117, 134 Bradycardia, 117, 128 Bradykinin, 117, 143 Brain Stem, 82, 117 Buccal, 117, 136 Bypass, 117, 153 C Calcium, 17, 69, 113, 117, 121, 146, 150, 154 Capillary, 117, 144, 155 Carbohydrate, 117, 122, 129, 144 Carbon Dioxide, 118, 143, 155 Carcinogenic, 118, 134 Carcinoma, 76, 118 Cardiac, 25, 33, 44, 115, 118, 125, 139 Cardiolipins, 114, 118 Cardiomyopathy, 118 Cardiopulmonary, 16, 118 Cardiovascular, 5, 13, 14, 28, 43, 66, 99, 118, 136 Cardiovascular disease, 118, 136 Carotene, 118, 148 Carrier Proteins, 118, 143, 147
Case report, 23, 27, 33, 35, 38, 39, 49, 54, 118 Catalytic Domain, 20, 118 Catheter, 118, 126 Cathode, 116, 118, 125 Cell Adhesion, 11, 52, 118 Cell Adhesion Molecules, 52, 118 Cell Death, 114, 118, 139 Cell Division, 116, 118, 138, 143 Cell membrane, 118, 119, 137, 142 Central Nervous System, 119, 128, 129, 130, 132, 139, 144 Central Nervous System Infections, 119, 130, 132 Central retinal artery, 28, 119, 148 Cerebral, 35, 66, 71, 76, 113, 117, 119, 122, 128, 131 Cerebral hemispheres, 117, 119 Cerebral Infarction, 35, 119, 132 Cerebrovascular, 45, 56, 118, 119 Cerebrum, 119 Cervical, 82, 119 Cervix, 119 Chemotactic Factors, 119, 121 Chest wall, 58, 119 Cholesterol, 4, 10, 116, 119, 120, 122, 136, 137 Cholesterol Esters, 119, 136 Chromatin, 115, 119, 136 Chromosomal, 119, 131 Chronic, 3, 27, 48, 120, 126, 131, 133, 135, 141, 146, 149, 151, 152, 154, 155 Chronic renal, 48, 120, 154 Chylomicrons, 120, 136 Ciliary, 120, 140 CIS, 120, 148 Clinical trial, 5, 11, 93, 120, 147 Cloning, 116, 120 Clot Retraction, 120, 143 Coagulation, 6, 8, 12, 13, 16, 17, 18, 30, 36, 76, 77, 78, 114, 117, 120, 130, 143, 155 Cofactor, 7, 23, 120, 146, 153 Colitis, 26, 120 Collagen, 32, 120, 122, 145 Colloidal, 112, 120, 125, 149 Colon, 120 Combinatorial, 18, 120 Complement, 15, 24, 37, 59, 113, 120, 121, 143 Complement Activation, 15, 113, 121 Complementary and alternative medicine, 69, 72, 121
159
Complementary medicine, 69, 121 Complete remission, 121, 148 Computational Biology, 93, 121 Conception, 121, 122, 128, 144, 145, 151 Concomitant, 4, 71, 121 Cones, 121, 148 Congestion, 121, 127, 136 Connective Tissue, 82, 114, 120, 121, 122, 123, 128, 129, 136, 142, 149, 152 Connective Tissue Cells, 121 Connective Tissue Diseases, 82, 114, 122 Constriction, 122, 135, 140, 146 Contraception, 39, 122 Contraindications, ii, 122 Convulsions, 116, 122, 124, 144 Coronary, 5, 10, 33, 49, 76, 118, 122, 132, 139 Coronary heart disease, 5, 118, 122 Coronary Thrombosis, 122, 139 Cortex, 122, 126 Cortical, 56, 122 Corticosteroid, 9, 122 Cranial, 27, 82, 122, 130, 134, 140, 142 Craniocerebral Trauma, 122, 130, 132 Criterion, 16, 122 Curative, 122, 152 Cutaneous, 4, 19, 45, 63, 66, 70, 122, 136 Cyclic, 122, 145 Cyclophosphamide, 11, 123 Cystathionine beta-Synthase, 123, 132 Cytokine, 15, 51, 123, 152 Cytoplasm, 115, 119, 123, 126, 127, 130, 136 Cytoskeleton, 11, 123 Cytotoxicity, 10, 123 D De novo, 11, 123 Decidua, 123, 143 Degenerative, 123, 131, 148 Deletion, 115, 123 Delusions, 123, 146 Denaturation, 123, 144 Dendrites, 123, 139 Dendritic, 11, 123 Dendritic cell, 11, 123 Dentate Gyrus, 123, 131 Dermis, 113, 123 Desensitization, 123, 133 Diagnostic procedure, 73, 84, 124 Diastolic, 124, 132 Diathesis, 8, 124 Diffusion, 124, 132, 134
Digestion, 116, 117, 124, 134, 136, 142, 151 Dihydrotestosterone, 124, 148 Dilated cardiomyopathy, 21, 124 Direct, iii, 18, 87, 124, 138, 148 Discoid, 21, 82, 124 Dissection, 27, 124 Dissociation, 111, 124 Dorsal, 124, 127, 144 Drug Interactions, 88, 124 Duct, 112, 124, 126, 127, 131, 136, 151 Duodenum, 116, 124, 126, 141, 142, 151 Dura mater, 124, 137, 141 E Echocardiography, 16, 33, 48, 56, 124 Eclampsia, 124, 144 Edema, 113, 124, 134, 139, 144, 154 Effector, 11, 78, 120, 124 Efficacy, 16, 124 Elastic, 125, 152 Elastin, 120, 122, 125 Electrocoagulation, 120, 125 Electrolyte, 122, 125, 138, 154 Electrons, 76, 114, 116, 118, 125, 135, 137, 141, 147 Electrophoresis, 125, 132 Elementary Particles, 125, 137, 146 Emboli, 71, 125, 151, 155 Embolism, 125, 147, 155 Embolization, 125, 155 Embolus, 125, 133 Embryo, 117, 125, 133, 145, 151 Embryo Transfer, 125, 145 Encephalopathy, 36, 125 Endocarditis, 44, 52, 125 Endocardium, 125 Endocrine Glands, 125, 126 Endocrine System, 126, 139 Endogenous, 18, 115, 117, 126 Endoscope, 126 Endoscopic, 4, 126 Endoscopic retrograde cholangiopancreatography, 4, 126 Endothelial cell, 11, 19, 30, 45, 125, 126, 153 Endotoxins, 121, 126 End-stage renal, 120, 126 Entorhinal Cortex, 126, 131 Environmental Exposure, 116, 126 Environmental Health, 92, 94, 126 Enzymatic, 117, 118, 121, 126, 128, 137, 144, 148
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Antiphospholipid Syndrome
Enzyme, 4, 10, 16, 74, 75, 116, 118, 123, 124, 126, 131, 143, 144, 146, 148, 149, 150, 151, 152, 155 Enzyme Inhibitors, 126, 143 Enzyme-Linked Immunosorbent Assay, 75, 126 Epidemiologic Studies, 116, 126 Epidemiological, 27, 127 Epidermal, 127, 138 Epidermis, 123, 127, 147 Epigastric, 127, 141 Epithelial, 111, 123, 127, 131 Epithelium, 127, 141 Erythema, 47, 127 Erythema Multiforme, 47, 127 Erythrocytes, 113, 127, 148 Esophageal, 127, 149 Esophageal Varices, 127, 149 Ethnic Groups, 39, 127 Excitotoxicity, 10, 127 Exocrine, 127, 141 Exogenous, 74, 111, 126, 127 Exons, 5, 127 Extracellular, 17, 121, 127 Extracellular Matrix, 121, 127 Extremity, 127, 135 F Family Planning, 28, 93, 127 Fat, 111, 115, 118, 122, 125, 127, 129, 135, 136, 152, 154 Fatty acids, 112, 127, 129, 137, 145 Fertilization in Vitro, 127, 145 Fetal Blood, 128, 143 Fetal Death, 6, 128 Fetal Distress, 17, 128 Fetal Growth Retardation, 19, 128 Fetal Viability, 17, 128 Fetus, 48, 128, 137, 143, 144, 145, 151, 154 Fever of Unknown Origin, 55, 128 Fibrin, 12, 42, 43, 117, 120, 128, 143, 152 Fibrinogen, 77, 128, 143, 152 Fibrinolysis, 6, 27, 32, 38, 40, 42, 128 Fibrinolytic, 12, 36, 58, 128, 153 Fibrinolytic Agents, 128, 153 Fibrosis, 128, 149 Fistula, 3, 128 Free Radicals, 76, 114, 124, 128 Frontal Lobe, 113, 119, 128 G Gadolinium, 29, 128 Gallbladder, 111, 116, 126, 128 Ganglia, 128, 139, 142
Ganglion, 128, 140 Gas, 118, 124, 129, 132, 140, 155 Gastric, 115, 129, 142, 149 Gene, 5, 15, 34, 61, 112, 116, 129, 134 Gene Expression, 15, 129 Genetic testing, 129, 144 Genotype, 61, 129, 142 Gestation, 129, 143, 144, 145, 151 Gestational, 128, 129 Gland, 111, 129, 136, 141, 143, 146, 149, 151, 153 Glomerular, 129, 148 Glomeruli, 129 Glomerulonephritis, 48, 129 Glomerulus, 129, 139 Glucocorticoids, 111, 122, 129 Glucose, 4, 129, 130, 134 Glucuronic Acid, 129, 130 Glutamate, 10, 127, 129 Glycerol, 118, 129, 142 Glycerophospholipids, 129, 142 Governing Board, 130, 144 Granulocytes, 130, 135, 150, 155 Granuloma, 82, 130 H Habitual, 78, 130 Haptens, 111, 130, 147 Headache, 38, 130, 131 Headache Disorders, 130 Hemoglobin, 113, 127, 130 Hemolytic, 43, 130 Hemorrhage, 23, 28, 30, 38, 47, 62, 122, 125, 130, 147, 151 Hemorrhoids, 130, 149 Hemostasis, 12, 13, 43, 45, 61, 130, 134, 153 Heparin, 36, 38, 46, 61, 70, 77, 78, 88, 130 Hepatic, 38, 112, 126, 130, 144 Hepatic Duct, Common, 126, 130 Hepatitis, 27, 66, 71, 131 Hepatitis C, 66, 131 Hepatocytes, 131 Hereditary, 38, 81, 122, 131 Heredity, 129, 131 Heterogeneity, 8, 111, 131 Heterogenic, 131 Heterogenous, 12, 131 Hippocampus, 10, 123, 131, 151 Histones, 32, 119, 131 Homeostasis, 17, 131 Homologous, 112, 113, 131 Hormonal, 39, 115, 122, 131
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Hormone, 116, 122, 131, 134, 149, 150, 152, 153 Horseradish Peroxidase, 126, 131 Humoral, 74, 131 Humour, 131 Hydrocephalus, 131, 134 Hydrogen, 111, 116, 117, 123, 132, 136, 138, 141, 146 Hydrogen Peroxide, 132, 136 Hydrolysis, 132, 144, 146 Hydrophobic, 129, 132, 136 Hydroxylysine, 120, 132 Hydroxyproline, 120, 132 Hyperhomocysteinemia, 40, 57, 66, 123, 132 Hyperlipidemia, 4, 132 Hypersensitivity, 81, 123, 132, 149 Hypertension, 4, 40, 50, 118, 132, 134, 144, 154 Hypnotic, 116, 132, 152 I Immune response, 5, 8, 41, 74, 114, 115, 122, 130, 132, 133, 155 Immune system, 8, 76, 114, 115, 132, 133, 155 Immunity, 74, 132, 133 Immunoassay, 74, 113, 126, 132 Immunodeficiency, 40, 132 Immunodiffusion, 74, 112, 132, 133 Immunoelectrophoresis, 74, 112, 132 Immunofluorescence, 133, 138 Immunogenic, 6, 133, 147 Immunoglobulins, 75, 133, 143 Immunologic, 11, 25, 119, 132, 133 Immunology, 25, 33, 39, 41, 60, 111, 131, 133 Immunosuppression, 27, 70, 133, 136 Immunosuppressive, 10, 34, 56, 123, 133 Immunosuppressive Agents, 133 Immunosuppressive therapy, 56, 133 Impairment, 17, 133, 137, 146 In situ, 85, 133 In vitro, 5, 6, 8, 11, 13, 17, 18, 32, 125, 133, 144 In vivo, 6, 9, 11, 15, 17, 130, 133, 136 Incontinence, 132, 133, 139 Induction, 8, 22, 23, 74, 113, 133, 141 Infantile, 133, 136 Infarction, 23, 59, 66, 119, 133, 143 Infection, 27, 28, 40, 71, 119, 120, 132, 133, 135, 136, 139, 142, 149, 151, 155 Inferior vena cava, 66, 134
Infiltration, 129, 134 Infusion, 17, 134, 149, 153 Initiation, 10, 134 Insulin, 45, 134 Insulin-dependent diabetes mellitus, 134 Insulin-like, 45, 134 Intensive Care, 26, 134 International Normalized Ratio, 24, 134 Interstitial, 134, 137, 139, 148 Intestine, 117, 134, 150 Intracellular, 11, 133, 134, 137, 145, 150 Intracranial Hypertension, 22, 130, 131, 134 Intrathecal, 51, 134 Intravascular, 76, 78, 134 Intravenous, 52, 61, 134 Intrinsic, 14, 58, 112, 134 Introns, 5, 134 Invasive, 132, 135, 137 Ions, 116, 124, 125, 132, 135, 138, 146 Ischemia, 49, 115, 135, 139 Ischemic stroke, 46, 69, 135 K Kb, 92, 135 Kidney Transplantation, 57, 135 L Labile, 120, 135 Latent, 135, 144 Leg Ulcer, 55, 135 Leprosy, 30, 135 Lesion, 130, 135, 154 Leucocyte, 42, 135 Libido, 113, 135 Life cycle, 116, 135 Ligaments, 122, 135 Ligands, 118, 135 Linkages, 130, 131, 135 Lipid, 6, 114, 129, 134, 135, 136, 154 Lipid Peroxidation, 6, 136 Lipodystrophy, 22, 136 Lipoprotein, 28, 32, 78, 136 Lipoprotein(a), 32, 136 Livedo, 4, 45, 136 Liver, 18, 25, 37, 98, 111, 112, 115, 116, 123, 127, 128, 129, 130, 131, 136 Liver Transplantation, 25, 37, 136 Lobe, 113, 119, 136 Localized, 45, 113, 133, 136, 139, 143, 149, 154 Low-density lipoprotein, 5, 54, 136 Lymph, 119, 126, 131, 136 Lymph node, 119, 136
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Antiphospholipid Syndrome
Lymphadenitis, 39, 136 Lymphatic, 134, 136 Lymphocyte Depletion, 133, 136 Lymphocytes, 114, 123, 129, 135, 136, 137, 155 Lymphoid, 113, 135, 136, 137 Lymphoma, 55, 71, 76, 137 Lysine, 131, 132, 137 M Magnetic Resonance Imaging, 9, 66, 137 Magnetic Resonance Spectroscopy, 10, 137 Malignant, 111, 114, 137 Manic, 137, 146 Manic-depressive psychosis, 137, 146 Meconium, 128, 137 Mediate, 118, 137 Medical Records, 137, 149 MEDLINE, 93, 137 Membrane, 7, 11, 16, 17, 113, 119, 121, 127, 137, 138, 140, 142, 143, 148, 150 Membrane Fusion, 113, 137 Membrane Lipids, 137, 142 Memory, 38, 137 Meninges, 119, 122, 124, 137 Meningitis, 44, 137 Mental, iv, 4, 92, 94, 124, 137, 146, 154 Mental Disorders, 137, 146 Mentors, 12, 138 Meta-Analysis, 39, 57, 138 Metastasis, 118, 138 Microorganism, 120, 138, 155 Mineralocorticoids, 111, 122, 138 Miscarriage, 70, 138 Mitochondrial Swelling, 138, 139 Mitosis, 115, 138 Mixed Connective Tissue Disease, 74, 138 Modification, 138, 147 Molecular, 7, 11, 13, 17, 46, 49, 93, 95, 114, 116, 121, 123, 128, 130, 138, 143, 154 Molecular Structure, 114, 138 Molecule, 11, 114, 116, 118, 121, 124, 132, 138, 141, 148, 150 Monoclonal, 6, 18, 19, 23, 32, 33, 58, 138 Monocyte, 9, 138 Mononuclear, 130, 138, 154 Motor nerve, 138, 140 Mucosa, 136, 138 Mutagenesis, 5, 139 Mutagens, 139 Myelin, 139, 149 Myelitis, 82, 139
Myocardial infarction, 6, 18, 49, 69, 76, 122, 139, 155 Myocardium, 139 Myosin, 139, 154 N Necrosis, 45, 63, 66, 115, 119, 133, 139 Neonatal, 48, 50, 139 Nephritis, 11, 139 Nephrosis, 139 Nephrotic, 66, 139 Nephrotic Syndrome, 66, 139 Nervous System, 14, 82, 119, 139, 142 Neural, 77, 131, 139 Neuroendocrine, 51, 139 Neuronal, 10, 51, 139, 142 Neurons, 123, 127, 128, 139 Neuropathy, 53, 139 Neuropsychological Tests, 9, 139 Neurotransmitter, 117, 129, 140, 150 Nitrogen, 112, 113, 123, 140, 154 Nonmalignant, 16, 140 Normotensive, 16, 140 Nuclear, 56, 125, 128, 138, 139, 140 Nuclei, 113, 125, 127, 131, 134, 137, 138, 140, 146 Nucleus, 113, 115, 116, 119, 123, 125, 136, 138, 140, 146, 151 O Observational study, 15, 55, 140 Obstetrics, 15, 21, 24, 31, 45, 47, 52, 60, 66, 67, 140 Ocular, 53, 62, 140 Oculomotor, 44, 53, 140 Oculomotor Nerve, 44, 140 Opsin, 140, 148, 149 Oral Health, 81, 140 Osmotic, 112, 138, 140, 149 Osteonecrosis, 49, 140 Ovulation, 42, 140, 141 Ovulation Induction, 42, 141 Oxidation, 5, 6, 7, 111, 114, 136, 141 P Pachymeningitis, 137, 141 Paediatric, 31, 141 Palliative, 141, 152 Palsy, 44, 53, 141 Pancreas, 3, 57, 111, 116, 134, 141, 154 Pancreatic, 3, 126, 141 Pancreatic Ducts, 126, 141 Pancreatic Pseudocyst, 3, 141 Pancreatitis, 3, 55, 141 Panniculitis, 37, 141
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Papilla, 126, 141 Partial remission, 141, 148 Parturition, 140, 141 Patch, 136, 141 Pathologic, 9, 62, 115, 122, 132, 141 Pathologic Processes, 115, 141 Pathophysiology, 8, 60, 141 Patient Education, 98, 104, 106, 109, 141 Pelvis, 111, 134, 141, 154 Penicillin, 142, 154 Peptic, 142, 149 Peptic Ulcer, 142, 149 Peptic Ulcer Hemorrhage, 142, 149 Peptide, 18, 41, 142, 144, 146 Perfusion, 32, 56, 142 Pericardium, 142, 152 Perioperative, 22, 142 Peripheral Nerves, 135, 142 Peripheral Nervous System, 140, 141, 142 Peritoneal, 115, 142 Peritoneal Cavity, 115, 142 Pharmacologic, 113, 142, 153 Phenotype, 13, 116, 142 Phospholipids, 5, 8, 16, 34, 77, 85, 113, 114, 118, 127, 136, 137, 142 Phosphorus, 117, 142 Photocoagulation, 120, 142 Physicochemical, 74, 142 Physiologic, 112, 142, 145, 148 Physiology, 116, 143 Pigments, 118, 137, 143, 148 Pilot study, 70, 143 Pituitary Gland, 122, 143 Placenta, 52, 53, 128, 143, 147 Placental tissue, 8, 143 Plants, 118, 129, 143, 153 Plasma cells, 113, 143 Plasma protein, 8, 12, 112, 143, 146, 149 Plasmapheresis, 27, 143 Plasmin, 6, 42, 128, 143 Plasminogen Activators, 143 Platelet Activation, 11, 34, 42, 143, 150 Platelets, 11, 31, 34, 36, 143, 152, 153 Pneumonia, 122, 143 Polyarteritis Nodosa, 51, 82, 143 Polymerase, 5, 144 Polymerase Chain Reaction, 5, 144 Polymorphic, 13, 123, 144 Polymorphism, 34, 57, 144 Polypeptide, 75, 112, 120, 128, 143, 144, 146 Polysaccharide, 112, 114, 144
Pons, 117, 144 Portal System, 3, 144 Posterior, 124, 141, 144 Postnatal, 17, 144 Practice Guidelines, 94, 144 Precursor, 115, 123, 124, 126, 144, 146, 154 Predisposition, 39, 99, 144 Preeclampsia, 17, 24, 144 Pre-Eclampsia, 69, 144 Pregnancy Complications, 15, 16, 144 Pregnancy Outcome, 7, 15, 31, 58, 60, 145 Pregnancy, High-Risk, 15, 145 Prenatal, 48, 52, 125, 145 Prenatal Care, 145 Prevalence, 5, 6, 7, 12, 34, 39, 41, 145 Primary tumor, 48, 145 Probe, 13, 145 Prognostic factor, 51, 145 Progression, 11, 145 Progressive, 70, 71, 74, 120, 139, 143, 145, 148 Proline, 120, 132, 145 Prone, 5, 6, 145 Prophylaxis, 39, 55, 62, 70, 145, 155 Prostaglandin, 60, 145 Prostaglandins A, 145 Prostate, 116, 146, 154 Protein C, 6, 112, 114, 136, 146, 154 Protein Conformation, 112, 146 Protein S, 11, 116, 146 Proteinuria, 139, 144, 146 Proteolytic, 121, 128, 143, 146 Prothrombin, 13, 16, 42, 58, 146, 152 Protons, 132, 137, 146, 147 Pseudotumor Cerebri, 134, 146 Psychiatric, 14, 116, 137, 146 Psychiatry, 25, 36, 146 Psychosis, 14, 129, 146 Public Policy, 93, 147 Publishing, 18, 147 Puerperium, 140, 147 Pulmonary, 16, 43, 47, 76, 117, 147, 152, 155 Pulmonary Artery, 117, 147, 155 Pulmonary Embolism, 16, 43, 147, 155 Pulmonary hypertension, 76, 147 Pulse, 16, 147 Purpura, 26, 55, 147 Q Quality of Life, 9, 147 R Race, 9, 147
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Antiphospholipid Syndrome
Radiation, 125, 126, 128, 133, 147, 156 Radioimmunoassay, 74, 75, 147 Randomized, 31, 35, 125, 147 Randomized clinical trial, 35, 147 Reagent, 76, 77, 134, 147 Reality Testing, 146, 147 Receptor, 10, 11, 12, 57, 78, 114, 147, 148, 150 Recombinant, 13, 148 Red blood cells, 127, 130, 148 Reductase, 10, 16, 148 Refer, 1, 117, 120, 136, 146, 148 Refraction, 148, 151 Regimen, 124, 148 Remission, 11, 137, 148 Renal Artery, 40, 148 Renal failure, 33, 148 Respiratory distress syndrome, 55, 148 Retina, 28, 119, 121, 148, 149 Retinal, 26, 66, 148, 149 Retinal Artery, 148 Retinol, 148, 149 Retinopathy, 46, 57, 142, 148 Retrograde, 148 Retrospective, 33, 42, 149 Retrospective study, 33, 42, 149 Rheumatic Diseases, 22, 25, 37, 40, 42, 45, 47, 49, 54, 57, 58, 82, 149 Rheumatoid, 39, 42, 74, 76, 149 Rheumatoid arthritis, 39, 42, 74, 76, 149 Rhodopsin, 140, 148, 149 Ribonuclease, 138, 149 Risk factor, 4, 5, 10, 14, 46, 54, 126, 132, 149 Rods, 128, 148, 149 S Saline, 138, 149 Scleroderma, 82, 98, 138, 149 Sclerosis, 39, 70, 74, 82, 149 Sclerotherapy, 58, 149 Screening, 16, 78, 120, 149 Secretion, 111, 122, 129, 131, 134, 138, 149 Secretory, 18, 149 Segmental, 59, 149 Segmentation, 149 Sensory loss, 82, 139, 149 Sequencing, 5, 144, 149 Serologic, 132, 149 Serum, 14, 15, 16, 45, 48, 74, 112, 113, 120, 121, 136, 138, 147, 149, 154 Serum Albumin, 74, 147, 149 Sex Characteristics, 113, 150, 152
Shock, 16, 150, 153 Side effect, 87, 111, 123, 150, 153 Signal Transduction, 113, 150 Signs and Symptoms, 143, 148, 150, 154 Skeletal, 113, 150, 154 Skeleton, 111, 145, 150 Skull, 122, 150, 152 Small intestine, 120, 124, 126, 131, 134, 150, 155 Social Environment, 147, 150 Somatic, 131, 138, 142, 150 Specialist, 100, 150 Species, 41, 131, 138, 147, 150, 151, 153, 154 Specificity, 7, 8, 18, 33, 111, 114, 150 Spectrum, 8, 13, 14, 27, 30, 59, 151 Sperm, 113, 151 Spinal cord, 82, 117, 119, 124, 128, 134, 137, 139, 141, 142, 151 Spinal Cord Vascular Diseases, 139, 151 Spirochete, 151, 152 Spontaneous Abortion, 76, 145, 151 Stenosis, 44, 151 Sterility, 23, 123, 151 Steroids, 122, 151 Stillbirth, 145, 151 Stimulant, 151, 154 Stimulus, 151, 152 Stomach, 111, 115, 127, 129, 131, 142, 150, 151 Strand, 144, 151 Stress, 16, 53, 144, 149, 151 Stricture, 151 Stroke, 6, 10, 14, 18, 42, 58, 76, 92, 118, 135, 151 Subacute, 133, 151 Subarachnoid, 130, 151 Subclinical, 5, 58, 133, 151 Subcutaneous, 113, 124, 136, 141, 151 Subiculum, 131, 151 Subspecies, 150, 151 Substrate, 118, 126, 151 Supplementation, 69, 152 Suppression, 122, 152 Surfactant, 74, 152 Symptomatic, 141, 152 Syphilis, 29, 85, 99, 118, 152 Systemic, 4, 5, 9, 14, 15, 20, 27, 28, 29, 32, 34, 37, 38, 39, 41, 42, 43, 46, 48, 49, 52, 53, 54, 57, 58, 62, 70, 74, 78, 82, 88, 113, 114, 117, 134, 138, 144, 149, 152, 155 Systolic, 16, 132, 152
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Systolic blood pressure, 16, 152 T Tachycardia, 128, 152 Telangiectasia, 38, 152 Temporal, 15, 130, 131, 152 Testosterone, 148, 152 Thalidomide, 21, 152 Therapeutics, 88, 152 Thermal, 124, 144, 152 Threshold, 77, 132, 152 Thrombin, 6, 13, 41, 128, 146, 152, 153 Thrombocytes, 143, 152 Thrombocytopenia, 4, 6, 12, 17, 36, 42, 61, 76, 78, 82, 152 Thromboembolism, 43, 56, 62, 152 Thrombolytic, 43, 152, 153 Thrombolytic Therapy, 43, 153 Thrombomodulin, 52, 146, 153 Thrombopenia, 114, 153 Thrombophilia, 57, 153 Thrombophlebitis, 58, 153 Thromboses, 24, 49, 114, 153 Thyroid, 39, 153 Tone, 140, 153 Torsion, 133, 153 Toxaemia, 144, 153 Toxic, iv, 123, 126, 132, 139, 153 Toxicity, 124, 153 Toxicology, 94, 153 Toxins, 114, 126, 129, 133, 153 Trachea, 153 Transfection, 116, 153 Transfusion, 131, 153 Transplantation, 57, 70, 120, 125, 136, 153 Trauma, 48, 139, 141, 153 Triglyceride, 23, 154 Tropomyosin, 154 Troponin, 16, 154 Tryptophan, 120, 154 Tuberculosis, 136, 154 Tumor marker, 116, 154 Tumor Necrosis Factor, 152, 154 U Ulcer, 19, 36, 142, 154, 155 Uraemia, 141, 154
Uremia, 148, 154 Ureters, 148, 154 Urethra, 146, 154 Urine, 15, 117, 133, 146, 154 Uterus, 119, 123, 154 V Vaccines, 154, 155 Valine, 61, 154 Varicose, 135, 149, 154, 155 Varicose Ulcer, 135, 155 Varicose vein, 149, 155 Vascular, 10, 11, 13, 15, 18, 24, 61, 62, 76, 113, 123, 130, 132, 133, 134, 143, 151, 155 Vasculitis, 47, 62, 99, 141, 143, 155 VE, 29, 155 Vein, 28, 48, 53, 134, 140, 153, 155 Vena, 155 Venereal, 152, 155 Venom, 75, 155 Venous, 3, 4, 5, 8, 12, 17, 26, 35, 43, 62, 76, 114, 119, 130, 135, 146, 155 Venous blood, 119, 155 Venous Thrombosis, 4, 8, 12, 35, 43, 76, 155 Ventral, 140, 144, 155 Ventricle, 131, 147, 152, 155 Ventricular, 16, 56, 132, 155 Veterinary Medicine, 93, 155 Villi, 16, 132, 155 Villous, 17, 53, 155 Viral, 27, 76, 155 Virus, 27, 40, 71, 119, 131, 155 Vitro, 5, 18, 130, 155 Vivo, 11, 15, 17, 136, 155 W Warfarin, 35, 46, 55, 78, 85, 155 White blood cell, 114, 136, 137, 138, 143, 155 Windpipe, 153, 156 Wound Healing, 118, 156 X X-ray, 113, 118, 126, 140, 156 Y Yeasts, 142, 156
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Antiphospholipid Syndrome
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Antiphospholipid Syndrome
