VASCULITIS 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., 1960Vasculitis: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-84678-2 1. Vasculitis-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 vasculitis. 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 VASCULITIS ............................................................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Vasculitis ...................................................................................... 6 E-Journals: PubMed Central ....................................................................................................... 40 The National Library of Medicine: PubMed ................................................................................ 41 CHAPTER 2. NUTRITION AND VASCULITIS ..................................................................................... 85 Overview...................................................................................................................................... 85 Finding Nutrition Studies on Vasculitis ..................................................................................... 85 Federal Resources on Nutrition ................................................................................................... 90 Additional Web Resources ........................................................................................................... 91 CHAPTER 3. ALTERNATIVE MEDICINE AND VASCULITIS ............................................................... 93 Overview...................................................................................................................................... 93 National Center for Complementary and Alternative Medicine.................................................. 93 Additional Web Resources ........................................................................................................... 97 General References ....................................................................................................................... 98 CHAPTER 4. PATENTS ON VASCULITIS ............................................................................................ 99 Overview...................................................................................................................................... 99 Patents on Vasculitis ................................................................................................................... 99 Patent Applications on Vasculitis ............................................................................................. 104 Keeping Current ........................................................................................................................ 106 CHAPTER 5. BOOKS ON VASCULITIS ............................................................................................. 109 Overview.................................................................................................................................... 109 Book Summaries: Federal Agencies............................................................................................ 109 Book Summaries: Online Booksellers......................................................................................... 110 Chapters on Vasculitis ............................................................................................................... 111 CHAPTER 6. MULTIMEDIA ON VASCULITIS ................................................................................... 113 Overview.................................................................................................................................... 113 Video Recordings ....................................................................................................................... 113 CHAPTER 7. PERIODICALS AND NEWS ON VASCULITIS ................................................................ 115 Overview.................................................................................................................................... 115 News Services and Press Releases.............................................................................................. 115 Newsletters on Vasculitis .......................................................................................................... 117 Newsletter Articles .................................................................................................................... 118 Academic Periodicals covering Vasculitis.................................................................................. 118 CHAPTER 8. RESEARCHING MEDICATIONS .................................................................................. 121 Overview.................................................................................................................................... 121 U.S. Pharmacopeia..................................................................................................................... 121 Commercial Databases ............................................................................................................... 122 Researching Orphan Drugs ....................................................................................................... 122 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 127 Overview.................................................................................................................................... 127 NIH Guidelines.......................................................................................................................... 127 NIH Databases........................................................................................................................... 129 Other Commercial Databases..................................................................................................... 131 The Genome Project and Vasculitis ........................................................................................... 131 APPENDIX B. PATIENT RESOURCES ............................................................................................... 135 Overview.................................................................................................................................... 135 Patient Guideline Sources.......................................................................................................... 135 Finding Associations.................................................................................................................. 140
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APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 143 Overview.................................................................................................................................... 143 Preparation................................................................................................................................. 143 Finding a Local Medical Library................................................................................................ 143 Medical Libraries in the U.S. and Canada ................................................................................. 143 ONLINE GLOSSARIES................................................................................................................ 149 Online Dictionary Directories ................................................................................................... 149 VASCULITIS DICTIONARY ...................................................................................................... 151 INDEX .............................................................................................................................................. 223
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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 vasculitis 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 vasculitis, 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 vasculitis, 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 vasculitis. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to vasculitis, 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 vasculitis. 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 VASCULITIS Overview In this chapter, we will show you how to locate peer-reviewed references and studies on vasculitis.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and vasculitis, 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 “vasculitis” (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: •
Systemic Vasculitis: Diagnostic Clues to This Confusing Array of Diseases Source: Postgraduate Medicine. 103(2): 68-69, 74, 79-81, 85-86. February 1998. Contact: Available from McGraw-Hill, Inc. 1221 Avenue of the Americas, New York, NY 10020. (612) 832-7869. Summary: This article on systemic vasculitis is one in a series of five articles on rheumatologic diseases. Systemic vasculitides are characterized by aberrant immune responses that result in inflammation and necrosis (death) of blood vessels. Systemic vasculitis can be difficult to recognize because of the many types of the disease and the conditions that can mimic it. However, early identification and initiation of treatment are important to avoid severe morbidity. In this article, the author describes the most common types of vasculitis according to current nomenclature based on the size of
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affected vessels. The article also includes illustrations of the most common signs of the various types of vasculitis. Hallmarks of vasculitis include renal dysfunction, skin rashes (palpable purpura, necrotic ulcers), and neurologic involvement, especially footdrop and wristdrop. Malaise, arthralgia, and anemia are also common. Initial evaluation in patients in whom vasculitis is suspected should include a detailed history of drug exposures and risk factors for hepatitis B, hepatitis C, and HIV infection. Some clinical features, such as fever and renal disease, are common to both systemic lupus erythematosus (SLE) and systemic vasculitis. Types of vasculitis discussed include small vessel vasculitis, Wegener's granulomatosis, Churg Strauss syndrome, microscopic polyangitis, medium vessel vasculitis, polyarteritis nodosa, Kawasaki syndrome, large vessel vasculitis, temporal arteritis, Takayasu's arteritis, and vasculitis related to connective tissue disease. Prompt consultation of the primary care physician with a rheumatologist is generally warranted to assist in thorough diagnostic workup and initiation of therapy. In addition, careful monitoring is needed to manage secondary complications, such as hypertension and chronic renal failure. 5 figures. 25 references. •
Systemic Vasculitis Source: Postgraduate Medicine. 103(2):68-70,74,79-81,85; February 1998. Summary: This journal article for health professionals reviews the most common types of vasculitis, focusing on important diagnostic features. It highlights the general diagnostic clues to vasculitis and describes the characteristics of small-vessel vasculitis, Wegener's granulomatosis, Churg-Strauss syndrome, microscopic polyangiitis, polyarteritis nodosa, Kawasaki syndrome, temporal arteritis, Takayasu's arteritis, and vasculitis related to connective tissue disease. These conditions are also discussed in terms of their diagnosis and treatment. 17 references, 5 figures, and 2 tables.
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Systemic Vasculitis: A Difficult Diagnosis in the Elderly Source: Physician Assistant. 25(1): 37-38,47-53. January 2001. Summary: This journal article provides health professionals with information on diagnosing systemic vasculitis in the elderly. Illnesses in geriatric patients are often difficult to diagnose because they may not present with the typical pattern for many common diseases. Their atypical presentation, compounded by the fact that vasculitides present with vague symptomatology, have nonspecific diagnostic testing, and are difficult to differentiate because of their overlapping presentations, makes the diagnosis of systemic vasculitis difficult for the clinician. In addition, geriatric patients often delay seeing a physician because they attribute their symptoms to aging. The physician must first rule out disorders that mimic vasculitis by taking a complete history, performing a physical examination, and conducting appropriate diagnostic tests. The most common differential diagnoses for vasculitis in the elderly are infection and malignancy. Caution must be used when interpreting laboratory values because some of them normally change with aging. Diseases that mimic vasculitis include antiphospholipid antibody syndrome, cholesterol emboli syndrome, venous stasis, and thrombotic thrombocytopenic purpura. Diagnosis of a specific vascular syndrome is based on clinical features, angiography, biopsy results, the presence of antineutrophil cytoplasmic autoantibodies, and viral testing. Vascular syndromes include giant cell arteritis, polyarteritis nodosa, microscopic polyangitis, and Wegener's granulomatosis. The article presents the etiology, signs and symptoms, diagnostic findings, and treatment of these vasculitides. 3 tables and 17 references. (AA-M).
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ANCA-Associated Small-Vessel Vasculitis Source: American Family Physician. 65(8): 1615-1620. April 15, 2002. Contact: Available from American Academy of Family Physicians. 11400 Tomahawk Creek Parkway, Leawood, KS 66211-2672. (800) 274-2237 or (913) 906-6000. E-mail:
[email protected]. Website: www.aafp.org. Summary: This journal article uses a question and answer format to provide health professionals with information on the diagnosis and treatment of antineutrophil cytoplasmic antibodies (ANCA) associated small vessel vasculitis. This disease is the most common primary systemic small vessel vasculitis to occur in adults. Although the etiology is not always known, the incidence of vasculitis is increasing, and diagnosis and patient management may be challenging because of the relative infrequency, changing nomenclature, and variability of clinical expression of the disease. Advances in clinical management have been achieved during the past few years, and many ongoing studies are pending. Vasculitis may affect the large, medium, or small blood vessels. Small vessel vasculitis may be further classified as ANCA associated or non ANCA associated vasculitis. ANCA associated small vessel vasculitis includes microscopic polyangiitis, Wegener's granulomatosis, Churg Strauss syndrome, and drug induced vasculitis. Better definition criteria and technological advancement make these diagnoses increasingly common. Features that may aid in defining the specific type of vasculitic disorder include the type of organ involvement, the presence and type of ANCA (myeloperoxidase ANCA or proteinase 3 ANCA), the presence of serum cryoglobulins, and the presence of evidence for granulomatous inflammation. Family physicians should be familiar with this group of vasculitis disorders to reach a prompt diagnosis and initiate treatment to prevent end organ damage. Treatment usually includes corticosteroid and immunosuppressive therapy. 2 figures, 2 tables, and 11 references. (AA-M).
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Early Diagnosis and Effective Therapy for Vasculitis Source: Journal of Musculoskeletal Medicine. 16(2): 79-82,85-86,95-99. February 1999. Summary: This journal article, the last in a series of special overview articles on major areas of musculoskeletal medicine, provides health professionals with information on the diagnosis and treatment of vasculitis. The article reviews the pathology, signs, symptoms, diagnosis, and treatment of each of the major vasculitic syndromes, focusing on Takayasu's arteritis, giant cell arteritis, polymyalgia rheumatica, PAN, and Wegener's granulomatosis. Vasculitic syndromes are characterized by inflammation and necrosis in the walls of blood vessels, resulting in narrowing or occlusion of the lumen or formation of aneurysms that may rupture. The pathogenesis is only beginning to be understood, but it is probably varied and complex. A detailed history, careful physical examination, and selected laboratory tests help determine the type of onset, course of illness, organ systems affected, and extent of involvement. Biopsy examination of involved tissues is nearly always essential for accurate diagnosis, except in Takayasu's arteritis, when arteriography of the aorta and its branches is indicated. Therapy depends on the nature and severity of the vasculitis. With a mild hypersensitivity vasculitis caused by a drug reaction, discontinuing the offending drug may be adequate. Patients with broader vasculitic involvement usually need corticosteroid therapy. When the organ involvement is widespread and progressive, a combination of a cytotoxic drug and corticosteroids is recommended. Available data reveal a generally good outcome for patients with vasculitis. 8 figures, 4 tables, and 28 references. (AA-M).
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Use of Cytotoxic Agents and Cyclosporine in the Treatment of Autoimmune Disease. Part 2: Inflammatory Bowel Disease, Systemic Vasculitis, and Therapeutic Toxicity Source: Annals of Internal Medicine. 129(1): 49-58. July 1, 1998. Summary: When cytotoxic (cell-damaging) agents were introduced, their ability to disrupt nucleic acid and protein synthesis led to their effective use for the treatment of neoplastic disease (cancer). It then became apparent that these agents also suppress the immune system. This usually unwelcome effect was subsequently studied and beneficially directed toward treating non-neoplastic diseases in which autoimmune mechanisms play a role. This article discusses the use of cytotoxic agents and cyclosporine in the treatment of inflammatory bowel disease (IBD) and systemic vasculitis, and reviews the toxic effects of these agents. The authors caution that because these medications can cause treatment-induced illness or even death, it is imperative to weigh the benefits and risks of cytotoxic therapy when treating a non-neoplastic disease. The authors review research studies that investigated the use of these drugs. Drugs used for IBD include azathioprine and 6-mercaptopurine, methotrexate, and cyclosporine. These drugs are frequently used in combination with other agents and require careful monitoring. The authors stress that the optimal use of various drug combinations requires not only a knowledge of appropriate indications and dosage but also a thorough assessment of patient expectations and quality of life, a careful weighing of the various risks of medical and surgical therapies, the judicious use of other supportive measures, and extensive patient education. The section on toxicity discusses cyclophosphamide, chlorambucil, methotrexate, azathioprine, 6-mercaptopurine, and cyclosporine. The authors caution that infection is still an important cause of illness and death that is largely related to the nonspecific actions of these agents on the immune response. 3 tables. 75 references.
Federally Funded Research on Vasculitis The U.S. Government supports a variety of research studies relating to vasculitis. 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 vasculitis. 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 vasculitis. The following is typical of the type of information found when searching the CRISP database for vasculitis:
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Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
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Project Title: ANCA GLOMERULONEPHRITIS: FROM MOLECULES TO MAN Principal Investigator & Institution: Falk, Ronald J.; Chief of Nephrology and Hypertension; Medicine; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 Timing: Fiscal Year 2002; Project Start 01-SEP-2000; Project End 31-AUG-2005 Summary: Our program project consists of 5 projects and two cores focusing on antineutrophil cytoplasmic autoantibody (ANCA) necrotizing and crescentic glomerulonephritis (GN) and small vessel vasculitis (SVV). The scope of the investigation and the diversity of the investigators allow for an integrated evaluation of basic molecular and clinical immunological and epidemiological studies pertaining to both anti-myeloperoxidase (MPO) and proteinase 3 (PR3) autoimmune response. Project 1 considers the derivation of murine anti-MPO autoantibodies with respect to relative contributions of antibody heavy and light chains and somatic mutations within them using basic molecular immunologic techniques and transgenic mice. In parallel, Project 2 investigates the human ANCA autoimmune response with respect to the contribution of light and heavy chains and somatic mutations within them, and the fine specificity of specific epitopes responsible for the generation of ANCA during disease onset or relapse. A novel paradigm of autoimmune response with respect to the contribution of light and heavy chains and somatic mutations within them, and the fine specificity of specific epitopes considered; that is, that the ANCA immune response is directed not only to MPO or PR3, but also to peptides complimentary in translation to MPO or PR3. Project 3 tests the hypothesis that ANCA directly participate in the pathogenesis of the ANCA immune response, determines the mechanism by which ANCA activate neutrophils and monocytes, delineates the mechanism by which the ANCA antigens MPO and PR3 directly induce vascular damage. Project 4 studies in vitro development of ANCA GN using animal models in which circulating anti-myeloperoxidase antibodies conspire to produce to GN. Project 5 uses state of t he art epidemiological techniques in a large population of ANCA GN patients to ascertain those environmental factors that predispose to the development and exacerbation of the ANCA immune response. In particular the role of silica exposure in the induction of ANCA GN will be tested in animal studies as well as in man. These investigations are tightly interwoven using state of the art techniques. Together, these sharpy focused and integrated projects will shed light on the central question of the overall project. What causes ANCA GN? If we knew the causes of this most aggressive form of glomerular injury targeted therapy would be in the offing. The program involves investigators from the Department of Medicine, Pathology, Microbiology and Immunology in the School of Medicine, the Department of Epidemiology in the School of Public Health, the Department of Medicinal Chemistry in the School of Pharmacy, and the National Institute of Environmental Health Sciences. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: AUTOIMMUNE THYROIDITIS--INDUCTION AND RESOLUTION Principal Investigator & Institution: Mullen, Helen B.; Professor; Internal Medicine; University of Missouri Columbia 310 Jesse Hall Columbia, Mo 65211 Timing: Fiscal Year 2002; Project Start 30-SEP-1985; Project End 31-MAR-2003 Summary: T cells from mouse thyroglobulin (MTg)-sensitized donors activated in vitro with MTg, anti-IL-2R and/or IL-12 induce severe granulomatous experimental autoimmune thyroiditis (G-EAT) in recipient mice. Thyroid lesions reach maximal severity at 19-21 days and completely resolve by 35-50 days if all thyroid follicles are not
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damaged. Depletion of CD8+ T cells inhibits resolution. If most thyroid follicles are damaged at day 21, there is continuing inflammation, with decreased serum T4, fibrosis and atrophy of the thyroid. The objective is to define the mechanisms involved in resolution and fibrosis of G-EAT and to determine if resolution can be promoted by preventing or reversing fibrosis. MTg- specific CD4+ T cells initiate injury to the thyroid by releasing cytokines. Cytokine-deletion mutant mice will be used to determine how particular inflammatory mediators regulate induction and resolution of G-EAT. CD4+ T cells or cytokines also recruit other cells to the thyroid; these include other inflammatory cells which induce more damage, and CD8+ T cells which become activated and terminate the inflammatory response, possibly by inducing apoptosis of CD4+ T cells. When inflammation is very severe, CD8+ T cells are unable to terminate the inflammation and lesions progress to fibrosis. Excessive production of TGFbeta by inflammatory cells is hypothesized to play a major role in excessive collagen deposition resulting in fibrosis. These studies will test the hypothesis that CD8+ T cells promote resolution of G-EAT, in part, by inducing apoptosis of inflammatory cells and that fibrosis develops when TGFbeta is overproduced. TGFbeta inhibitors and depletion of CD4+ T cells or neutrophils will be used to attempt to promote resolution and prevent or reverse fibrosis. This murine G-EAT model is a well-characterized animal model of autoimmune disease in which the host's immune system promotes healing of lesions. Our studies are aimed at understanding the mechanisms that enable the host to regulate and resolve this autoimmune inflammatory response and understanding how to prevent or reverse more severe destructive inflammatory responses that result in a failure of resolution, and a fibrotic end-stage disease. Granulomatous inflammation and fibrosis occur in many human diseases with presumed autoimmune mechanisms. These studies should provide directions for new clinical investigations that may lead to more rational and specific forms of therapy and provide insight into recovery mechanisms for autoimmune diseases, particularly those associated with granulomatous immunopathology, vasculitis and fibrosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: AUTOMATED, QUANTITATIVE IMMUNOFLUORESCENT ASSAY Principal Investigator & Institution: Newton, Kenneth R.; Hyperion, Inc. 14100 Sw 136Th St Miami, Fl 33186 Timing: Fiscal Year 2003; Project Start 01-JUL-2000; Project End 30-JUN-2005 Summary: (provided by applicant): Diagnosis of auto-immune and connective tissue diseases such as Systemic Lupus Erythematosus, Sjorgren syndrome and scleroderma often makes use of an Immunofluorescent assay (IFA) for antinuclear antibodies (ANA). More detailed diagnostic support may also utilize an IFA test for double-stranded DNA (dsDNA). IFA tests detecting Anti-Neutrophil Cytoplasmic Autoantibodies (ANCA) are diagnostic for systemic necrotizing vasculitis and glomerulonephritis. All these IFA tests require significant laboratory preparation time from highly trained technicians using current, manual techniques. The VisiQuant system developed as a prototype in Phase I, combined with Hyperion's Hyprep automated assay preparation system will automate both preparation and reading of the IFA tests, achieving significant cost savings and potential error reduction. During the Phase II project period, an updated VisiQuant Microscope will be introduced along with improved ANA assay and preparation procedure. The assay will be improved by applying results of a study of assay parameters and conditions. The Microscope will be upgraded by incorporating engineering enhancements to the optics and electronics, including features to optimize the joint operation of the Microscope with the HyPrep, and software improvements to
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the fluorescence intensity algorithm. New test kits for dsDNA based on Crithidia luciliae and for ANCA will be developed, tested and brought to market. Development work in automated image classification will lead to a complementary product that finds the best match to each sample image from a standard ANA image pattern library. Further development of the image classification software will be done based on input from the consultants. This will lead to an advanced Image Classification system to be brought to market at the end of the Phase II period. Image classification to support ANCA test will be started but is not expected to be ready for market until after completion of this project. These developments will result in Hyperion obtaining more than 18% share of the global market for autoimmune IFA based IVD tests by 2010. The development team includes personnel with many years of experience in dye chemistry, immunology in vitro device development, instrument development and image processing. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: B CELL HYPERACTIVITY IN AUTOIMMUNITY Principal Investigator & Institution: Marshak-Rothstein, Ann M.; Professor; Microbiology; Boston University Medical Campus 715 Albany St, 560 Boston, Ma 02118 Timing: Fiscal Year 2002; Project Start 22-SEP-1986; Project End 28-FEB-2006 Summary: (Adapted from the Investigator's abstract): Rheumatoid factors autologous IgG present in the synovial fluid of patients with rheumatoid arthritis. High levels of RF-containing immune complexes and/or cryoglobulins have also been found in patients with microbial infections such as infectious endocarditis, in individuals presenting with hepatitis C-related essential mixed cryogloblulinemia, and in Fas/FasLdeficient (lpr/gld) mice. These immune complexes can deposit in blood vessel walls, fix complement, and thereby promote the vasculitis and glomerulonephritis associated with these diseases. Thus the contribution of RF to the effector arm of systemic autoimmune disease is well documented. Nevertheless, exactly how RF+ B cells become activated, why RF so frequently present as monoclonal gammopathies, and what role RF+ B cells might play in the initiation and propagation of the autoimmune cascade are questions that remain unresolved. The intent of the current application is to address these questions by using an RF+ B cell receptor transgenic mouse line, developed from a prototypic MRL/lpr-derived autoantibody, to evaluate the role RF+ B cells might play in the presentation of autoantigens. Specifically, the project will be organized to: (1) determine the ability of monomeric IgG2a and different types of IgG2a-containing immune complexes to activate RF+ B cells and evaluate the ability of activated and nonactivated RF+ B cells to process and present autoantigenic epitopes; (2) evaluate the ability of RF+ B cells to stimulate autoreactive T cells in vitro and determine the specificity of the RF-activated ART; and (3) assess the ability of RF+ B cells and/or RF activated ART to trigger and propagate systemic autoimmune disease. While dealing with RF in particular, the results of these experiments should be applicable to a more general understanding of the principles governing self/nonself recognition and tolerance induction. Moreover, this experimental strategy should also have direct relevance to human clinical syndromes associated with excessive RF production. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: B CELL SPECIFICITY IN HEPATIC LYMPHOID FOLLICLES Principal Investigator & Institution: Bridges, S Louis.; Associate Professor; Medicine; University of Alabama at Birmingham Uab Station Birmingham, Al 35294
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Timing: Fiscal Year 2002; Project Start 30-SEP-1999; Project End 30-JUN-2004 Summary: Over 4 million individuals in the U.S. are infected with the hepatitis C virus (HCV). Essential mixed cryoglobulinemia (EMC) is an extra-hepatic manifestation of chronic HCV characterized by a systemic vasculitis resulting from production of coldprecipitable immunoglobulins largely composed of monoclonal (Type II) or polyclonal (Type III) IgM rheumatoid factors (RF). More than 80 percent of patients with EMC have chronic HCV and this complication of infection is difficult to treat and results in substantial morbidity. The pathogenesis of HCV-associated EMC is poorly understood and the antigenic stimulus for and site(s) of production of RF/cryoglobulins remain undefined. Hepatic lymphoid follicles (LF), present in approximately 90 percent of HCV patients are likely sites of generation of antibodies with RF and cryoglobulin activity. These LF resemble germinal centers, the sites of normal affinity maturation of the B cell response and contain B cells that are predominantly monoclonal, consistent with an antigen-driven response. In other chronic inflammatory conditions, similar LF in nonlymphoid tissue are known sites of antigen-driven B cell affinity maturation. Monoclonal RF (mRF)from patients with HCV-associated type II cryoglobulinemia have been found to bind HCV particles directly and infection with particular HCV genotypes appears to correlate with the presence and clonality of cryoglobulins, and clinical manifestations of EMC. These studies support the hypothesis that EMC results from mRF/cryoglobulin production in hepatic LF in response to chronic stimulation of a subset of B cells by HCV antigens. To test this hypothesis, the antigen specificity and clonality of individual B cells in particular hepatic LF from HCV patients with and without EMC must be assessed. We will utilize micromanipulation and single cell PCR techniques, to determine if a clonal/cryoglobulin B cell response occurs in hepatic LF, and whether particular HCV antigens drive antibody production and influence clinical manifestations. This proposal is directly applicable to RFA DK-98-017: Hepatitis C: Natural History, Pathogenesis, Therapy, and Prevention, as it addresses whether particular HCV antigens are involved in the pathogenesis of HCV-associated EMC. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BIOLOGY OF THE HUMAN PLATELET FC(GAMMA) RECEPTOR Principal Investigator & Institution: Schreiber, Alan D.; Professor; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: The human platelet Fcgamma receptor plays an important role in several hematologic disorders characterized by thrombocytopenia, thrombosis or vasculitis. Over the past 15 years, knowledge of the platelet Fcgamma receptor has grown. Aspects of its genetics, regulated expression and structure/function relationships, as well as its function in rive in immune pathology, have been studied by our group and others. The long term goai of our project is to more fully decipher the molecular mechanisms underlying piatelet Fcgamma, receptor biology in order to provide safer and more rational therapy for the immune platelet disorders, in addition, studies of the genetics, regulated expression, and signaling pathways of the platelet Fcgamma receptor remain synergistic with the other projects of our Program Project. The Specific Aims of this proposal are: 1. To examine the role of platelet FcgammaRIIA vs macrophage FcgammaRIIA in immune clearance in vivo. Our hypothesis is that the expression of FcgammaRllA ptays a major rote in regulating the fate of immune complexes in vivo, and that abrogation of ptatelet Fcgamma receptors, despite continued macrophage expression, will lead to aberrant clearance of immune complexes. Platetet-specific FcgammaRIIA transgenic mice as well as macrophage-specific FcgammaRIIA transgenic
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mice will be generated by use of DNA constructs with celt-specific promoter sequences appended to the coding region of the FcgammaRIIA gene. 2. To examine the regulation of expression of the platelet Fcgamma receptor. The level of platetet FcgammaRIIA correlates with its function in health and disease. Our hypothesis is that genetic variation in FcgammaRllA gene regulatory sequences, such as the promoter single nucleotide polymorphisms (SNPs) we recently identified, determine differences in the level of FcgammaRIlA expression. The mechanism of the SNP effects on FcgammaRllA expression will be studied in vitro with transfected reporter genes driven by genetic isoforms of the FcgammaRllA gene in megakaryocytic ceils, and in vivo in new transgenic mouse lines created with FcgammaRlIA variants. 3. To examine the role of Cbl in immune clearance, endocytosis and platelet activation. We have established the importance of Cbl in FcgammaRIIA mediated endocytosis in vitro and have crossbred Cbl knockout mice to our FcgammaRIIA transgenic mice. Our hypothesis is that Cbl is important for both FcgammaRIIA endocytosis in rive and FcgammaRIIA subcellutar localization. Continued progress in platelet Fcgamma, receptor biology should permit better diagnosis and therapy for patients with immune ptatelet disorders. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CHARACTERIZATION OF FRACTALKINE IN VITRO AND IN VIVO Principal Investigator & Institution: Feng, Lili; Professor; Medicine; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-JUL-2004 Summary: (Adapted from Investigator's Abstract): Fractalkine, a newly cloned CX3C chemokine, is an endothelium-derived lymphoctye and macrophage chemoattractant, and is unique as the only chemokine mounted on a mucin stalk and having a transmembrane domain. This structure may optimize its function in high-flow vascular circuits such as the renal glomerulus. The Principal Investigator has shown that a neutralizing antibody (Ab) against the receptor for fractalkine, CX3CR1, almost completely prevented CD8+ lymphocyte-dependent and monocyte/macrophage-related anti-glomerular basement membrane (GBM) Ab-induced glomerulonephritis (GN) in the Wistar-Kyoto (WKY) rat. This suggests that the fractalkine/CX3CR1 ligand/receptor pair play a central role in immune-mediated inflammation in the glomerulus. The Principal Investigator proposes to explore the mechanisms of fractalkine regulation and signaling in glomerular endothelial cells (GenC), as well as how fractalkine-expressing GenC cross-communicate with CX3CR1-bearing cells, mainly monocytes/macrophages. The Principal Investigator will study when fractalkine can be induced, what fractalkine can regulate, and how fractalkine can function. The Principal Investigator will, by dissecting the individual domains of fractalkine (including its chemokine, mucin, transmembrane, and cytoplasmic domains), study the role of the molecule in fractalkine-mediated cellular events, including chemotaxis, cell adhesion, activation of macrophage proliferation in vitro in GenC and in vivo in renal inflammation. The Principal Investigator will continue to develop a fractalkine antagonist for better indepth understanding of the relationship between the structure and activity of the molecule, which in addition will provide insightful information for drug design. Finally, the Principal Investigator will use the antagonist, along with other chemokine antagonist controls and blockers, to determine the in vivo effects of fractalkine on acute inflammation and also on the proliferation of monocytes/macrophages as they contribute to continued injury and destruction in experimental glomerular and tubulointestinal renal injury. The Principal Investigator believes that these studies will provide new drug targets for many human disorders that may be fractalkine/CX3CR1-
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Vasculitis
associated, including GN, vasculitis, allograft rejection, ischemia/reperfusion injury, thrombotic angiopathies, and atherosclerosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CHARACTERIZATION OF THE GAMMA HV68 V CYCLIN Principal Investigator & Institution: Speck, Samuel H.; Professor; Microbiology and Immunology; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2002; Project Start 01-JUL-2000; Project End 30-JUN-2005 Summary: This is a new RO1 grant proposal to investigate the mechanisms by which cyclin homologs encoded by gamma-Herpesviruses (v-cyclin) contribute to gammaherpesvirus pathogenesis and latency. The human gamma-herpesviruses, KSHV and EBV, are important causes of cancer especially in immunocompromised individuals. Because of the species specificity of these viruses, in vivo studies of their pathogenesis have been limited. This proposal makes use of a small animal model system, infection of inbred mice with gammaHV68, for analysis of the pathogenesis of gamma-herpesvirus infection and the role of individual gamma-herpesvirus genes in latency and tumor induction. GammaHV68 infection is associated with the development of lymphoma and lymphoproliferative disease, severe vasculitis of the great elastic vessels and splenic fibrosis. Studies to date indicate the gammaHV68 shares pathogenetic mechanisms with EBV, KSHV, and HVS, validating it as a model for analysis of important questions in gammaherpesvirus pathogenesis. This grant is focused on the role of the gammaHV68 v-cyclin in disease pathogenesis. Notably, the gamma2- herpesviruses (HVS, KSHV and gammaHV68) all encode homologs of D-type cyclins, while EBV infection upregulates expression of host D-type cyclins. The investigators have shown that the gammaHV68 v-cyclin is an oncogene that promotes cell cycle progression in primary lymphocytes and that a gammaHV68 v-cyclin mutant reactivates inefficiently from latently infected Msigma and/or B cells. These observations lead to the following 3 specific aims of this proposal: 1) Determine the role(s) of the gammaHV68 v-cyclin in latency and reactivation. 2) Characterize regulation of gammaHV68 v-cyclin expression. 3) Determine the structural and biochemical basis of differences in the functions of the gammaHV68 v-cyclin and host D and E type cyclins. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CORE--CLINICAL AND PATHOLOGIC DATA AND SPECIMENS Principal Investigator & Institution: Hogan, Susan L.; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 Timing: Fiscal Year 2002 Summary: The purpose of the clinical core is to provide pathologic data, clinical information and blood and tissue samples on ANCA glomerulonephritis (ANCA-GN) patients for three of the five proposed projects. The clinical core consists of five components that already exist and that have an ongoing establish and interconnected working relationship. The five components include 1) the UNC Nephropathology Laboratory, 2) the UNC Glomerulonephritis and Vasculitis 5) a statistician/epidemiologist. Working together, the components of this core have established the ability to public abstracts and manuscripts. The UNC Nephropathology Laboratory evaluates approximately 1,500 renal biopsy specimens per year with approximately 15% from the UNCS Glomerulonephritis have joined together with Drs. Ronald J. Falk and J. Charles Jeanette of UNC to form a research collaboration called the GDCN. The mainstay of the GDCN has been the maintenance an ANCA- GN patient
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registry. Clinical information is collected on over 250 patients diagnosed since 1986. Registry patients are followed from the onset of symptoms until death. Registry data has provided information for manuscripts on clinical presentation, disease associations, treatment response, environmental associations, and on prognostic markers for dialysis, death and disease relapses. The core will identify patients for participation in the Environmental Factors in ANCA-GN study (Project #5) and will maintain long-term follow-up of these patients to evaluate the role of environmental factors in disease progression. The registry provides a pool of patients for collecting blood samples. Samples can be collected at the UNC Glomerulonephritis and Vasculitis Clinic and from the GDCN practices for collecting blood samples. Samples can be collected at the UNC Glomerulonephritis and Vasculitis Clinic and from the GDCN practices. Blood samples will be needed on numerous patients during various stages of Vitro Analysis of ANCAInduced Glomerular Inflammation (Project 3). In summary, the core will play a critical role in identifying patients and obtaining blood samples and clinical information at these various clinical stages of the disease. The core will also provide support for statistical analysis. The core has demonstrated the ability to work collaboratively and can meet the clinical research needs of the program project. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: COX-2 MEDIATED INFLAMMATION OF CEREBRAL BLOOD VESSELS Principal Investigator & Institution: Brian, Johnny E.; Anesthesia; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2002; Project Start 30-SEP-2001; Project End 31-AUG-2003 Summary: (provided by the applicant): The overall goal of this application is to provide new insight into changes in the regulation of brain vascular tone following brain injury. Specifically, the proposed studies will investigate the mechanisms that subserve the delayed dilatation of brain arterioles that occurs after transient exposure to the acute vasodilators bradykinin or arachidonic acid. In brain, both bradykinin and arachidonic acid produce acute, reversible vasodilatation mediated by reactive oxygen species, most likely hydrogen peroxide. Reactive oxygen species have been shown in isolated tissues and cells to cause expression of cyclooxygenase-2 (COX-2), an inducible isoform of cyclooxygenase. We hypothesize that transient exposure of brain to bradykinin or arachidonic acid produces a delayed vasodilatation that occurs hours later. We also hypothesize that this delayed vasodilatation is mediated almost exclusively by COX-2, whose expression is upregulated by reactive oxygen species. The studies proposed in this application will use a cranial window model in anesthetized rats. Cranial windows offer the unique ability to study the cerebral circulation where it remains integrated brain tissue. Initial studies will undertake a systematic exploration of the concentrationand time-dependence of the delayed dilatation produced by acute exposure to bradykinin or arachidonic acid. Subsequent studies will use pharmacologic antagonists to establish the role of COX-2 and inducible NO-synthase in the delayed vasodilatation. Immunohistochemical studies will verify the expression of COX-2 protein and also identify the cell type expressing COX-2 by use of double labeling with confocal microscopy. The final series of projects will investigate the role of reactive oxygen species in bradykinin- and arachidonic acid-mediated delayed expression of COX-2. The specific role of hydrogen peroxide will be investigated, as well as the ability of hydrogen peroxide alone to induce delayed, COX-2 dependent dilatation. These studies will introduce an important new concept in the cerebral circulation - that acute dilators such
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as bradykinin and arachidonic acid can cause changes in gene expression that underlie delayed vascular effects. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: D XYLOSE & METHYLPREDNISOLONE HYPERSENSITITIVITY VASTICULITIS
ABSORPTION
IN
Principal Investigator & Institution: Pachman, Lauren; Northwestern University Office of Sponsored Research Chicago, Il 60611 Timing: Fiscal Year 2003 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ENVIRONMENTAL GLOMERULONEPHRITIS
RISK
FACTORS
FOR
ANCA
Principal Investigator & Institution: Savitz, David A.; Professor and Chair; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 Timing: Fiscal Year 2002 Summary: Small vessel vasculitis results in significant organ damage, most often involving the kidney and lungs. ANCA glomerulonephritis (ANCA-GN) is a form of small vessel vasculitis with renal involvement, with or without involvement of the lungs of other organs. ANCA GN is a serious with a short-term (< 3 mortality of 5-10% and a clinical course that often includes periods of remission and relapse that frequently progresses to chronic dialysis. Exposure to silica dust has been associated with a 4-fold increase in risk of ANA GN in three case-control studies. Deficiencies in these studies include small sample size and limited exposure assessment techniques. Smoking may also play a role in the involvement and progression of vasculitis, especially in the upper airways, lungs and kidney, but has never been examined as a risk factor. The purpose of this study is to evaluate the role of environmental exposures, specifically silica and smoking, in the development and progression of ANCA-GN. The proposed study is population-based case control study using a detailed telephone interview to evaluate the intensity and duration of silica and smoking exposures. The study will include 200 patients diagnosed with ANCA GN and 400 controls. ANCA GN cases will be identified through Nephropathology services in NC, SC and Southern Virginia by renal biopsy diagnosis and positive ANCA evaluation. Cases will be contacted with their nephrologist and will be followed prospectively to evaluate the role of silica and smoking on clinical outcomes. Controls will be identified by random digit telephone dialing for those age 18 to 64, and by Health Care Financing Administration database records for those age 65. Controls will be frequency matched on gender, and age group. Exposure to silica dust will be assessed by and experienced Industrial Hygienist. Given the sample size in this study statistical power of 0.80 and a two-sided alpha-0.05, the minimum detectable odds ratio is 1.7 and 1.8 for the relatively common exposures will be 3.4 for high silica exposure and 2.6 for moderate silica exposure. In summary, this study will expand the knowledge of the role of silica dust and smoking in ANCA-GN. This is an aggressive disease for which little is known about etiology. Exposure to silica dust and smoking are modifiable exposures, therefore understanding their role in ANCA-GN may lead to interventions to improve patient outcomes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: EPIDEMIOLOGY OF SYSTEMIC LUPUS & CARDIOVASCULAR DISEASE Principal Investigator & Institution: Manzi, Susan M.; Associate Professor; Medicine; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2002; Project Start 01-JUL-2001; Project End 30-JUN-2005 Summary: Systemic lupus erythematosus (SLE) is the prototypic systemic inflammatory autoimmune disease that affects predominantly young premenopausal women. AfricanAmerican women are afflicted 3 to 4 times more frequently than Caucasian women. The risk of myocardial infarction in women with SLE is up to 50 times higher than expected in women aged 35-44 years, a population of women that should otherwise be protected from such risks. SLE presents unique challenges to studying cardiovascular disease. In SLE, there are several potential mechanisms for ischemia, such as overt vasculitis, vasospasm, microvascular disease, or thrombosis with or without atherosclerosis. Thus, one cannot assume that all ischemic events in SLE are due to atherosclerosis. We do not know the burden of atherosclerosis in SLE or the most predictive risk factors. In addition to traditional factors, inflammatory, immunological, and treatment-related factors specific to SLE are likely involved. Specifically, we plan to: (1) compare the prevalence and extent of subclinical vascular disease in 200 SLE patients and matched controls. Subclinical disease will be defined by calcification of the coronary arteries and aorta as measured by electron beam CT, and carotid plaque and intima media thickness as measured by B mode ultrasound. Patients will be recruited from the Pittsburgh Lupus Registry; (2) determine whether the risk factors associated with subclinical vascular disease in patients with SLE are different from controls. Traditional, inflammatory and immunological factors will be measured; (3) determine the risk factors associated with progression of carotid atherosclerosis over a 3-year period in women with SLE. It is important to determine the burden of atherosclerosis in this unique population, examine potential risk factors, and ultimately design intervention and prevention trials. More far reaching is that SLE may be an ideal experiment of nature' in which to further examine the role of inflammation and immune mechanisms in atherogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GENETIC INFLUENCES & GENE EXPRESSION IN KAWASAKI DISEASE Principal Investigator & Institution: Burns, Jane L.; Professor of Pediatrics; Pediatrics; University of California San Diego La Jolla, Ca 920930934 Timing: Fiscal Year 2002; Project Start 01-DEC-2001; Project End 30-NOV-2004 Summary: (provided by applicant): Kawasaki disease (KD) is the most common cause of acquired cardiovascular disease in childhood in the United States. This acute vasculitis primarily affects children under the age of 5 yrs. who present with fever, rash, conjunctival injection, red mucosal membranes, cervical lymphadenopathy, and swollen extremities. The cause of KD remains unknown and there is no specific laboratory test to identify affected children. Nonetheless, high dose intravenous gamma globulin administered within the first 10 days of fever significantly reduces the risk of coronary artery damage by unknown mechanisms. Without treatment, one in four children will develop permanent damage to the coronary arteries that may lead to ischemic heart disease, myocardial infarction, and death. KD thus presents a unique dilemma: the disease may be difficult to recognize, there is no diagnostic laboratory test, there is an extremely effective therapy, and there is a 25 percent chance of serious cardiovascular
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damage or death if the therapy is not administered. Recent advances in the field of functional genomics allow the analysis of gene expression in complex biologic events such as the response to infection or vascular injury. These advances coincide with the emerging recognition that the hosts innate immune system responds to pathogenassociated molecular patterns with stereotypic patterns of gene expression. Thus, a survey of the transcriptional response can yield clues about the nature of the stimulus. This proposal brings together clinicians with expertise in KD, molecular biologists skilled in the application of these new genomic tools, and a statistical genetics team expert in evaluating genetic influences on disease susceptibility and outcome. This interdisciplinary team will discover the pattern of gene expression in acute KD and in patients with similar appearing, non-KD illness using DNA microarray techniques and mRNA quantitation by kinetic reverse transcriptase-polymerase chain reaction. Unique features of the transcriptional response in KD children will be used to develop a diagnostic test for KD. The role that genetic polymorphisms play in these gene expression patterns and their influence on disease susceptibility, response to therapy, and outcome will also be examined. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENETIC MOUSE MODELS FOR CHRONIC INFLAMMATORY DISEASE Principal Investigator & Institution: Bullard, Daniel C.; Assistant Professor; Genetics; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2007 Summary: Systemic lupus erythematosus, Wegener's granulomatosis, and polyarteritis nodosa are chronic inflammatory diseases that have vasculitis as a major component. The pathogenesis of vasculitis in these and other disorders involves a complex interaction among inflammatory, genetic, and environmental factors. Evidence from both patient studies and in vitro models supports a central role for leukocyte/endothelial cell adhesion molecules, such as ICAM-1 and its beta2 integrin counterreceptors, in the development of vasculitis. However, the specific mechanisms by which ICAM-1 mediates vasculititic lesion formation are not clear. This project will use a straightforward genetic approach using the MRL/MpJ-Faslpr mouse model to define the ICAM-1-dependent pathways responsible for mediating vasculitis. MRL/MpJ-Faslpr mice containing mutations in ICAM-1, LFA-l, Mac-1 and P150/95 have now been generated and will be used to investigate the roles of leukocyte/endothelial interactions in lesion formation in vivo. The specific aims are to: (i) define, by comprehensive qualitative and quantitative analysis, the effects of ICAM-1 deficiency on development and progression, organ distribution, and inflammatory characteristics of lesions of vasculitis in MRL/MpJ-Faslpr mice; (ii) define the relative contributions of ICAM-1 in mediating neutrophil, lymphocyte, and monocyte adhesion to MRL/MpJ-Faslpr endothelial cells; (iii) determine the roles of ICAM-1 in neutrophilmediated damage to MRL/MpJ-Faslpr endothelial cells; and (iv) determine whether MRL/MpJ-Faslpr mice with null mutations in the ICAM-1 ligands CD11a (LFA-1), CD11b (Mac-1), or CD11c (p150/95) will alter development and progression, organ distribution, or inflammatory characteristics of lesions of vasculitis. Upon successful completion of these aims, detailed mechanistic information regarding the roles of ICAM-1 in mediating leukocyte/endothelial adhesion and damage during the development of vasculitis will be obtained. In addition, new insights will be gained towards the general understanding of the pathogenesis of vasculitis as well as other leukocyte-mediated vascular injuries such as transplantation arteriosclerosis, and other
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reperfusion injuries. There have been many requests for these mutant mice or materials derived from these models; therefore, these models are contributing significantly to ongoing research that is relevant to several NIH institutes, including NIAMS, NHLBI, and NIAID. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENETIC POLYMORPHISMS IN RHEUMATOID ARTHRITIS Principal Investigator & Institution: Matteson, Eric L.; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2002; Project Start 15-SEP-2002; Project End 30-JUN-2005 Summary: (provided by applicant): About one-third of patients who have rheumatoid arthritis (RA) develop symptoms of inflammation outside the synovium, so-called extraarticular manifestations (ExRA), such as pericarditis, pleuritis, interstitial lung disease, Felty's syndrome, scleritis, keratitis, and vasculitis including mononeuritis multiplex as well as vasculitis involvement of internal organs, and the central nervous system. ExRA manifestations have been reported to occur mainly in patients with severe articular disease and are associated with an excess morbidity for disease related and other conditions, and increased mortality. Suggested predictors of ExRA features include genetic, clinical and serologic factors. The highest frequencies of RA-associated HLA-DR molecules are seen in patients with extraarticular RA. This study seeks to identify genetic risk factors predisposing patients who develop ExRA. Special emphasis will be put on the effect of different HLA polymorphisms and allelic combinations on the targeting of RA to different organ systems. The specific aims are to: 1. Expand a DNA bank from patients and ethnically matched controls to create the facility for large scale association studies in RA. The genetic information from the DNA bank will be linked to a database of clinical parameters collected during long-term follow-up of RA patients seen at Mayo Clinic. 2. Evaluate the impact of a series of candidate genes on the clinical phenotype of RA, including HLA class I genes, HLA class II genes and polymorphisms of inflammatory cytokines. 3. Assess the use of phenotypic immunologic markers as predictors of the clinical course of RA including deficiency for CD28, and aberrant expression of CD158 and 161 on T lymphocytes. The long-term goal is to establish profiles of genetic risk determinants associated with different patterns of RA to eventually be used as biomarkers in risk assessment and clinical management. This proposal is meant as the cornerstone for a long-term investigative initiative into the nature of RA, and will provide the resources and foundation for the development of a series of clinician-investigators at the beginning of their careers. The mentorship program proposed in this grant is critical to this long-term goal. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: HELIOBACTER INDUCED HEPATITIS AND TUMORIGENESIS Principal Investigator & Institution: Fox, James G.; Director and Professor; Div of Comparative Medicine; Massachusetts Institute of Technology Room E19-750 Cambridge, Ma 02139 Timing: Fiscal Year 2002; Project Start 01-MAY-1995; Project End 31-DEC-2003 Summary: Helicobacter hepaticus is responsible for a new murine disease, "H. hepaticus induced hepatitis". We have reproduced this type of chronic active hepatitis experimentally in both SPF inbred mice and outbred germfree mice and determined that H. hepaticus is widespread in mouse colonies and causes a persistent hepatitis in susceptible strains of mice. H. hepaticus also persistently colonizes the lower
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gastrointestinal tract of both A/JCr susceptible and resistant C57Bl/6 mice but does not cause liver lesions in resistant strains of mice. In the A/JCr and B6C3F1 the organism induces hepatic adenomas and hepatocellular carcinomas. We have determined the morphological stages of the H. hepaticus induced liver lesions in the A/JCr which consist of a series of progressive changes beginning with chronic active hepatitis and vasculitis leading to bile duct and oval cell hyperplasia with increased hepatocyte proliferation and hepatomegaly, development of clear cell foci and nodular hyperplasia and finally culminating in adenomas and hepatocellular carcinoma. Several key features of H.hepaticus' role in carcinogenesis have been recently elucidated which strongly suggest H. hepaticus acts as a tumor promoter. Experiments designed to further characterize and elucidate mechanisms responsible for H. hepaticus biological effects will continue to explore in vivo molecular events operable in establishing chronic hepatitis and promotion of tumorigenesis. In this proposal we plan to 1) Utilize isogenic mutants of H. hepaticus lacking putative virulence determinants to determine effects of these bacterial gene products on chronic hepatic inflammation and promotion of tumorigenesis. 2) Utilize congenic recombinant mice to characterize and map the genetic difference(s) responsible for determining the differential susceptibility of strains A/J and C57BL/6 to H. hepaticus induced hepatitis and liver tumors and 3) Determine if H. hepaticus infection promotes onset and progression of hepatitis and tumor formation in mice initiated with hepatic carcinogens and ascertain whether the sequential events operable in tumor induction can be interrupted by eradication of H. hepaticus at different stages of infection. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: IN PATHOGENESIS
VITRO
STUDIES
OF
ANCA
GLOMERULONEPHRITIS
Principal Investigator & Institution: Jennette, J. Charles.; Brinkhous Distinguished Professor and Ch; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 Timing: Fiscal Year 2002 Summary: The proposed research will investigate experimental animal models that elucidate afferent (immunogenic) and efferent (pathogenic) mechanisms of the autoimmune process that cause glomerulonephritis and vasculitis in patients with antineutrophil cytoplasmic autoantibodies (ANCA). The efferent mechanisms will be investigated by testing the hypothesis that ANCA induce disease by synergistic interactions with other pro- inflammatory stimuli. This possibility is supported by clinical observations that suggest that infectious processes prompt the onset and exacerbation of ANCA- disease, and by in vitro experimental observations indicating that neutrophil activation by ANCA requires synergistic neutrophil priming by proinflammatory cytokines. Mice with circulating anti-MPO antibodies will be generated by active immunization with MPO, passive administration of monoclonal murine antiMPO antibodies, and introduction of immunoglobulin transgenes that produce antiMPO antibodies. Mice with circulating anti-MPO, MPO-knockout mice with circulating anti-MPO, and control mice will be challenged with sub-neophritogenic doses of antiGBM, low dose neophritogenic heterologous antigen (horse apoferritin) that induces only mild glomerular inflammation in normal mice, and systemic injection of proinflammatory cytokines. Measuring urine protein, serum creatine, and pathologic changes in renal and other tissues will monitor the onset of renal disease by the synergistic interaction of ANCA with changes in renal and other tissues will monitor the onset of renal disease by the synergistic interaction of ANCA with pro-inflammatory
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stimuli. Afferent mechanisms of ANCA induction (ANCA immunogenesis) will be studied by testing the hypothesis that certain environmental factors induce the ANCA autoimmune response. This hypothesis is supported by the clinical observation that the development of ANCA and of ANCA-disease can be correlated with environmental exposures, for example silica and certain drugs. BALB/c, C57B6, autoimmune prone mice (MRL/lpr, NOD), and transgenic mice expressing anti-MPO will be exposed to silica or aminoguanidine. Control and exposed mice will be monitored for anti- MPO production and development of ANCA-disease. When models of ANCA immunogenesis and ANCA pathogenesis are established, the underlying mechanisms can be evaluated using experimental tools developed to investigate the immune system and inflammatory mediator systems in mice (measuring mRNA expression and protein levels of inflammatory mediators, evaluating effects of cellular and humoral immune and inflammatory effector depletion, and assessing the effects of targeted gene knock outs (e.g. of chemokines and cytokines, and their receptors. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: IN INFLAMMATION
VIVO
STUDIES
OF
ANCA
INDUCED
GLOMERULAR
Principal Investigator & Institution: Preston, Gloria A.; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 Timing: Fiscal Year 2002 Summary: ANCA-associated glomerular injury may be mediated by ANCA binding to neutrophils/monocytes, resulting in enhanced neutrophil granule release and endothelial cell damage. Our experimental approach is based on the premise that ANCA are pathogenic and are responsible for mediating the most common forms of systemic necrotizing vasculitis and crescentic glomerulonephritis. The first Specific Aim focuses on the mechanism/s of ANCA-induced neutrophil/monocyte activation. The proposed in vitro and in vivo studies are complementary and will be done in parallel. The in vitro studies will examine the relative contribution of the F(ab')2 portion of the antibody versus the Fc portion, by treating cells from healthy individuals. We will engineer anti-PR3 and MPO F(ab')2- like molecules, with and without Fc regions to determine this. The in vivo studies will investigate changes in circulating cells from patients with active disease, in remission and at relapse, i.e., examine the surface expression ANCA antigens, and examine the changes in transcription of genes associated with inflammation. The second Specific Aim will test the effects of ANCA and its antigens, PR3 and MPO, on the endothelium. These studies will be done in parallels with Specific Aim 1. We known that PR3 and MPO are translocated into endothelial cells and PR3 induced apoptosis but MPO did not. We will determine the mechanism of cell entry and the effects on cell signaling pathways that lead to apoptosis. Be deletion analysis we will determine the domain of PR3 responsible for the pro-apoptotic activity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INTERACTION OF CIQ ON PHAGOCYTIC CELLS Principal Investigator & Institution: Tenner, Andrea J.; Professor; Molecular Biology and Biochem; University of California Irvine Irvine, Ca 926977600 Timing: Fiscal Year 2002; Project Start 01-JUL-1996; Project End 30-JUN-2005 Summary: (adapted from investigator's abstract): The innate immune system is composed of "hard-wired" elements of immunity, such as natural killer cells,
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phagocytes, defensins, and complement, that mount an initial protective response to kill, clear and/or limit deleterious invaders. A relatively newly defined family of proteins, designated as defense collagens, is an example of the constitutive recognition components of the innate system. Each of these defense collagens recognizes selective motifs displayed on pathogenic material, and mediates a protective response. Interaction of several soluble defense collagens with a novel transmembrane protein, C1qRP, has been shown to facilitate the rapid ingestion of suboptimally opsonized particles, a potentially critical mechanism in host defense particularly at early stages of infection/disease when little or no adaptive response is yet present. In addition, this receptor, which is selectively expressed on monocytes, macrophages, neutrophils, endothelial cells and platelets, may contribute to the rapid clearance of apoptotic and/or damaged cells, a critical process during tissue remodeling. This would be particularly advantageous, as ligation of this receptor by monocytes does not trigger proinflammatory cytokine production. This proposal will focus, first, on determining the physiologic role of this receptor by generating, characterizing, and testing specific hypotheses in a murine model in which this gene has been ablated, and secondly, on the intracellular signaling mechanisms involved in triggering enhanced phagocytosis and in regulating proinflammatory cytokine induction. The ability of C1qRP to regulate the phagocytic capacity of myeloid cells could be extremely valuable as a prophylactic treatment for individuals at risk for infection, such as individuals with genetic immunodeficiencies or pathogen-induced immunosuppression, patients undergoing cancer chemotherapy, or patients undergoing high risk surgery. However, this surface molecule also has the potential for modulation of processes contributing to damaging inflammation (such as vasculitis, nephritis, neurodegeneration), and understand physiologic clearance of apoptotic cells and/or cellular debris which would be potentially relevant to both inflammation and certain types of autoimmunity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CYTOTOXICITY
MAC-1(CR3)
IN
IMMUNE-MEDIATED
NEUTROPHIL
Principal Investigator & Institution: Mayadas-Norton, Tanya N.; Associate Professor; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-MAY-2007 Summary: (provided by applicant): Neutrophil cytotoxicity is implicated in the microvascular damage observed in a number of autoimmune diseases. Basement membrane disruption contributes not only to the pathogenesis of vasculitis but may also expose neoepitopes that induce humoral immunity. Mac-I(CD11b/CD18,CR3), a leukocyte specific beta-2 integrin, supports adhesion and cytotoxic functions in phagocytes. It is also the primary receptor for complement fragment C3bi. Two studies on Mac-1 deficient mice (Mac1-/-) revealed that Mac-1 is required for inflammationinduced cytotoxicity leading to basement membrane damage. Mac1-/- lacked complementdependent proteinuria in response to anti-glomerular basement membrane nephritis despite glomerular neutrophil accumulation. Furthermore, in response to the Shwartzman reaction in the skin, a model of hemorrhagic vasculitis, mice deficient in Mac-1 exhibited no hemorrhage which correlated with an absence of laminin degradation in the vessel wall. This was despite neutrophil accumulation in Mac1-/that was comparable to wild-type animals. Studies in relevant knock-out mice revealed that complement C3 was required for hemorrhage but not neutrophil accumulation and that NADPH oxidase derived oxygen radicals did not play a significant role in the pathology. The goal of this proposal is to understand cellular and molecular
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mechanisms that underly Mac-l's role in complement-dependent, neutrophil cytotoxicity. We will test our hypothesis that Mac-1 adhesion to C3bi in the vessel wall generates a sealed compartment ("immunological synapse") for focalized protease release, and stimulates degranulation, two steps likely required for neutrophil cytotoxicity. Furthermore we propose that these two steps require the CD1 lb cytoplasmic tail and select downstream integrin signaling molecules. In Aim I we will elucidate the intracellular sequences required for Mac-1 mediated cytotoxicity and the role of select signaling molecules in this process. In Aim II, evidence for degranulation leading to protease release and formation of an immunological synapse in the Shwartzman reaction that is Mac-1 dependent will be sought. The role of signaling molecules src, syk and vav in the Shwartzman reaction will be evaluated. In Aim III, the in vivo role of the complement binding and the cytoplasmic domain of Mac-t in the pathogenesis of Shwartzman will be elucidated. The results of these studies will greatly extend our understanding of Mac-l's role in neutrophil cytotoxicity and could lead to the identification of therapeutic targets that can interfere with this function. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MECHANISMS OF IMMUNE MEDIATED LUNG INJURY Principal Investigator & Institution: Clark, Joan; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2002 Summary: Acute lung injury is associated with systemic immune responses involving both cellular and cytokine components. Graft-vs.-host disease is such an immune response generated by donor T cells. In this project, we will use a novel murine model in which a systemic immune reaction initiated by transfer of cloned T lymphocytes of Th1 phenotype culminates in a remarkably selective inflammatory response (including vasculitis, alveolitis, and interstitial inflammation) is comprised of host derived mononuclear cells and activated alveolar macrophages. The central hypothesis that we propose to investigate in this model is hat Th1 cell activation initiates a multi-step sequence of signals that results in selective adherence of activated effector T cells in lung, amplification by selective recruitment of mononuclear cells, and accumulation of activated mononuclear cells and alveolar macrophages. Understanding what controls these events is crucial to defining strategies for modifying these fundamental biologic responses in patients. Our work in progress leads us to postulate that Th1 cell activation results in release of critical pro-inflammatory cytokines and expression of T cell integrins that initiate and direct lung specific inflammation, determined in part by selective up-regulation of vascular adhesion molecules in lung. The mechanisms that confer lung specificity in this model and specify mononuclear cell recruitment to lung are of primary interest to us. We think that the initial Th1 cell derived pro-inflammatory cytokine signals may not only influence vascular adhesion molecules, but also promote a subsequently set of host-derived signals that include chemokines/chemoattractants for mononuclear cells and pro-inflammatory cytokines. The regulation of these "downstream" events, may have important consequences in terms of a sustained inflammatory responses, and susceptibility to further lung injury. Our specific aims in this project are as follows: Aim 1. To identify mechanisms by which Th1 cells initiate lung inflammation. Aim 2. To determine mechanisms by which Th1 ell transfer results in selective mononuclear cell (host-derived) recruit to lung. Aim 3. To examine the effects of T cell transfer on alveolar macrophage function. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISMS OF VIRUS-INDUCED ELASTIC ARTERITIS Principal Investigator & Institution: Virgin, Herbert W.; Associate Professor; Pathology and Immunology; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2002; Project Start 15-DEC-1998; Project End 29-SEP-2002 Summary: We have developed a novel small animal model of virus induced elastic arteritis that will allow us to define fundamental mechanisms of vascular injury and the role of virus infection and the immune system in controlling or promoting chronic vascular pathology [Nature Medicine, 1997, 3(12):1346-1353]. Little is known about mechanisms that initiate inflammatory lesions of large elastic arteries, and the mechanisms underlying vasculitis are incompletely defined. Recently, attention has been paid to herpesviruses and activated lymphocytes as possible causes or cofactors in vascular injury. Mechanistic studies in a tractable model system have not been performed to determine how herpesvirus infection and the immune system interact to generate or control vascular pathology. We discovered that a newly characterized murine gamma-herpesvirus (gammaHV68) causes striking elastic arteritis in normal mice, and that interferon-gamma (IFNgamma) unresponsive mice and B cell deficient mice are much more susceptible than normal mice to induction of arteritis by gammaHV68. Further analysis revealed (i) a novel tropism of gammaHV68 for vascular smooth muscle cells, (ii) that productive replication is occurring in arteritic lesions, (iii) that IFNgamma acts primarily at the level of somatic cells, and (iv) the pathology of arteritic lesions in IFN-unresponsive and B cell deficient mice are strikingly different. To provide molecular tools for analysis of viral contributions to chronic arteritis we sequenced the genome of gammaHV68 (119,450 bp), demonstrating that gammaHV68 is closely related to the human gamma- herpesviruses Epstein-Barr virus and Kaposi's sarcoma herpesvirus. We have recently isolated mutant and marker rescue gammaHV68, and identified candidate latency-associated gammaHV68 genes. The availability of genetic tools for analysis of the host immune response arid the role of specific viral genes, will allow us to define mechanisms of gammaHV68 induced arteritis as follows. Aim 1. Determine the contribution of latent and productive gammaHV68 infection to chronic arteritis. Aim 2. Determine the mechanism by which IFNgamma regulates arteritis. Aim 3. Determine the mechanism by which B cells regulate arteritis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MICROVASCULAR HAEMOPHILUS
ENDOTHELIAL
CELL
REPONSE
TO
Principal Investigator & Institution: Behling-Kelly, Erica L.; Pathobiological Sciences; University of Wisconsin Madison 750 University Ave Madison, Wi 53706 Timing: Fiscal Year 2004; Project Start 01-MAY-2004; Project End 29-FEB-2008 Summary: (provided by applicant): This proposal incorporates a phased career development plan for a candidate with a long-standing interest in research and basic investigation skills. Under this phased plan, the first two years of training will incorporate methods development, preliminary experimentation, and didactic coursework selected to build on the candidate's background in clinical veterinary medicine. The following two years will be spent using the previously developed methods to intensively investigate aspects of bacterial infection of the central nervous system (CNS). The candidate will develop an in-vitro primary cell culture system to serve as a model for infection of the vasculature at the level of the blood-brain barrier. The system will be used to investigate the pathogenesis of a bovine CNS pathogen, Haemophilus somnus,
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(H. somnus). This pathogenic bacterium will serve as a model for infection at the bloodbrain barrier by related human CNS pathogens that are difficult to study as a result of host-restriction. The blood-brain barrier protects the brain parenchyma from foreign agents and inflammatory mediators and aids in the regulation of intravascular coagulation. The endothelial cell is the central cellular constituent of the blood-brain barrier. This project will focus on the role of the cerebral microvascular endothelial cell (CMVEC) in H. somnus cerebrovascular pathology. H. somnus infection can result in an acute neurological disease, pathologically similar to meningococcemia, characterized by a fibrinopurulent meningitis, haemorrhage with abscessation and a thrombotic vasculitis of the CNS. We will specifically investigate the interactions of H. somnus with the CMVEC relative to alterations in endothelial cell derived mediators of intravascular coagulation and inflammation, the role of the cytoskeleton in regulating vascular permeability, and apoptosis. Determining the mechanisms involved in destruction of the blood-brain barrier and localized coagulation in the CNS as a result of H. somnus infection could elucidate common pathogenic mechanisms used by other neurotropic bacteria, (i.e. Neisseria meningitides) to invade the CNS. Completion of this research project will also provide the candidate with the means to further build on her current research techniques and cognitive abilities, and acquire new technical laboratory skills that will assist in the candidate's progression to independence as a scientist. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MIDCAREER INVESTIGATOR AWARD IN PATIENT-ORIENTED RESEAR 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 01-MAY-2002; Project End 30-APR-2007 Summary: (provided by the applicant): Systemic lupus erythematosus (SLE) is a systemic inflammatory autoimmune disease that affects predominantly young, minority, pre-menopausal women. Up to 75% of patients with SLE experience some type of nervous system manifestations during their disease course (termed neuropsychiatric lupus or NPSLE). The most common manifestations include cognitive dysfunction, psychiatric disease and stroke, although the full range of NS involvement has not been well characterized. Two major areas of the candidate's research have been the study of 1) clinical and serologic predictors for the development of NPSLE, and 2) immune-mediated thrombosis related to antiphospholipid antibodies (aPL). The major thrust of this proposal will be to expand a strong clinical research program studying NPSLE in a cohort of predominantly Mexican-American SLE patients by 1) determining the frequency of and risk factors for accelerated atherosclerosis in this well-defined cohort and 2) evaluating the frequency and of microembolic signals (MES) by transcranial doppler (TCD) and the relationship between MES and cerebrovascular ischemia and cognitive dysfunction in 2 cohorts of SLE patients (UTHSCSA and Dusseldorf, Germany) with and without aPL. SLE patients are at increased risk for thrombotic events, including both myocardial infarction and stroke. Several NPSLE manifestations may have cerebral ischemia as a common underlying pathophysiologic mechanism, e.g. cognitive dysfunction and stroke. Potential causes of ischemia in SLE include vasospasm, microvascular disease, thrombosis with or without atherosclerosis, and rarely, vasculitis. The frequency of atherosclerosis in SLE, the importance of atherosclerosis in SLE-related stroke risk, or whether there are important genetic or racial influences are unknown. Traditional vascular risk factors, inflammatory, immunological, and treatment-related factors specific to SLE are all likely to be
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Vasculitis
involved. With the support of the Mid-Career Investigator Award, the candidate will work with a multidisciplinary team of established investigators and fellows in the areas of stroke, vascular and brain imaging, immunogenetics, epidemiology, psychiatry and neuropsychology. This collaborative effort will provide very important information regarding prevalence and extent of sub-clinical vascular disease and associated risk factors in SLE. Much will be learned about the relative importance of genetic factors and autoantibodies on vascular disease risk in SLE that is likely to apply to other populations also at increased risk for cerebral ischemia and vascular dementia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOLECULAR BIOLOGY OF ANTINEUTROPHIL CYTOPLASMIC AUTOANTIBODIES Principal Investigator & Institution: Nachman, Patrick H.; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 Timing: Fiscal Year 2002; Project Start 01-DEC-2001; Project End 30-NOV-2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: MOLECULAR ETIOLOGY OF FAMILIAL MEDITERRANEAN FEVER Principal Investigator & Institution: Gumucio, Deborah L.; Associate Professor; Cell and Developmental Biology; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 31-DEC-2007 Summary: (provided by applicant): Patients with the autosomal recessive disease, Familial Mediterranean fever (FMF), suffer periodic, unpredictable attacks of fever associated with severe pain; the pain is localized most commonly in joints (arthritis), abdomen (peritonitis) or chest (pleuritis). Occasionally, this disease presents with skin manifestations (erysipeloid erythema), pericarditis, vasculitis, or myalgia. In many patients, amyloidosis is a complication, and if untreated, this can be life-threatening. FMF is caused by missense mutations in pyrin, a protein of unknown function expressed in neutrophils, monocytes, eosinophils, dendritic cells, synovial cells and skin and peritoneal fibroblasts. Pyrin expression in these cells is induced by proinflammatory cytokines and by LPS. Thus, it has been speculated that pyrin modulates the inflammatory response. Evolutionary studies of the pyrin molecule indicate that it has been under positive Darwinian selection during evolution of the primates. Moreover, the high frequency of mutant pyrin alleles in several human ethnic groups supports a heterozygote (selective) advantage for the mutant allele. Mutant forms of pyrin may enhance the body's ability to clear important pathogen(s). Indeed, acute phase reactants, important agents of innate immunity, are up-regulated not only in patients but in carriers of mutant alleles. Structural analysis of the pyrin molecule revealed that exon 1 encodes a death-domain related structural motif (known as the pyrin domain or PyD) that is found in a growing family of proteins involved in inflammation and innate immunity. Identification of pyrin-interacting proteins as well as additional functional studies reveal that pyrin is linked directly to apoptotic and cytoskeletal signaling cascades, and that it modulates cytokine secretion. Experiments described in this proposal are designed to further explore these functions of pyrin and determine the effects of pyrin mutations on apoptosis (Aim 1); cytoskeletal signaling (Aim 2); and cytokine production (Aim 3). Recently identified pyrin isoforms will also be examined in these functional assays, since preliminary studies indicate that the
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various isoforms may function differently. Such studies could provide clues to understanding of the molecular pathogenesis of FMF, and may reveal new information about inflammatory pathways in general. In fact, pyrin-interacting proteins and pyrin domain-containing family members have already been connected to several human diseases, including inflammatory bowel disease, PAPA syndrome, Muckle-Wells syndrome, familial cold urticaria, Blau syndrome and Bechet's disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NIAMS MULTIDISCIPLINARY CLIN RES CTR: RHEUMATIC DISEASES Principal Investigator & Institution: Jordan, Joanne M.; Associate Professor; Medicine; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 Timing: Fiscal Year 2003; Project Start 09-MAY-2003; Project End 31-DEC-2007 Summary: (provided by applicant): The proposed Multidisciplinary Clinical Research Center (MCRC) is a natural outgrowth of the Epidemiology Education/Health Services Research Component of the Multipurpose Arthritis and Musculoskeletal Diseases Center of the Thurston Arthritis Research Center at the University of North Carolina at Chapel Hill. The center has a large cadre of experienced researchers and administrators with direct linkages to the Schools of Medicine, Public Health, Dentistry, Pharmacy, and Nursing and to the Departments of Medicine, Pediatrics, Orthopaedics, Family Medicine, Social Medicine, Radiology, Epidemiology, Health Behavior and Health Education, Health Policy and Administration, and Biostatistics. The objectives of the MCRC are 1) to conduct rigorous interdisciplinary clinical research in a variety of musculoskeletal conditions; 2) to direct a Methodology Core to support the methodological, analytical, and statistical needs of the funded projects and other future projects; and 3) to foster the development of new research ideas and the funding of new research projects in arthritis and musculoskeletal diseases. In order to achieve these goals, the proposed MCRC will consist of a Methodology Core, three clinical projects, and an Administrative Core. The Methodology Core will form the foundation of the Center and will serve the following functions: 1) methodological and biostatistical consultation and review; 2) measurement development; 3) data support services including data collection, data management, and analysis; 4) data and safety monitoring; and 5) teaching. The three proposed projects are 1) The role of metals in osteoarthritis in a multi-ethnic, rural population (Principal Investigator: Dr. Joanne Jordan); 2) Individual and Community Social Determinants of Arthritis Outcomes (Principal Investigator: Dr. Leigh Callahan); and 3) Social support, perceived control, and psychological adjustment in vasculitis patients and their partners (Principal Investigator: Dr. Robert DeVellis). The projects include epidemiologic and biobehavioral approaches to distinct patient populations: osteoarthritis in a specific rural community in North Carolina; arthritis in community family practices spanning the state of North Carolina; and small vessel vasculitis from practices across the Southeast. Each project is innovative and addresses issues which have rarely or never been examined in the context of arthritis and rheumatic diseases. A common theme to the area of inquiry of each project is that of influences and issues outside the realm of the individual. In the first project, environmental exposures are the forces outside the individual. In the second project, the focus is the impact of the socioeconomic status of the community in which one lives upon arthritis outcomes. Finally, the interaction of the individual and his/her spouse is the focus of inquiry of the third project. An Administrative Core will provide financial and scientific oversight and direction to the Center and will be
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Vasculitis
composed of a Director, an Associate Director, an Executive Committee, and support staff. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NICOTINIC RECEPTORS IN NONNEURONAL CELLS AS TARGETS FOR NICTOINE TOXICITY Principal Investigator & Institution: Conti-Fine, Bianca M.; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, Mn 554552070 Timing: Fiscal Year 2002 Summary: Bronco epithelial cells, endothelial cells and esophagus keratinocytes express nicotinic acetylcholine receptors of neuronal type (nAChR) sensitive to nicotine (Nic): the overall goal of the proposed studies is to identify new mechanisms of Nic toxicity resulting from a direct effect on those nAChRs. Block of the nAChR in bronchial epithelial and endothelial cells causes cell paralysis and cell-cell detachment. Long term exposure to Nic causes nAChR desensitization, and will likely result in cell-cell detachment, leading to bronchitis and esophagitis, atherosclerotic lesions, and facilitated entrance of carcinogenic compounds. Acute exposure of bronchial epithelial cells to Nic causes apoptosis, that might be an additional mechanism of Nic toxicity. The proposed studies will have three major (1 to 3), and three minor (4-6) specific aims: 1) to investigate the structural and functional properties of nAChRs expressed by bronchial epithelial cells, endothelial cells and esophagus keratinocytes; to extend these studies to lung alveolar epithelial cells; by patch clamp and binding studies using ligands specific for different nAChR subtypes; by immunohistochemistry, using antibodies and protein probes specific for different nAChR subtypes; by PCR using subunit specific primers, followed by cloning and sequencing of the products; by in situ hybridization using subunit specific probes. 2) to demonstrate in these cells the presence of the enzymes that metabolize ACh; by immunohistochemical and to demonstrate in these cells the presence of the enzymes that metabolize ACh; by immunohistochemical and biochemical assays of the enzymes choline acetyltransferase and acetylcholinesterase. 3) to investigate the cellular functions modulated by Nic and ACh binding , and the effects of acute and chronic Nic exposure in vitro, using functional assays of cell adhesion, motility, and proliferation, and by measuring the rate of cell death and apoptosis after exposure to Nic. 4) to investigate the possibility that the nAChRs expressed by bronchial epithelial cells are a port of entry for rabies virus, explained rabies cases that result from airborne exposure. 5) to investigate the characteristics of the endothelia nAChRs expressed in patients with Buerger's disease, a vasculitis of the limb blood vessels caused or triggered by tobacco usage. 6) to do pilot investigations to test whether nAChRs are expressed at other non-neuronal locations involved in tobacco toxicity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: OCULAR DISEASE IN GIANT CELL ARTERITIS Principal Investigator & Institution: Weyand, Cornelia M.; Professor; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2002; Project Start 01-AUG-1997; Project End 31-JUL-2006 Summary: (provided by applicant): Giant cell arteritis (GCA) is a sight-threatening systemic vasculitis with an immune-mediated pathogenesis. Vascular lesions, composed of activated T cells and macrophages, induce progressive, insidious vascular occlusion of medium-size arteries, resulting in tissue ischemia, such as ischemic optic neuropathy. Our long-term objective has been to unravel the mechanisms by which
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lymphocytes and macrophages are recruited to the vessel wall, differentiate into specialized effector cells, and promote GCA. During the last four years, we have made progress towards these goals by dissecting macrophage effector pathways that lead to arterial injury and the artery's response-to-injury program. Most importantly, we have provided evidence that the primary defect in GCA is a breach of T-cell tolerance and that T-cell activation occurs in the adventitia where dendritic cells (DC) initiate and maintain T-cell stimulation. We hypothesize that adventitial DC are key players in generating immunological privilege for the artery and that breakdown of this immune protection causes GCA. This hypothesis includes that structural and cellular components of the adventitia create the unique target-tissue susceptibility and agedependence of GCA. Experiments to test this hypothesis will use a temporal arteryNOD/LtSz-Rag1 (tm1 Mom) mouse chimera model. The specific aims of this proposal are to: 1) Examine the heterogeneity of adventitial DC and vasa vasorum networks in different vascular beds and at different ages. Three-dimensional rendering of capillary networks in the adventitia and their relationship to DC indigenous to the adventitia will be examined by microcomputed-CT to define a model for the targeting of GCA to extracranial arteries in elderly individuals. 2) Determine the mechanisms of immune tolerance promoted by adventitial DC. These experiments will use adoptively transferred T cells in mouse chimeras. 3) Investigate the functional profile of adventitial DC in GCA and polymyalgia rheumatica (PMR), a forme fruste of GCA. Diseaserelevant defects in DC function will be identified by gene expression profiling. 4) Explore the mechanisms of inappropriate arrest and premature differentiation of DC in PMR and GCA arteries. These studies will focus on pathways regulating the life cycle of DC and deviations leading to vasculitis. 5) Explore the therapeutic implications of modulating DC function in GCA. We will proceed with two approaches, TNF-alpha inhibitors and tolerogenic DC, in the attempt to disrupt persistent DC and T-cell activation in GCA. These experiments will help us understand the immunobiology of healthy and inflamed arteries, advance our understanding of the events initiating vasculitis, and may provide new avenues for therapeutic intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PATHOGENESIS KAWASAKI DISEASE Principal Investigator & Institution: Rowley, Anne H.; Pediatrics; Northwestern University Office of Sponsored Research Chicago, Il 60611 Timing: Fiscal Year 2002; Project Start 01-FEB-2000; Project End 31-DEC-2003 Summary: Kawasaki Disease (KD) is an acute, potentially fatal vasculitis of young children which predominately affects the coronary arteries. KD affects children of all nations and ethnic groups, and has replaced acute rheumatic fever as the most common cause of acquired heart disease in children in the U.S. and Japan. At Children's Memorial Hospital in Chicago alone, 65 new acute KD cases were diagnosed in 1998. Despite the fact that KD has become a significant pediatric problem in the U.S. the etiology and pathogenesis remain undefined. Our long-term objective is to determine the pathogenesis of KD. The overall goal of this proposal is to investigate the role of IgA and IgA plasma cells in the development of KD vasculitis. Recent studies from our laboratory indicate that IgA1 plasma cells infiltrate the vascular wall in acute KD. Preliminary data indicate that IgA genes in the vascular wall in acute KD are oligoclonal, suggesting that the IgA response in KD is directed toward specific antigens, either those of the potential pathogen(s) causing the illness, or host antigens by a molecular mimicry mechanism. Preliminary data also indicate that IgA plasma cells are present in markedly increased numbers in the respiratory and GI tracts of KD patients
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when compared with age-matched controls. Other preliminary data indicate that serum IgA1 in acute KD sera is aberrently glycosylated and therefore is likely to have altered properties. Our hypothesis is that KD is an immune-mediated vasculitis triggered by a mucosal pathogen, and that IgA plays a prominent role in pathogenesis. We propose to determine whether an oligoclonal IgA response is characteristic of KD. We will also determine glycosylation profiles of IgA l in KD sera. We will determine the distribution of IgA plasma cells in KD tissues using our established tissue repository of acute fatal KD cases. We will also characterize glycosylation profiles of IgA in the infiltrating plasma cells and determine whether these plasma cells produce matrix metalloproteinases (MMPs), matrix-degrading enzymes that participate in abdominal aortic aneurysm formation and that are produced by plasma cells in inflammatory diseases. These studies will elucidate the role of IgA and IgA plasma cells in the pathogenesis of KD, and will have important implications for potential diagnostic and treatment strategies for this increasingly recognized, potentially fatal childhood illness. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PATHOGENESIS OF COCAETHYLENE-INDUCED VASCULITIS Principal Investigator & Institution: Tacker, Danyel P.; Pathology; University of Texas Medical Br Galveston 301 University Blvd Galveston, Tx 77555 Timing: Fiscal Year 2002; Project Start 01-JUN-2002 Summary: (provided by applicant): Vasculitis is a common pathological outcome in cocaine addicts, 80% of whom co-abuse cocaine and ethanol. We believe that the use of cocaethylene (CE, a conjugate of cocaine and ethanol, produced in vivo) in studies of cocaine abuse will accurately represent pathogenic sequelae. Our long-term goal is to better understand the cellular and subcellular mechanisms of CE-associated vasculotoxicity, and propose to demonstrate the role of cations in CE-associated vasculotoxicity. Aim #1: CE exposure in human umbilical vein endothelial cells (HUVEC) induces pro-inflammatory activation and permeability. HUVEC monolayers exposed to CE or saline will be analyzed for CE (Gas Chromatography-Mass Spectrometry), and electrolyte (electrolyte analyzers) and oxygen/carbon dioxide levels (gas analyzers). Fixed monolayers will be stained for counting of intercellular gap formations (silver stain), and surface markers of activation (immunohistochemistry). Aim #2: CE exposure in HUVEC activates pro-inflammatory signaling/gene expression pathways. CE or saline treated monolayers will be tested for RNA and protein expression and activity changes utilizing electrophoretic mobility shift assay and supershift, RNAse protection assay, and Western blot. Targets are signaling and activation markers, and include Nuclear Factor kB, interleukin-8, and Vascular Cell Adhesion Molecule-1. Aim #3: HUVEC activation after exposure to CE is associated with high sustained cytoplasmic cation flux. Monolayers of HUVEC will be treated with CE and intracellular cation flux (calcium, magnesium, and hydronium) recorded utilizing fluorescence spectrometry. Flow cytometry and/or Western blotting will be used to monitor changes in calcium channel density over time. The proposed Aims will provide further insight into the pathogenic sequelae resulting from production of CE in humans. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PET ENCEPHALOPATHY
AND
MRI
IMAGING
OF
PERSISTENT
29
LYME
Principal Investigator & Institution: Fallon, Brian A.; Associate Professor of Clinical Psychiat; Psychiatry; Columbia University Health Sciences Po Box 49 New York, Ny 10032 Timing: Fiscal Year 2002; Project Start 08-DEC-1999; Project End 30-NOV-2003 Summary: This project tests specific hypotheses about functional and structural brain abnormalities in patients with Persistent Lyme Encephalopathy (PLE) and it cvaluates the efficacy of 10 weeks of IV ceftriaxone among patients previously treated with shorter courses of Iv antibiotics. Prior planar rCBF and SPECT studies of PLE reveal diffuse deficits affecting cortical and subcortical areas, primarily the white matter. These scans are often interpreted as consistent with vasculitis, multi-infarct dementia, or Lyme Disease. MRI series demonstrate that between 20-400/o of patients have hyperintensities, suggestive of inadequate arteriolar perftision resulting in demyelination and gliosis. To understand better the significance of these imaging abnormalities, this project will employ MRI and PET imaging and cognitive testing: a) to examine whether the functional imaging deficits are primarily vascular or metabolic in nature; b) to evaluate whether time course of improvement in MRI and PET scans correlates with clinical cognitive improvement; c) to identify whether deficits in blood flow (CBF), cerebral metabolism (CMR), and extent of MRI hyperintensities have prognostic significance; and d) to determine whether a subgroup of patients with poor outcome PLE have impaired vascular reserve 60 patients with PLE and 20 matched controls will be studied over 4 years. A second major goal is to determine the efficacy of a 10 week placebo-controlled trial of IV ceftriaxone in PLE using objective behavioral and imaging measures. After treatment, patients will be monitored off antibiotics to week 24. Durability of response will be examined by cognitive retesting at wk 48. Imaging procedures include MRI (T1 sagittal, 3D volumetric, T2 spin echo, FLAIR, and magnetization transfer sequences), O15. H2O PET during rest and hypercapnia, and FDG PET assessment of resting rCMR. We will test specific hypotheses about reversible and fixed functional and structural abnormalities that may account for antibiotic responsive and -unresponsive PLE. These hypotheses derive from histopathological studies indicating that a subgroup of patients with PLE have evidence of a vasculitic process that may lead to a syphilis-like endarteritis obliterans, with impairment in hcmodynamic reserve. This study will enhance our understanding of the pathophysiology and treatment of patients suffering with the disabling effects of persistent Lyme encephalopathy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PILOT-CHARACTERIZATION INFLAMMATION
OF
CXCL
16
IN
RENAL
Principal Investigator & Institution: Garcia, Gabriela E.; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: CXCL16 is a novel, unique CXC chemokine with characteristics of CC chemokines and structurally related to CX3CL1 since both are membrane bound chemokines. CXCL16 is expressed in antigen presenting cells including CD19 + B cells and CD14 + monocyte/macrophages. We have found that this chemokines is also expressed in glomerular endothelial cells. This chemokine was markedly induced in the glomeruli of Wistar-Kyoto rats with anti-glomerular basement membrane (GBM)
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antibody (Ab) glomerulonephritis (GN) throughout the disease and CXCL16 induced migratory response of glomerular infiltrate isolated from this model of GN. This data suggest that CXCL16 may play a critical role in the leukocyte influx in immunemediated inflammation in the kidney. We propose to study the mechanism of CXCL16 regulation and signaling in glomerular endothelial cells as well as the CXCL16/CXCR6 interactions mainly between glomerlular endothelial cells and monocyte/macrophages. We will study the potential role of CXCL16 in leukocyte capture and firm adhesion and whether this effects can be mediated under physiological flow conditions. We will further dissect this multidomain chemokine to determine the functional domain(s) in CXCL16-mediated adhesion. In in vivo studies we will analyze the functional role of CXCL16 during the progression of acute injury to renal fibrosis in a model of GN and tubulointerstitial nephritis by generating blocking antibodies. Further we will investigate whether blocking CXCL16 could intervene in the progressive phase of established GN and tubulointerstitial nephritis. These findings are expected to offer an approach to therapy that influences the regulation of chemokine/chemokine receptor to modulate renal diseases that may be CXCL16 associated, including tubulointerstitial nephritis, GN and endothelium-related inflammatory diseases such as vasculitis, allograft rejection, ischemia/reperfusion injury and atherosclerosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: POST PROCESSING FOR IMPROVED VESSEL DETAIL IN MRA Principal Investigator & Institution: Parker, Dennis L.; Professor; Radiology; University of Utah Salt Lake City, Ut 84102 Timing: Fiscal Year 2003; Project Start 01-SEP-1995; Project End 31-JAN-2005 Summary: Our intent in this project has been to improve the small vessel visibility in MIP images of 3D TOF MRA studies. During the first 3 years we tested the effectiveness of a non-linear vessel enhancing filter applied to the original 3D TOF MRA image data. In trying to understand the strength of the MIP algorithm in vessel display and to understanding the properties of vessels, we noticed the striking difference between the nature of "vessels" and background in the MIP depth buffer (the matrix of z-locations of points projected in the MIP). Vessels are predominantly smooth and connected while background is "rough". In trying to utilize this property to enhance the probability of vessel pixels, we have developed an algorithm which nearly completed extracts vessel voxels from the 3D MRA data, and excludes nearly all background. Using these extracted voxels, we have been able to generate X-ray like projection images of the 3D MRA image data which inherently contained more information than the MIP, leading to a striking improvement in vessel appearance. Nearly every vessel seen in the original MAP and some not seen are visible in these reproject images with the exact appearance of a digital subtraction X-ray angiogram (DSA). In the next funding period we will perform a large series of tasks designed at refining this new depth buffer segmentation (DBS) algorithm. After refining the algorithm, we will test the extent to which the DBS algorithm improves the accuracy and efficiency of detection and management of a variety of intracranial pathologies such as aneurysms and vasculitis. We will also study the application to other vascular systems. Because the algorithm extracts the image coordinates of the voxels that make up the vessels for which segments are visible in the MIP, we will develop algorithms which convert these lists of segmented voxels to a cubic spline representation, where the anatomic labels of the vessels are included. We will study methods to use this knowledge of the patients vascular anatomy to develop techniques to assist in the optimized presentation of the MRA information for improved diagnostic accuracy and efficiency. We will also test the application of the 3D vessel
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structure obtained from the DBS algorithm to improve surgical procedure planning and other applications. We believe that an improved version of this exciting new algorithm will improve the efficiency and accuracy of MRA in general. Experiments to characterize, improve and clinically evaluate this algorithm are described in this proposal. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PR3-ANCA SUBSETS AND DISEASE PHENOTYPE Principal Investigator & Institution: Specks, Ulrich; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2002; Project Start 15-SEP-2002; Project End 31-JUL-2006 Summary: (provided by applicant): Wegener's granulomatosis (WG) is the prototype of vasculitides associated with antineutrophil cytoplasmic antibodies (ANCA). The determinants of specific organ involvement and disease relapses remain unclear. A large body of experimental evidence supports the hypothesis of a pathogenic role of ANCA in the development of vasculitis. Yet not every patient with persistent ANCA following treatment has active disease, and recurrent ANCA do not invariably herald vasculitis flares. The most prominent target antigen for ANCA in WG is proteinase 3 (PR3), a serine protease contained within azurophilic granules of the neutrophil. Preliminary studies indicate that not only the type of ANCA (e.g., anti-PR3 or anti-myeloperoxidase antibodies), but particularly PR3-ANCA subsets may influence the prognosis and spectrum of clinical presentations. The development of novel, mechanism-based therapeutic interventions requires detailed understanding of the specific pathogenetic interactions of these antibodies with their target antigen. Consequently, the proposed studies are designed to test the following general hypothesis: PR3-ANCA subtypes, reacting with different structural epitopes of PR3, modulate PR3 functions and thereby affect clinical disease expression. To address this hypothesis, we will pursue the following specific aims. (1) We will determine the predictive value for disease relapse of PR3-ANCA reacting with pro-PR3, compared to that of ANCA reacting with mature PR3. (2) We will determine the clinical relevance of PR3-ANCA reactivity with different glycosylation variants of PR3. (3) We will identify PR3-ANC reactivity with specific epitopes and their relationship to organ manifestations, disease activity and duration of disease. (4) We will determine the functional impact of PR3-ANCA subsets on PR3 and its relation to organ manifestations, disease activity and duration of disease. The proposed studies will be performed using samples collected in the context of the Wegener's Granulomatosis Etanercept Trial (WGET). By investigating samples from this unique patient population, rigorously characterized in a prospective fashion according to disease activity and organ manifestations, we will be able to identify clinically relevant PR3-ANCA subsets and determine their impact upon disease manifestations. This study will provide new insights into the potential pathogenic role of PR3-ANCA that are not obtainable in any other way, and will constitute the most definitive study of these antibodies to date. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PROTEINASE MODULATION DURING T-CELL-ENDOTHELIAL ADHESION Principal Investigator & Institution: Madri, Joseph A.; Professor; Pathology; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2002; Project Start 01-AUG-1995; Project End 31-MAR-2005
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Summary: (Applicant's abstract): Our hypothesis is that adhesion molecule-dependent modulation of T cells and endothelia modulates not only adhesive functions, but also initiates specific protease induction, surface assembly, and activation which facilitates transmigration, as well as changes in adhesive properties of the T cells which affects residency of the cells at the site of inflammation. T cell transmigration through the endothelial cell layer and migration into the underlying and surrounding extracellular matrix is initiated by T cell adhesion to the endothelium, mediated by specific ligands resident on the surfaces of both the T cell [VLA-4 (a4B1)] and the endothelial cell (VCAM-1). We have demonstrated that engagement of this receptor/ligand pair evokes changes in MMP-2 expression and activation, consistent with the manifestation of an invasive phenotype in the adherent T cell population and an "activated" phenotype in the endothelial cells. Resultant proteolysis of basement membrane and interstitial matrix components is thought to facilitate T cell extravasation out of the affected vessel and toward the site of inflammation and angiogenesis. In this proposal we will: 1) determine, compare and contrast the MT1-MMP/TIMP-2/MMP-2 ternary complex characteristics in T lymphocytes and endothelial cells following their stimulation. 2) continue our characterizations of the MT1-MMP and MMP-2 promoters and their respective pertinent transcription factors. 3) identify, characterize, compare and contrast the signal transduction pathways involved in MT1-MMP and MMP-2 induction, complex formation, activation and clustering in T lymphocytes and endothelial cells. These aims will be accomplished with a combination of methodologies including an in vitro culture model utilizing antigen-specific murine T cell clones and lines; an in vivo adoptive transfer murine model of experimental allergic encephalomyelitis (EAE) and a variety of cellular and molecular biological techniques including cell culture, zymography, reverse zymography, immunoprecipitation, Western blotting, Northern blotting, transfection and stable expression of selected gene products, histology, immunohistochemistry, MALDI-TOF, DNA array analyses and the use of selected transgenic and knockout mice. These experiments will lead to a better understanding of T cell migration through and interaction with local extracellular matrix and the development of new and novel therapies directed at modulating selected proteinase/proteinase inhibitor cascade systems in the inflammatory processes of arthritis, vasculitis, and tissue rejection organ. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PULSE IV GLUCOCORTICOID INFUSION AS INITIAL TREATMENT OF GIANT CELL ARTERITIS Principal Investigator & Institution: Mazlumzadeh, Mehrdad; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2002 Summary: Giant Cell Arteritis (GCA, temporal arteritis) is a vasculitis of the medium and large-sized arteries that usually presents with headache and visual disturbances in patients over the age of fifty. Conventional treatment with oral glucocorticoid (GC, steroid, prednisone) for up to two to three years has been the only known efficacious therapy to suppress the inflammatory process and prevent associated vascular complications. However, the long duration and the cumulative dose of GC therapy frequently results in multiple adverse effect. Recent studies have shown several relapses and persistence of inflammation based on elevated inflammatory markers such as interleulin-6 despite timely oral GC therapy. Investigations on animal models suggest the need for much higher doses of GC to appropriately treat the vasculitic process. This forms the basis of our proposed study which is a randomized, double-blinded, placebo-
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controlled, prospective clinical trial where biopsy proven GCA patients will be treated with high dose pulse intravenous (IV) GC initially followed by lower doses of oral GC. We hypothesize that this will result in shorter length of therapy with lower dose of GC and hence reduced adverse effects. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF ANTI-PROTEINASE-3 IN WEGENER'S VASCULOPATHY Principal Investigator & Institution: James, Judith A.; Associate Professor; Oklahoma Medical Research Foundation Oklahoma City, Ok 731045005 Timing: Fiscal Year 2002; Project Start 30-SEP-1999; Project End 30-JUN-2004 Summary: Wegener's granulomatosis (WG) is a multisystem disease of unknown etiology which is characterized by small to medium vessel vasculitis, pauci-immune glomerulonephritis, necrosis/granuloma formation of the respiratory tracts and autoantibodies to neutrophilic components. Although the underlying pathophysiology of this disorder remains an enigma, several lines of evidence strongly support c-ANCA, particularly anti-PR3, has a role in disease pathogenesis. Unfortunately, the specific mechanisms that initiate and perpetuate this anti-PR3 response remain to be elucidated. One approach to delineate a potential etiology for these autoantibodies, and/or to understand their role in the pathogenesis of vasculitis would be to fully characterize the antigenic determinants of the PR3 autoantigen. By defining the common autoantigenic targets of PR3 we could arrive at molecular mimicry triggers for this autoimmune response. An animal model of WG autoimmunity could show to what tissues particular epitopes are targeted. Over the past decade our lab has conducted extensive work on the immunochemistry of lupus autoantigens (1-7). These previous studies provide the technical background for this proposal. Epitope mapping experiments of the spliceosomal autoantigens have led to our peptide induced model of lupus autoimmunity (8,9). We will now apply these well-honed techniques, as well as a similar scientific strategy, to analyze the humoral fine specificity of the WG reponse to PR3. Early work in the lab of Ralph Williams suggests that sequential eptiopes are common targets of PR3. Exciting new results from our co-PI's lab uncover a potential mechanism of anti-PR3 vascular damage. He has observed that PR3 can bind to endothelial protein C receptor (EPCR), a regulatory protein in the protein C anticoagulant pathway and that this binding is inhibited by c-ANCA. He has also observed that EPCR can inhibit tight neutrophil to activated endothelium and the subsequent spreading/activation. These observations lead to the hypothesis that EPCR plays a role in regulating leukocyte adhesion and activation, in part through interactions with PR3, and that antibodies to PR3 disrupt this physiological regulation contributing to the vascular damage in WG. This RFA response seeks to integrate the strengths of two labs to build on these early observations and to identify the common humoral epitopes of PR3, to track the development of the humoral autoimmune response of WG patients to PR3 over time, to develop an animal model of vasculitis, to evaluate EPCRs influence on the c-ANCA-PR3 interaction, and to identify the common T cell targets in WG. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ROLE OF COMPLEMENT FACTOR B IN THE PATHOGENESIS OF SLE Principal Investigator & Institution: Gilkeson, Gary S.; Professor; Medicine; Medical University of South Carolina 171 Ashley Ave Charleston, Sc 29425 Timing: Fiscal Year 2002; Project Start 01-APR-2000; Project End 31-MAR-2005
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Summary: (Adapted from the Investigator's abstract): The complement cascade plays an important role in the pathogenesis of immune complex mediated diseases, including lupus nephritis. The alternative complement pathway is activated in lupus nephritis, though its role in the pathogenesis of disease is unclear. To provide insight into the role of the alternative pathway, and specifically the role of Factor B (Bf), in disease, mice deficient in Bf were derived. Bf deficient mice were found to have normal immune function despite being unable to activate the alternative pathway. To determine what role Bf and the alternative pathway play in autoimmune disease, we bred the Bf knockout genotype to the lupus prone MRL/lpr background. Compared to Bf expressing litter mates, the Bf deficient MRL/lpr mice developed significantly less proteinuria, pathologic renal disease, glomerular IgG immune deposits and vasculitis. Surprisingly, C3 levels were normal in the MRL/lpr Bf deficient mice in contrast to significantly, depressed levels in the Bf producing litter mates, typical of disease in MRL/lpr mice. These findings suggest Bf has a key pathogenic role in lupus nephritis in MRL/lpr mice and that the alternative pathway is an important mechanism for C3 activation and consumption in MRL/lpr disease. Our central hypothesis is that Factor B and the alternative pathway are pro-inflammatory in lupus and that blocking Factor B activity provides a novel approach to treating this disease. To further define the role of Factor B in immune complex mediated diseases and activation of C3, the following specific aims are proposed: Aim 1- Determine the mechanisms by which renal damage is diminished in Bf deficient MRL/lpr mice. Aim 2 - Determine the mechanism for the maintenance of normal serum C3 levels in MRL/lpr Bf-/- mice. Aim 3 - Identify the effects of Bf deficiency on autoimmune B cell function including isotype switching and tolerance as well as macrophage/mesangial cell function. Aim 4 - Determine the potential for disease modification by inhibition of Bf activation using additional therapeutic strategies and models of glomerular injury. These studies will provide new insight into the role of the alternative pathway in disease and potentially provide a new therapeutic target (Factor B) in immune complex mediated diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF MAC-1/ICAM-1 INTERACTIONS IN VASCULITIS Principal Investigator & Institution: Kevil, Christopher G.; Genetics; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2002; Project Start 01-MAR-2002; Project End 31-MAY-2002 Summary: The role of leukocyte activation and leukocyte-endothelial cell interactions remains poorly understood and characterized in vasculitic pathologies. This laboratory has recently reported that ICAM-1 deficient MRL/MpJ-Fas/lpr mice demonstrate reduced vasculitic lesion formation and vessel necrosis. This project will investigate the hypothesis that ICAM-1/Mac-1 interactions between leukocytes and arterial endothelial cells mediate leukocyte activation, arterial endothelial cell damage, and subsequent arterial vessel necrosis observed in vasculitic lesions. The hypothesis will be examined using both Mac-1 and ICAM-1 mutant mice that have been backcrossed onto the MRL/MpJ-Fas/lpr background, a strain that spontaneously develops vasculitis. The first specific aim is to compare vasculitic lesion formation between Mac-1 mutant and Mac-1 wild type MRL/MpJ-Fas/lpr mice. The role of Mac-1 expression will be determined during various stages of vasculitis development using pathological grading studies. The second specific aim will determine the role of Mac-1/ICAM-1 interactions in leukocyte activation and endothelial cell damage in vitro. Mesenteric arterial endothelial cell cultures will be used to measure neutrophil adhesion of Mac-1- mutant and wild type neutrophils to both ICAM-1 mutant and wild type MRL/MpJ-Fas
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measure neutrophil adhesion of Mac-1 mutant and wild neutrophils to both ICAM-1 mutant and wild type MRL/MpJ-Fas lpr endothelial cells. Leukocyte activation and endothelial cell cytotoxicity will also be determined using Mac-1 mutant and wild type neutrophils with this in vitro model. The combined in vivo and in vitro approach of this project will significantly advance our understanding of the role of leukocyte adhesion and leukocyte mediated vessel necrosis in vasculitis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SKIN DISEASES RESEARCH CORE CENTER Principal Investigator & Institution: Caughman, Stewart W.; Professor and Chair; Dermatology; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2002; Project Start 01-MAR-1994; Project End 30-APR-2004 Summary: The Emory Skin Disease Research Core Center (ESDRC) will foster, coordinate and enhance collaborative efforts among 24 clinical and basic scientistic from a wide range of research disciplines. Their expertise will be focused on mechanisms of cutaneous disease as well as cutaneous biology, with special emphasis on the role of the cutaneous microvasculature in these processes. This emphasis will take advantage of an outstanding, multidisciplinary group of endothelial cell biologists, many of whom have never before focused their expertise on the skin. Combined with the expertise and experience of the investigators in the Department of Dermatology, this group of scientists centered at the ESDRC will provide novel insights into the role of cutaneous microvascular endothelial cells in a variety of skin-related biologic and pathologic processes, including acute and chronic inflammation, wound healing, angiogenesis, vasculitis, Kaposi's sarcoma, and tumor metastasis. Capitalizing upon the diversity of expertise and existing Emory research centers and services, the ESDRC will be organized into three scientific cores: 1) the Tissue Culture and Antibody Production Core; 2) the Microchemical Component; and c) a Flow Cytometry/Cell Sorting Component; and finally 3) the analytical approaches, a diversity of expertise, and continuous training for all ESDRC investigators and the research fellows in their laboratories. As a consequence, these facilities will greatly enhance the productivity of participating investigators. Additionally, six pilot and feasibility studies have been selected from a group of 13 submitted for review. All of them are focused on dermal microvascular cells and demonstrate application of a broad spectrum of expertise, techniques,and scientific rationale not currently being utilized in the study of cutaneous biology in general, and the dermal microvasculature in particular. Additionally, a comprehensive and multidisciplinary Enrichment Program will provide regular seminars, workshops, and visiting scientist presentations that will greatly enhance the research and educational environment at Emory. The long term goals of the ESDRC are to provide novel insights and approaches into cutaneous pathologic and physiologic processes through fostering and coordinating a multidisciplinary research approach among a variety of nationally recognized investigators and their laboratories. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SOCIAL SUPPORT AND PERCEIVED CONTROL IN VASCULITIS Principal Investigator & Institution: Devellis, Robert F.; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 Timing: Fiscal Year 2003; Project Start 01-JAN-2003; Project End 31-DEC-2007 Summary: Until recently, few successful treatment options existed for patients with ANCA (anti-neutrophil cytoplasmic antibodies) positive vasculitis and the illness was
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associated with high mortality rates. Advances in medical treatment have improved rates of survival substantially. Psychosocial aspects of the illness, however, remain largely unexplored. Yet, the course of the illness and its treatment with effective but potentially toxic drugs raise significant challenges for patients and their spouses. Paralleling the advances in the medical treatment of ANCA vasculitis, are advances in the conceptualization and operationalization of important psychological constructs including social support and perceived control. Although these variables have been studied for decades, they have often been approached in a nonspecific way that paid little attention to underlying processes. More recently, approaches have been developed that capture the true transactional nature of social support and perceived control and have provided new insights concerning how they can be beneficial. This study proposes to examine these processes among patients with ANCA vasculitis. We hypothesize that disease activity will have an adverse effect on psychological adjustment in both patients and spouses. We further hypothesize that this effect will be mediated by aspects of support and perceived control. More specifically, we believe that two specific, processoriented facets of support, empathic accuracy and transformation of motivation, and an interpersonally-defined facet of perceived control, dyadic efficacy, will attenuate the adverse affects of illness severity. To test these hypotheses, we will study 120 couples in which one partner has ANCA vasculitis. At two time periods, we will assess empathic accuracy behaviorally using the "dyadic interaction paradigm" technique and transformation of motivation by two different self-report methods. On these same occasions, we will also assess dyadic efficacy, using a scale currently under development as part of a related research project. In addition to testing these hypotheses, a further aim of the proposed study is to develop a self-report measure of perceived empathy that avoids the limitations of existing instruments and that can be validated against the gold-standard, behaviorally-based, dyadic interaction paradigm procedure. Such a tool would greatly enhance the utility of empathic accuracy by making its assessment less demanding to investigators. In summary, the proposed research will apply novel, state-of-the-art methods of assessing process-oriented features of social support and perceived control to a patient population that has been largely overlooked by social and behavioral scientists. Through this research, we hope to gain new insights into how these patients and their spouses adjust to ANCA vasculitis that will eventually lead to improvements in their quality of life. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SYSTEMIC VASCULITIS--HOST FACTORS IN TISSUE INJURY Principal Investigator & Institution: Kimberly, Robert P.; Professor; Medicine; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2002; Project Start 15-SEP-1994; Project End 31-AUG-2004 Summary: (adapted from the Investigator's abstract): In the systemic vasculitides, recent genetic and mechanism-based observations have emphasized the role of immune complexes (IC) and anti-neutrophil cytoplasmic autoantibodies (ANCA) as two major pathogenic mediators. Both play a central role in the recruitment and activation of neutrophils and mononuclear phagocytes, which is critical in the tissue injury in vasculitis. While the process of vascular injury in vivo is no doubt complex, new insights into the genetics, structure, and function of human Fc-gamma receptors (Fcgamma R), which interact with IC and ANCA and into the cell programs initiated by these receptors on phagocytes have brought critical new areas of research into clear focus. These new areas provide an opportunity to define genetic risk factors for disease predisposition and to develop targeted therapeutic strategies. The molecular complexity
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of human Fc-gamma R includes allelic polymorphisms that are genetically distinct. For example, the Fc-gamma RIIa-H131 allele is the only human Fc-gamma R that recognizes human IgG2 efficiently, thus establishing the precedent for interaction between the qualitative and quantitative nature of the humoral immune response and defined Fcgamma R genotypes. This molecula complexity also includes distinct receptor isoforms that, on neutrophils, engage different signal transduction pathways. These observations, coupled with new insights into complement receptor 1 (CR1; CD35), provide 1) a genetic basis for individual differences in patient responses in vasculitis; 2) a framework for understanding how the properties of autoantibodies, such as IC or ANCA antibodies, interplay with Fc-gamma R in phagocytes to lead to tissue damage, and 3) a potential strategy for selective modulation of receptor function. It is hypothesized that: 1) Fcgamma RIIIb expressed on neutrophils engages a distinct signal transduction pathway and elicits a unique cell program; 2) that, like KIR in NK cells, Fc-gamma RIIb and CR1 function as important negative regulators of Fc-gamma R-initiated programs in myeloid cells; 3) that participation of these negative regulators may explain the different biologies of ANCA and IC for neutrophils and mononuclear phagocytes, and 4) that allelic polymorphisms in expression and function will play an important role in disease risk and phenotype. Studies are proposed to characterize the pathways of neutrophil activation by the two neutrophil Fc-gamma R (Fc-gamma RIIIb and Fc-gamma RIIa) and define this differential activation at the levels of gene transcription and integrated cell programs. In addition, studies are proposed to characterize the mechanisms through which CR1 and Fc-gamma RIIb function as negative regulators in phagocytes, and these findings will be related to the representation of Fc-gamma R alleles, CR1 alleles, adhesion molecule alleles (E-selectin, ICAM-1) and clinical manifestations in two prototypic paradigms of systemic vasculitis; ANCA positive vasculitis (Wagener's granulomatosis, microscopic polyangiitis) and cryoglobulinemic leukocytoclastic vasculitis. These studies may identify risk factors for disease predisposition and new approaches for targeted therapeutics. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THE PROTEIN C RECEPTOR AND WEGENER'S VASCULOPATHY Principal Investigator & Institution: Kurosawa, Shinichiro; Oklahoma Medical Research Foundation Oklahoma City, Ok 731045005 Timing: Fiscal Year 2002; Project Start 10-MAY-2000; Project End 30-APR-2004 Summary: (Adapted from the Investigator's abstract): The investigators present a series of studies that link the soluble endothelial protein C receptor (EPCR), a member of the protein C anticoagulant pathway, with Wegener's granulomatosis, an autoimmune disease characterized by granulomatous inflammation and necrotizing vasculitis. They have observed that soluble EPCR can bind to activated neutrophils and this binding is mediated in large part by proteinase-3 (PR3), the target of the autoantibodies (cANCA) in Wegener's patients, and a beta2 integrin. EPCR binding to PR3 on cells or in purified systems is inhibited by cANCA. A monoclonal antibody to the beta2 chain of the leukocyte adhesion molecules (CD18) and an antibody to the unique alpha chain of Mac-1 (CD11b) also block binding of soluble EPCR to activated neutrophils. Finally, soluble EPCR can block tight adhesion of neutrophils to TNF alpha-activated endothelial cells. These observations elicit their working hypothesis that PR3 interaction with the beta2 integrin plays a role in leukocyte adhesion and soluble EPCR blocks this function by masking a key site on PR3. cANCA interferes with soluble EPCR binding to the PR3-beta2 integrin complex, thus preventing the negative regulatory function of EPCR. Their specific aims are to investigate the structure-function relationships of
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EPCR-PR3-beta2 integrin interactions by defining pair-wise interaction parameters and the influence of these complexes on neutrophil signaling and adhesion functions. The specific aims are to: 1) characterize the soluble EPCR-PR3 binding complex; 2) investigate the pair-wise interactions governing soluble EPCR-PR3-beta2 integrin complex formation; and 3) evaluate the influence of cANCA on the EPCR-PR3-beta2 integrin interaction with regard to neutrophil adhesion. Their studies focus on how soluble EPCR may influence leukocyte trafficking and the role of cANCA in modulating this process. Results from these studies will contribute to the identification of novel mechanisms of cANCA-mediated endothelial injury in vasculitis of Wegener's granulomatosis. In addition, the results will provide a foundation for future studies investigating potential therapeutic targets that modulate neutrophil-mediated endothelial injury, particularly for cANCA-mediated vasculitis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TRANSLATIONAL RESEARCH IN SYSTEMIC VASCULITIS Principal Investigator & Institution: Stone, John H.; Associate Professor; Medicine; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: (provided by applicant): Systemic vasculitis is a group of inflammatory disorders of blood vessels. Because knowledge of the pathophysiology of these conditions remains incomplete, their treatments are empiric, toxic, and often unsuccessful in inducing durable remissions. Insights derived from this translational research program described by Dr. John Stone, Director of the Johns Hopkins Vasculitis Center, may lead to novel methods of evaluating vasculitis patients. Dr. Stone's mentoring program for junior investigators interested in translational research provides access to a large database of well-characterized patients with vasculitis, outstanding institutional resources for clinical research training, committed mentoring, wellestablished collaborations within and outside of Johns Hopkins, and a research infrastructure that is essential to career development. As a programmatic research goal in the context of this application, Dr. Stone will employ current funding and existing collaborations to develop his work in proteomics. His co-investigators in this effort are collaborators at the National Cancer Institute/Food & Drug Administration (NCI/FDA) Clinical Proteomics Program, Dr. Emanuel Petricoin and Dr. Lance Liotta. Funding from the Maryland Arthritis Research Consortium (MARRC) and from the Food & Drug Administration's Office of Orphan Products Development will support these studies. The initial disease focus of this work will be Wegener's granulomatosis, using sera collected in the Wegener's Granulomatosis Etanercept Trial (A multicenter, NIAMSfunded trial in which Dr. Stone is the Principal Investigator). Other areas of research at the Vasculitis Center on which young investigators may choose to focus include: 1) the investigation of novel therapeutic approaches; 2) the role of microbial pathogens in the etiology of vasculitis; and, 3) molecular mechanisms of systemic vasculitis (under comentoring arrangements with colleagues whose expertise complements that of Dr. Stone), using patient samples and clinical data from the Vasculitis Center. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: VASCULITIS CLINICAL RESEARCH NETWORK (VCRN) Principal Investigator & Institution: Merkel, Peter A.; Assistant Professor; Medicine; Boston University Medical Campus 715 Albany St, 560 Boston, Ma 02118 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-JUL-2008
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Summary: (provided by applicant): AIM 1. Establish a multicenter Vasculitis clinical Research Network (VCRN) to foster and facilitate clinical investigation in the inflammatory vasculitides. The 4 major US vasculitis centers (Boston University, Cleveland Clinic, Johns Hopkins, and Mayo Clinic) will combine their clinical and research expertise with the resources of the General Clinical Research Centers at each site to form the core of the Network. Additionally, the combined strengths of several domestic and foreign secondary centers will be incorporated into the Network. The VCRN would serve as the focal point for vasculitis research in the United States and internationally for both clinical investigators and patients. To achieve this aim, the following activities are proposed: 1.1 Develop a clinical data repository in collaboration with other Rare Disease Clinical Research Networks and the Rare Disease Data and Technology Coordinating Center. 1.2 Build a vasculitis clinical specimen bank for storage of serum, plasma, DNA and tissue samples linked to the clinical data repository. 1.3 Enact a national recruitment program in cooperation with various vasculitis patient advocacy groups. 1.4 Utilize the extensive resources of the General Clinical Research Centers at each Primary Network Site AIM 2. Conduct a series of related longitudinal studies of novel biomarkers of vasculitis disease activity. Utilizing the VCRN Clinical Data Repository and Clinical Specimen Bank and in coordination with biostatistical support from the Data and Technology Coordinating Center, the VCRN Biomarkers Project will use several promising techniques to develop new markers of disease activity including: 2.1 Proteomics 2.2 Molecular Markers of Oxidative Stress and Inflammation 2.3 Additionally, this program will be established in a fashion that would easily allow for testing of future novel biomarkers by investigators both within and beyond the Network. AIM 3. Utilize the VCRN and patient base to conduct Phase I and II clinical trials within the proposed grant period and create the infrastructure to greatly facilitate the design and performance of other future trials. AIM 4. Establish the Vasculitis Clinical Investigator Fellowship as a core mission on the VCRN to provide a mechanism to support, train, and mentor fellows interested in establishing academic careers focused on vasculitis research. This aim will address the pressing need in academic medicine for the training and retaining of patient oriented clinical investigators. AIM 5. Build and contribute to an electronic website resource with substantive content for clinicians, researchers, and patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: VAV GDP/GTP EXCHANGE FACTORS IN CHEMOTAXIS Principal Investigator & Institution: Brugge, Joan S.; Professor; Cbr Institute for Biomedical Research 800 Huntington Ave Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 16-DEC-2002; Project End 30-NOV-2007 Summary: (provided by the Applicant): Leukocyte chemotaxis plays a critical in the body's defense against microorganisms and hyperactivity of these cells leads to a variety of pathologic states including inflammation, vasculitis, and glomerulonephritis. Chemotaxis is dependent on the dynamic activity of adhesive and actin cytoskeletal structures that regulate cell motility. Rho GTPases are central players in the regulation of cell adhesion and actin cytoskeletal polymerization and assembly into cytoskeletal structures. We have found that Vav family Rho GTPase exchange factors are required for chemotaxis mediated by the chemoattractant fMLP and for macrophage migration on an extracellular matrix. This conclusion was based on studies of mice deficient in two Vav family members, Vav1 and Vav3. This proposal will examine the mechanisms involved in activation of Vav by chemoattractants and integrins and establish the mechanisms whereby this multidomain scaffolding protein regulates actin cytoskeletal
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structures and controls cell migration. The latter will involve defining regions of Vav that are required for motility and identification of effectors that mediate the activity of these domains. In addition we will analyze neutrophil and macrophage motility in mice lacking all three Vav family members since they are all expressed in these two cell types. These studies promise to elucidate pathways that are important in the host defense again microorganisms and pathologic inflammatory states. 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 “vasculitis” (or synonyms) into the search box. This search gives you access to fulltext articles. The following is a sample of items found for vasculitis in the PubMed Central database: •
A case of central nervous system vasculitis related to an episode of Guillain-Barre syndrome. by Sinardi D, Spada A, Marino A, Mondello E.; 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=29044
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Antineutrophil cytoplasmic antibody and vasculitis: much more than a disease marker. by D'Agati V.; 2002 Oct 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151160
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Antineutrophil cytoplasmic autoantibodies specific for myeloperoxidase cause glomerulonephritis and vasculitis in mice. by Xiao H, Heeringa P, Hu P, Liu Z, Zhao M, Aratani Y, Maeda N, Falk RJ, Jennette JC.; 2002 Oct 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151154
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Circulating Immune Complexes in Cutaneous Vasculitis DETECTION WITH Clq AND MONOCLONAL RHEUMATOID FACTOR. by Mackel SE, Tappeiner G, Brumfield H, Jordon RE.; 1979 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=371319
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Cryoglobulinemia induced by a murine IgG3 rheumatoid factor: skin vasculitis and glomerulonephritis arise from distinct pathogenic mechanisms. by Reininger L, Berney T, Shibata T, Spertini F, Merino R, Izui S.; 1990 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=55310
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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Disseminated cryptococcosis presenting as cellulitis with necrotizing vasculitis. by Shrader SK, Watts JC, Dancik JA, Band JD.; 1986 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=269046
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Evidence for the role of platelet-activating factor in immune complex vasculitis in the rat. by Warren JS, Mandel DM, Johnson KJ, Ward PA.; 1989 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=303728
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Genetic Selection for Crescent Formation Yields Mouse Strain with Rapidly Progressive Glomerulonephritis and Small Vessel Vasculitis. by Kinjoh K, Kyogoku M, Good RA.; 1993 Apr 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=46310
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Hypersensitivity vasculitis induced by cefoperazone/sulbactam. by Islek I, Baris S, Katranci AO, Ariturk E, Gurses N.; 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=149382
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Immunoblot studies to analyze antibody to the Rickettsia typhi group antigen in sera from patients with acute febrile cerebrovasculitis. by Hechemy KE, Fox JA, Groschel DH, Hayden FG, Wenzel RP.; 1991 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=270373
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Monitoring Proteinase 3 Antineutrophil Cytoplasmic Antibodies for Detection of Relapses in Small Vessel Vasculitis. by Segelmark M, Phillips BD, Hogan SL, Falk RJ, Jennette JC.; 2003 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=193911
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Suppression of immune complex vasculitis in rats by prostaglandin. by Kunkel SL, Thrall RS, Kunkel RG, McCormick JR, Ward PA, Zurier RB.; 1979 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=371302
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Transduction of a Foreign Histocompatibility Gene into the Arterial Wall Induces Vasculitis. by Nabel EG, Plautz G, Nabel GJ.; 1992 Jun 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=49248
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What you should know about PR3-ANCA: Evidence for the role of T cells in the pathogenesis of systemic vasculitis. by Clayton AR, Savage CO.; 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130015
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 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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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 vasculitis, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “vasculitis” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for vasculitis (hyperlinks lead to article summaries): •
A case of ANCA-associated vasculitis with predominant involvement of central nervous system. Author(s): Caramaschi P, Biasi D, Carletto A, Bambara LM. Source: Joint, Bone, Spine : Revue Du Rhumatisme. 2003 September; 70(5): 380-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14563469
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A case of cutaneous leukocytoclastic vasculitis associated with gabapentin. Author(s): Poon DY, Law NM. Source: Singapore Med J. 2003 January; 44(1): 42-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12762564
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A case of recurrent cutaneous eosinophilic vasculitis: successful adjuvant therapy with suplatast tosilate. Author(s): Sakuma-Oyama Y, Nishibu A, Oyama N, Saito M, Nakamura K, Kaneko F. Source: The British Journal of Dermatology. 2003 October; 149(4): 901-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14616398
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A case suggesting lymphocytic vasculitis as a presenting sign of early undifferentiated connective tissue disease. Author(s): Oh CW, Lee SH, Heo EP. Source: The American Journal of Dermatopathology. 2003 October; 25(5): 423-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14501291
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A headache and a mass lesion: vasculitis or CNS sarcoid? Author(s): Calabrese LH. Source: Clin Exp Rheumatol. 2003 November-December; 21(6 Suppl 32): S131-2. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14740441
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A near fatal case of the dapsone hypersensitivity syndrome in a patient with urticarial vasculitis. Author(s): Leslie KS, Gaffney K, Ross CN, Ridley S, Barker TH, Garioch JJ. Source: Clinical and Experimental Dermatology. 2003 September; 28(5): 496-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12950336
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A prospective study of vasculitis patients collected in a five year period: evaluation of the Chapel Hill nomenclature. Author(s): Sorensen SF, Slot O, Tvede N, Petersen J. Source: Annals of the Rheumatic Diseases. 2000 June; 59(6): 478-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10834866
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ANCA glomerulonephritis and vasculitis: a Chapel Hill perspective. Author(s): Falk RJ, Nachman PH, Hogan SL, Jennette JC. Source: Semin Nephrol. 2000 May; 20(3): 233-43. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10855933
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ANCA-associated small vessel vasculitis presenting with ischemic optic neuropathy. Author(s): Duran E, Merkel PA, Sweet S, Swan N, Babikian VL. Source: Neurology. 2004 January 13; 62(1): 152-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14718724
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Annular leucocytoclastic vasculitis induced by chlorzoxazone. Author(s): Chiu CS, Chang YC, Chung WH, Yang LJ, Ho HC, Chen MJ, Hong HS. Source: The British Journal of Dermatology. 2004 January; 150(1): 153. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14746633
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Antagonist of monocyte chemoattractant protein 1 ameliorates the initiation and progression of lupus nephritis and renal vasculitis in MRL/lpr mice. Author(s): Hasegawa H, Kohno M, Sasaki M, Inoue A, Ito MR, Terada M, Hieshima K, Maruyama H, Miyazaki J, Yoshie O, Nose M, Fujita S. Source: Arthritis and Rheumatism. 2003 September; 48(9): 2555-66. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=13130475
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Antineutrophil cytoplasmic antibodies (ANCA) and small vessel vasculitis. Author(s): Mareen P, Van De Walle S, Bernaert P, Vanhouteghem H, Dierick J. Source: Acta Clin Belg. 2003 May-June; 58(3): 193-200. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12945480
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Antineutrophil cytoplasmic antibody-related vasculitis and liver diseases. Author(s): Hashimoto H. Source: Intern Med. 2000 June; 39(6): 449-50. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10852161
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Antiproteinase 3- and antimyeloperoxidase-associated vasculitis. Author(s): Franssen CF, Stegeman CA, Kallenberg CG, Gans RO, De Jong PE, Hoorntje SJ, Tervaert JW. Source: Kidney International. 2000 June; 57(6): 2195-206. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10844589
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Anti-tumor necrosis factor-alpha therapy-induced vasculitis: case series. Author(s): Jarrett SJ, Cunnane G, Conaghan PG, Bingham SJ, Buch MH, Quinn MA, Emery P. Source: The Journal of Rheumatology. 2003 October; 30(10): 2287-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14528531
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Asthma associated with worsening leg ulcer: a case of vasculitis in primary care. Author(s): Cakir B, Cykert S. Source: Southern Medical Journal. 2003 July; 96(7): 677-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12940319
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Atypical reginal vasculitis associated with ticlopidine hydrochloridine use. Author(s): Barak A, Morse LS, Schwab IR. Source: American Journal of Ophthalmology. 2000 May; 129(5): 684-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10844073
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Audit of the clinical usefulness of a rapid qualitative ELISA screen for antimyeloperoxidase and antiproteinase 3 antibodies in the assessment of patients with suspected vasculitis. Author(s): Aslam A, Newman TL, Misbah SA. Source: Journal of Clinical Pathology. 2003 October; 56(10): 775-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14514783
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Autoimmune testicular vasculitis. Author(s): Raj GV, Ellington KS, Polascik TJ. Source: Urology. 2003 May; 61(5): 1035. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12736037
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Azithromycin-induced leukocytoclastic vasculitis. Author(s): Odemis E, Kalyoncu M, Okten A, Yildiz K. Source: The Journal of Rheumatology. 2003 October; 30(10): 2292. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14528532
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Bacterial infection presenting as cutaneous vasculitis in adults. Author(s): Garcia-Porrua C, Gonzalez-Gay MA. Source: Clin Exp Rheumatol. 1999 July-August; 17(4): 471-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10464561
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Barraquer-Simons lipodystrophy, Raynaud's phenomenon and cutaneous vasculitis. Author(s): Porter WM, O'Gorman-Lalor O, Lane RJ, Francis N, Bunker CB. Source: Clinical and Experimental Dermatology. 2000 June; 25(4): 277-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10971484
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Basilar artery vasculitis secondary to sphenoid sinusitis--case report. Author(s): Sorimachi T, Kamada K, Ozawa T, Takeuchi S. Source: Neurol Med Chir (Tokyo). 2001 September; 41(9): 454-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11593974
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Basilar hyperlucency in a patient with emphysema due to hypocomplementemic urticarial vasculitis syndrome. Author(s): Ghamra Z, Stoller JK. Source: Respiratory Care. 2003 July; 48(7): 697-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12841861
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Behcet's disease with cerebral vasculitis. Author(s): Scardamaglia L, Desmond PM, Gonzales MF, Bendrups A, Brodtmann A, Kay TW. Source: Internal Medicine Journal. 2001 December; 31(9): 560-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11767874
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Behcet's disease: an enigmatic vasculitis. Author(s): Onder M, Gurer MA. Source: Clinics in Dermatology. 1999 September-October; 17(5): 571-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10590851
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Behcet's disease: an immune-mediated vasculitis involving vessels of all sizes. Author(s): Rizzi R, Bruno S, Dammacco R. Source: International Journal of Clinical & Laboratory Research. 1997; 27(4): 225-32. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9506265
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Bilateral adrenal enlargement as a first sign of systemic vasculitis. Author(s): Janssen M, Baggen MG, van Dekken H, Ouwendijk RJ. Source: The Netherlands Journal of Medicine. 1997 October; 51(4): 146-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9446926
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Bilateral facial nerve palsy associated with p-ANCA positive vasculitis in a patient with rheumatoid arthritis. Author(s): Stewart OG, Simmons IG, Martin MF, Morrell AJ. Source: The British Journal of Ophthalmology. 2001 October; 85(10): 1266-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11596584
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Bilateral leg pain and bruising. Hypersensitivity vasculitis. Author(s): Miller DW, Norton VC. Source: Academic Emergency Medicine : Official Journal of the Society for Academic Emergency Medicine. 1997 September; 4(9): 916-7; 922-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9305435
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Bilateral Parry-Romberg syndrome associated with retinal vasculitis. Author(s): Bellusci C, Liguori R, Pazzaglia A, Badiali L, Schiavi C, Campos EC. Source: Eur J Ophthalmol. 2003 November-December; 13(9-10): 803-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14700105
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Biopsy diagnosis of systemic vasculitis. Author(s): Lie JT. Source: Baillieres Clin Rheumatol. 1997 May; 11(2): 219-36. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9220076
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Birmingham vasculitis activity score, disease extent index and complement factor C3c reflect disease activity best in hepatitis C virus-associated cryoglobulinemic vasculitis. Author(s): Lamprecht P, Moosig F, Gause A, Herlyn K, Gross WL. Source: Clin Exp Rheumatol. 2000 May-June; 18(3): 319-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10895368
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Breathlessness in a patient with rheumatoid vasculitis. Author(s): Bascil N, Tutuncu T, Kisacik G, Sivri A, Coplu L. Source: Postgraduate Medical Journal. 1998 May; 74(871): 294-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9713616
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Brucella endocarditis associated with glomerulonephritis and renal vasculitis. Author(s): Elzouki AY, Akthar M, Mirza K. Source: Pediatric Nephrology (Berlin, Germany). 1996 December; 10(6): 748-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8971897
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Bullous pemphigoid associated with cutaneous leukocytoclastic vasculitis. Author(s): Beer TW, Smith HR. Source: International Journal of Dermatology. 1998 December; 37(12): 940-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9888339
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Central nervous system vasculitis. Author(s): Carolei A, Sacco S. Source: Neurological Sciences : Official Journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology. 2003 May; 24 Suppl 1: S8-S10. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12774201
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Central nervous system vasculitis. Author(s): West SG. Source: Curr Rheumatol Rep. 2003 April; 5(2): 116-27. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12628042
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Cerebral thrombosis and vasculitis: an uncommon complication of ulcerative colitis. Author(s): Carmona MA, Jaume Anselmi F, Ramirez Rivera J. Source: Bol Asoc Med P R. 2000 January-March; 92(1-3): 9-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10846281
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Cerebral vasculitis as the only manifestation of Borrelia burgdorferi infection in a 17year-old patient with basal ganglia infarction. Author(s): Heinrich A, Khaw AV, Ahrens N, Kirsch M, Dressel A. Source: European Neurology. 2003; 50(2): 109-12. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12944718
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Cerebral vasculitis in Henoch-Schonlein purpura: MRI and MRA findings, treated with plasmapheresis alone. Author(s): Eun SH, Kim SJ, Cho DS, Chung GH, Lee DY, Hwang PH. Source: Pediatrics International : Official Journal of the Japan Pediatric Society. 2003 August; 45(4): 484-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12911492
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Cerebral vasculitis with multiple infarcts caused by lyme disease. Author(s): Schmiedel J, Gahn G, von Kummer R, Reichmann H. Source: Cerebrovascular Diseases (Basel, Switzerland). 2004; 17(1): 79-81. Epub 2003 October 06. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14534380
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Churg-Strauss vasculitis diagnosed on muscle biopsy. Author(s): Suresh E, Dhillon VB, Smith C, Ironside JW. Source: Journal of Clinical Pathology. 2004 March; 57(3): 334. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14990615
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Circulating endothelial cells as markers for ANCA-associated small-vessel vasculitis. Author(s): Woywodt A, Streiber F, de Groot K, Regelsberger H, Haller H, Haubitz M. Source: Lancet. 2003 January 18; 361(9353): 206-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12547543
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Classification of vasculitis: comment on the review by Matteson. Author(s): Mercado U. Source: Arthritis Care and Research : the Official Journal of the Arthritis Health Professions Association. 2000 October; 13(5): 336; Author Reply 336. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14635306
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Clinical management issues in vasculitis. Angiographically defined angiitis of the central nervous system: diagnostic and therapeutic dilemmas. Author(s): Calabrese LH. Source: Clin Exp Rheumatol. 2003 November-December; 21(6 Suppl 32): S127-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14740440
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Clinical profile and treatment outcome of livedoid vasculitis: a case series. Author(s): Lee SS, Ang P, Tan SH. Source: Ann Acad Med Singapore. 2003 November; 32(6): 835-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14716957
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Cutaneous vasculitis - a case for laparotomy? Author(s): Willcocks L, Chelliah G, Brown R, Bacon P. Source: The Journal of Rheumatology. 2003 July; 30(7): 1621-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12858468
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Cutaneous vasculitis and reactive arthritis following respiratory infection due to Chlamydia pneumoniae: report of a case. Author(s): Cascina A, Marone Bianco A, Mangiarotti P, Montecucco CM, Meloni F. Source: Clin Exp Rheumatol. 2002 November-December; 20(6): 845-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12508779
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Cutaneous vasculitis associated with mixed cryoglobulinemia in adult Still's disease. Author(s): Elezoglou AV, Giamarelos-Bourboulis E, Katsilambros N, Sfikakis PP. Source: Clin Exp Rheumatol. 2003 May-June; 21(3): 405-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12846069
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Cutaneous vasculitis associated with rofecoxib. Author(s): Lillicrap MS, Merry P. Source: Rheumatology (Oxford, England). 2003 October; 42(10): 1267-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14508048
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Cutaneous vasculitis in primary Sjogren syndrome: classification and clinical significance of 52 patients. Author(s): Ramos-Casals M, Anaya JM, Garcia-Carrasco M, Rosas J, Bove A, Claver G, Diaz LA, Herrero C, Font J. Source: Medicine; Analytical Reviews of General Medicine, Neurology, Psychiatry, Dermatology, and Pediatrics. 2004 March; 83(2): 96-106. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15028963
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Cutaneous vasculitis secondary to ramipril. Author(s): Gupta S, Gandhi NM, Ferguson J. Source: J Drugs Dermatol. 2004 January-February; 3(1): 81-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14964753
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Cutaneous vasculitis. Author(s): Fiorentino DF. Source: Journal of the American Academy of Dermatology. 2003 March; 48(3): 311-40. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12637912
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Cutaneous vasculitis: a diagnostic approach. Author(s): Gonzalez-Gay MA, Garcia-Porrua C, Salvarani C, Lo Scocco G, Pujol RM. Source: Clin Exp Rheumatol. 2003 November-December; 21(6 Suppl 32): S85-8. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14740432
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Cutaneous vasculitis: a review. Author(s): Crowson AN, Mihm MC Jr, Magro CM. Source: Journal of Cutaneous Pathology. 2003 March; 30(3): 161-73. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12641775
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Dendritic cell uptake of human apoptotic and necrotic neutrophils inhibits CD40, CD80, and CD86 expression and reduces allogeneic T cell responses: relevance to systemic vasculitis. Author(s): Clayton AR, Prue RL, Harper L, Drayson MT, Savage CO. Source: Arthritis and Rheumatism. 2003 August; 48(8): 2362-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12905492
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Diagnosis and assessment of systemic vasculitis. Author(s): McLaren JS, McRorie ER, Luqmani RA. Source: Clin Exp Rheumatol. 2002 November-December; 20(6): 854-62. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12508782
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Diagnosis of vasculitis. Author(s): Mohan N, Kerr GS. Source: Best Practice & Research. Clinical Rheumatology. 2001 June; 15(2): 203-23. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11469818
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Diagnostic strategies for the histological examination of muscle biopsy specimens for the assessment of vasculitis in rheumatoid arthritis. Author(s): Zwinderman AH, Voskuyl AE, Schelhaas DD, van Duinen SG, van der Bas JM, Hazes JM. Source: Statistics in Medicine. 2000 December 30; 19(24): 3433-47. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11122506
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Diagnostic strategies in vasculitis affecting the central nervous system. Author(s): Calabrese LH. Source: Cleve Clin J Med. 2002; 69 Suppl 2: Sii105-8. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12086248
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Diagnostic strategy for the assessment of rheumatoid vasculitis. Author(s): Voskuyl AE, Hazes JM, Zwinderman AH, Paleolog EM, van der Meer FJ, Daha MR, Breedveld FC. Source: Annals of the Rheumatic Diseases. 2003 May; 62(5): 407-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12695150
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Diffuse endothelial dysfunction is common to ANCA associated systemic vasculitis and polyarteritis nodosa. Author(s): Filer AD, Gardner-Medwin JM, Thambyrajah J, Raza K, Carruthers DM, Stevens RJ, Liu L, Lowe SE, Townend JN, Bacon PA. Source: Annals of the Rheumatic Diseases. 2003 February; 62(2): 162-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12525387
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Diffuse large B cell lymphoma in a patient with hypocomplementemic urticarial vasculitis. Author(s): Calvo-Romero JM. Source: Journal of Postgraduate Medicine. 2003 July-September; 49(3): 252-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14597790
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Digital necrosis in a patient with hypereosinophilic syndrome in the absence of cutaneous eosinophilic vasculitis. Author(s): Oppliger R, Gay-Crosier F, Dayer E, Hauser C. Source: The British Journal of Dermatology. 2001 May; 144(5): 1087-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11359406
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Discordant uptake of F-18 FDG and In-111 WBC in systemic vasculitis. Author(s): Balan K, Voutnis D, Groves A. Source: Clinical Nuclear Medicine. 2003 June; 28(6): 485-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12917530
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Disease activity and survival in vasculitis: comment on the article by Gayraud et al. Author(s): Matteson EL. Source: Arthritis and Rheumatism. 2001 December; 44(12): 2943. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11762962
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Disseminated acanthamoebiasis presenting as lobular panniculitis with necrotizing vasculitis in a patient with AIDS. Author(s): Rosenberg AS, Morgan MB. Source: Journal of Cutaneous Pathology. 2001 July; 28(6): 307-13. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11401678
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Disseminated mucormycosis caused by Absidia corymbifera leading to cerebral vasculitis. Author(s): Eucker J, Sezer O, Lehmann R, Weber JR, Graf B, Denkert C, Bruck W, Schweigert M, Possinger K. Source: Infection. 2000 July-August; 28(4): 246-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10961535
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Do vasculitis categorization systems really matter? Author(s): Jennette JC, Falk RJ. Source: Curr Rheumatol Rep. 2000 October; 2(5): 430-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11123094
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Does infection play a role in the pathogenesis of pulmonary vasculitis? Author(s): Capizzi SA, Specks U. Source: Seminars in Respiratory Infections. 2003 March; 18(1): 17-22. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12652450
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Drug-induced acute interstitial nephritis and vasculitis or vasculary rejection in renal allografts. Author(s): Sen S, Bayrak R, Ok E, Basdemir G. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2001 January; 37(1): E4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11136193
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Drug-induced vasculitis. Author(s): Doyle MK, Cuellar ML. Source: Expert Opinion on Drug Safety. 2003 July; 2(4): 401-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12904096
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Drug-induced vasculitis. Author(s): Cuellar ML. Source: Curr Rheumatol Rep. 2002 February; 4(1): 55-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11798983
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Drug-induced vasculitis. Author(s): Merkel PA. Source: Rheumatic Diseases Clinics of North America. 2001 November; 27(4): 849-62. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11723768
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Dying neutrophils in ANCA-associated vasculitis: good or bad guys? Author(s): Kallenberg CG. Source: Kidney International. 2002 February; 61(2): 758-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11849420
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Echocardiographic and clinical characteristics of aortic regurgitation because of systemic vasculitis. Author(s): Song JK, Jeong YH, Kang DH, Song JM, Song H, Choo SJ, Lee JW, Song MG. Source: Journal of the American Society of Echocardiography : Official Publication of the American Society of Echocardiography. 2003 August; 16(8): 850-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12878994
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Efavirenz-induced leukocytoclastic vasculitis. Author(s): Domingo P, Barcelo M. Source: Archives of Internal Medicine. 2002 February 11; 162(3): 355-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11822931
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Effect of immune complexes in serum from patients with rheumatoid vasculitis on the expression of cell adhesion molecules on polymorphonuclear cells. Author(s): Haruta K, Kobayashi S, Tajima M, Sakai A, Tamura N, Bando H, Hara M, Kawashima S, Takasaki Y, Hashimoto H. Source: Clin Exp Rheumatol. 2001 January-February; 19(1): 59-68. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11247327
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Effector T cells and macrophages in urine as a hallmark of systemic vasculitis accompanied by crescentic glomerulonephritis. Author(s): Sakatsume M, Gejyo F. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 2003 March; 18(3): 607-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12584287
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Efficacy of corticosteroids and cyclosporin in the treatment of retinal vasculitis in patients with Behcet's disease. Author(s): Ermakova NA. Source: Advances in Experimental Medicine and Biology. 2003; 528: 563-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12918765
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Ehlers-Danlos syndrome mimicking mesenteric vasculitis: therapy, then diagnosis. Author(s): Bloch R, Hoffer E, Borsa J, Fontaine A. Source: Journal of Vascular and Interventional Radiology : Jvir. 2001 April; 12(4): 527-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11287544
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Elevated plasma levels of beta-thromboglobulin and platelet factor 4 in patients with rheumatic disorders and cutaneous vasculitis. Author(s): Yamamoto T, Chikugo T, Tanaka Y. Source: Clinical Rheumatology. 2002 November; 21(6): 501-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12447635
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Endothelial and platelet microparticles in vasculitis of the young. Author(s): Brogan PA, Shah V, Brachet C, Harnden A, Mant D, Klein N, Dillon MJ. Source: Arthritis and Rheumatism. 2004 March; 50(3): 927-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15022336
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Endothelial cell biology, perivascular inflammation, and vasculitis. Author(s): Cid MC. Source: Cleve Clin J Med. 2002; 69 Suppl 2: Sii45-9. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12086264
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Endothelial nitric oxide synthase gene polymorphisms in Behcet's disease and rheumatic diseases with vasculitis. Author(s): Kim JU, Chang HK, Lee SS, Kim JW, Kim KT, Lee SW, Chung WT. Source: Annals of the Rheumatic Diseases. 2003 November; 62(11): 1083-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14583572
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Eosinophilic heart disease with vasculitis: supported by HeartMate left ventricular assist device and heart transplantation. Author(s): Hsu CP, Chang SH, Wang JS, Shih CC, Lai ST, Yang AH. Source: The Annals of Thoracic Surgery. 2002 April; 73(4): 1307-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11996282
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Eosinophilic/T-cell chorionic vasculitis. Author(s): Fraser RB, Wright JR Jr. Source: Pediatric and Developmental Pathology : the Official Journal of the Society for Pediatric Pathology and the Paediatric Pathology Society. 2002 July-August; 5(4): 350-5. Epub 2002 May 21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12016525
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Epidemiology of vasculitis in Europe. Author(s): Watts RA, Lane SE, Scott DG, Koldingsnes W, Nossent H, Gonzalez-Gay MA, Garcia-Porrua C, Bentham GA. Source: Annals of the Rheumatic Diseases. 2001 December; 60(12): 1156-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11760724
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Erythema induratum with pulmonary tuberculosis: histopathologic features resembling true vasculitis. Author(s): Lee YS, Lee SW, Lee JR, Lee SC. Source: International Journal of Dermatology. 2001 March; 40(3): 193-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11422524
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Etanercept and infliximab associated with cutaneous vasculitis. Author(s): McCain ME, Quinet RJ, Davis WE. Source: Rheumatology (Oxford, England). 2002 January; 41(1): 116-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11792895
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Evaluation and treatment of vasculitis in the critically ill patient. Author(s): Merkel PA, Choi HK, Niles JL. Source: Critical Care Clinics. 2002 April; 18(2): 321-44. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12053837
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Evaluation of the Sorensen diagnostic criteria in the classification of systemic vasculitis. Author(s): Lane SE, Watts RA, Barker TH, Scott DG. Source: Rheumatology (Oxford, England). 2002 October; 41(10): 1138-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12364633
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Exercise-induced urticarial vasculitis as a paraneoplastic manifestation of cystic teratoma. Author(s): Di Stefano F, Siriruttanapruk S, Di Gioacchino M. Source: Rheumatology (Oxford, England). 2003 November; 42(11): 1418-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14578437
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Extensive dynamics in location, shape, and size of aneurysms in a patient with idiopathic retinal vasculitis, aneurysms, and neuroretinitis (IRVAN) syndrome. Idiopathic retinal vasculitis, aneurysms, and neuroretinitis. Author(s): Yeshurun I, Recillas-Gispert C, Navarro-Lopez P, Arellanes-Garcia L, Cervantes-Coste G. Source: American Journal of Ophthalmology. 2003 January; 135(1): 118-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12504719
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Extensive sterile abscess in an invasive fibrous thyroiditis (Riedel's thyroiditis) caused by an occlusive vasculitis. Author(s): Geissler B, Wagner T, Dorn R, Lindemann F. Source: J Endocrinol Invest. 2001 February; 24(2): 111-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11263468
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F-18-fluorodeoxyglucose positron emission tomography in diagnosis and follow-up of patients with different types of vasculitis. Author(s): Bleeker-Rovers CP, Bredie SJ, van der Meer JW, Corstens FH, Oyen WJ. Source: The Netherlands Journal of Medicine. 2003 October; 61(10): 323-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14708910
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Factor XIIIa+ dermal dendrocytes in erythema elevatum diutinum and ordinary cutaneous leukocytoclastic vasculitis lesions. Author(s): Pacheco LS, Sotto MN. Source: Journal of Cutaneous Pathology. 2000 March; 27(3): 136-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10728816
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Factors involved in the pathogenesis of neutrophilic vasculitis in MRL/Mp-lpr/lpr mice: a model for human microscopic angiitis. Author(s): Harper JM, Healey DG, Thiru S, Gordon C, Cook A. Source: Autoimmunity. 1999 October; 31(2): 133-45. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10680752
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Familial adenomatous polyposis coli associated arthritis and vasculitis. Author(s): Mattiuzzo M, Biscaro R, Scapinello A, Ferraccioli GF. Source: Clin Exp Rheumatol. 2003 November-December; 21(6): 800. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14740465
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Familial mediterranean fever and acute myocardial infarction secondary to coronary vasculitis. Author(s): Serrano R, Martinez MA, Andres A, Morales JM, Samartin R. Source: Histopathology. 1998 August; 33(2): 163-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9762550
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Familial occurrence of systemic vasculitis and rapidly progressive glomerulonephritis. Author(s): Nowack R, Lehmann H, Flores-Suarez LF, Nanhou A, van der Woude FJ. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1999 August; 34(2): 364-73. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10430990
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FasL autoantibodies in vasculitis are associated with the presence of anticorneal epithelial antibodies. Author(s): Gowen E, Tullo AB, Dixon J, Holt PJ, Hillarby MC. Source: Annals of the Rheumatic Diseases. 2002 June; 61(6): 538-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12006329
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Fatal allergic vasculitis associated with celecoxib. Author(s): Schneider F, Meziani F, Chartier C, Alt M, Jaeger A. Source: Lancet. 2002 March 9; 359(9309): 852-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11897288
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Fatal obliterative coronary vasculitis in Kawasaki disease. Author(s): McConnell ME, Hannon DW, Steed RD, Gilliland MG. Source: The Journal of Pediatrics. 1998 August; 133(2): 259-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9709716
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Fatal Pseudomonas septicemia and vasculitis in a premature infant. Author(s): Hughes JR, Newbould M, du Vivier AW, Greenough A. Source: Pediatric Dermatology. 1998 March-April; 15(2): 122-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9572696
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Fever and abdominal pain in a 45-year-old woman with cutaneous necrotising vasculitis. Author(s): Voulgarelis M, Chorti M, Kittas C, Karachristos A, Ikonomopoulos G, Skopouli FN. Source: Clin Exp Rheumatol. 1998 January-February; 16(1): 72-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9543567
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Fluorine 18 fluorodeoxyglucose positron emission tomography in the diagnosis and follow-up of three patients with vasculitis. Author(s): Bleeker-Rovers CP, Bredie SJ, van der Meer JW, Corstens FH, Oyen WJ. Source: The American Journal of Medicine. 2004 January 1; 116(1): 50-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14706666
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Fluticasone-associated cutaneous allergic granulomatous vasculitis. Author(s): English J 3rd, Greer KE, McCrone SA, Patterson JW, VanLoock JS. Source: J Drugs Dermatol. 2003 June; 2(3): 326-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12848118
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Focal cerebral vasculitis and stroke after chickenpox. Author(s): Alehan FK, Boyvat F, Baskin E, Derbent M, Ozbek N. Source: European Journal of Paediatric Neurology : Ejpn : Official Journal of the European Paediatric Neurology Society. 2002; 6(6): 331-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12401459
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Focal necrotising vasculitis with secondary myositis following fluoxetine administration. Author(s): Fisher A, McLean AJ, Purcell P, Herdson PB, Dahlstrom JE, Le Couteur DG. Source: Aust N Z J Med. 1999 June; 29(3): 375-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10868505
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Formation of new vasa vasorum in vasculitis. Production of angiogenic cytokines by multinucleated giant cells. Author(s): Kaiser M, Younge B, Bjornsson J, Goronzy JJ, Weyand CM. Source: American Journal of Pathology. 1999 September; 155(3): 765-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10487834
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Frequency of HLA in patients with Behcet's disease and association with occlusive retinal vasculitis. Author(s): Ermakova NA, Alekberova ZS, Prokaeva TB, Poljanskaja IB. Source: Advances in Experimental Medicine and Biology. 2003; 528: 231-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12918697
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Full panretinal photocoagulation and early vitrectomy improve prognosis of retinal vasculitis associated with tuberculoprotein hypersensitivity (Eales' disease). Author(s): El-Asrar AM, Al-Kharashi SA. Source: The British Journal of Ophthalmology. 2002 November; 86(11): 1248-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12386081
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Fulminant alveolar haemorrhage in a case of recurrent small vessel vasculitis after renal transplantation. Author(s): Blaschke S, Grunewald W, Strutz F, Sattler B, Muller GA, Reuss-Borst M. Source: Rheumatology (Oxford, England). 2000 September; 39(9): 1042-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10986314
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Funisitis and chorionic vasculitis: the histological counterpart of the fetal inflammatory response syndrome. Author(s): Pacora P, Chaiworapongsa T, Maymon E, Kim YM, Gomez R, Yoon BH, Ghezzi F, Berry SM, Qureshi F, Jacques SM, Kim JC, Kadar N, Romero R. Source: J Matern Fetal Neonatal Med. 2002 January;11(1):18-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12380603
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Gallbladder vasculitis associated with type-1 cryoglobulinemia. Author(s): Rajvanshi P, Atac BS, Seno R, Gupta S. Source: Digestive Diseases and Sciences. 2001 February; 46(2): 296-300. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11281178
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gamma/delta T lymphocytes and infection: pathogenesis of leukocytoclastic cutaneous necrotizing vasculitis. Author(s): Comacchi C, Ghersetich I, Katsambas A, Lotti TM. Source: Clinics in Dermatology. 1999 September-October; 17(5): 603-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10590857
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Gastrointestinal amyloidosis secondary to hypersensitivity vasculitis presenting with intestinal pseudoobstruction. Author(s): Hiramatsu K, Kaneko S, Shirota Y, Matsuda M, Kaji K, Kitano Y, Ikeda N, Terasaki S, Kawai H, Shimoda A, Yokoyama H, Matsushita E, Urabe T, Kobayashi K. Source: Digestive Diseases and Sciences. 1998 August; 43(8): 1824-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9724175
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Gastrointestinal and renal involvement in vasculitis: management strategies in Henoch-Schonlein purpura. Author(s): Szer IS. Source: Cleve Clin J Med. 1999 May; 66(5): 312-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10330784
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Gastrointestinal small vessel vasculitis in a patient with crescentic glomerulonephritis and longstanding idiopathic neutropaenia treated with G-CSF. Author(s): Hill PA. Source: Pathology. 2003 April; 35(2): 179-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12745472
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Gemcitabine associated vasculitis leading to necrotizing enterocolitis and death in women undergoing primary treatment for epithelial ovarian/peritoneal cancer. Author(s): Geisler JP, Schraith DF, Manahan KJ, Sorosky JI. Source: Gynecologic Oncology. 2004 February; 92(2): 705-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14766271
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Generalized vasculitis, thrombocytopenia, and transient lymphoproliferative disorder caused by idiopathic mixed cryoglobulinemia. Author(s): Schwartzenberg S, Levo Y, Averbuch M. Source: The American Journal of the Medical Sciences. 2003 July; 326(1): 47-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12861125
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Genetic background of Japanese patients with antineutrophil cytoplasmic antibodyassociated vasculitis: association of HLA-DRB1*0901 with microscopic polyangiitis. Author(s): Tsuchiya N, Kobayashi S, Kawasaki A, Kyogoku C, Arimura Y, Yoshida M, Tokunaga K, Hashimoto H. Source: The Journal of Rheumatology. 2003 July; 30(7): 1534-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12858454
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Genetic determinants of autoimmune disease and coronary vasculitis in the MRLlpr/lpr mouse model of systemic lupus erythematosus. Author(s): Gu L, Weinreb A, Wang XP, Zack DJ, Qiao JH, Weisbart R, Lusis AJ. Source: Journal of Immunology (Baltimore, Md. : 1950). 1998 December 15; 161(12): 69997006. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9862736
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Geoepidemiology of systemic vasculitis: comparison of the incidence in two regions of Europe. Author(s): Watts RA, Gonzalez-Gay MA, Lane SE, Garcia-Porrua C, Bentham G, Scott DG. Source: Annals of the Rheumatic Diseases. 2001 February; 60(2): 170-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11156552
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Giant cell arteritis presenting with proximal weakness and skeletal muscle vasculitis. Author(s): Lacomis D, Giuliani MJ, Wasko MC, Oddis CV. Source: Muscle & Nerve. 1999 January; 22(1): 142-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9883874
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Glomerular monocyte-macrophage features in ANCA-positive renal vasculitis and cryoglobulinemic nephritis. Author(s): Rastaldi MP, Ferrario F, Crippa A, Dell'Antonio G, Casartelli D, Grillo C, D'Amico G. Source: Journal of the American Society of Nephrology : Jasn. 2000 November; 11(11): 2036-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11053479
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Glomerulonephritis caused by Actinobacillus actinomycetemcomitans mimicking cANCA-positive vasculitis. Author(s): Viallard JF, Bonnet S, Couzi L, Deminiere C, Miossec V, Mercie P, Aparicio M, Pellegrin JL. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 2002 April; 17(4): 663-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11917062
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Glycopeptide-induced vasculitis--cross-reactivity between vancomycin and teicoplanin. Author(s): Marshall C, Street A, Galbraith K. Source: The Journal of Infection. 1998 July; 37(1): 82-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9733391
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Granuloma formation, implications for the pathogenesis of vasculitis. Author(s): Sneller MC. Source: Cleve Clin J Med. 2002; 69 Suppl 2: Sii40-3. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12086263
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Granulomatous cerebral vasculitis in systemic lupus erythematosus during systemic remission of disease. Author(s): Koerner C, Sommer C, Knauth M, Breitbart A, Wildemann B. Source: Journal of Neurology. 2000 September; 247(9): 722-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11081819
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Granulomatous vasculitis in diversion procto-colitis. Author(s): Rice AJ, Abbott CR, Mapstone NM. Source: Histopathology. 1999 March; 34(3): 276-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10217574
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Granulomatous vasculitis of the gallbladder. Author(s): Alam I, Salmo EN, Bennani F, Awad ZT. Source: Ir J Med Sci. 2002 January-March; 171(1): 59-60. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11993603
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Granulomatous vasculitis. Author(s): Marquez J, Flores D, Candia L, Espinoza LR. Source: Curr Rheumatol Rep. 2003 April; 5(2): 128-35. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12628043
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Granulomatous vasculitis: an unusual renal vasculitis. Author(s): Hailwood SJ, Scott DG, Barker TH, Heaton A. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1999 April; 14(4): 952-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10328477
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HCV and cryoglobulinemic vasculitis. Author(s): Ferri C, Zignego AL, Giuggioli D, Sebastiani M, Cazzato M, Antonelli A, La Civita L, Fadda P, Longombardo G, Pileri S. Source: Cleve Clin J Med. 2002; 69 Suppl 2: Sii20-3. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12086259
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HCV-related cryoglobulinemic vasculitis: an update on its etiopathogenesis and therapeutic strategies. Author(s): Ferri C, Giuggioli D, Cazzato M, Sebastiani M, Mascia MT, Zignego AL. Source: Clin Exp Rheumatol. 2003 November-December; 21(6 Suppl 32): S78-84. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14740431
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Hemophagocytosis associated with MPO-ANCA positive vasculitis in systemic sclerosis. Author(s): Kumakura S, Ishikura H, Kondo M, Murakawa Y, Kobayashi S. Source: Clin Exp Rheumatol. 2002 May-June; 20(3): 411-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12102482
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Hepatitis C virus infection and vasculitis: implications of antiviral and immunosuppressive therapies. Author(s): Vassilopoulos D, Calabrese LH. Source: Arthritis and Rheumatism. 2002 March; 46(3): 585-97. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11920393
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Hepatitis C virus: a common triggering factor for both nodular vasculitis and Sjogren's syndrome? Author(s): Cardinali C, Gerlini G, Caproni M, Pimpinelli N, Fabbri P. Source: The British Journal of Dermatology. 2000 January; 142(1): 187-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10819552
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Herpes zoster vasculitis presenting as giant cell arteritis with bilateral internuclear ophthalmoplegia. Author(s): Al-Abdulla NA, Rismondo V, Minkowski JS, Miller NR. Source: American Journal of Ophthalmology. 2002 December; 134(6): 912-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12470766
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Herpes zoster vasculitis presenting as giant cell arteritis with choroidal infarction. Author(s): Al-Abdulla NA, Kelley JS, Green WR, Miller NR. Source: Retina (Philadelphia, Pa.). 2003 August; 23(4): 567-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12972779
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Heterozygous prothrombin G20210A gene mutation in a patient with livedoid vasculitis. Author(s): Gotlib J, Kohler S, Reicherter P, Oro AE, Zehnder JL. Source: Archives of Dermatology. 2003 August; 139(8): 1081-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12925402
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High proteinase 3-anti-neutrophil cytoplasmic antibody (ANCA) level measured by the capture enzyme-linked immunosorbent assay method is associated with decreased patient survival in ANCA-associated vasculitis with renal involvement. Author(s): Westman KW, Selga D, Isberg PE, Bladstrom A, Olsson H. Source: Journal of the American Society of Nephrology : Jasn. 2003 November; 14(11): 2926-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14569103
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Historical perspective of vasculitis: polyarteritis nodosa and microscopic polyangiitis. Author(s): Matteson EL. Source: Curr Rheumatol Rep. 2002 February; 4(1): 67-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11798985
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Historical perspective on the classification of vasculitis. Author(s): Matteson EL. Source: Arthritis Care and Research : the Official Journal of the Arthritis Health Professions Association. 2000 April; 13(2): 122-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14635285
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HIV and vasculitis: case report. Author(s): Bhagat K, Mamutse G. Source: East Afr Med J. 2000 July; 77(7): 396-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12862162
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Homonymous hemianopia following a triplet pregnancy: post-natal cerebral vasculitis or atypical eclampsia. Author(s): Keay SD, Carroll SG, Scrutton M, Kelly A, Ormerod I, Cahill DJ. Source: European Journal of Obstetrics, Gynecology, and Reproductive Biology. 2002 June 10; 103(1): 92-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12039474
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Host and viral genes that control herpesvirus vasculitis. Author(s): Virgin HW 4th. Source: Cleve Clin J Med. 2002; 69 Suppl 2: Sii7-12. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12086270
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Human recombinant interferon-alpha2a (rhIFN alpha2a) for the treatment of Behcet's disease with sight-threatening retinal vasculitis. Author(s): Kotter I, Zierhut M, Eckstein A, Vonthein R, Ness T, Gunaydin I, Grimbacher B, Blaschke S, Peter HH, Kanz L, Stubiger N. Source: Advances in Experimental Medicine and Biology. 2003; 528: 521-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12918755
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Human T-cell lymphotropic virus type-1 associated t-cell leukemia/lymphoma masquerading as necrotizing retinal vasculitis. Author(s): Levy-Clarke GA, Buggage RR, Shen D, Vaughn LO, Chan CC, Davis JL. Source: Ophthalmology. 2002 September; 109(9): 1717-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12208722
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Hypersensitivity vasculitis and cytokines. Author(s): Nalbant S, Koc B, Top C, Kucukardali Y, Baykal Y, Danaci M, Kocer IH. Source: Rheumatology International. 2002 November; 22(6): 244-8. Epub 2002 September 06. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12426663
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Hypocomplementemic urticarial vasculitis with angioedema, a rare presentation of systemic lupus erythematosus: rapid response to rituximab. Author(s): Saigal K, Valencia IC, Cohen J, Kerdel FA. Source: Journal of the American Academy of Dermatology. 2003 November; 49(5 Suppl): S283-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14576655
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Hypocomplementemic urticarial vasculitis: report of a 12-year-old girl with systemic lupus erythematosus. Author(s): DeAmicis T, Mofid MZ, Cohen B, Nousari HC. Source: Journal of the American Academy of Dermatology. 2002 November; 47(5 Suppl): S273-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12399749
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Hypogalactosylation of serum IgG in patients with ANCA-associated systemic vasculitis. Author(s): Holland M, Takada K, Okumoto T, Takahashi N, Kato K, Adu D, Ben-Smith A, Harper L, Savage CO, Jefferis R. Source: Clinical and Experimental Immunology. 2002 July; 129(1): 183-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12100039
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Idiopathic retinal vasculitis, aneurysms, and neuroretinitis (IRVAN) with preserved perfusion. Author(s): DiLoreto DA Jr, Sadda SR. Source: Retina (Philadelphia, Pa.). 2003 August; 23(4): 554-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12972774
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Ig M class anticardiolipin antibody and anti-Ro/SS-A positivity in urticarial vasculitis associated with hepatitis C virus infection. Author(s): Sanli H, Ozdemir E. Source: International Journal of Dermatology. 2002 December; 41(12): 930-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12492994
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Immunohistochemical study of a case of uterine leiomyoma showing massive lymphoid infiltration and localized vasculitis after LH-RH derivant treatment. Author(s): Ohmori T, Wakamoto R, Lu LM, Okada K, Nose M. Source: Histopathology. 2002 September; 41(3): 276-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12207795
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Implications for pathogenesis of patterns of injury in small- and medium-sizedvessel vasculitis. Author(s): Jennette JC. Source: Cleve Clin J Med. 2002; 69 Suppl 2: Sii33-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12086262
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Incidence of selective IgG2 deficiency in patients with vasculitis. Author(s): Jimenez A, Lopez-Trascasa M, Fontan G. Source: Clinical and Experimental Immunology. 1989 November; 78(2): 149-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12412740
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Incidentally discovered asymptomatic necrotising intra-abdominal vasculitis after peripheral gastric bypass surgery for morbid obesity. Author(s): Bounas A, Melachrinou M, Giannopoulos G, Meimaris N, Aroukatos P, Kalfarentzos F, Andonopoulos AP. Source: Annals of the Rheumatic Diseases. 2004 February; 63(2): 211-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14722215
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Increased circulating levels of proteinase 3 in patients with anti-neutrophilic cytoplasmic autoantibodies-associated systemic vasculitis in remission. Author(s): Ohlsson S, Wieslander J, Segelmark M. Source: Clinical and Experimental Immunology. 2003 March; 131(3): 528-35. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12605707
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Increased incidence of hypercoagulability in patients with leg ulcers caused by leukocytoclastic vasculitis. Author(s): Mekkes JR, Loots MA, van der Wal AC, Bos JD. Source: Journal of the American Academy of Dermatology. 2004 January; 50(1): 104-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14699376
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Infectious complications of immunosuppressive treatment for anti-neutrophil cytoplasm antibody-related vasculitis. Author(s): Koselj-Kajtna M, Koselj M, Rott T, Kandus A, Bren A. Source: Transplantation Proceedings. 2002 November; 34(7): 3001-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12431683
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Infectious etiology of vasculitis: diagnosis and management. Author(s): Mohan N, Kerr G. Source: Curr Rheumatol Rep. 2003 April; 5(2): 136-41. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12628044
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Inflammation and arterial stiffness in systemic vasculitis: a model of vascular inflammation. Author(s): Booth AD, Wallace S, McEniery CM, Yasmin, Brown J, Jayne DR, Wilkinson IB. Source: Arthritis and Rheumatism. 2004 February; 50(2): 581-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14872502
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Influenza vaccination induced leukocytoclastic vasculitis and pauci-immune crescentic glomerulonephritis. Author(s): Yanai-Berar N, Ben-Itzhak O, Gree J, Nakhoul F. Source: Clinical Nephrology. 2002 September; 58(3): 220-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12356192
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Interferon-alpha and ribavirin treatment in patients with hepatitis C virus-related systemic vasculitis. Author(s): Cacoub P, Lidove O, Maisonobe T, Duhaut P, Thibault V, Ghillani P, Myers RP, Leger JM, Servan J, Piette JC. Source: Arthritis and Rheumatism. 2002 December; 46(12): 3317-26. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12483738
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Interleukin 8 gene polymorphism is associated with increased risk of nephritis in cutaneous vasculitis. Author(s): Amoli MM, Thomson W, Hajeer AH, Calvino MC, Garcia-Porrua C, Ollier WE, Gonzalez-Gay MA. Source: The Journal of Rheumatology. 2002 November; 29(11): 2367-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12415593
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Intravenous immunoglobulin in livedo vasculitis: a new treatment option? Author(s): Schanz S, Ulmer A, Fierlbeck G. Source: Journal of the American Academy of Dermatology. 2003 September; 49(3): 555-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12963934
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Intravenous immunoglobulins in peripheral neuropathy associated with vasculitis. Author(s): Levy Y, Uziel Y, Zandman GG, Amital H, Sherer Y, Langevitz P, Goldman B, Shoenfeld Y. Source: Annals of the Rheumatic Diseases. 2003 December; 62(12): 1221-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14644864
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Investigation of quality of life, mood, pain, disability, and disease status in primary systemic vasculitis. Author(s): Koutantji M, Harrold E, Lane SE, Pearce S, Watts RA, Scott DG. Source: Arthritis and Rheumatism. 2003 December 15; 49(6): 826-37. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14673970
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Involvement of oxidative and nitrosative stress in promoting retinal vasculitis in patients with Eales' disease. Author(s): Rajesh M, Sulochana KN, Punitham R, Biswas J, Lakshmi S, Ramakrishnan S. Source: Clinical Biochemistry. 2003 July; 36(5): 377-85. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12849870
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Is granuloma annulare related to intermediate uveitis with retinal vasculitis? Author(s): van Kooij B, van Dijk MC, de Boer J, Sigurdsson V, Rothova A. Source: The British Journal of Ophthalmology. 2003 June; 87(6): 763-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12770977
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Isolated testicular vasculitis presenting as a tumor-like lesion. Author(s): Joudi FN, Austin JC, Vogelgesang SA, Jensen CS. Source: The Journal of Urology. 2004 February; 171(2 Pt 1): 799. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14713819
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Juvenile dermatomyositis complicated with vasculitis and duodenal perforation. Author(s): Wang IJ, Hsu WM, Shun CT, Chiang BL, Ni YH. Source: J Formos Med Assoc. 2001 December; 100(12): 844-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11802528
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Juvenile neutrophilic eccrine hidradenitis: a vasculitis-like plantar dermatosis. Author(s): Drake M, Sanchez-Burson JM, Dona-Naranjo MA, Conde JM. Source: Clinical Rheumatology. 2000; 19(6): 481-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11147761
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Kidney transplantation and ANCA-associated vasculitis. Author(s): van der Woude FJ. Source: Cleve Clin J Med. 2002; 69 Suppl 2: Sii143-5. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12086254
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Kidney transplantation in patients with systemic vasculitis. Author(s): Nyberg G, Akesson P, Norden G, Wieslander J. Source: Transplantation Proceedings. 1997 February-March; 29(1-2): 235. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9122977
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Kidney transplantation in patients with vasculitis and predominant renal involvement. Author(s): Bayes B, Lauzurica R, Serra A, Bonet J, Bonal J, Teixido J, Mirapeix E, Romero R. Source: Transplantation Proceedings. 1999 September; 31(6): 2324-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10500600
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Kikuchi's disease with leukocytoclastic vasculitis in a 10-year-old girl. Author(s): Kawai H, Hasegawa M, Hagiwara S, Hosomura Y. Source: Pediatrics International : Official Journal of the Japan Pediatric Society. 1999 June; 41(3): 323-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10365589
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Klebsiella pneumoniae and leukocytoclastic vasculitis. Author(s): Lloret P, Redondo P, Molano E. Source: Lancet. 2002 October 5; 360(9339): 1062. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12383983
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Known causes of vasculitis in man. Author(s): Naides SJ. Source: Cleve Clin J Med. 2002; 69 Suppl 2: Sii15-9. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12086257
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Lack of association of alpha-1 antichymotrypsin gene polymorphism with PR3-ANCA and MPO-ANCA associated vasculitis. Author(s): Borgmann S, Haubitz M, Schwab SG. Source: Autoimmunity. 2002 November; 35(7): 435-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12685871
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Large vessel vasculitis. Author(s): Salvarani C. Source: Clin Exp Rheumatol. 2003 November-December; 21(6 Suppl 32): S133-4. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14740442
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Large-vessel vasculitis. Author(s): Seo P, Stone JH. Source: Arthritis and Rheumatism. 2004 February 15; 51(1): 128-39. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14872466
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Large-vessel vasculitis: unresolved issues. Author(s): Hoffman GS. Source: Arthritis and Rheumatism. 2003 September; 48(9): 2406-14. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=13130459
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Leflunomide induced vasculitis--a dose-response relationship. Author(s): Chan AT, Bradlow A, McNally J. Source: Rheumatology (Oxford, England). 2003 March; 42(3): 492-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12626811
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Leucocytoclastic vasculitis and influenza immunization. Author(s): Walker SL, Swindells KJ, Chalmers RJ. Source: Clinical and Experimental Dermatology. 2004 January; 29(1): 95-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14723736
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Leucocytoclastic vasculitis and influenza vaccination. Author(s): Tavadia S, Drummond A, Evans CD, Wainwright NJ. Source: Clinical and Experimental Dermatology. 2003 March; 28(2): 154-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12653702
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Leucocytoclastic vasculitis as onset symptom of ulcerative colitis. Author(s): Iannone F, Scioscia C, Musio A, Piscitelli D, Lapadula G. Source: Annals of the Rheumatic Diseases. 2003 August; 62(8): 785-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12860742
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Leukocyte scintigraphy with 99mTc-exametazime-labeled leukocytes is not useful for follow-up of systemic vasculitis. Author(s): Becherer A, Deicher R, Jilma B, Haas M, Staudenherz A, Horl WH, Dudczak R, Kletter K. Source: Wiener Klinische Wochenschrift. 2002 January 15; 114(1-2): 28-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12407932
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Leukocytoclastic (small vessel) vasculitis in multiple myeloma. Author(s): Bayer-Garner IB, Smoller BR. Source: Clinical and Experimental Dermatology. 2003 September; 28(5): 521-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12950344
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Leukocytoclastic vasculitis and interstitial nephritis with carbimazole treatment. Author(s): Day C, Bridger J, Rylance P, Jackson M, Nicholas J, Odum J. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 2003 February; 18(2): 429-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12543903
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Leukocytoclastic vasculitis induced by use of glyburide: a case of possible crossreaction of a sulfonamide and a sulfonylurea. Author(s): Bukhalo M, Zeitouni NC, Cheney RT. Source: Cutis; Cutaneous Medicine for the Practitioner. 2003 March; 71(3): 235-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12661752
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Leukocytoclastic vasculitis presenting as an erythema gyratum repens--like eruption on a patient with systemic lupus erythematosus. Author(s): Pique E, Palacios S, Santana Z. Source: Journal of the American Academy of Dermatology. 2002 November; 47(5 Suppl): S254-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12399742
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Leukocytoclastic vasculitis related to rofecoxib. Author(s): Palop-Larrea V, Melchor-Penella MA, Ortega-Monzo C, Martinez-Mir I. Source: The Annals of Pharmacotherapy. 2003 November; 37(11): 1731-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14565803
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Levels of matrix metalloproteinase-9 within cerebrospinal fluid in a rabbit model of coccidioidal meningitis and vasculitis. Author(s): Williams PL, Leib SL, Kamberi P, Leppert D, Sobel RA, Bifrare YD, Clemons KV, Stevens DA. Source: The Journal of Infectious Diseases. 2002 December 1; 186(11): 1692-5. Epub 2002 November 01. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12447750
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Livedoid vasculitis with ulcerations: the role of antithrombin III deficiency and its therapeutic consequences. Author(s): Hegemann B, Helmbold P, Marsch WC. Source: Archives of Dermatology. 2002 June; 138(6): 841-2. Erratum In: Arch Dermatol 2002 September; 138(9): 1212. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12056979
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Localized versus systemic vasculitis: diagnosis and management. Author(s): Quinet RJ, Zakem JM, McCain M. Source: Curr Rheumatol Rep. 2003 April; 5(2): 93-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12628039
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Long term follow up in a case of successfully treated idiopathic retinal vasculitis, aneurysms, and neuroretinitis (IRVAN). Author(s): Tomita M, Matsubara T, Yamada H, Takahashi K, Nishimura T, Sho K, Uyama M, Matsumura M. Source: The British Journal of Ophthalmology. 2004 February; 88(2): 302-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14736797
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Long-term follow-up of a patient with cutaneous vasculitis secondary to mixed cryoglobulinaemia and hepatitis C virus. Author(s): Kapur N, Tympanidis P, Colville C, Yu RC. Source: Clinical and Experimental Dermatology. 2002 January; 27(1): 37-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11952668
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Lupus-like syndrome and vasculitis induced by valpromide. Author(s): Bonnet F, Morlat P, De Witte S, Combe C, Beylot J. Source: The Journal of Rheumatology. 2003 January; 30(1): 208-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12508420
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Magnetic resonance imaging of skeletal muscle involvement in limb restricted vasculitis. Author(s): Gallien S, Mahr A, Rety F, Kambouchner M, Lhote F, Cohen P, Guillevin L. Source: Annals of the Rheumatic Diseases. 2002 December; 61(12): 1107-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12429545
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Maintenance therapy for vasculitis associated with antineutrophil cytoplasmic autoantibodies. Author(s): Sanders JS, Slot MC, Stegeman CA. Source: The New England Journal of Medicine. 2003 November 20; 349(21): 2072-3; Author Reply 2072-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14627795
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Medium- and large-vessel vasculitis. Author(s): Weyand CM, Goronzy JJ. Source: The New England Journal of Medicine. 2003 July 10; 349(2): 160-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12853590
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Membrane proteinase 3 expression on resting neutrophils as a pathogenic factor in PR3-ANCA-associated vasculitis. Author(s): van Rossum AP, Limburg PC, Kallenberg CG. Source: Clin Exp Rheumatol. 2003 November-December; 21(6 Suppl 32): S64-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14740429
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Membranoproliferative glomerulonephritis and leukocytoclastic vasculitis without cryoglobulin in chronic hepatitis C virus infection. Author(s): Nakajima A, Adachi M, Tanaka M, Suwa A, Yasuki Y, Imaeda H, Inada S. Source: Intern Med. 2003 October; 42(10): 1042-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14606724
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Monocyte activation and relationship to anti-proteinase 3 in acute vasculitis. Author(s): Wikman A, Fagergren A, Gunnar O Johansson S, Lundahl J, Jacobson SH. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 2003 September; 18(9): 1792-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12937226
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Mononeuropathy multiplex in association with livedoid vasculitis. Author(s): Toth C, Trotter M, Clark A, Zochodne D. Source: Muscle & Nerve. 2003 November; 28(5): 634-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14571469
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MPO-ANCA-associated pulmonary-renal vasculitis in a patient with diabetes mellitus. Author(s): Keven K, Akar H, Kutlay S, Nergizoglu G, Erbay B, Erturk S. Source: Journal of Nephrology. 2002 November-December; 15(6): 720-3. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12495292
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Multiple coronary aneurysms resulting from isolated coronary vasculitis in an elderly patient. Author(s): Shimizu M, Okada T, Kobayashi S, Yamamoto Y, Takahashi H, Kawata M, Nakamura T. Source: Circulation Journal : Official Journal of the Japanese Circulation Society. 2003 July; 67(7): 637-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12845190
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Mycotic cerebral vasculitis in a paediatric cardiac transplant patient excludes misadventure. Author(s): Rickert CH, Greiner C, Rellensmann G, Kehl HG, Scheld HH, Paulus W, Fechner G. Source: International Journal of Legal Medicine. 2002 August; 116(4): 233-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12420703
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Myocardial infarction caused by rheumatoid vasculitis: histological evidence of the involvement of T lymphocytes. Author(s): Takayanagi M, Haraoka H, Kikuchi H, Hirohata S. Source: Rheumatology International. 2003 November; 23(6): 315-8. Epub 2003 March 21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14634788
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Necrotizing granulomatous vasculitis in advanced HIV infection. Author(s): Garcia-Garcia JA, Macias J, Castellanos V, Fernandez-Rivera J, LozanoGutierrez F, Rivera JM, Pineda JA. Source: The Journal of Infection. 2003 November; 47(4): 333-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14556759
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Necrotizing vasculitis: a cause of aortic insufficiency and conduction system disturbance. Author(s): Gomez Perez M, Seres Garcia L, Olive Marques A, Lopez Ayerbe J, Larrousse Perez E, Aris A, Valle Tudela V. Source: Echocardiography (Mount Kisco, N.Y.). 2003 October; 20(7): 589-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14536006
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Neuroborreliosis with vasculitis causing stroke-like manifestations. Author(s): Romi F, Krakenes J, Aarli JA, Tysnes OB. Source: European Neurology. 2004; 51(1): 49-50. Epub 2003 November 21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14639033
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Neutrophil functions of patients with MPO-ANCA-related vasculitis. Author(s): Suzuki K. Source: Intern Med. 2003 July; 42(7): 552-3. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12879944
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Neutrophilic eccrine hidradenitis mimicking cutaneous vasculitis in a lupus patient: a complication of cyclophosphamide. Author(s): Lienesch DW, Mutasim DF, Singh RR. Source: Lupus. 2003; 12(9): 707-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14514135
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New developments in the pathogenesis of ANCA-associated vasculitis. Author(s): Day CJ, Hewins P, Savage CO. Source: Clin Exp Rheumatol. 2003 November-December; 21(6 Suppl 32): S35-48. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14740426
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Nitric oxide modulates MCP-1 expression in endothelial cells: implications for the pathogenesis of pulmonary granulomatous vasculitis. Author(s): Desai A, Miller MJ, Huang X, Warren JS. Source: Inflammation. 2003 August; 27(4): 213-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14527174
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Nodular vasculitis as a paraneoplastic presentation? Author(s): Khachemoune A, Longo MI, Phillips TJ. Source: International Journal of Dermatology. 2003 August; 42(8): 639-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12890111
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Notes on the history of eponymic idiopathic vasculitis: the diseases of Henoch and Schonlein, Wegener, Churg and Strauss, Horton, Takayasu, Behcet, and Kawasaki. Author(s): Matteson EL. Source: Arthritis Care and Research : the Official Journal of the Arthritis Health Professions Association. 2000 August; 13(4): 237-45. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14635278
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Nuclear medicine in vasculitis. Author(s): Peters AM. Source: Rheumatology (Oxford, England). 2000 May; 39(5): 463-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10852975
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Obstruction of the pulmonary artery by granulomatous vasculitis: a clinical, morphological, and immunological analysis. Author(s): Schett G, Winkler S, Hollenstein U, Amann G, Willheim M, Prokop M, Klepetko W, Becherer A, Smolen J, Graninger W. Source: Annals of the Rheumatic Diseases. 2002 May; 61(5): 463-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11959774
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Occlusive vasculitis in a patient with concomitant West Nile virus infection. Author(s): Kaiser PK, Lee MS, Martin DA. Source: American Journal of Ophthalmology. 2003 November; 136(5): 928-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14597052
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Ocular vasculitis. Author(s): Shepherd JB 3rd. Source: Curr Rheumatol Rep. 2003 April; 5(2): 100-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12628040
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Onset of acute respiratory distress syndrome following severe pulmonary hemorrhage in a patient with anti-neutrophil cytoplasmic antibody associated vasculitis. Author(s): Steinau F, Deja M, Weber-Carstens S, Busch T, Kaisers U. Source: Intensive Care Medicine. 2003 March; 29(3): 504. Epub 2003 February 08. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12577149
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Optic disk vasculitis associated with chronic active Epstein-Barr virus infection. Author(s): Yamamoto M, Ohga S, Ohnishi Y, Inomata H. Source: Ophthalmologica. Journal International D'ophtalmologie. International Journal of Ophthalmology. Zeitschrift Fur Augenheilkunde. 2002 May-June; 216(3): 221-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12065861
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Optic neuritis and retinal vasculitis as primary manifestations of systemic lupus erythematosus. Author(s): Barkeh HJ, Muhaya M. Source: Med J Malaysia. 2002 December; 57(4): 490-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12733176
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Orlistat-induced cutaneous leukocytoclastic vasculitis. Author(s): Gonzalez-Gay MA, Garcia-Porrua C, Lueiro M, Fernandez ML. Source: Arthritis and Rheumatism. 2002 October 15; 47(5): 567. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12382312
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Otolaryngologic manifestations of small vessel vasculitis. Author(s): Metaxaris G, Prokopakis EP, Karatzanis AD, Sakelaris G, Heras P, Velegrakis GA, Helidonis ES. Source: Auris, Nasus, Larynx. 2002 October; 29(4): 353-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12393040
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Outcome of ANCA-associated renal vasculitis: a 5-year retrospective study. Author(s): Booth AD, Almond MK, Burns A, Ellis P, Gaskin G, Neild GH, Plaisance M, Pusey CD, Jayne DR; Pan-Thames Renal Research Group. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2003 April; 41(4): 776-84. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12666064
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Outcome of renal transplantation in patients with pauci-immune small vessel vasculitis or anti-GBM disease. Author(s): Deegens JK, Artz MA, Hoitsma AJ, Wetzels JF. Source: Clinical Nephrology. 2003 January; 59(1): 1-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12572924
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P-ANCA positive renal vasculitis in association with renal cell carcinoma and prolonged hydralazine therapy. Author(s): Norris JH, Leeds J, Jeffrey RF. Source: Renal Failure. 2003 March; 25(2): 311-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12739838
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Plasmapheresis therapy for diffuse alveolar hemorrhage in patients with small-vessel vasculitis. Author(s): Klemmer PJ, Chalermskulrat W, Reif MS, Hogan SL, Henke DC, Falk RJ. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2003 December; 42(6): 1149-53. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14655185
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Primary pulmonary hypertension, Raynaud's phenomenon and generalised vasculitis in juvenile rheumatoid arthritis. Author(s): Banapurmath CR, Latha GS, Satishchandran VR, Manivannan MR. Source: Indian J Pediatr. 1996 May-June; 63(3): 396-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10830018
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Prognosis and outcome of 26 patients with systemic necrotizing vasculitis admitted to the intensive care unit. Author(s): Cruz BA, Ramanoelina J, Mahr A, Cohen P, Mouthon L, Cohen Y, Hoang P, Guillevin L. Source: Rheumatology (Oxford, England). 2003 October; 42(10): 1183-8. Epub 2003 May 30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12777637
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Pseudotumoral retroperitoneal fibrosis and localized vasculitis with very high serum levels of anti-PR3 ANCA. Author(s): Aslangul E, Ranque B, Papo T. Source: The American Journal of Medicine. 2003 August 15; 115(3): 250-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12935836
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PTU-associated cutaneous vasculitis with ANCA anti-MPO and anti-PR3 antibodies. Author(s): Jacobs EM, Hartkamp A, Kaasjager HA. Source: The Netherlands Journal of Medicine. 2003 September; 61(9): 296-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14692444
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PTU-associated vasculitis. Author(s): Bombassei GJ. Source: Endocrine Practice : Official Journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. 2003 March-April; 9(2): 167. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12917084
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Pulmonary embolism--or vasculitis? Author(s): Haydar AA, Goldsmith DJ. Source: Journal of the Royal Society of Medicine. 2004 January; 97(1): 27-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14702362
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Pulmonary vasculitis presenting as atypical asthma. Author(s): Chamarthy LM, de la Morena M, Lacson A, Cawkwell G, Good RA. Source: Annals of Allergy, Asthma & Immunology : Official Publication of the American College of Allergy, Asthma, & Immunology. 2000 May; 84(5): 495-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10831001
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Pustular vasculitis in a patient with T-cell large granular lymphocyte proliferation and myelodysplasia. Successful treatment by ciclosporin. Author(s): Sailler L, Joseph-Hein K, Astudillo L, Madaule S, Ecoiffier M, Dahan S, Delisle MB, Arlet P. Source: The British Journal of Dermatology. 2003 October; 149(4): 893-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14616392
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Radiologic features of vasculitis involving the gastrointestinal tract. Author(s): Ha HK, Lee SH, Rha SE, Kim JH, Byun JY, Lim HK, Chung JW, Kim JG, Kim PN, Lee MG, Auh YH. Source: Radiographics : a Review Publication of the Radiological Society of North America, Inc. 2000 May-June; 20(3): 779-94. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10835128
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Recombinant protein to analyze autoantibodies to proteinase 3 in systemic vasculitis. Author(s): Rarok AA, Huitema MG, van der Leij MJ, van der Geld YM, Berthold H, Schmitt J, Stegeman CA, Limburg PC, Kallenberg CG. Source: American Journal of Clinical Pathology. 2003 October; 120(4): 586-95. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14560570
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Regression of aneurysmal dilatations in a case of idiopathic retinal vasculitis, aneurysms and neuroretinitis (IRVAN) associated with allergic fungal sinusitis. Author(s): Abu El-Asrar AM, Jestaneiah S, Al-Serhani AM. Source: Eye (London, England). 2004 February; 18(2): 197-9; Discussion 199-201. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14762419
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Relapse rate and outcome of ANCA-associated small vessel vasculitis after transplantation. Author(s): Elmedhem A, Adu D, Savage CO. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 2003 May; 18(5): 1001-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12686678
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Renal survival and prognostic factors in patients with PR3-ANCA associated vasculitis with renal involvement. Author(s): Slot MC, Tervaert JW, Franssen CF, Stegeman CA. Source: Kidney International. 2003 February; 63(2): 670-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12631133
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Respiratory syncytial virus pneumonitis complicating immunosuppressive treatment for ANCA-positive vasculitis. Author(s): Jones R, Shah S, MacMahon EE, Goldsmith DJ. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 2003 September; 18(9): 1920-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12937244
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Retinal vasculitis due to secondary syphilis. Author(s): Yokoi M, Kase M. Source: Japanese Journal of Ophthalmology. 2004 January-February; 48(1): 65-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14767654
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Rheumatoid vasculitis following influenza vaccination. Author(s): Iyngkaran P, Limaye V, Hill C, Henderson D, Pile KD, Rischmueller M. Source: Rheumatology (Oxford, England). 2003 July; 42(7): 907-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12826713
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Ritodrine-induced leukocytoclastic vasculitis in pregnancy. Author(s): Cobeta-Garcia JC, Garcia-Enguita P, Pina-Latorre MA, Lerin-Sanchez FJ, Rodilla-Calvelo F. Source: The Annals of Pharmacotherapy. 2004 January; 38(1): 66-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14742797
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Rituximab induces remission in refractory HCV associated cryoglobulinaemic vasculitis. Author(s): Lamprecht P, Lerin-Lozano C, Merz H, Dennin RH, Gause A, Voswinkel J, Peters SO, Gutzeit O, Arlt AC, Solbach W, Gross WL. Source: Annals of the Rheumatic Diseases. 2003 December; 62(12): 1230-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14644867
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Silica exposure and systemic vasculitis. Author(s): Mulloy KB. Source: Environmental Health Perspectives. 2003 December; 111(16): 1933-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14644669
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SIR 2003 film panel case 1: Behcet vasculitis. Author(s): Papenhausen MD, Mendez R, Mauro MA. Source: Journal of Vascular and Interventional Radiology : Jvir. 2003 May; 14(5): 649-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12761321
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Small fiber neuropathy due to isolated vasculitis of the peripheral nervous system. Author(s): Zafrir B, Zimmerman M, Fellig Y, Naparstek Y, Reichman N, Flatau E. Source: Isr Med Assoc J. 2004 March; 6(3): 183-4. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15055280
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Small-bowel arteriovenous shunting due to systemic lupus erythematosus vasculitis. Author(s): Inyang AN, Ulrrich H. Source: American Journal of Critical Care : an Official Publication, American Association of Critical-Care Nurses. 2003 May; 12(3): 242-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12751399
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Subarachnoid hemorrhages in vasculitis. Author(s): Thompson B, Burns A. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2003 September; 42(3): 582-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12955688
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Subclinical pulmonary haemorrhage causing a restrictive lung defect in three siblings with a unique urticarial vasculitis syndrome. Author(s): Al Riyami BM, Al Kaabi JK, Elagib EM, Khatim HS, Woodhouse NJ. Source: Clinical Rheumatology. 2003 October; 22(4-5): 309-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14579162
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Successful response to infliximab in a patient with undifferentiated spondyloarthropathy coexisting with polyarteritis nodosa-like cutaneous vasculitis. Author(s): Garcia-Porrua C, Gonzalez-Gay MA. Source: Clin Exp Rheumatol. 2003 November-December; 21(6 Suppl 32): S138. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14740443
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Successful treatment of severe rheumatoid vasculitis by infliximab. Author(s): Unger L, Kayser M, Nusslein HG. Source: Annals of the Rheumatic Diseases. 2003 June; 62(6): 587-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12759302
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Sweet's syndrome with arthritis and vasculitis. Author(s): Gouliaris Y, Papadakis P, Kranias D, Sambatziotis D, Kaklamanis P. Source: Clinical Rheumatology. 2003 September; 22(3): 244-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14505221
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Systemic vasculitis presenting with acute gastrointestinal hemorrhage: case report and review of the literature. Author(s): Sisk CM, Parker C, Cassidy T, Parker A. Source: Digestive Diseases and Sciences. 2003 September; 48(9): 1782-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14561001
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Temporal arteritis associated with systemic necrotizing vasculitis. Author(s): Hamidou MA, Moreau A, Toquet C, El Kouri D, de Faucal P, Grolleau JY. Source: The Journal of Rheumatology. 2003 October; 30(10): 2165-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14528512
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Temporal concurrence of vasculitis and cancer: a report of 12 cases. Author(s): Hutson TE, Hoffman GS. Source: Arthritis Care and Research : the Official Journal of the Arthritis Health Professions Association. 2000 December; 13(6): 417-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14635319
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The coexistence of cutaneous vasculitis and thrombosis in childhood-onset systemic lupus erythematosus with antiphospholipid antibodies. Author(s): Tomizawa K, Sato-Matsumura KC, Kajii N. Source: The British Journal of Dermatology. 2003 August; 149(2): 439-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12932270
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The ICAM1469*E is associated with susceptibility to ocular lesions and vasculitis in Korean patients with Behcet's disease. Author(s): Kim EH, Mok JW, Bang D, Lee ES, Lee S, Park KS. Source: Advances in Experimental Medicine and Biology. 2003; 528: 235-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12918698
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The pathology and pathogenesis of retinal vasculitis. Author(s): Hughes EH, Dick AD. Source: Neuropathology and Applied Neurobiology. 2003 August; 29(4): 325-40. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12887593
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The pulmonary physician in critical care * illustrative case 3: pulmonary vasculitis. Author(s): Griffith M, Brett S. Source: Thorax. 2003 June; 58(6): 543-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12775874
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The role of myeloperoxidase in the pathogenesis of systemic vasculitis. Author(s): Rutgers A, Heeringa P, Tervaert JW. Source: Clin Exp Rheumatol. 2003 November-December; 21(6 Suppl 32): S55-63. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14740428
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The use of (18F)fluoro-deoxyglucose positron emission tomography in the assessment of large vessel vasculitis. Author(s): Blockmans D. Source: Clin Exp Rheumatol. 2003 November-December; 21(6 Suppl 32): S15-22. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14740423
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Therapy of neurological disorders in systemic vasculitis. Author(s): Gold R, Fontana A, Zierz S. Source: Seminars in Neurology. 2003 June; 23(2): 207-14. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12894386
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Transfusion medicine illustrated. Cryoglobulinemia and cutaneous vasculitis. Author(s): Boctor FN, Sands C, Billett H. Source: Transfusion. 2004 February; 44(2): 145. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14962302
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Unihemispheric cerebral vasculitis mimicking Rasmussen's encephalitis. Author(s): Derry C, Dale RC, Thom M, Miller DH, Giovannoni G. Source: Neurology. 2002 January 22; 58(2): 327-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11805272
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Unilateral retinal vasculitis, branch retinal artery occlusion and subsequent retinal neovascularization in Crohn's disease. Author(s): Saatci OA, Kocak N, Durak I, Ergin MH. Source: International Ophthalmology. 2001; 24(2): 89-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12201349
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Unusual morphologic features of uterine leiomyomas treated with gonadotropinreleasing hormone agonists: massive lymphoid infiltration and vasculitis. Author(s): McClean G, McCluggage WG. Source: International Journal of Surgical Pathology. 2003 October; 11(4): 339-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14615835
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Urticaria and urticarial vasculitis. Author(s): Guha B, Youngberg G, Krishnaswamy G. Source: Compr Ther. 2003 Summer-Fall; 29(2-3): 146-56. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14606344
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Urticarial vasculitis and dermatomyositis in a patient with nasopharyngeal carcinoma. Author(s): Wang CC, Chen MJ, Ho HC, Hong HS. Source: Cutis; Cutaneous Medicine for the Practitioner. 2003 November; 72(5): 399-402. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14655782
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Urticarial vasculitis with asymptomatic chronic hepatitis C infection: response to doxepin, interferon-alfa, and ribavirin. Author(s): Kelkar PS, Butterfield JH, Kalaaji AN. Source: Journal of Clinical Gastroenterology. 2002 September; 35(3): 281-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12192209
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Urticarial vasculitis. Author(s): Venzor J, Lee WL, Huston DP. Source: Clinical Reviews in Allergy & Immunology. 2002 October; 23(2): 201-16. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12221865
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Urticarial vasculitis: a paraneoplastic presentation of B-cell non-Hodgkin's lymphoma. Author(s): Wilson D, McCluggage WG, Wright GD. Source: Rheumatology (Oxford, England). 2002 April; 41(4): 476-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11961187
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Use of prostacyclin (iloprost) in digital vasculitis secondary to meningococcaemia. Author(s): Siddiqui K, Razak AR, Kneafsey B, Delanty N. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 2004 March; 75(3): 506. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14966179
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Using antineutrophil cytoplasmic antibody testing to diagnose vasculitis: can testordering guidelines improve diagnostic accuracy? Author(s): Mandl LA, Solomon DH, Smith EL, Lew RA, Katz JN, Shmerling RH. Source: Archives of Internal Medicine. 2002 July 8; 162(13): 1509-14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12090888
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Varicella-zoster vasculitis presenting with intracranial hemorrhage. Author(s): Jain R, Deveikis J, Hickenbottom S, Mukherji SK. Source: Ajnr. American Journal of Neuroradiology. 2003 May; 24(5): 971-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12748105
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Vascular endothelial growth factor may provide additional values to C-reactive protein and anti-myeloperoxidase titer as a parameter for evaluating disease activity in anti-myeloperoxidase associated vasculitis. Author(s): Peng CH, Lin CL, Yang CW, Shueh S, Huang CC. Source: Renal Failure. 2003 November; 25(6): 1057-66. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14669866
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Vasculitis and the gastrointestinal tract. Author(s): Geboes K, Dalle I. Source: Acta Gastroenterol Belg. 2002 October-December; 65(4): 204-12. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12619427
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Vasculitis associated with all trans retinoic acid (ATRA) in a case with acute promyelocytic leukemia. Author(s): Paydas S, Yavuz S, Disel U, Sahin B, Canbolat T, Tuncer I. Source: Leukemia & Lymphoma. 2003 March; 44(3): 547-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12688331
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Vasculitis in a dog resembling isolated angiitis of the central nervous system in humans. Author(s): Sasaki M, Pool R, Summers BA. Source: Veterinary Pathology. 2003 January; 40(1): 95-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12627719
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Vasculitis in children. Author(s): Kumar L, Singh S. Source: Indian J Pediatr. 1996 May-June; 63(3): 323-34. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10830007
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Vasculitis mimicking bacterial endocarditis. Author(s): Calachanis M, Ferrero P, Orzan F, Marchisio F, Trevi G. Source: Ital Heart J. 2003 November; 4(11): 816-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14699714
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Vasculitis of the spinal cord. Author(s): Ropper AH, Ayata C, Adelman L. Source: Archives of Neurology. 2003 December; 60(12): 1791-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14676059
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Vasculitis with digital gangrene in a patient with HIV infection. Author(s): Kakrani AL, Basavraj A, Madraki R. Source: J Assoc Physicians India. 2003 March; 51: 299-301. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12839357
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Vasculitis: the true and near-true. Author(s): Ackerman AB. Source: The American Journal of Dermatopathology. 2002 December; 24(6): 521-2; Author Reply 522-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12454607
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What is new in systemic vasculitis? Author(s): Kallenberg CG, Tervaert JW. Source: Annals of the Rheumatic Diseases. 2000 November; 59(11): 924-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11053075
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What is Vasculitis? Author(s): Nadeau SE. Source: Journal of Neuro-Ophthalmology : the Official Journal of the North American Neuro-Ophthalmology Society. 2003 June; 23(2): 113-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12782921
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What is your diagnosis? Bywaters lesions of rheumatoid vasculitis. Author(s): Herron MD, Florell S. Source: Cutis; Cutaneous Medicine for the Practitioner. 2003 June; 71(6): 439, 462, 464. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12839252
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What you should know about PR3-ANCA. Evidence for the role of T cells in the pathogenesis of systemic vasculitis. Author(s): Clayton AR, Savage CO. Source: Arthritis Research. 2000; 2(4): 260-2. Epub 2000 June 12. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11094438
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When should you consider vasculitis? Author(s): Conn DL. Source: Bulletin on the Rheumatic Diseases. 1998 October; 47(6): 1-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9805403
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CHAPTER 2. NUTRITION AND VASCULITIS Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and vasculitis.
Finding Nutrition Studies on Vasculitis 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 “vasculitis” (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 “vasculitis” (or a synonym): •
A case of frosted branch angiitis with yellowish-white placoid lesions: fluorescein and indocyanine green angiography findings. Author(s): Department of Ophthalmology, Hamamatsu University School of Medicine, Shizuoka, Japan. Source: Masuda, K Ueno, M Watanabe, I Jpn-J-Ophthalmol. 1998 Nov-December; 42(6): 484-9 0021-5155
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Acute febrile neutrophilic vasculitis of the skin of young Shar-Pei dogs. Author(s): University Veterinary Centre Sydney, Faculty of Veterinary Science, The University of Sydney, New South Wales.
[email protected] Source: Malik, R Foster, S F Martin, P Canfield, P J Mason, K V Bosward, K L Gough, A Rippon, G Aust-Vet-J. 2002 April; 80(4): 200-6 0005-0423
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Acute meningococcaemia complicated by late onset gastrointestinal vasculitis. Author(s): Infection and Immunodeficiency Unit, Kings Cross Hospital, Dundee, UK. Source: Seaton, R A Nathwani, D Dick, J Smith, D J-Infect. 2000 September; 41(2): 190-1 0163-4453
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Acute transverse myelitis and primary urticarial vasculitis. Author(s): Department of Internal Medicine, Centre Hospitalo-Universitaire Timone, Marseille, France. Source: Bolla, G Disdier, P Verrot, D Swiader, L Andrac, L Harle, J R Pouget, J Weiller, P J Clin-Rheumatol. 1998; 17(3): 250-2 0770-3198
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Adjuvant treatment of patients with antineutrophil cytoplasmic antibody-associated vasculitis with vitamins E and C reduces superoxide production by neutrophils. Author(s): MRC Centre for Immune Regulation, Department of Medicine, The Medical School, Birmingham University, Edgbaston, Birmingham B15 2TT, UK. Source: Harper, L Nuttall, S L Martin, U Savage, C O S Rheumatology-(Oxford). 2002 Mar; 41(3): 274-8 1462-0324
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All trans retinoic acid as the possible cause of necrotizing vasculitis. Author(s): Department of Oncology, Cukurova University Faculty of Medicine, Adana, Turkey. Source: Paydas, S Sahin, B Zorludemir, S Hazar, B Leuk-Res. 1998 July; 22(7): 655-7 01452126
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An immunohistopathologic study in cutaneous necrotizing vasculitis. Author(s): Department of Dermatology, Hospital Universitari Germans Trias i Pujol, Badalona, Spain. Source: Bielsa, I Carrascosa, J M Hausmann, G Ferrandiz, C J-Cutan-Pathol. 2000 March; 27(3): 130-5 0303-6987
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ANCA-positive vasculitis. Author(s): Renal Immunobiology, Division of Medical Sciences, The Medical School, University of Birmingham, Birmingham B15 277, UK. Source: Kamesh, L Harper, L Savage, C O J-Am-Soc-Nephrol. 2002 July; 13(7): 1953-60 1046-6673
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Antigen inhalation as a triggering factor in systemic small-sized-vessel vasculitis. Four cases. Author(s): Service de Medecine Interne, Hopital Avicenne, Universite Paris-Nord, Bobigny, Cedex, France.
[email protected]
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Source: Mouthon, L Khaled, M Cohen, P Subra, J F Guillevin, L Ann-Med-Interne(Paris). 2001 April; 152(3): 152-6 0003-410X •
Antigen specificity in hydralazine associated ANCA positive systemic vasculitis. Author(s): Department of Medicine, School of Clinical Medicine, University of Cambridge, UK. Source: Short, A K Lockwood, C M QJM. 1995 November; 88(11): 775-83 1460-2725
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Antioxidants inhibit mercuric chloride-induced early vasculitis. Author(s): Division of Renal Medicine, St George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK.
[email protected] Source: Wu, Zhonglin Turner, David R Oliveira, David B G Int-Immunol. 2002 March; 14(3): 267-73 0953-8178
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Association of cerebral vasculitis with a lupus anticoagulant. A case with brain pathology. Author(s): Department of Internal Medicine, CHU La Timone Marseille, France. Source: Toussirot, E Figarella Branger, D Disdier, P Harle, J R Weiller, P J ClinRheumatol. 1994 December; 13(4): 624-7 0770-3198
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Asthma and vasculitis. Response to intravenous immunoglobulins. Author(s): Allergy Section, Hospital Rio Hortega, Valladolid, Spain. Source: Armentia, A Fernandez, A Sanchez, P de la Fuente, R Sanchis, E Mendez, J Parra, I Puyo, M Allergol-Immunopathol-(Madr). 1993 Mar-April; 21(2): 47-52 0301-0546
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Birdshot retinochoroidopathy and HLA-A29+ and HLA-A29- idiopathic retinal vasculitis: comparative study of 56 cases. Author(s): Unite d'Immunopathologie Oculaire, Centre Hospitalo-universitaire de Bicetre, Faculte de Medecine, Paris Sud, France. Source: Bloch Michel, E Frau, E Can-J-Ophthalmol. 1991 December; 26(7): 361-6 00084182
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Chronic immunosuppressive therapy for systemic vasculitis. Author(s): Immunologic Diseases Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892, USA. Source: Langford, C A Curr-Opin-Rheumatol. 1997 January; 9(1): 41-7 1040-8711
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Clinical image: occult large vessel vasculitis diagnosed by PET imaging. Author(s): Department of Internal Medicine I, University of Regensburg, Germany.
[email protected] Source: Wiest, R Gluck, T Schonberger, J Scholmerich, J Eilles, C Muller Ladner, U Rheumatol-Int. 2001 August; 20(6): 250 0172-8172
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Clinical management and treatment of vasculitis. Author(s): Box 157, Department of Medicine, Addenbrooke's Hospital, Cambridge CB1 2SP, UK. Source: Jayne, D Springer-Semin-Immunopathol. 2001; 23(3): 267-86 0172-6641
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Clinical trials review: vasculitis. Author(s): Department of Medicine, Clinical and Laboratory Immunology, University of South Florida and the James A. Haley VA Hospital, 13000 Bruce B. Downs Blvd., VAR 111D, Tampa, FL 33612, USA.
[email protected] Source: Ledford, D K Curr-Rheumatol-Repage 2000 October; 2(5): 365-8 1523-3774
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CT findings at lupus mesenteric vasculitis. Author(s): Department of Radiology, Chang Gung Medical College and Memorial Hospital, Kaohsiung Hsien, Taiwan.
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Source: Ko, S F Lee, T Y Cheng, T T Ng, S H Lai, H M Cheng, Y F Tsai, C C Acta-Radiol. 1997 January; 38(1): 115-20 0284-1851 •
Cutaneous vasculitis and its relationship to systemic disease. Source: Callen, J P Australas-J-Dermatol. 1987 August; 28(2): 49-55 0004-8380
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Diagnosis and treatment of the systemic and cutaneous necrotizing vasculitis syndromes. Author(s): Division of Rheumatology, Allergy and Immunology, Duke University Medical Center, Durham, North Carolina, USA. Source: Allen, N B Bressler, P B Med-Clin-North-Am. 1997 January; 81(1): 243-59 00257125
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Effects of chronic intracutaneous administration of arachidonic acid and its metabolites. Induction of leukocytoclastic vasculitis by leukotriene B4 and 12hydroxyeicosatetraenoic acid and its prevention by prostaglandin E2. Source: Ruzicka, T Burg, G J-Invest-Dermatol. 1987 February; 88(2): 120-3 0022-202X
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Elastin degradation in systemic vasculitis. Author(s): Department of Rheumatology, Moscow Medical Academy, Russia. Source: Bokarewa, M BaraNovember, A Nassonov, E Robert, L Pathol-Biol-(Paris). 1996 April; 44(4): 254-8 0369-8114
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Elimination diet in the treatment of selected patients with hypersensitivity vasculitis. Author(s): Institute of Clinical Medicine, University of Verona, Italy. Source: Lunardi, C Bambara, L M Biasi, D Zagni, P Caramaschi, P Pacor, M L Clin-ExpRheumatol. 1992 Mar-April; 10(2): 131-5 0392-856X
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Granulomatous angiitis of the nervous system. Author(s): Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, New York, USA. Source: Younger, D S Calabrese, L H Hays, A P Neurol-Clin. 1997 November; 15(4): 82134 0733-8619
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Hemorrhagic stroke due to cerebral vasculitis and the role of immunosuppressive therapy. Author(s): Northwestern University Medical School, Chicago, Illinois. Source: Cohen, B A Biller, J Neurosurg-Clin-N-Am. 1992 July; 3(3): 611-24 1042-3680
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Isotretinoin-induced vasculitis imitating polyarteritis nodosa, with perinuclear antineutrophil cytoplasmic antibody in titers correlated with clinical symptoms. Author(s): Internal Medicine Department, Tournai Medical and Surgical Institute, Belgium. Source: Chochrad, D Langhendries, J P Stolear, J C Godin, J Rev-Rhum-Engl-Ed. 1997 February; 64(2): 129-31 1169-8446
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Less common treatment in cutaneous vasculitis. Author(s): Department of Dermatology, University of Cagliari, Italy. Source: Atzori, L Ferreli, C Biggio, P Clin-Dermatol. 1999 Nov-December; 17(6): 641-7 0738-081X
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Lessons from animal models of vasculitis. Author(s): University of Maryland School of Medicine and Baltimore VA Medical Center, 10 North Greene Street, Baltimore, MD 21201, USA.
[email protected] Source: Luzina, I G Handwerger, B S Curr-Rheumatol-Repage 2000 October; 2(5): 369-75 1523-3774
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Leukocytoclastic vasculitis and long-term remission in a patient with secondary AML and post-remission treatment with low-dose interleukin-2. Author(s): Medizinische Klinik I, University of Freiburg, Germany. Source: Engelhardt, M Rump, J A Hellerich, U Mertelsmann, R Lindemann, A AnnHematol. 1995 April; 70(4): 227-30 0939-5555
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Microscopic polyangiitis presenting as schizophrenia. Author(s): Medical School, Jordan University of Science and Technology, Irbid, Jordan. Source: Askari, A Saadeh, A Buheis, N I Rheumatol-Int. 1999; 18(5-6): 215-7 0172-8172
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Necrotising vasculitis associated with captopril therapy. Source: Laaban, J Marie, J P Wallach, D Blanchard, D Lafay, M Gruffaz, F Eur-Heart-J. 1987 Mar; 8(3): 319 0195-668X
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Necrotizing peripheral nerve vasculitis. Author(s): Service de Neurologie, Hopital de Bicetre, Universite Paris Sud, Paris, France. Source: Said, G Neurol-Clin. 1997 November; 15(4): 835-48 0733-8619
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New concepts in treatment protocols for severe systemic vasculitis. Author(s): Dep. Rheumatologie des Universitat Lubeck und Rheumaklinik Bad Bramstedt GmbH, Germany. Source: Gross, W L Curr-Opin-Rheumatol. 1999 January; 11(1): 41-6 1040-8711
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New developments in the treatment of systemic vasculitis. Author(s): Universitat zu Lubeck, Germany. Source: Gross, W L Curr-Opin-Rheumatol. 1994 January; 6(1): 11-9 1040-8711
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Novel therapies for anti-neutrophil cytoplasmic antibody-associated vasculitis. Author(s): University Hospital Maastricht, Department of Clinical and Experimental Immunology, Maastricht, the Netherlands.
[email protected] Source: Cohen Tervaert, J W Stegeman, C A Kallenberg, C G Curr-Opin-NephrolHypertens. 2001 March; 10(2): 211-7 1062-4821
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Optic disk vasculitis associated with chronic active Epstein-Barr virus infection. Author(s): Department of Ophthalmology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
[email protected] Source: Yamamoto, M Ohga, S Ohnishi, Y Inomata, H Ophthalmologica. 2002 May-June; 216(3): 221-5 0030-3755
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Polyarteritis nodosa, microscopic polyangiitis, and Churg-Strauss syndrome: clinical aspects, neurologic manifestations, and treatment. Author(s): Service de Medecine Interne, Hopital Avicenne, Faculte de Medecine ParisNord, Bobigny, France. Source: Guillevin, L Lhote, F Gherardi, R Neurol-Clin. 1997 November; 15(4): 865-86 0733-8619
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Primary vasculitis in a Norwegian community hospital: a retrospective study. Author(s): Department of Rheumatology, Vest-Agder Community Hospital, Kristiansand S, Norway. Source: Haugeberg, G Bie, R Bendvold, A Larsen, A S Johnsen, V Clin-Rheumatol. 1998; 17(5): 364-8 0770-3198
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Retinal vasculitis as a complication of rheumatoid arthritis. Author(s): Department of Ophthalmology, Okayama University Medical School, Japan. Source: Matsuo, T Koyama, T Morimoto, N Umezu, H Matsuo, N Ophthalmologica. 1990; 201(4): 196-200 0030-3755
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Rheumatoid arthritis complicated by vasculitis. Author(s): Division of Immunology, University of Cincinnati, College of Medicine. Source: Hess, E V Hosp-Pract-(Off-Ed). 1988 October 30; 23(10A): 50-4, 57, 61-4 passim 8750-2836
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Sixth nerve palsies, temporal artery biopsy, and necrotizing vasculitis. Author(s): Department of Ophthalmology, University of South Florida, Tampa. Source: Sedwick, L A Margo, C E J-Clin-Neuroophthalmol. 1989 June; 9(2): 119-21 0272846X
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Small cell pleomorphic T-cell lymphoma presenting with cutaneous vasculitis. Author(s): Department of Rheumatology, Central Hospital of Aust Agder, Arendal. Source: Gran, J T Sund, S Langholm, R Clin-Rheumatol. 1994 December; 13(4): 628-30 0770-3198
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Suppression of coronary vasculitis in a murine model of Kawasaki disease using an angiogenesis inhibitor. Author(s): UCLA School of Medicine, Los Angeles, California, 90095-1670, USA. Source: Brahn, E Lehman, T J Peacock, D J Tang, C Banquerigo, M L Clin-Immunol. 1999 January; 90(1): 147-51 1521-6616
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The carbohydrate sialyl Lewis(x) (sLe(x)) sulfated glycomimetic GM2941 attenuates glucan-induced pulmonary granulomatous vasculitis in the rat. Author(s): Department of Pathology, University of Michigan Medical School, Ann Arbor, USA. Source: Kilgore, K S Powers, K L Imlay, M M Malani, A Allen, D I Beyer, J T Anderson, M B Warren, J S J-Pharmacol-Exp-Ther. 1998 July; 286(1): 439-46 0022-3565
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Therapy of systemic vasculitis. Author(s): Department of Rheumatic and Immunologic Disease, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA. Source: Calabrese, L H Neurol-Clin. 1997 November; 15(4): 973-91 0733-8619
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Vasculitis and leukemia. Author(s): Faculty of Medicine, Department of Oncology, Cukurova University, Balcali, Adana, Turkey.
[email protected] Source: Paydas, S Zorludemir, S Sahin, B Leuk-Lymphoma. 2000 December; 40(1-2): 10512 1042-8194
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 MEDICINE AND VASCULITIS Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to vasculitis. 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 vasculitis 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 “vasculitis” (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 vasculitis: •
“Living with Behcet”--a young patients' group. Author(s): Muller A. Source: Advances in Experimental Medicine and Biology. 2003; 528: 619-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12918778
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A report on the use of pulvis resinae in the treatment of thromboangiitis obliterans. Author(s): Zhu BG, Sun YY, Liu TP, Gao CZ, Feng LZ, Dong YF. Source: J Tradit Chin Med. 1985 December; 5(4): 237-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3834234
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Adjuvant treatment of patients with antineutrophil cytoplasmic antibody-associated vasculitis with vitamins E and C reduces superoxide production by neutrophils. Author(s): Harper L, Nuttall SL, Martin U, Savage CO.
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Source: Rheumatology (Oxford, England). 2002 March; 41(3): 274-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11934963 •
Alternative therapies for vasculitis and proliferative nephritides: the role of cyclic AMP elevating agents. Author(s): Wardle EN. Source: Renal Failure. 1998 January; 20(1): 7-13. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9509556
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Characterization of C1q found in a patient with hypocomplementemic vasculitisurticaria syndrome. Author(s): Sasaki T, Yonemasu K, Matsumoto M, Nagaki K. Source: Microbiology and Immunology. 1989; 33(5): 413-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2502705
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Etoposide: more effective and less bone-marrow toxic than standard immunosuppressive therapy in systemic vasculitis? Author(s): Pedersen RS, Bistrup C. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1996 June; 11(6): 1121-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8671979
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Hyperbaric oxygen in acute ischaemia due to allergic vasculitis. Author(s): Monies-Chass I, Herer D, Alon U, Birkhahn HJ. Source: Anaesthesia. 1976 November; 31(9): 1221-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1015606
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Less common treatment in cutaneous vasculitis. Author(s): Atzori L, Ferreli C, Biggio P. Source: Clinics in Dermatology. 1999 November-December; 17(6): 641-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10631524
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Leukocytoclastic vasculitis with IgA deposits in angioimmunoblastic T cell lymphoma. Author(s): Sugaya M, Nakamura K, Asahina A, Tamaki K. Source: The Journal of Dermatology. 2001 January; 28(1): 32-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11280462
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Multiple angiitis of mesenterial arteries in guinea pigs induced by intraperitoneal administration high doses of Na2EDTA. I. Light microscopic study. Author(s): Yamaguchi H, Usui H, Tajima T.
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Source: Exp Pathol. 1981; 20(1): 26-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6799317 •
Multiple angiitis of mesenterial arteries in guinea pigs induced by intraperitoneal administration of high doses of Na2 EDTA. II. Electron microscopic study. Author(s): Yamaguchi H, Usui H, Tajima T, Sakaguchi H. Source: Exp Pathol. 1981; 20(1): 31-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6799318
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Necrotizing angiitis associated with drug abuse. Author(s): Halpern M, Citron BP. Source: Am J Roentgenol Radium Ther Nucl Med. 1971 April; 111(4): 663-71. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4397122
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Nodular vasculitis associated with chronic hepatitis C. Author(s): Ural I, Erel A, Ozenirler S, Tekin NS, Gurert MA. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2002 May; 16(3): 298-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12195584
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Platelet satellitism, spurious neutropenia, and cutaneous vasculitis: casual or causal association? Author(s): Lazo-Langner A, Piedras J, Romero-Lagarza P, Lome-Maldonado C, SanchezGuerrero J, Lopez-Karpovitch X. Source: American Journal of Hematology. 2002 July; 70(3): 246-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12111772
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Pseudothrombocytopenia associated with vasculitis. Author(s): Boehme WM, Mahmood T, Phanuphak P. Source: The American Journal of the Medical Sciences. 1980 March-April; 279(2): 125-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6770687
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Purpura and vasculitis: unapproved treatments. Author(s): Katsambas A, Riga P. Source: Clinics in Dermatology. 2002 November-December; 20(6): 626-33. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12490355
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Purpuric vasculitis-like eruption in a patient sensitive to balsam of Peru. Author(s): Bruynzeel DP, van den Hoogenband HM, Koedijk F.
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Source: Contact Dermatitis. 1984 October; 11(4): 207-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6499422 •
Reversal of microvascular abnormalities in a successfully treated case of leukocytoclastic vasculitis. Author(s): Kitchens CS. Source: Johns Hopkins Med J. 1980 September; 147(3): 97-101. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7412072
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Systemic injection of products of activated neutrophils and H2O2 in myeloperoxidase-immunized rats leads to necrotizing vasculitis in the lungs and gut. Author(s): Heeringa P, Foucher P, Klok PA, Huitema MG, Tervaert JW, Weening JJ, Kallenberg CG. Source: American Journal of Pathology. 1997 July; 151(1): 131-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9212739
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Systemically induced vasculitis in children. Author(s): Peterson-Sweeney KL. Source: Aacn Clinical Issues. 1995 November; 6(4): 657-69. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7493267
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Traditional Chinese medicine anesthesia in severe thromboangiitis obliterans. Report of 30 cases. Author(s): Zheng P. Source: Chinese Medical Journal. 1988 March; 101(3): 221-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3136997
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Treatment of thromboangiitis obliterans with arterialization of the venous channel. Author(s): Pei YK, Lin MS, Jiang ZY, Wang XW. Source: Chinese Medical Journal. 1985 November; 98(11): 787-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3938707
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Urticarial vasculitis possibly induced by herbs. Author(s): Lee CW, Kim SJ. Source: International Journal of Dermatology. 1991 April; 30(4): 303-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2050464
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Vasculitis associated with herbal preparation containing Passiflora extract. Author(s): Smith GW, Chalmers TM, Nuki G. Source: British Journal of Rheumatology. 1993 January; 32(1): 87-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8422575
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Vasculitis induced by zafirlukast therapy. Author(s): Soy M, Ozer H, Canataroglu A, Gumurdulu D, Erken E. Source: Clinical Rheumatology.
Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •
Alternative Medicine Foundation, Inc.: http://www.herbmed.org/
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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
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Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMDHealth: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
The following is a specific Web list relating to vasculitis; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
General Overview Allergies and Sensitivities Source: Healthnotes, Inc.; www.healthnotes.com Hives Source: Healthnotes, Inc.; www.healthnotes.com Peripheral Vascular Disease Source: Healthnotes, Inc.; www.healthnotes.com
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Herbs and Supplements Cinnamomum Alternative names: Cinnamon; Cinnamomum zeylanicum Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Passiflora Alternative names: Passion Flower; Passiflora alata L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 4. PATENTS ON VASCULITIS 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 “vasculitis” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on vasculitis, we have not necessarily excluded non-medical patents in this bibliography.
Patents on Vasculitis By performing a patent search focusing on vasculitis, 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
8Adapted
from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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will tell you how to obtain this information later in the chapter. The following is an example of the type of information that you can expect to obtain from a patent search on vasculitis: •
Antibodies specific for E-selectin and the uses thereof Inventor(s): Gimbrone, Jr.; Michael A. (Jamaica Plain, MA) Assignee(s): Brigham & Women's Hospital (boston, Ma) Patent Number: 5,632,991 Date filed: December 29, 1994 Abstract: A method is provided for selectively targeting a therapeutic agent to a site of activated endothelium by administering a pharmaceutical composition comprising a therapeutically effective amount of an E-selectin (formerly called ELAM-1) specific monoclonal antibody conjugated to a therapeutic agent. An immunoconjugate comprising an E-selectin specific monoclonal antibody and a therapeutic agent is also provided. A method is also provided for the treatment of a vascular smooth muscle cell proliferative disorder, vasculitis, inflammation, post-reperfusion injury, microbial infections, acute or chronic allograft rejection, and leukemia, as well as for the inhibition of metastatic spread of tumor cells, by administering a pharmaceutical composition comprising a therapeutically effective amount of an E-selectin antibody, or antibody fragment, either alone, or conjugated to a therapeutic agent. Excerpt(s): The present invention relates to immunology and cellular adhesion. In particular, the invention relates to antibodies specific for endothelial leukocyte adhesion molecule-1 (formerly known as ELAM-1), which is now referred to as E-selectin (CD62E) (Schlossman et al., Blood 83:879-880 (1994); Bevilacqua and Nelson, J. Clin. Invest. 91:379-387 (1993); Bevilacqua et al., Cell 67:233 (1991)). More particularly, the invention relates to the use of E-selectin specific antibodies, both alone, and conjugated to a therapeutic agent, for the treatment of various disease states. Focal adhesion of leukocytes to the endothelial lining of blood vessels is a characteristic step in intimation and in certain vascular disease processes. Although it has long been suspected that alterations in the vessel wall could promote leukocyte adhesion (Cohnheim, J., Lectures in General Pathology (New Syndenham Society, London) Vol. 1, 2nd Ed. (1898)), until recently, potential mechanisms and modulators of this interaction have remained undefined (Harlan, J. M., Blood 65:513-525 (1985)). Certain inflammatory/immune cytokines including interleukin-1 (IL-1) and tumor necrosis factor (TNF), as well as bacterial endotoxin, have been shown to act directly on cultured human vascular endothelium to increase the adhesiveness of its surface for blood leukocytes and related cell lines (Bevilacqua et al., J. Clin. Invest. 76:2003-2011 (1985); Bevilacqua et al., Am. J. Pathol. 121:393-403 (1985); Bevilacqua et al., Leukocyte Emigration and Its Sequelae, Movat, H. Z., ed., Karger, N.Y. (1987), pp. 79-93; Gamble et at., Proc. Natl. Acad. Sci. (USA) 82:8667-8671 (1985); Schleimer et al., J. Immunol. 136:649-654 (1986); Dunn et al., The Physiologic, Metabolic and Immunologic Actions of Interleukin-1, Kluger et al., eds., Liss, N.Y. (1985), pp. 45-54; Cavender et al., J. Immunol. 136:203-207 (1986); Yu et al., J. Immunol. 136:571 (1986); and Pohlman et at., J. Immunol. 136:4548-4553 (1986)). A number of leukocyte and endothelial cell surface proteins participate in endothelial cellleukocyte adhesion. One example, ICAM-1, is expressed on a variety of hemopoietic cells and non-hemopoietic cells including vascular endothelium. ICAM-1 is a 90 kD glycoprotein which is induced by certain cytokines on endothelial cells. ICAM-1 expression is protein and mRNA synthesis-dependent and its induction is reversible
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(Dustin et al., J. Immunol. 137:245-254 (1986); Rothlein et al., J. Immunol. 137:1270-1274 (1986); and Pober et al., J. Immunol. 136:1680-1687 (1986)). Web site: http://www.delphion.com/details?pn=US05632991__ •
Cloned genes which encode ELAM-1 Inventor(s): Bevilacqua; Michael P. (Holbrook, MA), Gimbrone; Michael A. (Jamaica Plain, MA), Seed; Brian (Boston, MA), Stengelin; Siegfried (Hofheim, DE) Assignee(s): Brigham & Women's Hospital (boston, Ma) Patent Number: 5,081,034 Date filed: November 14, 1988 Abstract: The invention relates to cloned genes, or degenerate variants thereof, which encode endothelial-leukocyte adhesion molecule-1 (ELAM-1), or fragments thereof. Such fragments may be leukocyte or complement-binding. The invention also relates to cloned genes encoding fusion proteins comprising ELAM. The invention also relates to vectors containing the cloned genes of the invention, hosts transformed with the vectors, and the protein products expressed therefrom. The invention also relates to pharmaceutical compositions comprising the expressed proteins. The invention also relates to methods for the treatment of inflammation, post reperfusion injury, bacterial infections, vasculitis, leukemia, and methods of inhibiting metastatic spread of tumor cells by administering the pharmaceutical compositions of the invention. Excerpt(s): The invention is in the field of recombinant genetics. Focal adhesion of leukocytes to the endothelial lining of blood vessels is a characteristic step in inflammation and in certain vascular disease processes. Although it has long been suspected that alterations in the vessel wall could promote leukocyte adhesion (Cohnheim, J., Lectures in General Pathology. (New Syndenham Society, London) Vol. 1, 2nd Ed. (1898)), until recently, potential mechanisms and modulators of this interaction have remained undefined (Harlan, J. M., Blood. 65:513-525 (1985)). Certain inflammatory/immune cytokines including interleukin-1 (IL-1) and tumor necrosis factor (TNF), as well as bacterial endotoxin, have been shown to act directly on cultured human vascular endothelium to increase the adhesiveness of its surface for blood leukocytes and related cell lines. Bevilacqua, M. P. et al., J. Clin. Invest. 76:2003-2011 (1985); Bevilacqua, M. P. et al., Am. J. Pathol. 121:393-403 (1985); Bevilacqua, M. P. et al., Leukocyte Emigration and Its Sequelae, Movat, H. Z. (ed.), Karger, N.Y., pp. 79-93 (1987); Gamble, J. R. et al. Proc Natl. Acad. Sci. teu(USA) 82:8667-8671 (1985); Schleimer, R. P. et al., J. Immunol. 136:649-654 (1986); Dunn, C. J. et al., The Physiologic, Metabolic and Immunologic Actions of Interleukin-1, Kluger, M. J. et al., (eds.), Liss, N.Y. pp. 45-54 (1985); Cavender, D. E. et al., J. Immunol. 136:203-207 (1986); Yu, C. -L. et al., J. Immunol. 136:571 (1986); and Pohlman, T. H. et al., J. Immunol. 136:4548-4553 (1986). A number of leukocycte and endothelial cell surface proteins participate in endothelial cell-leukocyte adhesion. One example, ICAM-1, is expressed on a variety of hemopoetic cells and nonhemopoietic cells including vascular endothelium. ICAM-1 is a 90 kD glycoprotein which is induced by certain cytokines on endothelial cells. ICAM-1 expression is protein-and mRNA sythesis-dependent and its induction is reversible. Dustin, M. L., et al., J. Immunol. 137:245-254 (1986); Rothlein, R., et al., J. Immunol. 137:1270-1274 (1986); and Pober, J. S., et al., J. Immunol. 136:1680-1687 (1986). Web site: http://www.delphion.com/details?pn=US05081034__
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Method of treating diseases arising from platelet hyperactivation Inventor(s): Ahn; Yeon S. (Miami, FL), Harrington; William J. (Miami, FL), Haynes; Duncan H. (Miami, FL), Jy; Wenche (Miami, FL) Assignee(s): University of Miami (coral Gables, Fl) Patent Number: 4,728,660 Date filed: June 11, 1984 Abstract: Calcium (Ca.sup.2+) channel blockers, such as nifedipine and verapamil, are used in the treatment of thromboembolic diseases such as stroke and peripheral vascular occlusive diseases, especially arterial and venous thrombosis, vasculitis, myelofibrosis disease and hemolytic anemias. Such diseases arise from platelet hyperactivation and the Ca.sup.2+ channel blockers restore the platelets to their normal aggregation characteristics. Diagnostic procedures for detecting platelet hyperactivation and defective calcium handling/transport indicative of certain peripheral obstructive diseases using chlorotetracycline as a detectable fluorescent probe as a means of assessing a patient's response to Ca.sup.2+ channel blockers in the therapy of such diseases are also described. Excerpt(s): Current Therapy for Vascular Occlusive Diseases: Thrombosis and many related peripheral obstructive diseases are the result of abnormal activation of normal clotting mechanisms. Normal blood clotting is the result of a highly amplified chain reaction triggered by exposure of soluble factors and platelets to tissue factors, collagen and certain metabolites or hormones such as adenosine diphosphate (ADP), adrenaline and thromboxane. The clotting mechanism makes use of two systems: (a) soluble factors in the blood which activate each other in a serial manner causing hydrolysis of fibrinogen to fibrin which forms an insoluble crosslinked network, and (b) the circulating thrombocytes (platelets) which respond to the activating stimuli by releasing their own activators and by aggregating with each other. In normal clotting the soluble and platelet systems interact, with activation of one reinforcing the activation of the other. Abnormal activation of these systems can give rise to peripheral obstructive diseases. While the pathogenesis is very complex, current models involve a lesion of the vein or artery wall, local activation of the clotting system, recruitment of activated soluble factors and platelets into the region, homeostasis, local ischemia, and reinforced activation recruitment. The platelet plays a central role in the formation and extension of clot in both venous and arterial thrombosis. In venous thrombosis, the activation of platelet initiates shape changes and release reactions of platelet contents such ADP, arachidonic acid derivatives, clotting factors which promote platelet recruitment and aggregation and activate coagulation cascade leading to fibrin formation. The activated platelet also provides an activated surface (platelet factor III) which serves as a binding site for soluble clotting factors thereby increasing their interaction and further accelerating the rate of fibrin formation. Current therapy for venous thrombosis relies mainly on the inhibition of fibrin formation; little attention was given to inhibition of the platelet which plays central role in activation. Conventional therapy for venous thrombosis makes use of heparin which actively neutralizes several of the activated soluble clotting factors. Conventional therapy also makes use of the so-called "oral anticoagulants" (dicumarol and related compounds) which inhibit the synthesis of these factors. Direct platelet activation is not affected by these drugs. In arterial thrombosis, platelets adhere to injured or diseased vessel wall and transform their shapes, release ADP and other platelet granule content, convert arachidonic acid to thromboxane A.sub.2, which promotes more platelet aggregation and vasconstriction and consolidation of platelet plugs. The use of antiplatelet drugs is, therefore, the mainstay
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of treatment and prevention of arterial thrombosis. Two classes of drug target the platelet and are used to treat arterial thrombosis: aspirin and dipyridamole. Aspirin inhibits the activation of arachidonic acid, which is one of the pathways for platelet activation. This offers some protection against activation. Dipyridamole is a phosphodiesterase inhibitor which increases the platelets' cyclic AMP level. This offers further protection against activation. Web site: http://www.delphion.com/details?pn=US04728660__ •
Regulation of neural enzymes Inventor(s): Gluckman; Peter D (Remuera, NZ), Guan; Jian (Avondale, NZ), Williams; Christopher E. (Grafton, NZ) Assignee(s): Neuronz Ltd. (nz) Patent Number: 6,365,573 Date filed: May 10, 1999 Abstract: This invention relates to the use of the tripeptide Gly-Pro-Glu (GPE) or analogs thereof for the treatment of conditions of the central nervous system (e.g. cerebral vasculitis) in which the amount of the neural enzymes nitric oxide synthetase (NOS) and/or glutamic acid decarboxylase (GAD) is reduced. Excerpt(s): This application is a 371 of PCT/NZ97/00132, filed Oct. 6, 1997. This invention relates to methods of regulating the effect of neural enzymes. It particularly relates to increasing the effective amount of the neural enzymes choline acetyltransferase (ChAT), glutamic acid decarboxylase (GAD) and nitric oxide synthetase (NOS) in the central nervous system (CNS). To date however, there has been no teaching or suggestion of GPE or its analogs having any direct effect on the effective amount of neural enzymes present in the CNS. There has certainly been no suggestion of GPE having the ability to upregulate expression of the neural enzymes, ChAT, GAD and NOS, and/or of their receptors. Web site: http://www.delphion.com/details?pn=US06365573__
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Specific inhibitors of hyaluronidase 2, and methods of identifying and using same Inventor(s): Frost; Gregory I. (Solana Beach, CA) Assignee(s): Deliatroph Pharmaceuticals, Inc. (san Diego, Ca) Patent Number: 6,682,904 Date filed: August 15, 2002 Abstract: Methods for identifying a hyaluronidase 2 (HYAL2) specific inhibitor, which selectively inhibits HYAL2 activity, but does not substantially affect the activity of noninflammatory hyaluronidases, are provided. Also provided are HYAL2 specific inhibitors obtained using such a method. In addition, methods for ameliorating an inflammatory disorder or vasculitis condition by specifically inhibiting HYAL2 is provided. Excerpt(s): The invention generally relates to hyaluronidase 2 (HYAL2) inhibition and, more specifically, to molecules that specifically inhibit HYAL2 activity, to methods of identifying HYAL2-specific inhibitors, and to methods for ameliorating a condition
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associated with the pro-inflammatory activity of HYAL2, including, for example, chronic inflammation or vasculitis, by specifically inhibiting HYAL2 activity and, therefore, HYAL2 mediated generation of pro-inflammatory and pro-angiogenic hyaluronan intermediate fragments. Inflammation and necrosis of blood vessels (vasculitis), including arteries, veins, and capillaries, can occur in connection with exposure to infectious agents, mechanical trauma, radiation, or toxins, and in association with immunological responses or disorders. In many cases, however, no etiology can be determined for a vasculitis (Rubin and Farber, "Pathology" 3d ed. (Lippincott-Raven 1999); pages 514-520). Numerous vasculitis disorders have been identified, and have been classified based on the size of the blood vessels that primarily are affected, i.e., small vessel, medium vessel, or large vessel, or based on general similarities of the disorders, e.g hypersensitivity vasculitis, which includes serum sickness and some, but not all, other disorders that involve, at least in part, an undesirable immune response. Despite these attempted classifications of vasculitis disorders, however, there is considerable overlap of signs and symptoms associated with the vasculitis disorders in different classification groups, and, therefore, it has been difficult to prescribe general treatment protocols. Web site: http://www.delphion.com/details?pn=US06682904__
Patent Applications on Vasculitis 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 vasculitis: •
Aldosterone blocker therapy to prevent or treat inflammation-related disorders Inventor(s): Rocha, Ricardo; (Flemington, NJ), Zack, Marc D.; (Winnetka, IL) Correspondence: Pharmacia Corporation; Global Patent Department; Post Office Box 1027; ST. Louis; MO; 63006; US Patent Application Number: 20040037806 Date filed: January 24, 2003 Abstract: A method of preventing or treating an inflammation-related disorder such as myocarditis, cardiomyopathy, vasculitis, and Behcet's disease in a subject, comprising treating the subject with a therapeutically-effective amount of an aldosterone blocker sufficient to alter the expression of one or more expression products involved, directly or indirectly, in the regulation of inflammation or cardiac remodeling in the subject. Excerpt(s): This invention is in the field of preventing or treating inflammation-related disorders, and more particularly inflammation-related cardiovascular disorders. More specifically, this invention relates to the use of aldosterone blocker therapy in preventing or treating cardiovascular disease including atherosclerosis. Prostaglandins play a major role in the inflammation process and the inhibition of prostaglandin production, especially production of PGG.sub.2, PGH.sub.2 and PGE.sub.2, has been a common target of anti-inflammatory drug discovery. However, common non-steroidal anti-inflammatory drugs (NSAID's) that are active in reducing the prostaglandin-
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This has been a common practice outside the United States prior to December 2000.
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induced pain and swelling associated with the inflammation process are also active in affecting other prostaglandin-regulated processes not associated with the inflammation process. Thus, use of high doses of most common NSAID's can produce severe side effects, including life threatening ulcers, that limit their therapeutic potential. An alternative to NSAID's is the use of corticosteroids, which also produce severe adverse effects, especially when long term therapy is involved. NSAIDs have been found to prevent the production of prostaglandins by inhibiting enzymes in the human arachidonic acid/prostaglandin pathway, including the enzyme cyclooxygenase (COX). The recent discovery of an inducible enzyme associated with inflammation (named "cyclooxygenase-2 (COX-2)" or "prostaglandin G/H synthase II") provides a viable target of inhibition which more effectively reduces inflammation and produces fewer and less drastic side effects. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method of treating immune-mediated diseases by administration of IgM Inventor(s): Drew, Hazel P.; (Laurelton, NY), Joks, Rauno; (Glen Cove, NY), Mueller, Patricia; (Miami, FL), Nowakowski, Maja; (Port Washington, NY) Correspondence: Scully Scott Murphy & Presser, PC; 400 Garden City Plaza; Garden City; NY; 11530 Patent Application Number: 20040043019 Date filed: May 14, 2003 Abstract: Human polyclonal immunoglobulin M may be administered to patients suffering from a variety of immune-mediated diseases, including asthma, Common Variable Immunodeficiency (CVID), rheumatoid arthritis (RA), Systemic Lupus Erythmatosus (SLE), serum sickness and vasculitis, to treat the disease condition of those patients. Administration of immunoglobulin M results in a direct inhibitory effect on complement activity and a significant clinical improvement in the level of disease activity in patients with immune-mediated diseases. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/380,789, filed on May 15, 2002. The present invention relates to the treatment of immune-mediated diseases, including autoimmune diseases, especially those resulting from immune complex formation and deposition. The invention relates to the treatment of asthma, Common Variable Immunodeficiency (CVID), rheumatoid arthritis (RA), and Systemic Lupus Erythmatosus (SLE). The invention also relates to the treatment of spondyloarthopathies including, inflammatory bowel disease, psoriatic arthritis, Reiter's Syndrome and ankylosing spondylitis, temporal arteritis, polymyalgia rheumatica and agammaglobulinemia. In accordance with the present invention immune-mediated diseases are treated by administration of a pharmaceutical composition comprising polyclonal IgM. The present invention relates to a method for the treatment of immunemediated diseases by administering a pharmaceutical composition comprising polyclonal IgM. Polyclonal IgM, and in particular human polyclonal IgM, is commonly obtained from commercial sources such as Chemicon International (Temecula, Calif.). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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THERAPEUTIC APPLICATIONS FOR THE ANTI-T-BAM (CD40L) MONOCLONAL ANTIBODY 5C8 IN THE TREATMENT OF VASCULITIS Inventor(s): CHESS, LEONARD; (SCARSDALE, NY), KARPUSAS, MIHAIL N.; (ROSLINDALE, MA), LEDERMAN, SETH; (NEW YORK, NY), THOMAS, DAVID W.; (WELLESLEY, MA), YELLIN, MICHAEL J.; (RIVERDALE, NY) Correspondence: James F Haley JR; Fish & Neave; 1251 Avenue OF The Americas; New York; NY; 10020 Patent Application Number: 20030099642 Date filed: June 29, 1999 Abstract: Activation of cells bearing CD40 on their cell surface by CD40 ligand is inhibited by contacting the cells with an agent capable of inhibiting interaction between CD40 ligand and the cells, in an amount effective to inhibit activation of the cells. Activation of cells bearing CD40 on their surface by CD40 ligand in a subject is inhibited by administering to the subject an agent capable of inhibiting interaction between CD40 ligand and the cells, in an amount effective to inhibit activation of the cells. Conditions dependent on CD40 ligand-induced activation of CD40-bearing cells are treated. Excerpt(s): This application is a continuation-in-part of U.S. application Ser. Nos. 08/566,258 and 08/567,391, both filed Dec. 1, 1995, the contents of which are hereby incorporated by reference. Throughout this application, various references are referred to within parentheses. Disclosures of these publications in their entireties are hereby incorporated by reference into this application to more fully describe the state of the art to which this invention pertains. Full bibliographic citation for these references may be found in the text or at the end of this application, preceding the sequence listing and claims. CD40 is a 50 kDa cell surface molecule originally described as being expressed on B cells and some epithelial carcinomas (1, 2). CD40 interacts with CD40L (T-BAM, gp39, TRAP), a 30 kDa cell surface molecule transiently expressed on activated CD4.sup.+ T cells (3-8). CD40L-CD40 interactions have been extensively studied in the context of T cell-B cell interactions. CD40 ligation plays key roles in B cell activation, proliferation, differentiation, Ig production and rescue from apoptotic signals (9-11). The critical in vivo role of CD40 ligation in B cell differentiation is highlighted by the hyperIgM syndrome, a humoral immunodeficiency due to mutations in the gene encoding CD40L (12-16). Murine CD40 (17) or CD40L (18) "knockouts" have similar phenotypes to patients with the hyper-IgM syndrome. 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 vasculitis, you can access the U.S. Patent Office archive via the Internet at the following Web address: http://www.uspto.gov/patft/index.html. You will see two broad options: (1) Issued Patent, and (2) Published Applications. To see a list of issued patents, perform the following steps: Under “Issued Patents,” click “Quick Search.” Then, type “vasculitis” (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 vasculitis.
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You can also use this procedure to view pending patent applications concerning vasculitis. 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 VASCULITIS Overview This chapter provides bibliographic book references relating to vasculitis. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on vasculitis include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.
Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “vasculitis” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on vasculitis: •
Atlas of Diseases of the Kidney. Volume 2: Glomerulonephritis and Vasculitis/Tubulointerstitial Disease Source: Philadelphia, PA: Current Medicine, Inc. 1999. [204 p.]. Contact: Available from Blackwell Science, Inc. 350 Main Street, Malden, MA 02148. (800) 215-1000 or (781) 388-8250. Fax (781) 388-8270. E-mail:
[email protected]. PRICE: $75.00 plus shipping and handling. ISBN: 0632043873. Summary: This volume is one in a series of five in the Atlas of Diseases of the Kidney, a set that offers educational images including colored photographs, schematics, tables, and algorithms. In this volume, the first section covers glomerulonephritis and vasculitis; the second section covers tubulointerstitial disease. Twelve chapters cover normal vascular and glomerular anatomy; the primary glomerulopathies; heredofamilial and congenital glomerular disorders; infection associated glomerulopathies; vascular disorders; renal interstitium and major features of chronic
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tubulointerstitial nephritis; urinary tract infection; reflux and obstructive nephropathy; cystic diseases of the kidney; toxic nephropathies; metabolic causes of tubulointerstitial disease; and renal tubular disorders. Each chapter features a detailed introduction and lengthy captions for each of the illustrations and diagrams offered. The first section relies heavily on images provided by analysis of renal biopsy; the section on vascular diseases of the kidney emphasizes microscopic images that illustrate essential or characteristic features of disease. A subject index for Volume 2 and a section of full color plates concludes the book.
Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in Print). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “vasculitis” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “vasculitis” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “vasculitis” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •
Central Nervous System Angiitis by James W. Schmidley; ISBN: 075067153X; http://www.amazon.com/exec/obidos/ASIN/075067153X/icongroupinterna
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Mpd 10 Vasculitis by Mpd 10 Wolff; ISBN: 0853241511; http://www.amazon.com/exec/obidos/ASIN/0853241511/icongroupinterna
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Renal Involvement in Systemic Vasculitis: First Seminar on Renal Involvement in Systemic Vasculitis, Vimercate, September 22, 1990 (Contributions to) by A. Sessa, et al; ISBN: 3805554222; http://www.amazon.com/exec/obidos/ASIN/3805554222/icongroupinterna
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Systemic Lupus Erythematosus: Renal Vasculitis (Contributions to Nephrology, Vol 99) by A. Sessa, et al; ISBN: 3805556039; http://www.amazon.com/exec/obidos/ASIN/3805556039/icongroupinterna
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Systemic Vasculitis: The Biological Basis (Inflammatory Disease and Therapy, No 11) by E. Carwile Leroy (Editor); ISBN: 0824786505; http://www.amazon.com/exec/obidos/ASIN/0824786505/icongroupinterna
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The Official Patient's Sourcebook on Vasculitis with Temporal Arteritis: A Revised and Updated Directory for the Internet Age by Icon Health Publications; ISBN: 0597842043; http://www.amazon.com/exec/obidos/ASIN/0597842043/icongroupinterna
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Vasculitis by Gene V. Ball (Editor), et al; ISBN: 0192630539; http://www.amazon.com/exec/obidos/ASIN/0192630539/icongroupinterna
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Vasculitis by H. Yazici; ISBN: 0702022667; http://www.amazon.com/exec/obidos/ASIN/0702022667/icongroupinterna
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Vasculitis; ISBN: 0721695833; http://www.amazon.com/exec/obidos/ASIN/0721695833/icongroupinterna
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Vasculitis, Rheumatic Disease, and the Nervous System by Peter Berlit; ISBN: 354054853X; http://www.amazon.com/exec/obidos/ASIN/354054853X/icongroupinterna
Chapters on Vasculitis In order to find chapters that specifically relate to vasculitis, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and vasculitis 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 “vasculitis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on vasculitis: •
Classification of Vasculitis Source: in Maddison, P.J.; et al., Eds. Oxford Textbook of Rheumatology. Volume 2. New York, NY: Oxford University Press, Inc. 1993. p. 842-846. Contact: Available from Oxford University Press, Inc., New York, NY. Summary: This chapter for health professionals explains the classification of vasculitis. Vasculitis describes a heterogeneous group of uncommon diseases characterized by vascular inflammation. Problems involved in the classification of vasculitis are identified. The historical classification of vasculitis is discussed. The classification of vasculitis based on its pathological features and etiological agents is examined. The prognosis for patients with vasculitis is considered. 50 references and 2 figures.
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Chapter 21-B: Vasculitides: Wegener's Granulomatosis and Churg-Strauss Vasculitis Source: in Klippel, J.H., et al., eds. Primer on the Rheumatic Diseases. 12th ed. Atlanta, GA: Arthritis Foundation. 2001. p. 392-396. Contact: Available from Arthritis Foundation. P.O. Box 1616, Alpharetta, GA 300091616. (800) 207-8633. Fax (credit card orders only) (770) 442-9742. Website: www.arthritis.org. PRICE: $69.95 plus shipping and handling. ISBN: 0912423293. Summary: This chapter provides health professionals with information on the epidemiology, clinical features, and treatment of Wegener's granulomatosis (WG) and Churg Strauss Syndrome (CSS). Although WG can affect people of all ages and all ethnic and racial backgrounds, it is more common in Caucasian adults. The upper and lower respiratory tract and the kidneys are most commonly affected. Vascular injury is most evident in small and medium sized vessels. Musculoskeletal manifestations are common. Immunosuppressive therapy with cyclophosphamide has been effective in controlling disease progression, but such therapy may not achieve sustained remissions and is often associated with serious complications. Therefore, several prospective studies have evaluated intermittent high dose intravenous cyclophosphamide, trimethoprim/sulfamethoxazole therapy for less severe manifestations of WG, and corticosteroids plus intermittent low dose methotrexate (MTX) therapy. The most promising new approach is induction therapy with daily cyclophosphamide, followed by 3 to 6 months with maintenance MTX or azathioprine. Monitoring peripheral leukocyte counts can guide adjustment of cyclophosphamide, MTX, and azathioprine
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doses. CSS, an extremely rare inflammatory blood vessel disease, can affect people of any age or gender. Asthma usually precedes evidence of vasculitis by months to years. Although the presence of rhinitis, sinusitis, and occasionally pulmonary modules can lead to confusion with WG, the allergic nasal and sinus disease of CSS is usually not a destructive process, pulmonary nodules are less common than fleeting infiltrates, and nodules generally do not cavitate. CSS is generally responsive to corticosteroid therapy. Cytotoxic agents such as cyclophosphamide should be used for patients with severe, progressive disease. The chapter also discusses the use of antineutrophil cytoplasmic antibody studies in the diagnosis and treatment of patients who have WG and CSS. 1 figure, 2 tables, and 21 references.
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CHAPTER 6. MULTIMEDIA ON VASCULITIS Overview In this chapter, we show you how to keep current on multimedia sources of information on vasculitis. We start with sources that have been summarized by federal agencies, and then show you how to find bibliographic information catalogued by the National Library of Medicine.
Video Recordings An excellent source of multimedia information on vasculitis is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “vasculitis” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find video productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Videorecording (videotape, videocassette, etc.).” Type “vasculitis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on vasculitis: •
Update in Clinical Rheumatology 1992 Source: Cleveland, OH: Cleveland Clinic Educational Foundation. 1992. (videocassette, exam, proceedings). Contact: Available from CME Conference Video, Inc. 2000 Crawford Place, Mount Laurel, NJ 08054. (800) 284-8433 or (609) 866-9100. PRICE: $425.00 plus shipping and handling. Summary: These materials were produced in conjunction with a symposium designed to familiarize rheumatologists and other health care providers with advancements in the management of rheumatic diseases. Seventeen programs are presented on seven videotapes, covering juvenile rheumatoid arthritis; vasculitis and other connective tissue disorders in children; the rheumatic manifestations of endocrine and metabolic disease; Sjogren's syndrome; the effects of anti-rheumatic drugs on the liver; perplexity in rheumatic disease (case management); entrapment neuropathies; sports medicine for the rheumatologist; chronic fatigue syndrome; the medical management of spinal
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disease; anti-phospholipid antibody syndrome; systemic lupus erythematosus and pregnancy; pregnancy in scleroderma, rheumatoid athritis, and polymyositis; and Behcet's syndrome. The section on Behcet's syndrome covers diagnostic criteria, epidemiology, oral aphthous ulcers, genital ulcers, uveitis, synovitis, skin lesions, central nervous system involvement, arteritis, venous occlusions, other lesions, immunopathology, differential diagnosis, and treatment. The section on Sjogren's syndrome (SS) covers diagnostic criteria, prevalence, symptoms and clinical manifestations, the neurologic features of SS, interstitial nephritis, SS-related dysphagia, salivary gland involvement, and treatment issues. The package also includes a detailed syllabus and an examination booklet with which viewers can obtain continuing education credits.
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CHAPTER 7. PERIODICALS AND NEWS ON VASCULITIS Overview In this chapter, we suggest a number of news sources and present various periodicals that cover vasculitis.
News Services and Press Releases One of the simplest ways of tracking press releases on vasculitis 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 “vasculitis” (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 vasculitis. 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 “vasculitis” (or synonyms). The following was recently listed in this archive for vasculitis: •
IFN-alpha and ribavirin combo effective against hepatitis C-related systemic vasculitis Source: Reuters Industry Breifing Date: January 08, 2003
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Case of HIV-related CNS angiitis reported with no secondary infection Source: Reuters Medical News Date: March 19, 2002
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Death tied to celecoxib-related allergic vasculitis Source: Reuters Medical News Date: March 08, 2002
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FDA approves Hycor's p-ANCA assay for diagnosing vasculitis Source: Reuters Industry Breifing Date: October 10, 2000
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Refined histology facilitates vasculitis diagnosis in rheumatoid arthritis Source: Reuters Medical News Date: August 15, 2000 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 “vasculitis” (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 “vasculitis” (or synonyms). If you know the name of a company that is relevant to vasculitis, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for
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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 “vasculitis” (or synonyms).
Newsletters on Vasculitis Find newsletters on vasculitis using the Combined Health Information Database (CHID). You will need to use the “Detailed Search” option. To access CHID, go to the following hyperlink: http://chid.nih.gov/detail/detail.html. Limit your search to “Newsletter” and “vasculitis.” Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter.” Type “vasculitis” (or synonyms) into the “For these words:” box. The following list was generated using the options described above: •
Drug-Induced Rheumatic Syndromes Source: Bulletin on the Rheumatic Diseases. 51(4): 1-4. 2002. Contact: Available from Arthritis Foundation. 1330 West Peachtree Street, Atlanta, GA 30309. (800) 268-6942 or (404) 872-7100. Fax (404) 872-9559. Website: www.arthritis.org. Summary: This newsletter provides health professionals with information on drug induced rheumatic syndromes. Categories of drug induced rheumatic diseases are drug induced lupus (DIL), drug induced myopathy/myositis (DIM), and drug induced vasculitis (DIV). Although more than 100 drugs have been implicated in DIL, the drugs most studied have been procainamide and hydralazine. However, these drugs are not commonly prescribed today, and the illness they produce is often different from those recently implicated in DIL. Minocycline is a treatment used for acne and rheumatoid arthritis that has caused immune and autoimmune phenomena. Several of the new recombinant biologics have been implicated in DIL, including interferon alpha, interferon gamma, and antitumor necrosis factor therapies. It is not possible to predict who will develop DIL, so patients with idiopathic lupus should be allowed to take potentially lupus inducing drugs but with careful monitoring. Drugs associated with the development of DIV include hematopoietic growth factors such as G-CSF and GM-CSF; vaccines for hepatitis B, influenza, and others; and leukotriene inhibitors. The article concludes that the number of drugs that are capable of inducing rheumatic syndromes is growing. Elements in the assessment of a possible association between exposure and the development of a rheumatic disorder include temporal association, lack of likely alternative explanations, rechallenge, and biological plausibility. 1 table and 23 references.
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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 “vasculitis” (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 vasculitis: •
Vasculitis and Systemic Lupus Erythematosus Source: SLE Newsletter. 20(4):5; Winter 1997/1998. Contact: Bay Area Lupus Foundation, Inc., 2635 North First Street, Suite 206, San Jose, CA 95134. (408) 954-8600. Summary: This newsletter article for individuals with lupus presents an overview of vasculitis, which is an inflammation of both large and small blood vessels. It describes the clinical features of vasculitis, including raised red or purplish skin lesions on the fingertips, forearms, elbows, and toes; infarcts at the nailfold; urticaria; bluish discoloration of the fingers and toes; pain from poor circulation; an absent pulse in a digit; abdominal pain; or blood in the bowel. In addition, the article discusses the diagnosis and treatment of vasculitis.
•
When Should You Consider Vasculitis? Source: Bulletin on the Rheumatic Diseases. 47(6): 1-2. October 1998. Contact: Available from Arthritis Foundation. 1330 West Peachtree Street, Atlanta, GA 30309. (800) 268-6942 or (404) 872-7100. Fax (404) 872-9559. Website: www.arthritis.org. Summary: This newsletter article provides health professionals with an overview of vasculitis. This group of diseases is characterized by inflammation of the arteries. Clinical symptoms include fever, weight loss, fatigue, overall achiness that is worse in the morning, and possibly inflammatory arthritis in one or more joints. One or several organs may be involved. Laboratory abnormalities will indicate systemic inflammation. If detected early, vasculitis can be controlled and its progression limited. Diagnosis is established by tissue biopsy or angiography. The initial treatment is usually prednisone therapy at a dose of 40 to 60 milligrams per day. In severe cases, cytotoxic agents, either cyclophosphamide or methotrexate, should be initially used as well. 2 tables.
Academic Periodicals covering Vasculitis Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to vasculitis. In addition to these sources, you can search for articles covering vasculitis 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 8. 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 vasculitis. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a nonprofit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI Advice for the Patient can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP).
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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.
Researching Orphan Drugs Although the list of orphan drugs is revised on a daily basis, you can quickly research orphan drugs that might be applicable to vasculitis by using the database managed by the National Organization for Rare Disorders, Inc. (NORD), at http://www.rarediseases.org/. Scroll down the page, and on the left toolbar, click on “Orphan Drug Designation Database.” On this page (http://www.rarediseases.org/search/noddsearch.html), type “vasculitis” (or synonyms) into the search box, and click “Submit Query.” When you receive your results, note that not all of the drugs may be relevant, as some may have been withdrawn from orphan status. Write down or print out the name of each drug and the relevant contact information. From there, visit the Pharmacopeia Web site and type the name of each orphan drug into the search box at http://www.nlm.nih.gov/medlineplus/druginformation.html. You may need to contact the sponsor or NORD for further information. NORD conducts “early access programs for investigational new drugs (IND) under the Food and Drug Administration’s (FDA’s) approval ‘Treatment INDs’ programs which allow for a limited number of individuals to receive investigational drugs before FDA marketing approval.” If the orphan product about which you are seeking information is approved for
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marketing, information on side effects can be found on the product’s label. If the product is not approved, you may need to contact the sponsor. The following is a list of orphan drugs currently listed in the NORD Orphan Drug Designation Database for vasculitis: •
pVGI.(VEGF2) http://www.rarediseases.org/nord/search/nodd_full?code=1007
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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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
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National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
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National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
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National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
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National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
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National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
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National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
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National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
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These publications are typically written by one or more of the various NIH Institutes.
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National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
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National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
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National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
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National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
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National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
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National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
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National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
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National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
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National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
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National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
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National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
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National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
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National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
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Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
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National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
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National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
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Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
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Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.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
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HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
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NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
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Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
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Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
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Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
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Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
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Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
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Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
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Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
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MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
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
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Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html
The NLM 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 “vasculitis” (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 59273 88 77 49 182 59669
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 “vasculitis” (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.
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The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH). 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/.
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Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.
The Genome Project and Vasculitis In the following section, we will discuss databases and references which relate to the Genome Project and vasculitis. Online Mendelian Inheritance in Man (OMIM) The Online Mendelian Inheritance in Man (OMIM) database is a catalog of human genes and genetic disorders authored and edited by Dr. Victor A. McKusick and his colleagues at Johns Hopkins and elsewhere. OMIM was developed for the World Wide Web by the National Center for Biotechnology Information (NCBI).21 The database contains textual information, pictures, and reference information. It also contains copious links to NCBI’s Entrez database of MEDLINE articles and sequence information. 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. 21 Adapted from http://www.ncbi.nlm.nih.gov/. Established in 1988 as a national resource for molecular biology information, NCBI creates public databases, conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information--all for the better understanding of molecular processes affecting human health and disease.
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To search the database, go to http://www.ncbi.nlm.nih.gov/Omim/searchomim.html. Type “vasculitis” (or synonyms) into the search box, and click “Submit Search.” If too many results appear, you can narrow the search by adding the word “clinical.” Each report will have additional links to related research and databases. In particular, the option “Database Links” will search across technical databases that offer an abundance of information. The following is an example of the results you can obtain from the OMIM for vasculitis: •
Vasculitis, Hereditary Inflammatory, with Persistent Nodules Web site: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=192310 Genes and Disease (NCBI - Map)
The Genes and Disease database is produced by the National Center for Biotechnology Information of the National Library of Medicine at the National Institutes of Health. This Web site categorizes each disorder by system of the body. Go to http://www.ncbi.nlm.nih.gov/disease/, and browse the system pages to have a full view of important conditions linked to human genes. Since this site is regularly updated, you may wish to revisit it from time to time. The following systems and associated disorders are addressed: •
Cancer: Uncontrolled cell division. Examples: Breast and ovarian cancer, Burkitt lymphoma, chronic myeloid leukemia, colon cancer, lung cancer, malignant melanoma, multiple endocrine neoplasia, neurofibromatosis, p53 tumor suppressor, pancreatic cancer, prostate cancer, Ras oncogene, RB: retinoblastoma, von Hippel-Lindau syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Cancer.html
•
Immune System: Fights invaders. Examples: Asthma, autoimmune polyglandular syndrome, Crohn’s disease, DiGeorge syndrome, familial Mediterranean fever, immunodeficiency with Hyper-IgM, severe combined immunodeficiency. Web site: http://www.ncbi.nlm.nih.gov/disease/Immune.html
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Metabolism: Food and energy. Examples: Adreno-leukodystrophy, atherosclerosis, Best disease, Gaucher disease, glucose galactose malabsorption, gyrate atrophy, juvenile-onset diabetes, obesity, paroxysmal nocturnal hemoglobinuria, phenylketonuria, Refsum disease, Tangier disease, Tay-Sachs disease. Web site: http://www.ncbi.nlm.nih.gov/disease/Metabolism.html
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Muscle and Bone: Movement and growth. Examples: Duchenne muscular dystrophy, Ellis-van Creveld syndrome, Marfan syndrome, myotonic dystrophy, spinal muscular atrophy. Web site: http://www.ncbi.nlm.nih.gov/disease/Muscle.html
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Nervous System: Mind and body. Examples: Alzheimer disease, amyotrophic lateral sclerosis, Angelman syndrome, Charcot-Marie-Tooth disease, epilepsy, essential tremor, fragile X syndrome, Friedreich’s ataxia, Huntington disease, Niemann-Pick disease, Parkinson disease, Prader-Willi syndrome, Rett syndrome, spinocerebellar atrophy, Williams syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Brain.html
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Signals: Cellular messages. Examples: Ataxia telangiectasia, Cockayne syndrome, glaucoma, male-patterned
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baldness, SRY: sex determination, tuberous sclerosis, Waardenburg syndrome, Werner syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Signals.html •
Transporters: Pumps and channels. Examples: Cystic fibrosis, deafness, diastrophic dysplasia, Hemophilia A, long-QT syndrome, Menkes syndrome, Pendred syndrome, polycystic kidney disease, sickle cell anemia, Wilson’s disease, Zellweger syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Transporters.html Entrez
Entrez is a search and retrieval system that integrates several linked databases at the National Center for Biotechnology Information (NCBI). These databases include nucleotide sequences, protein sequences, macromolecular structures, whole genomes, and MEDLINE through PubMed. Entrez provides access to the following databases: •
3D Domains: Domains from Entrez Structure, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
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Books: Online books, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=books
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Genome: Complete genome assemblies, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Genome
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NCBI’s Protein Sequence Information Survey Results: Web site: http://www.ncbi.nlm.nih.gov/About/proteinsurvey/
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Nucleotide Sequence Database (Genbank): Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Nucleotide
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OMIM: Online Mendelian Inheritance in Man, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=OMIM
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PopSet: Population study data sets, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Popset
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ProbeSet: Gene Expression Omnibus (GEO), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
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Protein Sequence Database: Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Protein
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PubMed: Biomedical literature (PubMed), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
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Structure: Three-dimensional macromolecular structures, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Structure
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Taxonomy: Organisms in GenBank, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Taxonomy
To access the Entrez system at the National Center for Biotechnology Information, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=genome, and then select the database that you would like to search. The databases available are listed in the
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drop box next to “Search.” Enter “vasculitis” (or synonyms) into the search box and click “Go.” Jablonski’s Multiple Congenital Anomaly/Mental Retardation (MCA/MR) Syndromes Database22 This online resource has been developed to facilitate the identification and differentiation of syndromic entities. Special attention is given to the type of information that is usually limited or completely omitted in existing reference sources due to space limitations of the printed form. At http://www.nlm.nih.gov/mesh/jablonski/syndrome_toc/toc_a.html, you can search across syndromes using an alphabetical index. Search by keywords at http://www.nlm.nih.gov/mesh/jablonski/syndrome_db.html. The Genome Database23 Established at Johns Hopkins University in Baltimore, Maryland in 1990, the Genome Database (GDB) is the official central repository for genomic mapping data resulting from the Human Genome Initiative. In the spring of 1999, the Bioinformatics Supercomputing Centre (BiSC) at the Hospital for Sick Children in Toronto, Ontario assumed the management of GDB. The Human Genome Initiative is a worldwide research effort focusing on structural analysis of human DNA to determine the location and sequence of the estimated 100,000 human genes. In support of this project, GDB stores and curates data generated by researchers worldwide who are engaged in the mapping effort of the Human Genome Project (HGP). GDB’s mission is to provide scientists with an encyclopedia of the human genome which is continually revised and updated to reflect the current state of scientific knowledge. Although GDB has historically focused on gene mapping, its focus will broaden as the Genome Project moves from mapping to sequence, and finally, to functional analysis. To access the GDB, simply go to the following hyperlink: http://www.gdb.org/. Search “All Biological Data” by “Keyword.” Type “vasculitis” (or synonyms) into the search box, and review the results. If more than one word is used in the search box, then separate each one with the word “and” or “or” (using “or” might be useful when using synonyms).
22
Adapted from the National Library of Medicine: http://www.nlm.nih.gov/mesh/jablonski/about_syndrome.html. 23 Adapted from the Genome Database: http://gdbwww.gdb.org/gdb/aboutGDB.html - mission.
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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 vasculitis 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 vasculitis. 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 vasculitis. 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 “vasculitis”:
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Guides on vasculitis Vasculitis http://www.nlm.nih.gov/medlineplus/tutorials/vasculitisloader.html
•
Other guides Behcet's Syndrome http://www.nlm.nih.gov/medlineplus/behcetssyndrome.html Lupus http://www.nlm.nih.gov/medlineplus/lupus.html Polymyalgia Rheumatica http://www.nlm.nih.gov/medlineplus/polymyalgiarheumatica.html Vasculitis http://www.nlm.nih.gov/medlineplus/vasculitis.html Wegener's Granulomatosis http://www.nlm.nih.gov/medlineplus/wegenersgranulomatosis.html
Within the health topic page dedicated to vasculitis, the following was listed: •
General/Overviews Overview of Vasculitis Source: UpToDate http://patients.uptodate.com/topic.asp?file=arth_rhe/4492 Vasculitis http://www.nlm.nih.gov/medlineplus/tutorials/vasculitisloader.html Vasculitis Center: Frequently Asked Questions Source: Johns Hopkins Vasculitis Center http://vasculitis.med.jhu.edu/faqs/faqs.html What You Need to Know about Vasculitis Source: Cleveland Clinic Foundation http://www.clevelandclinic.org/arthritis/treat/facts/vasculitis.htm
•
Diagnosis/Symptoms Computed Tomography Angiography (CTA) Source: American College of Radiology, Radiological Society of North America http://www.radiologyinfo.org/content/ct-angiography.htm How Do We Diagnose Vasculitis? Source: Johns Hopkins Vasculitis Center http://vasculitis.med.jhu.edu/whatis/diagnosis.html MR Angiography (MRA) Source: American College of Radiology, Radiological Society of North America http://www.radiologyinfo.org/content/mr-angiography.htm
Patient Resources
Ultrasound-Vascular Source: American College of Radiology, Radiological Society of North America http://www.radiologyinfo.org/content/ultrasound-vascular.htm What Are the Symptoms of Vasculitis? Source: Johns Hopkins Vasculitis Center http://vasculitis.med.jhu.edu/whatis/symptoms.html What You Need to Know about Your Angiography Test Source: Cleveland Clinic Foundation http://www.clevelandclinic.org/health/healthinfo/docs/0100/0147.asp?index=4977 •
Treatment Cytoxan Source: Johns Hopkins Vasculitis Center http://vasculitis.med.jhu.edu/treatments/cytoxan.html Prednisone Source: Johns Hopkins Vasculitis Center http://vasculitis.med.jhu.edu/treatments/prednisone.html
•
Specific Conditions/Aspects Buerger's Disease Source: Johns Hopkins Vasculitis Center http://vasculitis.med.jhu.edu/typesof/buergers.html Churg-Strauss Syndrome Source: Johns Hopkins Vasculitis Center http://vasculitis.med.jhu.edu/typesof/churgstrauss.html Cryoglobulinemia Source: Johns Hopkins Vasculitis Center http://vasculitis.med.jhu.edu/typesof/cryoglobulinemia.html Henoch-Schönlein Purpura Source: American Academy of Family Physicians http://familydoctor.org/312.xml Lupus and Vasculitis Source: Lupus Foundation of America http://www.lupus.org/education/brochures/vasculitis.html Polyarteritis Nodosa Source: Johns Hopkins Vasculitis Center http://vasculitis.med.jhu.edu/typesof/polyarteritis.html Rheumatoid Vasculitis Source: Johns Hopkins Vasculitis Center http://vasculitis.med.jhu.edu/typesof/rheumatoid.html What You Need to Know about Central Nervous System Vasculitis Source: Cleveland Clinic Foundation http://www.clevelandclinic.org/arthritis/treat/facts/cns.htm
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What You Need to Know about Takayasu's Arteritis Source: Cleveland Clinic Foundation http://www.clevelandclinic.org/arthritis/treat/facts/takayasu.htm •
Children Kawasaki Disease Source: Nemours Foundation http://kidshealth.org/parent/medical/heart/kawasaki.html
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From the National Institutes of Health Vasculitis Including Temporal Arteritis Source: National Institute of Neurological Disorders and Stroke http://www.ninds.nih.gov/health_and_medical/disorders/vasculitis_doc.htm
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Organizations American Autoimmune Related Diseases Association http://www.aarda.org/ National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov/ National Institute of Allergy and Infectious Diseases http://www.niaid.nih.gov/ National Institute of Neurological Disorders and Stroke http://www.ninds.nih.gov/
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 vasculitis. 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: •
Lupus and Vasculitis Source: Washington, DC: Lupus Foundation of America. March 2000. 6 p. Contact: Available from Lupus Foundation of America. 2000 L. St., Suite 710, Washington, DC 20036-4916. (202) 349-1155 or (800) 558-0121. (800) 558-0231 (information in Spanish). Fax: (202) 349-1156. Website: www.lupus.org.
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Summary: This brochure provides information about vasculitis to patients with lupus. Vasculitis is an inflammation of the blood vessels that can be caused by immune or allergic reactions in the blood vessel walls or, in rare cases, by infection of the vessel walls. The diseases associated with vasculitis are listed. The brochure outlines the symptoms of vasculitis, and includes systemic, skin, joint, brain, peripheral nerve, intestinal, heart, lung, kidney, and eye manifestations. Patients should consult a physician if vasculitis is suspected. Diagnosis is based on medical history, current symptoms, physical examination, and specialized laboratory tests. Cortisone-type medications are the initial treatment for vasculitis. Cytotoxic drugs are used for patients with severe vasculitis or vasculitis that does not respond well to cortisone-type drugs. Experimental treatments such as plasmapheresis, intravenous gamma globulin, and cyclosporin are helpful in treating some forms of vasculitis. •
Temporal Arteritis/Giant Cell Vasculitis Source: Detroit, MI: American Autoimmune Related Diseases Association, Inc. 1998. 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. Summary: This fact sheet for people with temporal arteritis/giant cell vasculitis discusses the affected population, causes, symptoms, diagnosis, and treatment of this chronic inflammatory autoimmune disease. It is two to three times more prevalent in women than men and usually occurs after the age of 50. It is characterized by generalized vasculitis, but headache is the most common localized symptom. Systemic flu-like symptoms may also appear. The underlying cause of the inflammation is an autoimmune reaction to the lining of the blood vessels found in the aortic arch. Diagnosis is based on medical history, physical examination, clinical findings, and biopsy of the affected artery. Early diagnosis and treatment are important to prevent or control serious complications, and prednisone is the drug of choice. The fact sheet also explains what autoimmunity is, lists other autoimmune diseases, and outlines the activities of the American Autoimmune Related Diseases Association. 2 references. 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 vasculitis. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. NORD (The National Organization of Rare Disorders, Inc.) NORD provides an invaluable service to the public by publishing short yet comprehensive guidelines on over 1,000 diseases. NORD primarily focuses on rare diseases that might not
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be covered by the previously listed sources. NORD’s Web address is http://www.rarediseases.org/. A complete guide on vasculitis can be purchased from NORD for a nominal fee. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/specific.htm
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Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
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Med Help International: http://www.medhelp.org/HealthTopics/A.html
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Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
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Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
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WebMDHealth: http://my.webmd.com/health_topics
Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to vasculitis. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with vasculitis. 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 vasculitis. 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 “vasculitis” (or a synonym), and you will receive information on all relevant organizations listed in the database.
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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 “vasculitis”. 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 “vasculitis” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months. The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “vasculitis” (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.24
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
24
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)25: •
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)
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Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
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California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
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California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
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California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html
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California: Gateway Health Library (Sutter Gould Medical Foundation)
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California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
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California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
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California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
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California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
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California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
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California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
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California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
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California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
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Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
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Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
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Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
25
Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
Finding Medical Libraries
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•
Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
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Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm
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Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
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Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm
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Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp
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Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/
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Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm
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Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html
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Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/
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Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
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Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
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Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
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Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
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Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm
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Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html
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Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm
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Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
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Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
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Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
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Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
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•
Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html
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Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp
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Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp
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Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/
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Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
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Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
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Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
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Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
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Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
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Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
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Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
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Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
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Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html
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Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm
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Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
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Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
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National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
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National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/
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National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
Finding Medical Libraries
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Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
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New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
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New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
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New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
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New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
•
New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
•
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
•
MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
•
Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
•
Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
•
On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
•
Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
•
Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm
Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a).
Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •
Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical
•
MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html
•
Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/
•
Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
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VASCULITIS DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 6-Mercaptopurine: An antimetabolite antineoplastic agent with immunosuppressant properties. It interferes with nucleic acid synthesis by inhibiting purine metabolism and is used, usually in combination with other drugs, in the treatment of or in remission maintenance programs for leukemia. [NIH] Abdomen: That portion of the body that lies between the thorax and the pelvis. [NIH] Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Abdominal Pain: Sensation of discomfort, distress, or agony in the abdominal region. [NIH] Aberrant: Wandering or deviating from the usual or normal course. [EU] Abscess: A localized, circumscribed collection of pus. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acetylcholinesterase: An enzyme that catalyzes the hydrolysis of acetylcholine to choline and acetate. In the CNS, this enzyme plays a role in the function of peripheral neuromuscular junctions. EC 3.1.1.7. [NIH] Acne: A disorder of the skin marked by inflammation of oil glands and hair glands. [NIH] Actin: Essential component of the cell skeleton. [NIH] Acute myeloid leukemia: AML. A quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. Also called acute myelogenous leukemia or acute nonlymphocytic leukemia. [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] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adenine: A purine base and a fundamental unit of adenine nucleotides. [NIH] Adenocarcinoma: A malignant epithelial tumor with a glandular organization. [NIH] Adenomatous Polyposis Coli: An autosomal dominant polyposis syndrome in which the colon contains few to thousands of adenomatous polyps, often occurring by age 15 to 25. [NIH]
Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adenosine Diphosphate: Adenosine 5'-(trihydrogen diphosphate). An adenine nucleotide containing two phosphate groups esterified to the sugar moiety at the 5'-position. [NIH] Adenovirus: A group of viruses that cause respiratory tract and eye infections.
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Adenoviruses used in gene therapy are altered to carry a specific tumor-fighting gene. [NIH] Adipose Tissue: Connective tissue composed of fat cells lodged in the meshes of areolar tissue. [NIH] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH] Adjuvant: A substance which aids another, such as an auxiliary remedy; in immunology, nonspecific stimulator (e.g., BCG vaccine) of the immune response. [EU] Adjuvant Therapy: Treatment given after the primary treatment to increase the chances of a cure. Adjuvant therapy may include chemotherapy, radiation therapy, or hormone therapy. [NIH]
Adoptive Transfer: Form of passive immunization where previously sensitized immunologic agents (cells or serum) are transferred to non-immune recipients. When transfer of cells is used as a therapy for the treatment of neoplasms, it is called adoptive immunotherapy (immunotherapy, adoptive). [NIH] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Adrenal Glands: Paired glands situated in the retroperitoneal tissues at the superior pole of each kidney. [NIH] Adrenaline: A hormone. Also called epinephrine. [NIH] Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Adverse Effect: An unwanted side effect of treatment. [NIH] Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Agammaglobulinemia: An immunologic deficiency state characterized by an extremely low level of generally all classes of gamma-globulin in the blood. [NIH] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]
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]
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Airways: Tubes that carry air into and out of the lungs. [NIH] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Aldosterone: (11 beta)-11,21-Dihydroxy-3,20-dioxopregn-4-en-18-al. A hormone secreted by the adrenal cortex that functions in the regulation of electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alkaline: Having the reactions of an alkali. [EU] Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Some alkaloids have been shown to work against cancer. [NIH] Alkylating Agents: Highly reactive chemicals that introduce alkyl radicals into biologically active molecules and thereby prevent their proper functioning. Many are used as antineoplastic agents, but most are very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. They have also been used as components in poison gases. [NIH]
Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Allergen: An antigenic substance capable of producing immediate-type hypersensitivity (allergy). [EU] Allogeneic: Taken from different individuals of the same species. [NIH] Allograft: An organ or tissue transplant between two humans. [NIH] Alopecia: Absence of hair from areas where it is normally present. [NIH] Alpha Particles: Positively charged particles composed of two protons and two neutrons, i.e., helium nuclei, emitted during disintegration of very heavy isotopes; a beam of alpha particles or an alpha ray has very strong ionizing power, but weak penetrability. [NIH] Alpha-1: A protein with the property of inactivating proteolytic enzymes such as leucocyte collagenase and elastase. [NIH] Alpha-Defensins: Defensins found in azurophilic granules of neutrophils and in the secretory granules of intestinal paneth cells. [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] Ameliorating: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This
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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] Amphetamines: Analogs or derivatives of amphetamine. Many are sympathomimetics and central nervous system stimulators causing excitation, vasopression, bronchodilation, and to varying degrees, anorexia, analepsis, nasal decongestion, and some smooth muscle relaxation. [NIH] Amplification: The production of additional copies of a chromosomal DNA sequence, found as either intrachromosomal or extrachromosomal DNA. [NIH] Amyloidosis: A group of diseases in which protein is deposited in specific organs (localized amyloidosis) or throughout the body (systemic amyloidosis). Amyloidosis may be either primary (with no known cause) or secondary (caused by another disease, including some types of cancer). Generally, primary amyloidosis affects the nerves, skin, tongue, joints, heart, and liver; secondary amyloidosis often affects the spleen, kidneys, liver, and adrenal glands. [NIH] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Analog: In chemistry, a substance that is similar, but not identical, to another. [NIH] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anastomosis: A procedure to connect healthy sections of tubular structures in the body after the diseased portion has been surgically removed. [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] Aneurysm: A sac formed by the dilatation of the wall of an artery, a vein, or the heart. [NIH] Angiitis: Inflammation of a vessel, chiefly of a blood or a lymph vessel; called also
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vasculitis. [EU] Anginal: Pertaining to or characteristic of angina. [EU] Angiogenesis: Blood vessel formation. Tumor angiogenesis is the growth of blood vessels from surrounding tissue to a solid tumor. This is caused by the release of chemicals by the tumor. [NIH] Angiogenesis inhibitor: A substance that may prevent the formation of blood vessels. In anticancer therapy, an angiogenesis inhibitor prevents the growth of blood vessels from surrounding tissue to a solid tumor. [NIH] Angiogram: An x-ray of blood vessels; the person receives an injection of dye to outline the vessels on the x-ray. [NIH] Angiography: Radiography of blood vessels after injection of a contrast medium. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Annealing: The spontaneous alignment of two single DNA strands to form a double helix. [NIH]
Antagonism: Interference with, or inhibition of, the growth of a living organism by another living organism, due either to creation of unfavorable conditions (e. g. exhaustion of food supplies) or to production of a specific antibiotic substance (e. g. penicillin). [NIH] 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] 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-Dependent Cell Cytotoxicity: The phenomenon of antibody-mediated target cell destruction by non-sensitized effector cells. The identity of the target cell varies, but it must possess surface IgG whose Fc portion is intact. The effector cell is a "killer" cell possessing Fc receptors. It may be a lymphocyte lacking conventional B- or T-cell markers, or a monocyte, macrophage, or polynuclear leukocyte, depending on the identity of the target cell. The reaction is complement-independent. [NIH] Anticholinergic: An agent that blocks the parasympathetic nerves. Called also parasympatholytic. [EU] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Antidepressant: A drug used to treat depression. [NIH] Antidiabetic: An agent that prevents or alleviates diabetes. [EU] Antigen: Any substance which is capable, under appropriate conditions, of inducing a
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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] Antihypertensive: An agent that reduces high blood pressure. [EU] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antimetabolite: A chemical that is very similar to one required in a normal biochemical reaction in cells. Antimetabolites can stop or slow down the reaction. [NIH] Antimicrobial: Killing microorganisms, or suppressing their multiplication or growth. [EU] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antiseptic: A substance that inhibits the growth and development of microorganisms without necessarily killing them. [EU] Antithrombotic: Preventing or interfering with the formation of thrombi; an agent that so acts. [EU] Antiviral: Destroying viruses or suppressing their replication. [EU] Anus: The opening of the rectum to the outside of the body. [NIH] Aorta: The main trunk of the systemic arteries. [NIH] Aortic Aneurysm: Aneurysm of the aorta. [NIH] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Aqueous: Having to do with water. [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Arrhythmia: Any variation from the normal rhythm or rate of the heart beat. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH]
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Arteriography: A procedure to x-ray arteries. The arteries can be seen because of an injection of a dye that outlines the vessels on an x-ray. [NIH] Arteriolar: Pertaining to or resembling arterioles. [EU] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Arteriolosclerosis: Sclerosis and thickening of the walls of the smaller arteries (arterioles). Hyaline arteriolosclerosis, in which there is homogeneous pink hyaline thickening of the arteriolar walls, is associated with benign nephrosclerosis. Hyperplastic arteriolosclerosis, in which there is a concentric thickening with progressive narrowing of the lumina may be associated with malignant hypertension, nephrosclerosis, and scleroderma. [EU] Arteriosclerosis: Thickening and loss of elasticity of arterial walls. Atherosclerosis is the most common form of arteriosclerosis and involves lipid deposition and thickening of the intimal cell layers within arteries. Additional forms of arteriosclerosis involve calcification of the media of muscular arteries (Monkeberg medial calcific sclerosis) and thickening of the walls of small arteries or arterioles due to cell proliferation or hyaline deposition (arteriolosclerosis). [NIH] Arteriosus: Circle composed of anastomosing arteries derived from two long posterior ciliary and seven anterior ciliary arteries, located in the ciliary body about the root of the iris. [NIH]
Arteriovenous: Both arterial and venous; pertaining to or affecting an artery and a vein. [EU] Arteriovenous Fistula: An abnormal communication between an artery and a vein. [NIH] Arteritis: Inflammation of an artery. [NIH] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Arthralgia: Pain in the joint. [NIH] Articular: Of or pertaining to a joint. [EU] 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] Astrocytes: The largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the blood brain barrier. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with microglia) respond to injury. Astrocytes have high- affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitter, but their role in signaling (as in many other functions) is not well understood. [NIH] Asymptomatic: Having no signs or symptoms of disease. [NIH] Ataxia: Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharnyx, larnyx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or peripheral nerve diseases. Motor ataxia may be associated with cerebellar diseases; cerebral cortex diseases; thalamic diseases; basal ganglia diseases; injury to the red nucleus; and other conditions. [NIH] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a
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variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Attenuated: Strain with weakened or reduced virulence. [NIH] Atypical: Irregular; not conformable to the type; in microbiology, applied specifically to strains of unusual type. [EU] 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] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autoimmunity: Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by autoimmune diseases. [NIH] Autologous: Taken from an individual's own tissues, cells, or DNA. [NIH] Autonomic: Self-controlling; functionally independent. [EU] Autonomic Nervous System: The enteric, parasympathetic, and sympathetic nervous systems taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the central nervous system, especially the hypothalamus and the solitary nucleus, which receive information relayed from visceral afferents; these and related central and sensory structures are sometimes (but not here) considered to be part of the autonomic nervous system itself. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacterial Infections: Infections by bacteria, general or unspecified. [NIH] Bactericidal: Substance lethal to bacteria; substance capable of killing bacteria. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Basal Ganglia Diseases: Diseases of the basal ganglia including the putamen; globus pallidus; claustrum; amygdala; and caudate nucleus. Dyskinesias (most notably involuntary movements and alterations of the rate of movement) represent the primary clinical manifestations of these disorders. Common etiologies include cerebrovascular disease; neurodegenerative diseases; and craniocerebral trauma. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components
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such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its subdivisions is the basal (basement) lamina. [NIH] Basophils: Granular leukocytes characterized by a relatively pale-staining, lobate nucleus and cytoplasm containing coarse dark-staining granules of variable size and stainable by basic dyes. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]
Benign tumor: A noncancerous growth that does not invade nearby tissue or spread to other parts of the body. [NIH] Beta-Defensins: Defensins found mainly in epithelial cells. [NIH] Beta-Lactamases: Enzymes found in many bacteria which catalyze the hydrolysis of the amide bond in the beta-lactam ring. Well known antibiotics destroyed by these enzymes are penicillins and cephalosporins. EC 3.5.2.6. [NIH] Beta-Thromboglobulin: A platelet-specific protein which is released when platelets aggregate. Elevated plasma levels have been reported after deep venous thrombosis, preeclampsia, myocardial infarction with mural thrombosis, and myeloproliferative disorders. Measurement of beta-thromboglobulin in biological fluids by radioimmunoassay is used for the diagnosis and assessment of progress of thromboembolic disorders. [NIH] Bewilderment: Impairment or loss of will power. [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 Acids: Acids made by the liver that work with bile to break down fats. [NIH] Bile Acids and Salts: Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones. [NIH] Bile duct: A tube through which bile passes in and out of the liver. [NIH] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biological response modifier: BRM. A substance that stimulates the body's response to infection and disease. [NIH] Biological therapy: Treatment to stimulate or restore the ability of the immune system to fight infection and disease. Also used to lessen side effects that may be caused by some cancer treatments. Also known as immunotherapy, biotherapy, or biological response modifier (BRM) therapy. [NIH] Biomarkers: Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Biopsy specimen: Tissue removed from the body and examined under a microscope to determine whether disease is present. [NIH]
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Biosynthesis: The building up of a chemical compound in the physiologic processes of a living organism. [EU] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Bladder: The organ that stores urine. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blood Volume: Volume of circulating blood. It is the sum of the plasma volume and erythrocyte volume. [NIH] Blood-Brain Barrier: Specialized non-fenestrated tightly-joined endothelial cells (tight junctions) that form a transport barrier for certain substances between the cerebral capillaries and the brain tissue. [NIH] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [NIH]
Body Fluids: Liquid components of living organisms. [NIH] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bone Marrow Cells: Cells contained in the bone marrow including fat cells, stromal cells, megakaryocytes, and the immediate precursors of most blood cells. [NIH] Bone scan: A technique to create images of bones on a computer screen or on film. A small amount of radioactive material is injected into a blood vessel and travels through the bloodstream; it collects in the bones and is detected by a scanner. [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] 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] Branch: Most commonly used for branches of nerves, but applied also to other structures. [NIH]
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Breakdown: A physical, metal, or nervous collapse. [NIH] Broad-spectrum: Effective against a wide range of microorganisms; said of an antibiotic. [EU] Bronchi: The larger air passages of the lungs arising from the terminal bifurcation of the trachea. [NIH] Bronchial: Pertaining to one or more bronchi. [EU] Bronchitis: Inflammation (swelling and reddening) of the bronchi. [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] Calcification: Deposits of calcium in the tissues of the breast. Calcification in the breast can be seen on a mammogram, but cannot be detected by touch. There are two types of breast calcification, macrocalcification and microcalcification. Macrocalcifications are large deposits and are usually not related to cancer. Microcalcifications are specks of calcium that may be found in an area of rapidly dividing cells. Many microcalcifications clustered together may be a sign of cancer. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calcium channel blocker: A drug used to relax the blood vessel and heart muscle, causing pressure inside blood vessels to drop. It also can regulate heart rhythm. [NIH] Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU] Capillary Permeability: Property of blood capillary walls that allows for the selective exchange of substances. Small lipid-soluble molecules such as carbon dioxide and oxygen move freely by diffusion. Water and water-soluble molecules cannot pass through the endothelial walls and are dependent on microscopic pores. These pores show narrow areas (tight junctions) which may limit large molecule movement. [NIH] Captopril: A potent and specific inhibitor of peptidyl-dipeptidase A. It blocks the conversion of angiotensin I to angiotensin II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the renin-angiotensin system and inhibits pressure responses to exogenous angiotensin. [NIH] Carbimazole: An imidazole antithyroid agent. Carbimazole is metabolized to methimazole, which is responsible for the antithyroid activity. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH]
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Carcinogenesis: The process by which normal cells are transformed into cancer cells. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinogens: Substances that increase the risk of neoplasms in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included. [NIH] Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]
Cardiac: Having to do with the heart. [NIH] Cardiac Output: The volume of blood passing through the heart per unit of time. It is usually expressed as liters (volume) per minute so as not to be confused with stroke volume (volume per beat). [NIH] Cardiomyopathy: A general diagnostic term designating primary myocardial disease, often of obscure or unknown etiology. [EU] 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] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Case series: A group or series of case reports involving patients who were given similar treatment. Reports of case series usually contain detailed information about the individual patients. This includes demographic information (for example, age, gender, ethnic origin) and information on diagnosis, treatment, response to treatment, and follow-up after treatment. [NIH] Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group. [NIH] Cathode: An electrode, usually an incandescent filament of tungsten, which emits electrons in an X-ray tube. [NIH] Cations: Postively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis. [NIH] Causal: Pertaining to a cause; directed against a cause. [EU] Cefoperazone: Semisynthetic broad-spectrum cephalosporin with a tetrazolyl moiety that is resistant to beta-lactamase. It has been proposed especially against Pseudomonas infections. [NIH]
Ceftriaxone: Broad-spectrum cephalosporin antibiotic with a very long half-life and high penetrability to usually inaccessible infections, including those involving the meninges, eyes, inner ears, and urinary tract. [NIH] Celecoxib: A drug that reduces pain. Celecoxib belongs to the family of drugs called
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nonsteroidal anti-inflammatory agents. It is being studied for cancer prevention. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Adhesion: Adherence of cells to surfaces or to other cells. [NIH] Cell Adhesion Molecules: Surface ligands, usually glycoproteins, that mediate cell-to-cell adhesion. Their functions include the assembly and interconnection of various vertebrate systems, as well as maintenance of tissue integration, wound healing, morphogenic movements, cellular migrations, and metastasis. [NIH] Cell Cycle: The complex series of phenomena, occurring between the end of one cell division and the end of the next, by which cellular material is divided between daughter cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell Division: The fission of a cell. [NIH] Cell motility: The ability of a cell to move. [NIH] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. [NIH] Cellular adhesion: The close adherence (bonding) to adjoining cell surfaces. [NIH] Cellulitis: An acute, diffuse, and suppurative inflammation of loose connective tissue, particularly the deep subcutaneous tissues, and sometimes muscle, which is most commonly seen as a result of infection of a wound, ulcer, or other skin lesions. [NIH] 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] Cerebellar: Pertaining to the cerebellum. [EU] Cerebellar Diseases: Diseases that affect the structure or function of the cerebellum. Cardinal manifestations of cerebellar dysfunction include dysmetria, gait ataxia, and muscle hypotonia. [NIH] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebrospinal: Pertaining to the brain and spinal cord. [EU] Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU]
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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] Chemokines: Class of pro-inflammatory cytokines that have the ability to attract and activate leukocytes. They can be divided into at least three structural branches: C (chemokines, C), CC (chemokines, CC), and CXC (chemokines, CXC), according to variations in a shared cysteine motif. [NIH] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chemotaxis: The movement of cells or organisms toward or away from a substance in response to its concentration gradient. [NIH] Chemotherapy: Treatment with anticancer drugs. [NIH] Chickenpox: A mild, highly contagious virus characterized by itchy blisters all over the body. [NIH] Chimera: An individual that contains cell populations derived from different zygotes. [NIH] Chin: The anatomical frontal portion of the mandible, also known as the mentum, that contains the line of fusion of the two separate halves of the mandible (symphysis menti). This line of fusion divides inferiorly to enclose a triangular area called the mental protuberance. On each side, inferior to the second premolar tooth, is the mental foramen for the passage of blood vessels and a nerve. [NIH] Chlorambucil: An anticancer drug that belongs to the family of drugs called alkylating agents. [NIH] Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Choline: A basic constituent of lecithin that is found in many plants and animal organs. It is important as a precursor of acetylcholine, as a methyl donor in various metabolic processes, and in lipid metabolism. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Fatigue Syndrome: Fatigue caused by the combined effects of different types of prolonged fatigue. [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
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transplantation to replace the work of the kidneys. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Clamp: A u-shaped steel rod used with a pin or wire for skeletal traction in the treatment of certain fractures. [NIH] Clear cell carcinoma: A rare type of tumor of the female genital tract in which the inside of the cells looks clear when viewed under a microscope. [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] CNS: Central nervous system. The brain and spinal cord. [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] Coca: Any of several South American shrubs of the Erythroxylon genus (and family) that yield cocaine; the leaves are chewed with alum for CNS stimulation. [NIH] Cocaethylene: Hard drug formed by cocaine and alcohol. [NIH] Cocaine: An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake. [NIH] 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] Collagen disease: A term previously used to describe chronic diseases of the connective tissue (e.g., rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis), but now is thought to be more appropriate for diseases associated with defects in collagen, which is a component of the connective tissue. [NIH] Collapse: 1. A state of extreme prostration and depression, with failure of circulation. 2. Abnormal falling in of the walls of any part of organ. [EU]
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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] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] 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] Computed tomography: CT scan. A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized tomography and computerized axial tomography (CAT) scan. [NIH] Computerized axial tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called CAT scan, computed tomography (CT scan), or computerized
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tomography. [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] Conduction: The transfer of sound waves, heat, nervous impulses, or electricity. [EU] Cones: One type of specialized light-sensitive cells (photoreceptors) in the retina that provide sharp central vision and color vision. [NIH] Confusion: A mental state characterized by bewilderment, emotional disturbance, lack of clear thinking, and perceptual disorientation. [NIH] Congestion: Excessive or abnormal accumulation of blood in a part. [EU] Conjugated: Acting or operating as if joined; simultaneous. [EU] Conjunctiva: The mucous membrane that lines the inner surface of the eyelids and the anterior part of the sclera. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue Cells: A group of cells that includes fibroblasts, cartilage cells, adipocytes, smooth muscle cells, and bone cells. [NIH] 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] Consciousness: Sense of awareness of self and of the environment. [NIH] Consolidation: The healing process of a bone fracture. [NIH] Constipation: Infrequent or difficult evacuation of feces. [NIH] Constriction: The act of constricting. [NIH] Consultation: A deliberation between two or more physicians concerning the diagnosis and the proper method of treatment in a case. [NIH] Consumption: Pulmonary tuberculosis. [NIH] Contamination: The soiling or pollution by inferior material, as by the introduction of organisms into a wound, or sewage into a stream. [EU] 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] Conus: A large, circular, white patch around the optic disk due to the exposing of the sclera as a result of degenerative change or congenital abnormality in the choroid and retina. [NIH] Convulsions: A general term referring to sudden and often violent motor activity of cerebral or brainstem origin. Convulsions may also occur in the absence of an electrical cerebral discharge (e.g., in response to hypotension). [NIH] Coordination: Muscular or motor regulation or the harmonious cooperation of muscles or groups of muscles, in a complex action or series of actions. [NIH] Cornea: The transparent part of the eye that covers the iris and the pupil and allows light to enter the inside. [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
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pathologic involvement of them. [EU] Coronary Aneurysm: A saclike dilatation of the walls of a blood vessel, usually an artery. [NIH]
Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Corticosteroid: Any of the steroids elaborated by the adrenal cortex (excluding the sex hormones of adrenal origin) in response to the release of corticotrophin (adrenocorticotropic hormone) by the pituitary gland, to any of the synthetic equivalents of these steroids, or to angiotensin II. They are divided, according to their predominant biological activity, into three major groups: glucocorticoids, chiefly influencing carbohydrate, fat, and protein metabolism; mineralocorticoids, affecting the regulation of electrolyte and water balance; and C19 androgens. Some corticosteroids exhibit both types of activity in varying degrees, and others exert only one type of effect. The corticosteroids are used clinically for hormonal replacement therapy, for suppression of ACTH secretion by the anterior pituitary, as antineoplastic, antiallergic, and anti-inflammatory agents, and to suppress the immune response. Called also adrenocortical hormone and corticoid. [EU] Cortisone: A natural steroid hormone produced in the adrenal gland. It can also be made in the laboratory. Cortisone reduces swelling and can suppress immune responses. [NIH] Cost Savings: Reductions in all or any portion of the costs of providing goods or services. Savings may be incurred by the provider or the consumer. [NIH] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Craniocerebral Trauma: Traumatic injuries involving the cranium and intracranial structures (i.e., brain; cranial nerves; meninges; and other structures). Injuries may be classified by whether or not the skull is penetrated (i.e., penetrating vs. nonpenetrating) or whether there is an associated hemorrhage. [NIH] Creatine: An amino acid that occurs in vertebrate tissues and in urine. In muscle tissue, creatine generally occurs as phosphocreatine. Creatine is excreted as creatinine in the urine. [NIH]
Creatinine: A compound that is excreted from the body in urine. Creatinine levels are measured to monitor kidney function. [NIH] Critical Care: Health care provided to a critically ill patient during a medical emergency or crisis. [NIH] Cryoglobulinemia: A condition characterized by the presence of abnormal or abnormal quantities of cryoglobulins in the blood. They are precipitated into the microvasculature on exposure to cold and cause restricted blood flow in exposed areas. [NIH] Cryptococcosis: Infection with a fungus of the species Cryptococcus neoformans. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Cutaneous: Having to do with the skin. [NIH]
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Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cyclin: Molecule that regulates the cell cycle. [NIH] Cyclin A: A 33-kD protein identical to adenovirus E1A-associated protein p60. Cyclin A regulates p33cdk2 and p34cdc2, and is necessary for progression through the S phase of the cell cycle. [NIH] Cyclin E: A 50-kD protein that complexes with cdk2 in the late G1 phase of the cell cycle. [NIH]
Cyclophosphamide: Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the liver to form the active aldophosphamide. It is used in the treatment of lymphomas, leukemias, etc. Its side effect, alopecia, has been made use of in defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer. [NIH] Cyclosporine: A drug used to help reduce the risk of rejection of organ and bone marrow transplants by the body. It is also used in clinical trials to make cancer cells more sensitive to anticancer drugs. [NIH] Cysteine: A thiol-containing non-essential amino acid that is oxidized to form cystine. [NIH] 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] Cytotoxic: Cell-killing. [NIH] Cytotoxicity: Quality of being capable of producing a specific toxic action upon cells of special organs. [NIH] Data Collection: Systematic gathering of data for a particular purpose from various sources, including questionnaires, interviews, observation, existing records, and electronic devices. The process is usually preliminary to statistical analysis of the data. [NIH] Databases, Bibliographic: Extensive collections, reputedly complete, of references and citations to books, articles, publications, etc., generally on a single subject or specialized subject area. Databases can operate through automated files, libraries, or computer disks. The concept should be differentiated from factual databases which is used for collections of data and facts apart from bibliographic references to them. [NIH] Defense Mechanisms: Unconscious process used by an individual or a group of individuals in order to cope with impulses, feelings or ideas which are not acceptable at their conscious level; various types include reaction formation, projection and self reversal. [NIH] Defensins: Family of antimicrobial peptides that have been identified in humans, animals, and plants. They are thought to play a role in host defenses against infections, inflammation, wound repair, and acquired immunity. Based on the disulfide pairing of their characteristic six cysteine residues, they are divided into alpha-defensins and beta-defensins. [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]
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Dementia: An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness. [NIH] Denaturation: Rupture of the hydrogen bonds by heating a DNA solution and then cooling it rapidly causes the two complementary strands to separate. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Dendritic: 1. Branched like a tree. 2. Pertaining to or possessing dendrites. [EU] Dendritic cell: A special type of antigen-presenting cell (APC) that activates T lymphocytes. [NIH]
Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Deoxyglucose: 2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity. [NIH] Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Dermal: Pertaining to or coming from the skin. [NIH] Dermatosis: Any skin disease, especially one not characterized by inflammation. [EU] DES: Diethylstilbestrol. A synthetic hormone that was prescribed from the early 1940s until 1971 to help women with complications of pregnancy. DES has been linked to an increased risk of clear cell carcinoma of the vagina in daughters of women who used DES. DES may also increase the risk of breast cancer in women who used DES. [NIH] Desensitization: The prevention or reduction of immediate hypersensitivity reactions by administration of graded doses of allergen; called also hyposensitization and immunotherapy. [EU] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diabetic Retinopathy: Retinopathy associated with diabetes mellitus, which may be of the background type, progressively characterized by microaneurysms, interretinal punctuate macular edema, or of the proliferative type, characterized by neovascularization of the retina and optic disk, which may project into the vitreous, proliferation of fibrous tissue, vitreous hemorrhage, and retinal detachment. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Dicumarol: An oral anticoagulant that interferes with the metabolism of vitamin K. It is also used in biochemical experiments as an inhibitor of reductases. [NIH] Diffusion: The tendency of a gas or solute to pass from a point of higher pressure or concentration to a point of lower pressure or concentration and to distribute itself throughout the available space; a major mechanism of biological transport. [NIH] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Dilatation: The act of dilating. [NIH]
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Dilation: A process by which the pupil is temporarily enlarged with special eye drops (mydriatic); allows the eye care specialist to better view the inside of the eye. [NIH] Dipyridamole: A drug that prevents blood cell clumping and enhances the effectiveness of fluorouracil and other chemotherapeutic agents. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Disease Progression: The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis. [NIH] Disease Susceptibility: 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 individual more than usually susceptible to certain diseases. [NIH] Disinfectant: An agent that disinfects; applied particularly to agents used on inanimate objects. [EU] Disorientation: The loss of proper bearings, or a state of mental confusion as to time, place, or identity. [EU] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Domesticated: Species in which the evolutionary process has been influenced by humans to meet their needs. [NIH] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Double-blind: Pertaining to a clinical trial or other experiment in which neither the subject nor the person administering treatment knows which treatment any particular subject is receiving. [EU] Double-blinded: A clinical trial in which neither the medical staff nor the person knows which of several possible therapies the person is receiving. [NIH] Doxepin: A dibenzoxepin tricyclic compound. It displays a range of pharmacological actions including maintaining adrenergic innervation. Its mechanism of action is not fully understood, but it appears to block reuptake of monoaminergic neurotransmitters into presynaptic terminals. It also possesses anticholinergic activity and modulates antagonism of histamine H(1)- and H(2)-receptors. [NIH] Drive: A state of internal activity of an organism that is a necessary condition before a given
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stimulus will elicit a class of responses; e.g., a certain level of hunger (drive) must be present before food will elicit an eating response. [NIH] Drug Combinations: Single preparations containing two or more active agents, for the purpose of their concurrent administration as a fixed dose mixture. It is differentiated from combination drug therapy in which two or more drugs are administered separately for a combined effect. [NIH] Drug Design: The molecular designing of drugs for specific purposes (such as DNAbinding, enzyme inhibition, anti-cancer efficacy, etc.) based on knowledge of molecular properties such as activity of functional groups, molecular geometry, and electronic structure, and also on information cataloged on analogous molecules. Drug design is generally computer-assisted molecular modeling and does not include pharmacokinetics, dosage analysis, or drug administration analysis. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH] Duct: A tube through which body fluids pass. [NIH] Duodenum: The first part of the small intestine. [NIH] Dura mater: The outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain and spinal cord; called also pachymeninx. [EU] Dysphagia: Difficulty in swallowing. [EU] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [NIH] Dystrophy: Any disorder arising from defective or faulty nutrition, especially the muscular dystrophies. [EU] Eclampsia: Onset of convulsions or coma in a previously diagnosed pre-eclamptic patient. [NIH]
Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Effector cell: A cell that performs a specific function in response to a stimulus; usually used to describe cells in the immune system. [NIH] Efferent: Nerve fibers which conduct impulses from the central nervous system to muscles and glands. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Effusion: The escape of fluid into a part or tissue, as an exudation or a transudation. [EU] Elastic: Susceptible of resisting and recovering from stretching, compression or distortion applied by a force. [EU] Elasticity: Resistance and recovery from distortion of shape. [NIH] Elastin: The protein that gives flexibility to tissues. [NIH] Elective: Subject to the choice or decision of the patient or physician; applied to procedures that are advantageous to the patient but not urgent. [EU]
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Electrocoagulation: Electrosurgical procedures used to treat hemorrhage (e.g., bleeding ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. [NIH] Electrolysis: Destruction by passage of a galvanic electric current, as in disintegration of a chemical compound in solution. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] 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] 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] 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] Emphysema: A pathological accumulation of air in tissues or organs. [NIH] Empiric: Empirical; depending upon experience or observation alone, without using scientific method or theory. [EU] Encephalitis: Inflammation of the brain due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see encephalitis, viral) are a relatively frequent cause of this condition. [NIH] Encephalitis, Viral: Inflammation of brain parenchymal tissue as a result of viral infection. Encephalitis may occur as primary or secondary manifestation of Togaviridae infections; Herpesviridae infections; Adenoviridae infections; Flaviviridae infections; Bunyaviridae infections; Picornaviridae infections; Paramyxoviridae infections; Orthomyxoviridae infections; Retroviridae infections; and Arenaviridae infections. [NIH] Encephalomyelitis: A general term indicating inflammation of the brain and spinal cord, often used to indicate an infectious process, but also applicable to a variety of autoimmune and toxic-metabolic conditions. There is significant overlap regarding the usage of this term and encephalitis in the literature. [NIH] 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] Endocytosis: Cellular uptake of extracellular materials within membrane-limited vacuoles or microvesicles. Endosomes play a central role in endocytosis. [NIH]
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Endophthalmitis: Suppurative inflammation of the tissues of the internal structures of the eye; not all layers of the uvea are affected. Fungi, necrosis of intraocular tumors, and retained intraocular foreign bodies often cause a purulent endophthalmitis. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium, Lymphatic: Unbroken cellular lining (intima) of the lymph vessels (e.g., the high endothelial lymphatic venules). It is more permeable than vascular endothelium, lacking selective absorption and functioning mainly to remove plasma proteins that have filtered through the capillaries into the tissue spaces. [NIH] Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components from interstitium to lumen; this function has been most intensively studied in the blood capillaries. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxin: Toxin from cell walls of bacteria. [NIH] End-stage renal: Total chronic kidney failure. When the kidneys fail, the body retains fluid and harmful wastes build up. A person with ESRD needs treatment to replace the work of the failed kidneys. [NIH] 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-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] Eosinophilic: A condition found primarily in grinding workers caused by a reaction of the pulmonary tissue, in particular the eosinophilic cells, to dust that has entered the lung. [NIH] Eosinophils: Granular leukocytes with a nucleus that usually has two lobes connected by a slender thread of chromatin, and cytoplasm containing coarse, round granules that are uniform in size and stainable by eosin. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum
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lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Episcleritis: Inflammation of the episclera and/or the outer layers of the sclera itself. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial carcinoma: Cancer that begins in the cells that line an organ. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Epitopes: Sites on an antigen that interact with specific antibodies. [NIH] Epoprostenol: A prostaglandin that is biosynthesized enzymatically from prostaglandin endoperoxides in human vascular tissue. It is a potent inhibitor of platelet aggregation. The sodium salt has been also used to treat primary pulmonary hypertension. [NIH] Erysipeloid: An infection caused by Erysipelothrix rhusiopathiae that is almost wholly restricted to persons who in their occupation handle infected fish, shellfish, poultry, or meat. Three forms of this condition exist: a mild localized form manifested by local swelling and redness of the skin; a diffuse form that might present with fever; and a rare systemic form associated with endocarditis. [NIH] Erythema: Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Esophagitis: Inflammation, acute or chronic, of the esophagus caused by bacteria, chemicals, or trauma. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]
Essential Tremor: A rhythmic, involuntary, purposeless, oscillating movement resulting from the alternate contraction and relaxation of opposing groups of muscles. [NIH] Estrogens: A class of sex hormones associated with the development and maintenance of secondary female sex characteristics and control of the cyclical changes in the reproductive cycle. They are also required for pregnancy maintenance and have an anabolic effect on protein metabolism and water retention. [NIH] Ethanol: A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. [NIH] Ethnic Groups: A group of people with a common cultural heritage that sets them apart from others in a variety of social relationships. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Evoke: The electric response recorded from the cerebral cortex after stimulation of a peripheral sense organ. [NIH]
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Excitatory: When cortical neurons are excited, their output increases and each new input they receive while they are still excited raises their output markedly. [NIH] Excrete: To get rid of waste from the body. [NIH] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Exon: The part of the DNA that encodes the information for the actual amino acid sequence of the protein. In many eucaryotic genes, the coding sequences consist of a series of exons alternating with intron sequences. [NIH] Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extracellular Matrix Proteins: Macromolecular organic compounds that contain carbon, hydrogen, oxygen, nitrogen, and usually, sulfur. These macromolecules (proteins) form an intricate meshwork in which cells are embedded to construct tissues. Variations in the relative types of macromolecules and their organization determine the type of extracellular matrix, each adapted to the functional requirements of the tissue. The two main classes of macromolecules that form the extracellular matrix are: glycosaminoglycans, usually linked to proteins (proteoglycans), and fibrous proteins (e.g., collagen, elastin, fibronectins and laminin). [NIH] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extravasation: A discharge or escape, as of blood, from a vessel into the tissues. [EU] Extremity: A limb; an arm or leg (membrum); sometimes applied specifically to a hand or foot. [EU] Eye Manifestations: Ocular disorders attendant upon non-ocular disease or injury. [NIH] Facial: Of or pertaining to the face. [EU] Facial Nerve: The 7th cranial nerve. The facial nerve has two parts, the larger motor root which may be called the facial nerve proper, and the smaller intermediate or sensory root. Together they provide efferent innervation to the muscles of facial expression and to the lacrimal and salivary glands, and convey afferent information for taste from the anterior two-thirds of the tongue and for touch from the external ear. [NIH] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Family Practice: A medical specialty concerned with the provision of continuing, comprehensive primary health care for the entire family. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatal Outcome: Death resulting from the presence of a disease in an individual, as shown by a single case report or a limited number of patients. This should be differentiated from death, the physiological cessation of life and from mortality, an epidemiological or statistical concept. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]
Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH]
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Feasibility Studies: Studies to determine the advantages or disadvantages, practicability, or capability of accomplishing a projected plan, study, or project. [NIH] Febrile: Pertaining to or characterized by fever. [EU] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrin: A protein derived from fibrinogen in the presence of thrombin, which forms part of the blood clot. [NIH] Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three nonidentical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibroid: A benign smooth muscle tumor, usually in the uterus or gastrointestinal tract. Also called leiomyoma. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Flatus: Gas passed through the rectum. [NIH] Fluorescence: The property of emitting radiation while being irradiated. The radiation emitted is usually of longer wavelength than that incident or absorbed, e.g., a substance can be irradiated with invisible radiation and emit visible light. X-ray fluorescence is used in diagnosis. [NIH] Fluorouracil: A pyrimidine analog that acts as an antineoplastic antimetabolite and also has immunosuppressant. It interferes with DNA synthesis by blocking the thymidylate synthetase conversion of deoxyuridylic acid to thymidylic acid. [NIH] Fluoxetine: The first highly specific serotonin uptake inhibitor. It is used as an antidepressant and often has a more acceptable side-effects profile than traditional antidepressants. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Follicles: Shafts through which hair grows. [NIH] Fungi: A kingdom of eukaryotic, heterotrophic organisms that live as saprobes or parasites, including mushrooms, yeasts, smuts, molds, etc. They reproduce either sexually or asexually, and have life cycles that range from simple to complex. Filamentous fungi refer to those that grow as multicelluar colonies (mushrooms and molds). [NIH] Fungus: A general term used to denote a group of eukaryotic protists, including mushrooms, yeasts, rusts, moulds, smuts, etc., which are characterized by the absence of chlorophyll and by the presence of a rigid cell wall composed of chitin, mannans, and sometimes cellulose. They are usually of simple morphological form or show some reversible cellular specialization, such as the formation of pseudoparenchymatous tissue in the fruiting body of a mushroom. The dimorphic fungi grow, according to environmental conditions, as moulds or yeasts. [EU] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] 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
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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] Gangrene: Death and putrefaction of tissue usually due to a loss of blood supply. [NIH] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gastric: Having to do with the stomach. [NIH] Gastric Bypass: Surgical procedure in which the stomach is transected high on the body. The resulting proximal remnant is joined to a loop of the jejunum in an end-to-side anastomosis. This procedure is used frequently in the treatment of morbid obesity. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]
Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal Hemorrhage: Bleeding in the gastrointestinal tract. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]
Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Expression Profiling: The determination of the pattern of genes expressed i.e., transcribed, under specific circumstances or in a specific cell. [NIH] Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called codons (codon). [NIH] Genetic Engineering: Directed modification of the gene complement of a living organism by such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetic testing: Analyzing DNA to look for a genetic alteration that may indicate an increased risk for developing a specific disease or disorder. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genital: Pertaining to the genitalia. [EU] Genomics: The systematic study of the complete DNA sequences (genome) of organisms. [NIH]
Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Geriatric: Pertaining to the treatment of the aged. [EU] Germfree: Free from all living micro-organisms. [NIH] Germinal Center: The activated center of a lymphoid follicle in secondary lymphoid tissue where B-lymphocytes are stimulated by antigens and helper T cells (T-lymphocytes, helperinducer) are stimulated to generate memory cells. [NIH] Giant Cells: Multinucleated masses produced by the fusion of many cells; often associated with viral infections. In AIDS, they are induced when the envelope glycoprotein of the HIV
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virus binds to the CD4 antigen of uninfected neighboring T4 cells. The resulting syncytium leads to cell death and thus may account for the cytopathic effect of the virus. [NIH] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Gliosis: The production of a dense fibrous network of neuroglia; includes astrocytosis, which is a proliferation of astrocytes in the area of a degenerative lesion. [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] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glucose Intolerance: A pathological state in which the fasting plasma glucose level is less than 140 mg per deciliter and the 30-, 60-, or 90-minute plasma glucose concentration following a glucose tolerance test exceeds 200 mg per deciliter. This condition is seen frequently in diabetes mellitus but also occurs with other diseases. [NIH] Glucuronic Acid: Derivatives of uronic acid found throughout the plant and animal kingdoms. They detoxify drugs and toxins by conjugating with them to form glucuronides in the liver which are more water-soluble metabolites that can be easily eliminated from the body. [NIH] Glutamate: Excitatory neurotransmitter of the brain. [NIH] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH]
Glyburide: An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide. [NIH] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Glycosylation: The chemical or biochemical addition of carbohydrate or glycosyl groups to other chemicals, especially peptides or proteins. Glycosyl transferases are used in this biochemical reaction. [NIH] Gonadal: Pertaining to a gonad. [EU] Gonadotropin: The water-soluble follicle stimulating substance, by some believed to originate in chorionic tissue, obtained from the serum of pregnant mares. It is used to supplement the action of estrogens. [NIH]
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Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Grade: The grade of a tumor depends on how abnormal the cancer cells look under a microscope and how quickly the tumor is likely to grow and spread. Grading systems are different for each type of cancer. [NIH] Grading: A system for classifying cancer cells in terms of how abnormal they appear when examined under a microscope. The objective of a grading system is to provide information about the probable growth rate of the tumor and its tendency to spread. The systems used to grade tumors vary with each type of cancer. Grading plays a role in treatment decisions. [NIH]
Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Gram-positive: Retaining the stain or resisting decolorization by alcohol in Gram's method of staining, a primary characteristic of bacteria whose cell wall is composed of a thick layer of peptidologlycan with attached teichoic acids. [EU] Gram-Positive Bacteria: Bacteria which retain the crystal violet stain when treated by Gram's method. [NIH] Granule: A small pill made from sucrose. [EU] Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [NIH] Granuloma: A relatively small nodular inflammatory lesion containing grouped mononuclear phagocytes, caused by infectious and noninfectious agents. [NIH] Granuloma Annulare: Benign granulomatous disease of unknown etiology characterized by a ring of localized or disseminated papules or nodules on the skin and palisading histiocytes surrounding necrobiotic tissue resulting from altered collagen structures. [NIH] Growth: The progressive development of a living being or part of an organism from its earliest stage to maturity. [NIH] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Guanylate Cyclase: An enzyme that catalyzes the conversion of GTP to 3',5'-cyclic GMP and pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC 4.6.1.2. [NIH] Guinea Pigs: A common name used for the family Caviidae. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research. [NIH]
Haematoma: A localized collection of blood, usually clotted, in an organ, space, or tissue, due to a break in the wall of a blood vessel. [EU] Haemorrhage: The escape of blood from the vessels; bleeding. Small haemorrhages are classified according to size as petechiae (very small), purpura (up to 1 cm), and ecchymoses (larger). The massive accumulation of blood within a tissue is called a haematoma. [EU] Half-Life: The time it takes for a substance (drug, radioactive nuclide, or other) to lose half of its pharmacologic, physiologic, or radiologic activity. [NIH] 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]
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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] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Heart Transplantation: The transference of a heart from one human or animal to another. [NIH]
Hematopoietic growth factors: A group of proteins that cause blood cells to grow and mature. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemoglobinuria: The presence of free hemoglobin in the urine. [NIH] 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] 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] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatitis A: Hepatitis caused by hepatovirus. It can be transmitted through fecal contamination of food or water. [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]
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Hepatitis E: An acute form of hepatitis caused by a virus serologically distinct from the agents of hepatitis A, B, and C. Hepatitis E is associated with fecally-contaminated water, is enterically transmitted, and is commonly found in tropical or subtropical countries. [NIH] Hepatocellular: Pertaining to or affecting liver cells. [EU] Hepatocellular carcinoma: A type of adenocarcinoma, the most common type of liver tumor. [NIH] Hepatocyte: A liver cell. [NIH] Hepatomegaly: Enlargement of the liver. [NIH] Hepatovirus: A genus of Picornaviridae causing infectious hepatitis naturally in humans and experimentally in other primates. It is transmitted through fecal contamination of food or water. [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] Heterodimers: Zippered pair of nonidentical proteins. [NIH] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]
Heterozygote: An individual having different alleles at one or more loci in homologous chromosome segments. [NIH] Hidradenitis: The inflammation of a sweat gland (usually of the apocrine type). The condition can be idiopathic or occur as a result of or in association with another underlying condition. Neutrophilic eccrine hidradenitis is a relatively rare variant that has been reported in patients undergoing chemotherapy, usually for non-Hodgkin lymphomas or leukemic conditions. [NIH] Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] Histology: The study of tissues and cells under a microscope. [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] Hormone therapy: Treatment of cancer by removing, blocking, or adding hormones. Also called endocrine therapy. [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] Host: Any animal that receives a transplanted graft. [NIH]
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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] Hyaluronidase: An enzyme that splits hyaluronic acid and thus lowers the viscosity of the acid and facilitates the spreading of fluids through tissues either advantageously or disadvantageously. [NIH] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hybridization: The genetic process of crossbreeding to produce a hybrid. Hybrid nucleic acids can be formed by nucleic acid hybridization of DNA and RNA molecules. Protein hybridization allows for hybrid proteins to be formed from polypeptide chains. [NIH] Hydralazine: A direct-acting vasodilator that is used as an antihypertensive agent. [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] 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] Hypercapnia: A clinical manifestation of abnormal increase in the amount of carbon dioxide in arterial blood. [NIH] Hyperplasia: An increase in the number of cells in a tissue or organ, not due to tumor formation. It differs from hypertrophy, which is an increase in bulk without an increase in the number of cells. [NIH] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hypertrophy: General increase in bulk of a part or organ, not due to tumor formation, nor to an increase in the number of cells. [NIH] Hypesthesia: Absent or reduced sensitivity to cutaneous stimulation. [NIH] Id: The part of the personality structure which harbors the unconscious instinctive desires and strivings of the individual. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH] Ileostomy: Surgical creation of an external opening into the ileum for fecal diversion or drainage. Loop or tube procedures are most often employed. [NIH]
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Iloprost: An eicosanoid, derived from the cyclooxygenase pathway of arachidonic acid metabolism. It is a stable and synthetic analog of epoprostenol, but with a longer half-life than the parent compound. Its actions are similar to prostacyclin. Iloprost produces vasodilation and inhibits platelet aggregation. [NIH] Imidazole: C3H4N2. The ring is present in polybenzimidazoles. [NIH] Immune function: Production and action of cells that fight disease or infection. [NIH] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]
Immune Sera: Serum that contains antibodies. It is obtained from an animal that has been immunized either by antigen injection or infection with microorganisms containing the antigen. [NIH] Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immune Tolerance: The specific failure of a normally responsive individual to make an immune response to a known antigen. It results from previous contact with the antigen by an immunologically immature individual (fetus or neonate) or by an adult exposed to extreme high-dose or low-dose antigen, or by exposure to radiation, antimetabolites, antilymphocytic serum, etc. [NIH] Immunity: Nonsusceptibility to the invasive or pathogenic microorganisms or to the toxic effect of antigenic substances. [NIH]
effects
of
foreign
Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH] Immunoassay: Immunochemical assay or detection of a substance by serologic or immunologic methods. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance. [NIH] Immunochemistry: Field of chemistry that pertains to immunological phenomena and the study of chemical reactions related to antigen stimulation of tissues. It includes physicochemical interactions between antigens and antibodies. [NIH] Immunocompromised: Having a weakened immune system caused by certain diseases or treatments. [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunogenetics: A branch of genetics which deals with the genetic basis of the immune response. [NIH] Immunogenic: Producing immunity; evoking an immune response. [EU] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunology: The study of the body's immune system. [NIH] Immunosuppressant: An agent capable of suppressing immune responses. [EU]
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Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunosuppressive Agents: Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of suppressor T-cell populations or by inhibiting the activation of helper cells. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of interleukins and other cytokines are emerging. [NIH] Immunosuppressive therapy: Therapy used to decrease the body's immune response, such as drugs given to prevent transplant rejection. [NIH] Immunotherapy: Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In Situ Hybridization: A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes. [NIH] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incision: A cut made in the body during surgery. [NIH] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU] Indocyanine Green: A tricarbocyanine dye that is used diagnostically in liver function tests and to determine blood volume and cardiac output. [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] Induction therapy: Treatment designed to be used as a first step toward shrinking the cancer and in evaluating response to drugs and other agents. Induction therapy is followed by additional therapy to eliminate whatever cancer remains. [NIH] Infantile: Pertaining to an infant or to infancy. [EU] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]
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Infiltration: The diffusion or accumulation in a tissue or cells of substances not normal to it or in amounts of the normal. Also, the material so accumulated. [EU] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Inflammatory bowel disease: A general term that refers to the inflammation of the colon and rectum. Inflammatory bowel disease includes ulcerative colitis and Crohn's disease. [NIH]
Influenza: An acute viral infection involving the respiratory tract. It is marked by inflammation of the nasal mucosa, the pharynx, and conjunctiva, and by headache and severe, often generalized, myalgia. [NIH] Ingestion: Taking into the body by mouth [NIH] Inhalation: The drawing of air or other substances into the lungs. [EU] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Inner ear: The labyrinth, comprising the vestibule, cochlea, and semicircular canals. [NIH] Innervation: 1. The distribution or supply of nerves to a part. 2. The supply of nervous energy or of nerve stimulus sent to a part. [EU] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Integrins: A family of transmembrane glycoproteins consisting of noncovalent heterodimers. They interact with a wide variety of ligands including extracellular matrix glycoproteins, complement, and other cells, while their intracellular domains interact with the cytoskeleton. The integrins consist of at least three identified families: the cytoadhesin receptors, the leukocyte adhesion receptors, and the very-late-antigen receptors. Each family contains a common beta-subunit combined with one or more distinct alpha-subunits. These receptors participate in cell-matrix and cell-cell adhesion in many physiologically important processes, including embryological development, hemostasis, thrombosis, wound healing, immune and nonimmune defense mechanisms, and oncogenic transformation. [NIH] 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]
Interferon: A biological response modifier (a substance that can improve the body's natural response to disease). Interferons interfere with the division of cancer cells and can slow tumor growth. There are several types of interferons, including interferon-alpha, -beta, and gamma. These substances are normally produced by the body. They are also made in the laboratory for use in treating cancer and other diseases. [NIH] Interferon-alpha: One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells when exposed to live or inactivated virus, double-stranded RNA, or bacterial products. It is the major interferon produced by virus-induced leukocyte cultures and, in addition to its pronounced antiviral activity, it causes activation of NK cells. [NIH] Interleukin-1: A soluble factor produced by monocytes, macrophages, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. IL-1 consists of two distinct forms, IL-1 alpha and IL-1 beta which perform the same functions but are distinct proteins. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. The factor is distinct from interleukin-2. [NIH]
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Interleukin-2: Chemical mediator produced by activated T lymphocytes and which regulates the proliferation of T cells, as well as playing a role in the regulation of NK cell activity. [NIH] Interleukin-8: A cytokine that activates neutrophils and attracts neutrophils and Tlymphocytes. It is released by several cell types including monocytes, macrophages, Tlymphocytes, fibroblasts, endothelial cells, and keratinocytes by an inflammatory stimulus. IL-8 is a member of the beta-thromboglobulin superfamily and structurally related to platelet factor 4. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intestinal: Having to do with the intestines. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intracellular: Inside a cell. [NIH] Intraocular: Within the eye. [EU] Intraperitoneal: IP. Within the peritoneal cavity (the area that contains the abdominal organs). [NIH] Intravascular: Within a vessel or vessels. [EU] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Involuntary: Reaction occurring without intention or volition. [NIH] Ionizing: Radiation comprising charged particles, e. g. electrons, protons, alpha-particles, etc., having sufficient kinetic energy to produce ionization by collision. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Jejunum: That portion of the small intestine which extends from the duodenum to the ileum; called also intestinum jejunum. [EU] Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [NIH] Kallidin: A decapeptide bradykinin homolog produced by the action of tissue and glandular kallikreins on low-molecular-weight kininogen. It is a smooth-muscle stimulant and hypotensive agent that functions through vasodilatation. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Keratin: A class of fibrous proteins or scleroproteins important both as structural proteins and as keys to the study of protein conformation. The family represents the principal constituent of epidermis, hair, nails, horny tissues, and the organic matrix of tooth enamel. Two major conformational groups have been characterized, alpha-keratin, whose peptide backbone forms an alpha-helix, and beta-keratin, whose backbone forms a zigzag or pleated
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sheet structure. [NIH] Keratinocytes: Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell. [NIH] Keratitis: Inflammation of the cornea. [NIH] Kidney Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Killer Cells: Lymphocyte-like effector cells which mediate antibody-dependent cell cytotoxicity. They kill antibody-coated target cells which they bind with their Fc receptors. [NIH]
Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Lacrimal: Pertaining to the tears. [EU] Laminin: Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement membrane. Evidence suggests that the protein plays a role in tumor invasion. [NIH] Laparotomy: A surgical incision made in the wall of the abdomen. [NIH] Latency: The period of apparent inactivity between the time when a stimulus is presented and the moment a response occurs. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Left ventricular assist device: A mechanical device used to increase the heart's pumping ability. [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] Leiomyoma: A benign tumor derived from smooth muscle tissue, also known as a fibroid tumor. They rarely occur outside of the uterus and the gastrointestinal tract but can occur in the skin and subcutaneous tissues, probably arising from the smooth muscle of small blood vessels in these tissues. [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]
Leukemia: Cancer of blood-forming tissue. [NIH] Leukocyte Count: A count of the number of white blood cells per unit volume in venous blood. A differential leukocyte count measures the relative numbers of the different types of white cells. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Leukotrienes: A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and
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inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system. [NIH] Library Services: Services offered to the library user. They include reference and circulation. [NIH]
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] Ligament: A band of fibrous tissue that connects bones or cartilages, serving to support and strengthen joints. [EU] Ligands: A RNA simulation method developed by the MIT. [NIH] Ligation: Application of a ligature to tie a vessel or strangulate a part. [NIH] 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] 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] Litter: Appliance consisting of an oblong frame over which is stretched a canvas or other material, used for carrying an injured or disabled person. [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 scan: An image of the liver created on a computer screen or on film. A radioactive substance is injected into a blood vessel and travels through the bloodstream. It collects in the liver, especially in abnormal areas, and can be detected by the scanner. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Longitudinal Studies: Studies in which variables relating to an individual or group of individuals are assessed over a period of time. [NIH] Loop: A wire usually of platinum bent at one end into a small loop (usually 4 mm inside diameter) and used in transferring microorganisms. [NIH] Lucida: An instrument, invented by Wollaton, consisting essentially of a prism or a mirror through which an object can be viewed so as to appear on a plane surface seen in direct view and on which the outline of the object may be traced. [NIH] Lumen: The cavity or channel within a tube or tubular organ. [EU] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [NIH] Lupus Nephritis: Glomerulonephritis associated with systemic lupus erythematosus. It is classified into four histologic types: mesangial, focal, diffuse, and membranous. [NIH] Lyme Disease: An infectious disease caused by a spirochete, Borrelia burgdorferi, which is transmitted chiefly by Ixodes dammini and pacificus ticks in the United States and Ixodes
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ricinis in Europe. It is a disease with early and late cutaneous manifestations plus involvement of the nervous system, heart, eye, and joints in variable combinations. The disease was formerly known as Lyme arthritis and first discovered at Old Lyme, Connecticut. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH] Lymph node: A rounded mass of lymphatic tissue that is surrounded by a capsule of connective tissue. Also known as a lymph gland. Lymph nodes are spread out along lymphatic vessels and contain many lymphocytes, which filter the lymphatic fluid (lymph). [NIH]
Lymphadenopathy: Disease or swelling of the lymph nodes. [NIH] Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphocyte: A white blood cell. Lymphocytes have a number of roles in the immune system, including the production of antibodies and other substances that fight infection and diseases. [NIH] Lymphocytic: Referring to lymphocytes, a type of white blood cell. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Lymphoproliferative: Disorders characterized by proliferation of lymphoid tissue, general or unspecified. [NIH] Lyssavirus: A genus of the family Rhabdoviridae that includes rabies virus and other rabieslike viruses. [NIH] Lytic: 1. Pertaining to lysis or to a lysin. 2. Producing lysis. [EU] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH] 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] Malabsorption: Impaired intestinal absorption of nutrients. [EU] Malignancy: A cancerous tumor that can invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant tumor: A tumor capable of metastasizing. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]
Mammogram: An x-ray of the breast. [NIH] Matrix metalloproteinase: A member of a group of enzymes that can break down proteins,
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such as collagen, that are normally found in the spaces between cells in tissues (i.e., extracellular matrix proteins). Because these enzymes need zinc or calcium atoms to work properly, they are called metalloproteinases. Matrix metalloproteinases are involved in wound healing, angiogenesis, and tumor cell metastasis. [NIH] Meat: The edible portions of any animal used for food including domestic mammals (the major ones being cattle, swine, and sheep) along with poultry, fish, shellfish, and game. [NIH]
Meatus: A canal running from the internal auditory foramen through the petrous portion of the temporal bone. It gives passage to the facial and auditory nerves together with the auditory branch of the basilar artery and the internal auditory veins. [NIH] Medial: Lying near the midsaggital plane of the body; opposed to lateral. [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU] Medical Records: Recording of pertinent information concerning patient's illness or illnesses. [NIH] Medical Staff: Professional medical personnel who provide care to patients in an organized facility, institution or agency. [NIH] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Melanocytes: Epidermal dendritic pigment cells which control long-term morphological color changes by alteration in their number or in the amount of pigment they produce and store in the pigment containing organelles called melanosomes. Melanophores are larger cells which do not exist in mammals. [NIH] Melanoma: A form of skin cancer that arises in melanocytes, the cells that produce pigment. Melanoma usually begins in a mole. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Meningitis: Inflammation of the meninges. When it affects the dura mater, the disease is termed pachymeningitis; when the arachnoid and pia mater are involved, it is called leptomeningitis, or meningitis proper. [EU] Menopause: Permanent cessation of menstruation. [NIH] 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] Mercaptopurine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH] Mercuric Chloride: Mercury chloride (HgCl2). A highly toxic compound that volatizes slightly at ordinary temperature and appreciably at 100 degrees C. It is corrosive to mucous
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membranes and used as a topical antiseptic and disinfectant. [NIH] Mesenteric: Pertaining to the mesentery : a membranous fold attaching various organs to the body wall. [EU] Mesentery: A layer of the peritoneum which attaches the abdominal viscera to the abdominal wall and conveys their blood vessels and nerves. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH] Metastatic: Having to do with metastasis, which is the spread of cancer from one part of the body to another. [NIH] Methimazole: A thioureylene antithyroid agent that inhibits the formation of thyroid hormones by interfering with the incorporation of iodine into tyrosyl residues of thyroglobulin. This is done by interfering with the oxidation of iodide ion and iodotyrosyl groups through inhibition of the peroxidase enzyme. [NIH] Methotrexate: An antineoplastic antimetabolite with immunosuppressant properties. It is an inhibitor of dihydrofolate reductase and prevents the formation of tetrahydrofolate, necessary for synthesis of thymidylate, an essential component of DNA. [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microcalcifications: Tiny deposits of calcium in the breast that cannot be felt but can be detected on a mammogram. A cluster of these very small specks of calcium may indicate that cancer is present. [NIH] Micromanipulation: The performance of dissections, injections, surgery, etc., by the use of micromanipulators (attachments to a microscope that manipulate tiny instruments). [NIH] Micromanipulators: A high precision instrument used in microinjection or chromosome dissection activities. [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] Micro-organism: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [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] Mitochondrial Swelling: Increase in volume of mitochondria due to an influx of fluid; it
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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] Mobility: Capability of movement, of being moved, or of flowing freely. [EU] Modeling: A treatment procedure whereby the therapist presents the target behavior which the learner is to imitate and make part of his repertoire. [NIH] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] Monocyte: A type of white blood cell. [NIH] Mononuclear: A cell with one nucleus. [NIH] Morphological: Relating to the configuration or the structure of live organs. [NIH] Motility: The ability to move spontaneously. [EU] Mucociliary: Pertaining to or affecting the mucus membrane and hairs (including eyelashes, nose hair, .): mucociliary clearing: the clearance of mucus by ciliary movement ( particularly in the respiratory system). [EU] Mucosa: A mucous membrane, or tunica mucosa. [EU] Mucus: The viscous secretion of mucous membranes. It contains mucin, white blood cells, water, inorganic salts, and exfoliated cells. [NIH] Multiple Myeloma: A malignant tumor of plasma cells usually arising in the bone marrow; characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria, and anemia. [NIH] Muscle Fibers: Large single cells, either cylindrical or prismatic in shape, that form the basic unit of muscle tissue. They consist of a soft contractile substance enclosed in a tubular sheath. [NIH] Muscular Atrophy: Derangement in size and number of muscle fibers occurring with aging, reduction in blood supply, or following immobilization, prolonged weightlessness, malnutrition, and particularly in denervation. [NIH] Muscular Dystrophies: A general term for a group of inherited disorders which are characterized by progressive degeneration of skeletal muscles. [NIH] Musculoskeletal Diseases: Diseases of the muscles and their associated ligaments and other connective tissue and of the bones and cartilage viewed collectively. [NIH] Myalgia: Pain in a muscle or muscles. [EU] Myelitis: Inflammation of the spinal cord. Relatively common etiologies include infections;
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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] Myelodysplasia: Abnormal bone marrow cells that may lead to myelogenous leukemia. [NIH]
Myelofibrosis: A disorder in which the bone marrow is replaced by fibrous tissue. [NIH] Myelogenous: Produced by, or originating in, the bone marrow. [NIH] Myeloid Cells: Cells which include the monocytes and the granulocytes. [NIH] Myeloproliferative Disorders: Disorders in which one or more stimuli cause proliferation of hemopoietically active tissue or of tissue which has embryonic hemopoietic potential. [NIH] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Myocardial Reperfusion: Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing myocardial reperfusion injury. [NIH] Myocardial Reperfusion Injury: Functional, metabolic, or structural changes in ischemic heart muscle thought to result from reperfusion to the ischemic areas. Changes can be fatal to muscle cells and may include edema with explosive cell swelling and disintegration, sarcolemma disruption, fragmentation of mitochondria, contraction band necrosis, enzyme washout, and calcium overload. Other damage may include hemorrhage and ventricular arrhythmias. One possible mechanism of damage is thought to be oxygen free radicals. Treatment currently includes the introduction of scavengers of oxygen free radicals, and injury is thought to be prevented by warm blood cardioplegic infusion prior to reperfusion. [NIH]
Myocarditis: Inflammation of the myocardium; inflammation of the muscular walls of the heart. [EU] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myopathy: Any disease of a muscle. [EU] Myositis: Inflammation of a voluntary muscle. [EU] Myotonic Dystrophy: A condition presenting muscle weakness and wasting which may be progressive. [NIH] Nasal Cavity: The proximal portion of the respiratory passages on either side of the nasal septum, lined with ciliated mucosa, extending from the nares to the pharynx. [NIH] Nasal Mucosa: The mucous membrane lining the nasal cavity. [NIH] Natural killer cells: NK cells. A type of white blood cell that contains granules with enzymes that can kill tumor cells or microbial cells. Also called large granular lymphocytes (LGL). [NIH] 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]
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Necrotizing Enterocolitis: A condition in which part of the tissue in the intestines is destroyed. Occurs mainly in under-weight newborn babies. A temporary ileostomy may be necessary. [NIH] Need: A state of tension or dissatisfaction felt by an individual that impels him to action toward a goal he believes will satisfy the impulse. [NIH] Neoplasia: Abnormal and uncontrolled cell growth. [NIH] Neoplasm: A new growth of benign or malignant tissue. [NIH] Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] Nephritis: Inflammation of the kidney; a focal or diffuse proliferative or destructive process which may involve the glomerulus, tubule, or interstitial renal tissue. [EU] Nephrologist: A doctor who treats patients with kidney problems or hypertension. [NIH] Nephron: A tiny part of the kidneys. Each kidney is made up of about 1 million nephrons, which are the working units of the kidneys, removing wastes and extra fluids from the blood. [NIH] Nephropathy: Disease of the kidneys. [EU] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Networks: Pertaining to a nerve or to the nerves, a meshlike structure of interlocking fibers or strands. [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] Neuritis: A general term indicating inflammation of a peripheral or cranial nerve. Clinical manifestation may include pain; paresthesias; paresis; or hypesthesia. [NIH] Neuroglia: The non-neuronal cells of the nervous system. They are divided into macroglia (astrocytes, oligodendroglia, and schwann cells) and microglia. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the blood-brain and blood-retina barriers, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear. [NIH] Neurologic: Having to do with nerves or the nervous system. [NIH] Neurologic Manifestations: Clinical signs and symptoms caused by nervous system injury or dysfunction. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU] Neuromuscular Junction: The synapse between a neuron and a muscle. [NIH] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] 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]
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Neuropsychology: A branch of psychology which investigates the correlation between experience or behavior and the basic neurophysiological processes. The term neuropsychology stresses the dominant role of the nervous system. It is a more narrowly defined field than physiological psychology or psychophysiology. [NIH] Neuroretinitis: Inflammation of the optic nerve head and adjacent retina. [NIH] Neurotransmitters: Endogenous signaling molecules that alter the behavior of neurons or effector cells. Neurotransmitter is used here in its most general sense, including not only messengers that act directly to regulate ion channels, but also those that act through second messenger systems, and those that act at a distance from their site of release. Included are neuromodulators, neuroregulators, neuromediators, and neurohumors, whether or not acting at synapses. [NIH] Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH] Neutropenia: An abnormal decrease in the number of neutrophils, a type of white blood cell. [NIH] Neutrophil: A type of white blood cell. [NIH] Neutrophil Activation: The process in which the neutrophil is stimulated by diverse substances, resulting in degranulation and/or generation of reactive oxygen products, and culminating in the destruction of invading pathogens. The stimulatory substances, including opsonized particles, immune complexes, and chemotactic factors, bind to specific cellsurface receptors on the neutrophil. [NIH] Nicotine: Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke. [NIH] Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful antianginal agent that also lowers blood pressure. The use of nifedipine as a tocolytic is being investigated. [NIH] Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells. It is synthesized from arginine by a complex reaction, catalyzed by nitric oxide synthase. Nitric oxide is endothelium-derived relaxing factor. It is released by the vascular endothelium and mediates the relaxation induced by some vasodilators such as acetylcholine and bradykinin. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic guanylate cyclase and thus elevates intracellular levels of cyclic GMP. [NIH]
Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] 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] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by
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polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleic Acid Hybridization: The process whereby two single-stranded polynucleotides form a double-stranded molecule, with hydrogen bonding between the complementary bases in the two strains. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Occult: Obscure; concealed from observation, difficult to understand. [EU] Ocular: 1. Of, pertaining to, or affecting the eye. 2. Eyepiece. [EU] Odds Ratio: The ratio of two odds. The exposure-odds ratio for case control data is the ratio of the odds in favor of exposure among cases to the odds in favor of exposure among noncases. The disease-odds ratio for a cohort or cross section is the ratio of the odds in favor of disease among the exposed to the odds in favor of disease among the unexposed. The prevalence-odds ratio refers to an odds ratio derived cross-sectionally from studies of prevalent cases. [NIH] Oncogene: A gene that normally directs cell growth. If altered, an oncogene can promote or allow the uncontrolled growth of cancer. Alterations can be inherited or caused by an environmental exposure to carcinogens. [NIH] Oncogenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Ophthalmic: Pertaining to the eye. [EU] Ophthalmic Artery: Artery originating from the internal carotid artery and distributing to the eye, orbit and adjacent facial structures. [NIH] Ophthalmoplegia: Paralysis of one or more of the ocular muscles due to disorders of the eye muscles, neuromuscular junction, supporting soft tissue, tendons, or innervation to the muscles. [NIH] Opsin: A protein formed, together with retinene, by the chemical breakdown of metarhodopsin. [NIH] Optic Nerve: The 2nd cranial nerve. The optic nerve conveys visual information from the retina to the brain. The nerve carries the axons of the retinal ganglion cells which sort at the optic chiasm and continue via the optic tracts to the brain. The largest projection is to the lateral geniculate nuclei; other important targets include the superior colliculi and the suprachiasmatic nuclei. Though known as the second cranial nerve, it is considered part of the central nervous system. [NIH] Optic nerve head: The circular area (disc) where the optic nerve connects to the retina. [NIH] Organelles: Specific particles of membrane-bound organized living substances present in eukaryotic cells, such as the mitochondria; the golgi apparatus; endoplasmic reticulum; lysomomes; plastids; and vacuoles. [NIH] Osteoarthritis: A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans. [NIH] Ovaries: The pair of female reproductive glands in which the ova, or eggs, are formed. The ovaries are located in the pelvis, one on each side of the uterus. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH]
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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] Palsies: Disease of the peripheral nervous system occurring usually after many years of increased lead absorption. [NIH] 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 cancer: Cancer of the pancreas, a salivary gland of the abdomen. [NIH] Panniculitis: General term for inflammation of adipose tissue, usually of the skin, characterized by reddened subcutaneous nodules. [NIH] Paralysis: Loss of ability to move all or part of the body. [NIH] Paranasal Sinuses: Air-filled extensions of the respiratory part of the nasal cavity into the frontal, ethmoid, sphenoid, and maxillary cranial bones. They vary in size and form in different individuals and are lined by the ciliated mucous membranes of the nasal cavity. [NIH]
Parenchyma: The essential elements of an organ; used in anatomical nomenclature as a general term to designate the functional elements of an organ, as distinguished from its framework, or stroma. [EU] Paresis: A general term referring to a mild to moderate degree of muscular weakness, occasionally used as a synonym for paralysis (severe or complete loss of motor function). In the older literature, paresis often referred specifically to paretic neurosyphilis. "General paresis" and "general paralysis" may still carry that connotation. Bilateral lower extremity paresis is referred to as paraparesis. [NIH] Paresthesias: Abnormal touch sensations, such as burning or prickling, that occur without an outside stimulus. [NIH] Paroxysmal: Recurring in paroxysms (= spasms or seizures). [EU] Partial remission: The shrinking, but not complete disappearance, of a tumor in response to therapy. Also called partial response. [NIH] Particle: A tiny mass of material. [EU] Patch: A piece of material used to cover or protect a wound, an injured part, etc.: a patch over the eye. [NIH] Pathogen: Any disease-producing microorganism. [EU] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]
Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of
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tissues and organs. [NIH] Pathologies: The study of abnormality, especially the study of diseases. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Advocacy: Promotion and protection of the rights of patients, frequently through a legal process. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]
Pelvic: Pertaining to the pelvis. [EU] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Perforation: 1. The act of boring or piercing through a part. 2. A hole made through a part or substance. [EU] Perfusion: Bathing an organ or tissue with a fluid. In regional perfusion, a specific area of the body (usually an arm or a leg) receives high doses of anticancer drugs through a blood vessel. Such a procedure is performed to treat cancer that has not spread. [NIH] Pericarditis: Inflammation of the pericardium. [EU] Pericardium: The fibroserous sac surrounding the heart and the roots of the great vessels. [NIH]
Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Peripheral Neuropathy: Nerve damage, usually affecting the feet and legs; causing pain, numbness, or a tingling feeling. Also called "somatic neuropathy" or "distal sensory polyneuropathy." [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] Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] Peritonitis: Inflammation of the peritoneum; a condition marked by exudations in the peritoneum of serum, fibrin, cells, and pus. It is attended by abdominal pain and tenderness, constipation, vomiting, and moderate fever. [EU] Perivascular: Situated around a vessel. [EU] Peroxide: Chemical compound which contains an atom group with two oxygen atoms tied to each other. [NIH] Petechiae: Pinpoint, unraised, round red spots under the skin caused by bleeding. [NIH] Phagocytosis: The engulfing of microorganisms, other cells, and foreign particles by phagocytic cells. [NIH]
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Pharmacokinetics: Dynamic and kinetic mechanisms of exogenous chemical and drug absorption, biotransformation, distribution, release, transport, uptake, and elimination as a function of dosage, and extent and rate of metabolic processes. It includes toxicokinetics, the pharmacokinetic mechanism of the toxic effects of a substance. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Pharynx: The hollow tube about 5 inches long that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes to the stomach). [NIH] 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] Phosphodiesterase: Effector enzyme that regulates the levels of a second messenger, the cyclic GMP. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [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] Physical Examination: Systematic and thorough inspection of the patient for physical signs of disease or abnormality. [NIH] Physical Fitness: A state of well-being in which performance is optimal, often as a result of physical conditioning which may be prescribed for disease therapy. [NIH] Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]
Pigment: A substance that gives color to tissue. Pigments are responsible for the color of skin, eyes, and hair. [NIH] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] 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
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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] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelet Factor 4: A high-molecular-weight proteoglycan-platelet factor complex which is released from blood platelets by thrombin. It acts as a mediator in the heparin-neutralizing capacity of the blood and plays a role in platelet aggregation. At high ionic strength (I=0.75), the complex dissociates into the active component (molecular weight 29,000) and the proteoglycan carrier (chondroitin 4-sulfate, molecular weight 350,000). The molecule exists in the form of a dimer consisting of 8 moles of platelet factor 4 and 2 moles of proteoglycan. [NIH]
Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Pleomorphic: Occurring in various distinct forms. In terms of cells, having variation in the size and shape of cells or their nuclei. [NIH] Pneumonitis: A disease caused by inhaling a wide variety of substances such as dusts and molds. Also called "farmer's disease". [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Polyarteritis Nodosa: A form of necrotizing vasculitis involving small- and medium-sized arteries. The signs and symptoms result from infarction and scarring of the affected organ system. [NIH] Polycystic: An inherited disorder characterized by many grape-like clusters of fluid-filled cysts that make both kidneys larger over time. These cysts take over and destroy working kidney tissue. PKD may cause chronic renal failure and end-stage renal disease. [NIH] 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] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH] Polymyalgia Rheumatica: A syndrome in the elderly characterized by proximal joint and muscle pain, high erythrocyte sedimentation rate, and a self-limiting course. Pain is usually
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accompanied by evidence of an inflammatory reaction. Women are affected twice as commonly as men and Caucasians more frequently than other groups. The condition is frequently associated with temporal arteritis and some theories pose the possibility that the two diseases arise from a single etiology or even that they are the same entity. [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] Polyposis: The development of numerous polyps (growths that protrude from a mucous membrane). [NIH] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Port: An implanted device through which blood may be withdrawn and drugs may be infused without repeated needle sticks. Also called a port-a-cath. [NIH] Port-a-cath: An implanted device through which blood may be withdrawn and drugs may be infused without repeated needle sticks. Also called a port. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Potassium: An element that is in the alkali group of metals. It has an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte and it plays a significant role in the regulation of fluid volume and maintenance of the water-electrolyte balance. [NIH] Potentiates: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practicability: A non-standard characteristic of an analytical procedure. It is dependent on the scope of the method and is determined by requirements such as sample throughout and costs. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Predisposition: A latent susceptibility to disease which may be activated under certain conditions, as by stress. [EU] Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [NIH] Prednisone: A synthetic anti-inflammatory glucocorticoid derived from cortisone. It is biologically inert and converted to prednisolone in the liver. [NIH] 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,
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but it may develop before this time in the presence of trophoblastic disease. [NIH] Pre-eclamptic: A syndrome characterized by hypertension, albuminuria, and generalized oedema, occurring only in pregnancy. [NIH] Premenopausal: Refers to the time before menopause. Menopause is the time of life when a women's menstrual periods stop permanently; also called "change of life." [NIH] Presynaptic: Situated proximal to a synapse, or occurring before the synapse is crossed. [EU] Presynaptic Terminals: The distal terminations of axons which are specialized for the release of neurotransmitters. Also included are varicosities along the course of axons which have similar specializations and also release transmitters. Presynaptic terminals in both the central and peripheral nervous systems are included. [NIH] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Prickle: Several layers of the epidermis where the individual cells are connected by cell bridges. [NIH] 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] Procainamide: A derivative of procaine with less CNS action. [NIH] Procaine: A local anesthetic of the ester type that has a slow onset and a short duration of action. It is mainly used for infiltration anesthesia, peripheral nerve block, and spinal block. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1016). [NIH] Prodrug: A substance that gives rise to a pharmacologically active metabolite, although not itself active (i. e. an inactive precursor). [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] 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] Progressive disease: Cancer that is increasing in scope or severity. [NIH] Projection: A defense mechanism, operating unconsciously, whereby that which is emotionally unacceptable in the self is rejected and attributed (projected) to others. [NIH] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Promyelocytic leukemia: A type of acute myeloid leukemia, a quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. [NIH]
Prone: Having the front portion of the body downwards. [NIH] Prophylaxis: An attempt to prevent disease. [NIH]
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Proportional: Being in proportion : corresponding in size, degree, or intensity, having the same or a constant ratio; of, relating to, or used in determining proportions. [EU] Prospective Studies: Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group. [NIH] Prospective study: An epidemiologic study in which a group of individuals (a cohort), all free of a particular disease and varying in their exposure to a possible risk factor, is followed over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] Prostaglandin: Any of a group of components derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway that are extremely potent mediators of a diverse group of physiologic processes. The abbreviation for prostaglandin is PG; specific compounds are designated by adding one of the letters A through I to indicate the type of substituents found on the hydrocarbon skeleton and a subscript (1, 2 or 3) to indicate the number of double bonds in the hydrocarbon skeleton e.g., PGE2. The predominant naturally occurring prostaglandins all have two double bonds and are synthesized from arachidonic acid (5,8,11,14-eicosatetraenoic acid) by the pathway shown in the illustration. The 1 series and 3 series are produced by the same pathway with fatty acids having one fewer double bond (8,11,14-eicosatrienoic acid or one more double bond (5,8,11,14,17-eicosapentaenoic acid) than arachidonic acid. The subscript a or ß indicates the configuration at C-9 (a denotes a substituent below the plane of the ring, ß, above the plane). The naturally occurring PGF's have the a configuration, e.g., PGF2a. All of the prostaglandins act by binding to specific cell-surface receptors causing an increase in the level of the intracellular second messenger cyclic AMP (and in some cases cyclic GMP also). The effect produced by the cyclic AMP increase depends on the specific cell type. In some cases there is also a positive feedback effect. Increased cyclic AMP increases prostaglandin synthesis leading to further increases in cyclic AMP. [EU] Prostaglandins A: (13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE. PGA(1) and PGA(2) as well as their 19hydroxy derivatives are found in many organs and tissues. [NIH] Prostaglandins B: Physiologically active prostaglandins found in many tissues and organs. They are potent pressor substances and have many other physiological activities. [NIH] Prostaglandins F: (9 alpha,11 alpha,13E,15S)-9,11,15-Trihydroxyprost-13-en-1-oic acid (PGF(1 alpha)); (5Z,9 alpha,11,alpha,13E,15S)-9,11,15-trihydroxyprosta-5,13-dien-1-oic acid (PGF(2 alpha)); (5Z,9 alpha,11 alpha,13E,15S,17Z)-9,11,15-trihydroxyprosta-5,13,17-trien-1oic acid (PGF(3 alpha)). A family of prostaglandins that includes three of the six naturally occurring prostaglandins. All naturally occurring PGF have an alpha configuration at the 9carbon position. They stimulate uterine and bronchial smooth muscle and are often used as oxytocics. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] 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
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and VIIIa at the rate-limiting steps of thrombin formation. [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] Proteoglycan: A molecule that contains both protein and glycosaminoglycans, which are a type of polysaccharide. Proteoglycans are found in cartilage and other connective tissues. [NIH]
Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] 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] Protozoa: A subkingdom consisting of unicellular organisms that are the simplest in the animal kingdom. Most are free living. They range in size from submicroscopic to macroscopic. Protozoa are divided into seven phyla: Sarcomastigophora, Labyrinthomorpha, Apicomplexa, Microspora, Ascetospora, Myxozoa, and Ciliophora. [NIH] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychology: The science dealing with the study of mental processes and behavior in man and animals. [NIH] Psychophysiology: The study of the physiological basis of human and animal behavior. [NIH]
Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]
Pulmonary: Relating to the lungs. [NIH] Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs. [NIH] 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.
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[NIH]
Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include adenine and guanine, constituents of nucleic acids, as well as many alkaloids such as caffeine and theophylline. Uric acid is the metabolic end product of purine metabolism. [NIH] Purpura: Purplish or brownish red discoloration, easily visible through the epidermis, caused by hemorrhage into the tissues. [NIH] Putrefaction: The process of decomposition of animal and vegetable matter by living organisms. [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] Rabies: A highly fatal viral infection of the nervous system which affects all warm-blooded animal species. It is one of the most important of the zoonoses because of the inevitably fatal outcome for the infected human. [NIH] Rabies Virus: The type species of lyssavirus causing rabies in humans and other animals. Transmission is mostly by animal bites through saliva. The virus is neurotropic multiplying in neurons and myotubes of vertebrates. [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] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radioactive: Giving off radiation. [NIH] 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] Ramipril: A long-acting angiotensin-converting enzyme inhibitor. It is a prodrug that is transformed in the liver to its active metabolite ramiprilat. [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] Reactivation: The restoration of activity to something that has been inactivated. [EU] Reactive Oxygen Species: Reactive intermediate oxygen species including both radicals and non-radicals. These substances are constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been implicated in a number of diseases. Scientific data exist that link the reactive oxygen species produced by inflammatory phagocytes to cancer development. [NIH]
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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] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Red Nucleus: A pinkish-yellow portion of the midbrain situated in the rostral mesencephalic tegmentum. It receives a large projection from the contralateral half of the cerebellum via the superior cerebellar peduncle and a projection from the ipsilateral motor cortex. [NIH] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Reflux: The term used when liquid backs up into the esophagus from the stomach. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Refractory: Not readily yielding to treatment. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Regurgitation: A backward flowing, as the casting up of undigested food, or the backward flowing of blood into the heart, or between the chambers of the heart when a valve is incompetent. [EU] Relapse: The return of signs and symptoms of cancer after a period of improvement. [NIH] Remission: A decrease in or disappearance of signs and symptoms of cancer. In partial remission, some, but not all, signs and symptoms of cancer have disappeared. In complete remission, all signs and symptoms of cancer have disappeared, although there still may be cancer in the body. [NIH] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [NIH] Renal tubular: A defect in the kidneys that hinders their normal excretion of acids. Failure to excrete acids can lead to weak bones, kidney stones, and poor growth in children. [NIH] Renin: An enzyme which is secreted by the kidney and is formed from prorenin in plasma and kidney. The enzyme cleaves the Leu-Leu bond in angiotensinogen to generate angiotensin I. EC 3.4.23.15. (Formerly EC 3.4.99.19). [NIH] Renin-Angiotensin System: A system consisting of renin, angiotensin-converting enzyme, and angiotensin II. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming angiotensin I. The converting enzyme contained in the lung acts on angiotensin I in the plasma converting it to angiotensin II, the most powerful directly pressor substance known. It causes contraction of the arteriolar smooth muscle and has other indirect actions mediated through the adrenal cortex. [NIH] Reperfusion: Restoration of blood supply to tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. It is primarily a procedure for treating infarction or other ischemia, by enabling viable ischemic tissue to recover, thus limiting further necrosis. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing reperfusion injury. [NIH]
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Reperfusion Injury: Functional, metabolic, or structural changes, including necrosis, in ischemic tissues thought to result from reperfusion to ischemic areas of the tissue. The most common instance is myocardial reperfusion injury. [NIH] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Respiratory distress syndrome: A lung disease that occurs primarily in premature infants; the newborn must struggle for each breath and blueing of its skin reflects the baby's inability to get enough oxygen. [NIH] Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH] 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] Retinal Artery Occlusion: Occlusion or closure of the central retinal artery causing sudden, usually nearly complete, loss of vision in one eye. Occlusion of the branch retinal artery causes sudden visual loss in only a portion of the visual field. [NIH] Retinal Detachment: Separation of the inner layers of the retina (neural retina) from the pigment epithelium. Retinal detachment occurs more commonly in men than in women, in eyes with degenerative myopia, in aging and in aphakia. It may occur after an uncomplicated cataract extraction, but it is seen more often if vitreous humor has been lost during surgery. (Dorland, 27th ed; Newell, Ophthalmology: Principles and Concepts, 7th ed, p310-12). [NIH] Retinal Neovascularization: Formation of new blood vessels originating from the retinal veins and extending along the inner (vitreal) surface of the retina. [NIH] Retinal Vein: Central retinal vein and its tributaries. It runs a short course within the optic nerve and then leaves and empties into the superior ophthalmic vein or cavernous sinus. [NIH]
Retinoblastoma: An eye cancer that most often occurs in children younger than 5 years. It occurs in hereditary and nonhereditary (sporadic) forms. [NIH] Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous membranes. Retinol is being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Retroperitoneal: Having to do with the area outside or behind the peritoneum (the tissue
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that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Retroperitoneal Fibrosis: A slowly progressive condition of unknown etiology, characterized by deposition of fibrous tissue in the retroperitoneal space compressing the ureters, great vessels, bile duct, and other structures. When associated with abdominal aortic aneurysm, it may be called chronic periaortitis or inflammatory perianeurysmal fibrosis. [NIH]
Retroperitoneal Space: An area occupying the most posterior aspect of the abdominal cavity. It is bounded laterally by the borders of the quadratus lumborum muscles and extends from the diaphragm to the brim of the true pelvis, where it continues as the pelvic extraperitoneal space. [NIH] Retrospective: Looking back at events that have already taken place. [NIH] Retrospective study: A study that looks backward in time, usually using medical records and interviews with patients who already have or had a disease. [NIH] Rheumatic Diseases: Disorders of connective tissue, especially the joints and related structures, characterized by inflammation, degeneration, or metabolic derangement. [NIH] Rheumatism: A group of disorders marked by inflammation or pain in the connective tissue structures of the body. These structures include bone, cartilage, and fat. [NIH] Rheumatoid: Resembling rheumatism. [EU] Rheumatoid arthritis: A form of arthritis, the cause of which is unknown, although infection, hypersensitivity, hormone imbalance and psychologic stress have been suggested as possible causes. [NIH] Rhinitis: Inflammation of the mucous membrane of the nose. [NIH] Rhusiopathiae: Causal agent of the anthropozoonosis called erysipeloid. [NIH] Ribavirin: 1-beta-D-Ribofuranosyl-1H-1,2,4-triazole-3-carboxamide. A nucleoside antimetabolite antiviral agent that blocks nucleic acid synthesis and is used against both RNA and DNA viruses. [NIH] Ribose: A pentose active in biological systems usually in its D-form. [NIH] Ribosome: A granule of protein and RNA, synthesized in the nucleolus and found in the cytoplasm of cells. Ribosomes are the main sites of protein synthesis. Messenger RNA attaches to them and there receives molecules of transfer RNA bearing amino acids. [NIH] Rickettsiae: One of a group of obligate intracellular parasitic microorganisms, once regarded as intermediate in their properties between bacteria and viruses but now classified as bacteria in the order Rickettsiales, which includes 17 genera and 3 families: Rickettsiace. [NIH]
Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Ristocetin: An antibiotic mixture of two components, A and B, obtained from Nocardia lurida (or the same substance produced by any other means). It is no longer used clinically because of its toxicity. It causes platelet agglutination and blood coagulation and is used to assay those functions in vitro. [NIH] Rituximab: A type of monoclonal antibody used in cancer detection or therapy. Monoclonal antibodies are laboratory-produced substances that can locate and bind to cancer cells. [NIH] Rod: A reception for vision, located in the retina. [NIH] Rural Population: The inhabitants of rural areas or of small towns classified as rural. [NIH] Sagittal: The line of direction passing through the body from back to front, or any vertical plane parallel to the medial plane of the body and inclusive of that plane; often restricted to
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the medial plane, the plane of the sagittal suture. [NIH] Saline: A solution of salt and water. [NIH] Saliva: The clear, viscous fluid secreted by the salivary glands and mucous glands of the mouth. It contains mucins, water, organic salts, and ptylin. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] Sarcoid: A cutaneus lesion occurring as a manifestation of sarcoidosis. [NIH] Sarcoidosis: An idiopathic systemic inflammatory granulomatous disorder comprised of epithelioid and multinucleated giant cells with little necrosis. It usually invades the lungs with fibrosis and may also involve lymph nodes, skin, liver, spleen, eyes, phalangeal bones, and parotid glands. [NIH] Sarcoma: A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant. [NIH] Scans: Pictures of structures inside the body. Scans often used in diagnosing, staging, and monitoring disease include liver scans, bone scans, and computed tomography (CT) or computerized axial tomography (CAT) scans and magnetic resonance imaging (MRI) scans. In liver scanning and bone scanning, radioactive substances that are injected into the bloodstream collect in these organs. A scanner that detects the radiation is used to create pictures. In CT scanning, an x-ray machine linked to a computer is used to produce detailed pictures of organs inside the body. MRI scans use a large magnet connected to a computer to create pictures of areas inside the body. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Sclera: The tough white outer coat of the eyeball, covering approximately the posterior fivesixths of its surface, and continuous anteriorly with the cornea and posteriorly with the external sheath of the optic nerve. [EU] Scleritis: Refers to any inflammation of the sclera including episcleritis, a benign condition affecting only the episclera, which is generally short-lived and easily treated. Classic scleritis, on the other hand, affects deeper tissue and is characterized by higher rates of visual acuity loss and even mortality, particularly in necrotizing form. Its characteristic symptom is severe and general head pain. Scleritis has also been associated with systemic collagen disease. Etiology is unknown but is thought to involve a local immune response. Treatment is difficult and includes administration of anti-inflammatory and immunosuppressive agents such as corticosteroids. Inflammation of the sclera may also be secondary to inflammation of adjacent tissues, such as the conjunctiva. [NIH] 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] Screening: Checking for disease when there are no symptoms. [NIH]
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Secondary tumor: Cancer that has spread from the organ in which it first appeared to another organ. For example, breast cancer cells may spread (metastasize) to the lungs and cause the growth of a new tumor. When this happens, the disease is called metastatic breast cancer, and the tumor in the lungs is called a secondary tumor. Also called secondary cancer. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Segmentation: The process by which muscles in the intestines move food and wastes through the body. [NIH] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Semen: The thick, yellowish-white, viscid fluid secretion of male reproductive organs discharged upon ejaculation. In addition to reproductive organ secretions, it contains spermatozoa and their nutrient plasma. [NIH] Sensibility: The ability to receive, feel and appreciate sensations and impressions; the quality of being sensitive; the extend to which a method gives results that are free from false negatives. [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] Septicemia: Systemic disease associated with the presence and persistence of pathogenic microorganisms or their toxins in the blood. Called also blood poisoning. [EU] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [NIH] Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines, and other amino acids. [NIH] Serologic: Analysis of a person's serum, especially specific immune or lytic serums. [NIH] Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-tryptophan. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (receptors, serotonin) explain the broad physiological actions and distribution of this biochemical mediator. [NIH] Serous: Having to do with serum, the clear liquid part of blood. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Serum Sickness: Immune complex disease caused by the administration of foreign serum or serum proteins and characterized by fever, lymphadenopathy, arthralgia, and urticaria. When they are complexed to protein carriers, some drugs can also cause serum sickness when they act as haptens inducing antibody responses. [NIH] Sex Determination: The biological characteristics which distinguish human beings as female or male. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral
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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] Sinusitis: An inflammatory process of the mucous membranes of the paranasal sinuses that occurs in three stages: acute, subacute, and chronic. Sinusitis results from any condition causing ostial obstruction or from pathophysiologic changes in the mucociliary transport mechanism. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skin Manifestations: Dermatologic disorders attendant upon non-dermatologic disease or injury. [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]
Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Social Support: Support systems that provide assistance and encouragement to individuals with physical or emotional disabilities in order that they may better cope. Informal social support is usually provided by friends, relatives, or peers, while formal assistance is provided by churches, groups, etc. [NIH] Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation,
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maintenance of fluid volume, and electrolyte balance. [NIH] Solid tumor: Cancer of body tissues other than blood, bone marrow, or the lymphatic system. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] Soma: The body as distinct from the mind; all the body tissue except the germ cells; all the axial body. [NIH] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Somatic cells: All the body cells except the reproductive (germ) cells. [NIH] Somatic mutations: Alterations in DNA that occur after conception. Somatic mutations can occur in any of the cells of the body except the germ cells (sperm and egg) and therefore are not passed on to children. These alterations can (but do not always) cause cancer or other diseases. [NIH] Sound wave: An alteration of properties of an elastic medium, such as pressure, particle displacement, or density, that propagates through the medium, or a superposition of such alterations. [NIH] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Species Specificity: Restriction of a characteristic or response to the members of one species; it usually refers to that property of the immune response which differentiates one species from another on the basis of antigen recognition, but the concept is not limited to immunology and is used loosely at levels higher than the species. [NIH] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Sperm: The fecundating fluid of the male. [NIH] Sphenoid: An unpaired cranial bone with a body containing the sphenoid sinus and forming the posterior part of the medial walls of the orbits. [NIH] Sphenoid Sinus: One of the paired paranasal sinuses, located in the body of the sphenoid bone and communicating with the highest meatus of the nasal cavity on the same side. [NIH] Sphenoid Sinusitis: Inflammation of the sphenoid sinus. This condition usually is accompanied by pansinusitis and may present itself in an acute or chronic form. [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]
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Spinal Nerves: The 31 paired peripheral nerves formed by the union of the dorsal and ventral spinal roots from each spinal cord segment. The spinal nerve plexuses and the spinal roots are also included. [NIH] Spinous: Like a spine or thorn in shape; having spines. [NIH] Spirochete: Lyme disease. [NIH] Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Spondylitis: Inflammation of the vertebrae. [EU] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Sports Medicine: The field of medicine concerned with physical fitness and the diagnosis and treatment of injuries sustained in sports activities. [NIH] Staging: Performing exams and tests to learn the extent of the cancer within the body, especially whether the disease has spread from the original site to other parts of the body. [NIH]
Stasis: A word termination indicating the maintenance of (or maintaining) a constant level; preventing increase or multiplication. [EU] Steel: A tough, malleable, iron-based alloy containing up to, but no more than, two percent carbon and often other metals. It is used in medicine and dentistry in implants and instrumentation. [NIH] Sterile: Unable to produce children. [NIH] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Stroma: The middle, thickest layer of tissue in the cornea. [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
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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] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]
Substrate: A substance upon which an enzyme acts. [EU] Sulbactam: A beta-lactamase inhibitor with very weak antibacterial action. The compound prevents antibiotic destruction of beta-lactam antibiotics by inhibiting beta-lactamases, thus extending their spectrum activity. Combinations of sulbactam with beta-lactam antibiotics have been used successfully for the therapy of infections caused by organisms resistant to the antibiotic alone. [NIH] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Suppurative: Consisting of, containing, associated with, or identified by the formation of pus. [NIH] Sweat: The fluid excreted by the sweat glands. It consists of water containing sodium chloride, phosphate, urea, ammonia, and other waste products. [NIH] Symphysis: A secondary cartilaginous joint. [NIH] Symptomatology: 1. That branch of medicine with treats of symptoms; the systematic discussion of symptoms. 2. The combined symptoms of a disease. [EU] Synapse: The region where the processes of two neurons come into close contiguity, and the nervous impulse passes from one to the other; the fibers of the two are intermeshed, but, according to the general view, there is no direct contiguity. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Synaptic Transmission: The communication from a neuron to a target (neuron, muscle, or secretory cell) across a synapse. In chemical synaptic transmission, the presynaptic neuron releases a neurotransmitter that diffuses across the synaptic cleft and binds to specific synaptic receptors. These activated receptors modulate ion channels and/or secondmessenger systems to influence the postsynaptic cell. Electrical transmission is less common in the nervous system, and, as in other tissues, is mediated by gap junctions. [NIH] Syncytium: A living nucleated tissue without apparent cellular structure; a tissue composed of a mass of nucleated protoplasm without cell boundaries. [NIH] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Synovial: Of pertaining to, or secreting synovia. [EU] Synovial Fluid: The clear, viscous fluid secreted by the synovial membrane. It contains mucin, albumin, fat, and mineral salts and serves to lubricate joints. [NIH]
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Synovial Membrane: The inner membrane of a joint capsule surrounding a freely movable joint. It is loosely attached to the external fibrous capsule and secretes synovial fluid. [NIH] Synovitis: Inflammation of a synovial membrane. It is usually painful, particularly on motion, and is characterized by a fluctuating swelling due to effusion within a synovial sac. Synovitis is qualified as fibrinous, gonorrhoeal, hyperplastic, lipomatous, metritic, puerperal, rheumatic, scarlatinal, syphilitic, tuberculous, urethral, etc. [EU] Syphilis: A contagious venereal disease caused by the spirochete Treponema pallidum. [NIH]
Systemic: Affecting the entire body. [NIH] Systemic disease: Disease that affects the whole body. [NIH] Systemic lupus erythematosus: SLE. A chronic inflammatory connective tissue disease marked by skin rashes, joint pain and swelling, inflammation of the kidneys, inflammation of the fibrous tissue surrounding the heart (i.e., the pericardium), as well as other problems. Not all affected individuals display all of these problems. May be referred to as lupus. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Teicoplanin: Glycopeptide antibiotic complex from Actinoplanes teichomyceticus active against gram-positive bacteria. It consists of five major components each with a different fatty acid moiety. [NIH] Telangiectasia: The permanent enlargement of blood vessels, causing redness in the skin or mucous membranes. [NIH] Telencephalon: Paired anteriolateral evaginations of the prosencephalon plus the lamina terminalis. The cerebral hemispheres are derived from it. Many authors consider cerebrum a synonymous term to telencephalon, though a minority include diencephalon as part of the cerebrum (Anthoney, 1994). [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] Teratoma: A type of germ cell tumor that may contain several different types of tissue, such as hair, muscle, and bone. Teratomas occur most often in the ovaries in women, the testicles in men, and the tailbone in children. Not all teratomas are malignant. [NIH] Testicles: The two egg-shaped glands found inside the scrotum. They produce sperm and male hormones. Also called testes. [NIH] Testicular: Pertaining to a testis. [EU] Testis: Either of the paired male reproductive glands that produce the male germ cells and the male hormones. [NIH] Thalamic: Cell that reaches the lateral nucleus of amygdala. [NIH] Thalamic Diseases: Disorders of the centrally located thalamus, which integrates a wide range of cortical and subcortical information. Manifestations include sensory loss, movement disorders; ataxia, pain syndromes, visual disorders, a variety of neuropsychological conditions, and coma. Relatively common etiologies include cerebrovascular disorders; craniocerebral trauma; brain neoplasms; brain hypoxia; intracranial hemorrhages; and infectious processes. [NIH] 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] Thorax: A part of the trunk between the neck and the abdomen; the chest. [NIH]
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Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. [NIH] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] Thrombocytes: Blood cells that help prevent bleeding by causing blood clots to form. Also called platelets. [NIH] Thrombocytopenia: A decrease in the number of blood platelets. [NIH] Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thromboxanes: Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase. [NIH] Thrombus: An aggregation of blood factors, primarily platelets and fibrin with entrapment of cellular elements, frequently causing vascular obstruction at the point of its formation. Some authorities thus differentiate thrombus formation from simple coagulation or clot formation. [EU] Thymus: An organ that is part of the lymphatic system, in which T lymphocytes grow and multiply. The thymus is in the chest behind the breastbone. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Thyroid Gland: A highly vascular endocrine gland consisting of two lobes, one on either side of the trachea, joined by a narrow isthmus; it produces the thyroid hormones which are concerned in regulating the metabolic rate of the body. [NIH] Thyroiditis: Inflammation of the thyroid gland. [NIH] Ticks: Blood-sucking arachnids of the order Acarina. [NIH] Ticlopidine: Ticlopidine is an effective inhibitor of platelet aggregation. The drug has been found to significantly reduce infarction size in acute myocardial infarcts and is an effective antithrombotic agent in arteriovenous fistulas, aorto-coronary bypass grafts, ischemic heart disease, venous thrombosis, and arteriosclerosis. [NIH] Tin: A trace element that is required in bone formation. It has the atomic symbol Sn, atomic number 50, and atomic weight 118.71. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] Tone: 1. The normal degree of vigour and tension; in muscle, the resistance to passive elongation or stretch; tonus. 2. A particular quality of sound or of voice. 3. To make permanent, or to change, the colour of silver stain by chemical treatment, usually with a heavy metal. [EU] Tonus: A state of slight tension usually present in muscles even when they are not
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undergoing active contraction. [NIH] Topical: On the surface of the body. [NIH] Torsion: A twisting or rotation of a bodily part or member on its axis. [NIH] 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] Traction: The act of pulling. [NIH] Transcriptase: An enzyme which catalyses the synthesis of a complementary mRNA molecule from a DNA template in the presence of a mixture of the four ribonucleotides (ATP, UTP, GTP and CTP). [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transfer Factor: Factor derived from leukocyte lysates of immune donors which can transfer both local and systemic cellular immunity to nonimmune recipients. [NIH] Transferases: Transferases are enzymes transferring a group, for example, the methyl group or a glycosyl group, from one compound (generally regarded as donor) to another compound (generally regarded as acceptor). The classification is based on the scheme "donor:acceptor group transferase". (Enzyme Nomenclature, 1992) EC 2. [NIH] Transfusion: The infusion of components of blood or whole blood into the bloodstream. The blood may be donated from another person, or it may have been taken from the person earlier and stored until needed. [NIH] Transgenes: Genes that are introduced into an organism using gene transfer techniques. [NIH]
Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH] Transplantation: Transference of a tissue or organ, alive or dead, within an individual,
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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] Treatment Outcome: Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, practicability, etc., of these interventions in individual cases or series. [NIH]
Tremor: Cyclical movement of a body part that can represent either a physiologic process or a manifestation of disease. Intention or action tremor, a common manifestation of cerebellar diseases, is aggravated by movement. In contrast, resting tremor is maximal when there is no attempt at voluntary movement, and occurs as a relatively frequent manifestation of Parkinson disease. [NIH] Tricyclic: Containing three fused rings or closed chains in the molecular structure. [EU] Tropism: Directed movements and orientations found in plants, such as the turning of the sunflower to face the sun. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [NIH] Tuberous Sclerosis: A rare congenital disease in which the essential pathology is the appearance of multiple tumors in the cerebrum and in other organs, such as the heart or kidneys. [NIH] 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] TYPHI: The bacterium that gives rise to typhoid fever. [NIH] Typhoid fever: The most important member of the enteric group of fevers which also includes the paratyphoids. [NIH] Typhoid fever: The most important member of the enteric group of fevers which also includes the paratyphoids. [NIH] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH] Ulcerative colitis: Chronic inflammation of the colon that produces ulcers in its lining. This condition is marked by abdominal pain, cramps, and loose discharges of pus, blood, and mucus from the bowel. [NIH] Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [NIH] Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [NIH] Ureters: Tubes that carry urine from the kidneys to the bladder. [NIH]
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Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]
Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary tract: The organs of the body that produce and discharge urine. These include the kidneys, ureters, bladder, and urethra. [NIH] Urinary tract infection: An illness caused by harmful bacteria growing in the urinary tract. [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] Urticaria: A vascular reaction of the skin characterized by erythema and wheal formation due to localized increase of vascular permeability. The causative mechanism may be allergy, infection, or stress. [NIH] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH] Uvea: The middle coat of the eyeball, consisting of the choroid in the back of the eye and the ciliary body and iris in the front of the eye. [NIH] Uveitis: An inflammation of part or all of the uvea, the middle (vascular) tunic of the eye, and commonly involving the other tunics (the sclera and cornea, and the retina). [EU] Vaccination: Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vacuoles: Any spaces or cavities within a cell. They may function in digestion, storage, secretion, or excretion. [NIH] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vancomycin: Antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to ristocetin that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear. [NIH] Varicose: The common ulcer in the lower third of the leg or near the ankle. [NIH] Vasa Vasorum: Nutrient blood vessels which supply the walls of large arteries or veins. [NIH]
Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasculitis: Inflammation of a blood vessel. [NIH] Vasodilatation: A state of increased calibre of the blood vessels. [EU] Vasodilation: Physiological dilation of the blood vessels without anatomic change. For dilation with anatomic change, dilatation, pathologic or aneurysm (or specific aneurysm) is used. [NIH] Vasodilator: An agent that widens blood vessels. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venereal: Pertaining or related to or transmitted by sexual contact. [EU] Venous: Of or pertaining to the veins. [EU]
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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] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Verapamil: A calcium channel blocker that is a class IV anti-arrhythmia agent. [NIH] Vertebrae: A bony unit of the segmented spinal column. [NIH] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Viscera: Any of the large interior organs in any one of the three great cavities of the body, especially in the abdomen. [NIH] Viscosity: A physical property of fluids that determines the internal resistance to shear forces. [EU] Visual Acuity: Acuteness or clearness of vision, especially of form vision, which is dependent mainly on the sharpness of the retinal focus. [NIH] Visual field: The entire area that can be seen when the eye is forward, including peripheral vision. [NIH] Vitrectomy: Removal of the whole or part of the vitreous body in treating endophthalmitis, diabetic retinopathy, retinal detachment, intraocular foreign bodies, and some types of glaucoma. [NIH] Vitreous Body: The transparent, semigelatinous substance that fills the cavity behind the crystalline lens of the eye and in front of the retina. It is contained in a thin hyoid membrane and forms about four fifths of the optic globe. [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] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]
Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH] Wound Healing: Restoration of integrity to traumatized tissue. [NIH]
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Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] 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] Zoonoses: Diseases of non-human animals that may be transmitted to man or may be transmitted from man to non-human animals. [NIH] Zoster: A virus infection of the Gasserian ganglion and its nerve branches, characterized by discrete areas of vesiculation of the epithelium of the forehead, the nose, the eyelids, and the cornea together with subepithelial infiltration. [NIH]
223
INDEX 6 6-Mercaptopurine, 6, 151 A Abdomen, 24, 151, 160, 187, 188, 189, 198, 199, 209, 214, 216, 221 Abdominal, 28, 57, 65, 118, 151, 187, 189, 192, 198, 199, 209, 219 Abdominal Pain, 57, 118, 151, 199, 219 Aberrant, 3, 10, 17, 151 Abscess, 55, 151 Acetylcholine, 26, 151, 164, 196 Acetylcholinesterase, 26, 151 Acne, 117, 151 Actin, 39, 151 Acute myeloid leukemia, 151, 203 Acute renal, 151, 181 Adaptability, 151, 163 Adenine, 151, 206 Adenocarcinoma, 151, 182 Adenomatous Polyposis Coli, 56, 151 Adenosine, 102, 151, 200 Adenosine Diphosphate, 102, 151 Adenovirus, 151, 169 Adipose Tissue, 152, 198 Adjustment, 25, 36, 111, 152 Adjuvant, 42, 86, 93, 152 Adjuvant Therapy, 42, 152 Adoptive Transfer, 32, 152 Adrenal Cortex, 152, 153, 168, 203, 207 Adrenal Glands, 152, 154 Adrenaline, 102, 152 Adrenergic, 152, 171, 175 Adverse Effect, 32, 36, 105, 152, 212 Afferent, 18, 152, 176 Affinity, 10, 152, 157, 195, 212 Agammaglobulinemia, 105, 152 Agar, 152, 200 Agonist, 152, 171, 196 Airways, 14, 153 Albumin, 153, 200, 206, 215 Aldosterone, 104, 153 Algorithms, 30, 109, 153, 160 Alkaline, 153, 161 Alkaloid, 153, 165, 196 Alkylating Agents, 153, 164 Alleles, 24, 37, 153, 182 Allergen, 153, 170 Allogeneic, 49, 153
Allograft, 12, 30, 100, 153 Alopecia, 153, 169 Alpha Particles, 153, 206 Alpha-1, 68, 153 Alpha-Defensins, 153, 169 Alternative medicine, 93, 98, 116, 153 Alveolitis, 21, 153 Ameliorating, 103, 153 Amino Acid Sequence, 153, 155, 176, 178 Amino Acids, 153, 154, 178, 199, 202, 205, 209, 211, 218 Amphetamines, 154, 165 Amplification, 21, 154 Amyloidosis, 24, 58, 154 Anaesthesia, 94, 154, 185 Analog, 154, 177, 184 Analogous, 154, 172, 218 Anaphylatoxins, 154, 166 Anastomosis, 154, 178 Anatomical, 154, 164, 185, 198, 210 Androgens, 152, 154, 168 Anemia, 4, 133, 154, 193 Anesthesia, 13, 96, 154, 203 Aneurysm, 28, 154, 156, 220 Angiitis, 48, 55, 83, 86, 88, 94, 95, 110, 116, 154 Anginal, 155, 196 Angiogenesis, 32, 35, 90, 155, 191 Angiogenesis inhibitor, 90, 155 Angiogram, 30, 155 Angiography, 4, 86, 118, 136, 137, 155 Animal model, 7, 8, 12, 18, 22, 32, 33, 88, 155 Annealing, 155, 201 Antagonism, 155, 171 Antiallergic, 155, 168 Antibacterial, 155, 213, 215, 220 Antibiotic, 29, 155, 161, 162, 209, 213, 215, 216 Antibody, 4, 7, 10, 11, 19, 30, 35, 37, 40, 41, 43, 59, 62, 64, 65, 74, 82, 86, 88, 89, 93, 100, 112, 114, 152, 155, 156, 166, 174, 180, 182, 184, 185, 188, 191, 193, 206, 209, 211, 213 Antibody-Dependent Cell Cytotoxicity, 155, 188 Anticholinergic, 155, 171 Anticoagulant, 33, 37, 87, 155, 170, 204
224
Vasculitis
Antidepressant, 155, 177 Antidiabetic, 155, 179 Antigen-Antibody Complex, 156, 166 Antigen-presenting cell, 156, 170 Antihypertensive, 156, 183 Anti-infective, 156, 183 Anti-inflammatory, 104, 156, 157, 163, 168, 179, 202, 210 Anti-Inflammatory Agents, 156, 157, 163, 168 Antimetabolite, 151, 156, 170, 177, 192, 209 Antimicrobial, 156, 169 Antineoplastic, 151, 153, 156, 168, 169, 177, 192 Antiseptic, 156, 192 Antithrombotic, 156, 217 Antiviral, 61, 156, 170, 186, 209 Anus, 156, 166 Aorta, 5, 15, 156, 221 Aortic Aneurysm, 28, 156, 209 Apoptosis, 8, 19, 23, 24, 26, 156 Aqueous, 156, 158, 169, 183 Arachidonic Acid, 13, 88, 102, 105, 156, 184, 188, 204 Arginine, 154, 156, 196 Arrhythmia, 156, 221 Arterial, 27, 34, 41, 65, 102, 156, 157, 161, 183, 188, 205, 216 Arteries, 15, 22, 26, 27, 32, 94, 95, 104, 118 Arteriography, 5, 157 Arteriolar, 29, 157, 160, 207 Arterioles, 13, 157, 160, 161 Arteriolosclerosis, 157 Arteriosclerosis, 16, 157, 213, 217 Arteriosus, 157, 205 Arteriovenous, 78, 157, 217 Arteriovenous Fistula, 157, 217 Arteritis, 4, 5, 22, 26, 32, 59, 62, 79, 105, 110, 114, 138, 139, 157, 202 Artery, 15, 27, 45, 90, 102, 139, 154, 156, 157, 168, 173, 191, 194, 197, 205, 207, 208 Arthralgia, 4, 157, 211 Articular, 17, 157, 197 Aspirin, 103, 157 Assay, 8, 28, 116, 157, 184, 206, 209 Astrocytes, 157, 179, 195 Asymptomatic, 65, 81, 157, 181 Ataxia, 132, 157, 163, 216 Atrophy, 8, 132, 157, 189 Attenuated, 158 Atypical, 4, 44, 63, 76, 158
Autoantibodies, 4, 7, 8, 18, 24, 33, 36, 37, 40, 56, 65, 71, 77, 158 Autoantigens, 9, 33, 158 Autoimmune disease, 8, 9, 15, 20, 23, 34, 37, 59, 105, 139, 158, 194 Autoimmunity, 20, 33, 55, 68, 139, 158 Autologous, 9, 158 Autonomic, 151, 158, 194, 199 Autonomic Nervous System, 158, 199 B Bacteria, 23, 155, 156, 158, 159, 173, 174, 175, 180, 192, 206, 209, 213, 218, 220 Bacterial Infections, 101, 158, 163 Bactericidal, 158, 175 Bacteriophage, 158, 200, 218 Bacterium, 23, 158, 181, 219 Basal Ganglia, 47, 157, 158, 178 Basal Ganglia Diseases, 157, 158 Base, 39, 151, 158, 170, 178, 187, 216 Basement Membrane, 11, 20, 29, 32, 158, 176, 188 Basophils, 159, 180, 188 Benign, 157, 159, 177, 178, 180, 181, 188, 195, 210 Benign tumor, 159, 188 Beta-Defensins, 159, 169 Beta-Lactamases, 159, 215 Beta-Thromboglobulin, 53, 159, 187 Bewilderment, 159, 167 Bilateral, 45, 46, 62, 159, 198 Bile, 18, 159, 177, 183, 189, 209, 214 Bile Acids, 159, 214 Bile Acids and Salts, 159 Bile duct, 18, 159, 209 Biochemical, 12, 26, 153, 156, 159, 170, 179, 197, 211 Biological response modifier, 159, 186 Biological therapy, 159, 180 Biomarkers, 17, 39, 159 Biopsy, 4, 5, 12, 14, 33, 46, 48, 50, 90, 110, 118, 139, 159 Biopsy specimen, 12, 50, 159 Biosynthesis, 156, 160, 211 Biotechnology, 40, 41, 116, 129, 131, 132, 133, 160 Bladder, 160, 185, 204, 219, 220 Blood Coagulation, 160, 161, 209 Blood Platelets, 160, 201, 211, 217 Blood pressure, 156, 160, 161, 162, 183, 193, 196, 205, 212 Blood Volume, 160, 185 Blood-Brain Barrier, 22, 160
225
Blot, 28, 160 Body Fluids, 159, 160, 161, 172, 212, 219 Bone Marrow, 151, 160, 169, 184, 190, 193, 194, 203, 213 Bone Marrow Cells, 160, 194 Bone scan, 160, 210 Bowel, 6, 25, 78, 105, 118, 160, 186, 187, 199, 214, 219 Bradykinin, 13, 160, 187, 196, 200 Branch, 81, 86, 147, 160, 184, 190, 191, 196, 198, 208, 213, 215, 216 Breakdown, 27, 161, 170, 178, 197 Broad-spectrum, 161, 162 Bronchi, 161, 175, 218 Bronchial, 26, 161, 182, 204 Bronchitis, 26, 161 Buccal, 161, 189 Bypass, 161, 194, 217 C Calcification, 15, 157, 161 Calcium, 28, 102, 161, 166, 191, 192, 194, 196, 205, 212, 221 Calcium channel blocker, 161, 221 Capillary, 27, 160, 161, 221 Capillary Permeability, 160, 161 Captopril, 89, 161 Carbimazole, 69, 161 Carbohydrate, 90, 161, 168, 179, 202 Carbon Dioxide, 28, 161, 183, 208, 221 Carcinogenesis, 18, 162 Carcinogenic, 26, 153, 162, 186, 197, 203, 214 Carcinogens, 18, 162, 197 Carcinoma, 18, 75, 81, 162 Cardiac, 72, 104, 162, 173, 175, 185, 194, 214 Cardiac Output, 162, 185 Cardiomyopathy, 104, 162 Cardiovascular, 15, 104, 162, 189, 211 Cardiovascular disease, 15, 104, 162 Carotene, 162, 208 Case report, 62, 79, 162, 176 Case series, 44, 48, 162 Case-Control Studies, 14, 162 Cathode, 162, 173 Cations, 28, 162, 187 Causal, 95, 162, 209 Cefoperazone, 41, 162 Ceftriaxone, 29, 162 Celecoxib, 56, 116, 162 Cell, 4, 5, 6, 9, 10, 11, 12, 13, 16, 18, 19, 21, 22, 24, 26, 28, 32, 33, 34, 35, 36, 39, 49,
50, 53, 54, 59, 62, 63, 75, 76, 82, 90, 94, 100, 101, 106, 132, 133, 139, 151, 152, 154, 155, 156, 157, 158, 160, 163, 164, 166, 169, 170, 171, 172, 174, 176, 177, 178, 179, 180, 182, 184, 185, 186, 187, 188, 191, 193, 194, 195, 196, 197, 200, 201, 203, 204, 207, 208, 212, 215, 216, 218, 219, 220, 221 Cell Adhesion, 11, 16, 26, 28, 32, 39, 53, 163, 186 Cell Adhesion Molecules, 16, 53, 163 Cell Cycle, 12, 163, 169 Cell Death, 26, 156, 163, 179, 194 Cell Differentiation, 106, 163, 212 Cell Division, 132, 158, 163, 180, 193, 200 Cell motility, 39, 163 Cell proliferation, 157, 163, 212 Cell Survival, 163, 180 Cellular adhesion, 100, 163 Cellulitis, 41, 163 Central Nervous System, 17, 22, 40, 103, 110, 114, 137 Central Nervous System Infections, 163, 181 Central retinal artery, 163, 208 Cerebellar, 157, 163, 207, 219 Cerebellar Diseases, 157, 163, 219 Cerebral, 13, 23, 29, 87, 88, 103 Cerebrospinal, 70, 163 Cerebrospinal fluid, 70, 163 Cerebrovascular, 23, 47, 158, 162, 163, 216 Cerebrum, 163, 164, 216, 219 Cervical, 15, 164 Cervix, 164 Chemokines, 19, 21, 29, 164 Chemotactic Factors, 164, 166, 196 Chemotaxis, 11, 39, 164 Chemotherapy, 20, 152, 164, 182 Chickenpox, 57, 164 Chimera, 27, 164 Chin, 93, 164, 191 Chlorambucil, 6, 164 Cholesterol, 4, 159, 164, 168, 214 Choline, 26, 103, 151, 164 Cholinergic, 164, 196 Chromatin, 156, 164, 174 Chromosomal, 154, 164 Chromosome, 164, 182, 189, 192 Chronic Fatigue Syndrome, 113, 164 Chronic renal, 4, 164, 201 CIS, 165, 208 Clamp, 26, 165
226
Vasculitis
Clear cell carcinoma, 165, 170 Clinical trial, 6, 33, 39, 87, 129, 165, 169, 171, 206 Cloning, 26, 160, 165 CNS, 22, 42, 103, 116, 137, 151, 165, 203 Coagulation, 23, 102, 160, 165, 181, 200, 217 Coca, 165 Cocaethylene, 28, 165 Cocaine, 28, 165 Cofactor, 165, 205 Colitis, 60, 165 Collagen, 8, 102, 159, 165, 167, 176, 177, 180, 191, 201, 203, 210 Collagen disease, 165, 210 Collapse, 161, 165 Colon, 132, 151, 165, 166, 186, 219 Complement, 9, 20, 34, 37, 46, 101, 105, 154, 155, 166, 178, 186, 200 Complementary and alternative medicine, 93, 98, 166 Complementary medicine, 93, 166 Complete remission, 166, 207 Computational Biology, 129, 131, 166 Computed tomography, 166, 210 Computerized axial tomography, 166, 210 Conception, 167, 177, 213, 214 Concomitant, 74, 167 Conduction, 72, 167 Cones, 167, 208 Confusion, 112, 167, 171, 219 Congestion, 167, 175, 189 Conjugated, 100, 159, 167 Conjunctiva, 167, 186, 210 Connective Tissue, 4, 8, 42, 113, 160, 163, 165, 167, 177, 190, 193, 205, 209, 210, 216 Connective Tissue Cells, 167 Connective Tissue Diseases, 8, 167 Consciousness, 167, 170, 171 Consolidation, 102, 167 Constipation, 167, 199 Constriction, 167, 187 Consultation, 4, 25, 167 Consumption, 34, 167, 208 Contamination, 167, 181, 182 Contraindications, ii, 167 Conus, 167, 205 Convulsions, 167, 172 Coordination, 39, 167 Cornea, 167, 188, 210, 214, 220, 222 Coronary, 15, 27, 56, 59, 72, 90, 162, 167, 168, 192, 194, 217
Coronary Aneurysm, 72, 168 Coronary heart disease, 162, 168 Coronary Thrombosis, 168, 192, 194 Cortex, 157, 168, 175, 207 Cortical, 29, 168, 176, 211, 216 Corticosteroid, 5, 112, 168, 202 Cortisone, 139, 168, 202 Cost Savings, 8, 168 Cranial, 13, 168, 176, 181, 195, 197, 198, 199, 213 Craniocerebral Trauma, 158, 168, 181, 216 Creatine, 18, 168 Creatinine, 168 Critical Care, 54, 78, 80, 168 Cryoglobulinemia, 10, 40, 48, 58, 59, 81, 137, 168 Cryptococcosis, 41, 168 Curative, 168, 216 Cutaneous, 35, 40, 86, 88, 90, 94, 95 Cyclic, 94, 103, 169, 180, 196, 200, 204 Cyclin, 12, 169 Cyclin A, 12, 169 Cyclin E, 12, 169 Cyclophosphamide, 6, 73, 111, 118, 169 Cyclosporine, 6, 169 Cysteine, 164, 169 Cytokine, 8, 20, 21, 24, 169, 187 Cytoplasm, 65, 156, 159, 169, 174, 180, 209 Cytoskeleton, 23, 169, 186 Cytotoxic, 5, 6, 20, 112, 118, 139, 169, 185, 212 Cytotoxicity, 20, 35, 169 D Data Collection, 25, 169 Databases, Bibliographic, 129, 169 Defense Mechanisms, 169, 186 Defensins, 20, 153, 159, 169 Degenerative, 167, 169, 179, 181, 197, 208 Deletion, 8, 19, 156, 169 Dementia, 24, 29, 170 Denaturation, 170, 201 Dendrites, 170, 195 Dendritic, 24, 27, 49, 170, 191 Dendritic cell, 24, 27, 49, 170 Density, 28, 170, 197, 213 Deoxyglucose, 80, 170 Depolarization, 170, 212 Dermal, 35, 55, 170 Dermatosis, 67, 170 DES, 89, 154, 170 Desensitization, 26, 170 Deuterium, 170, 183
227
Diabetes Mellitus, 71, 170, 179, 181 Diabetic Retinopathy, 170, 200, 221 Diagnostic procedure, 99, 102, 116, 170 Diastolic, 170, 183 Dicumarol, 102, 170 Diffusion, 161, 170, 186 Digestion, 159, 160, 170, 187, 189, 214, 220 Dilatation, 13, 154, 168, 170, 203, 220 Dilation, 160, 171, 220 Dipyridamole, 103, 171 Direct, iii, 9, 21, 25, 26, 102, 103, 105, 171, 183, 189, 207, 215 Disease Progression, 13, 111, 171 Disease Susceptibility, 16, 171 Disinfectant, 171, 175, 192 Disorientation, 167, 171 Dissociation, 152, 171 Distal, 171, 199, 203, 205 Domesticated, 171, 180 Dopamine, 165, 171 Double-blind, 32, 171 Double-blinded, 32, 171 Doxepin, 81, 171 Drive, ii, vi, 7, 10, 12, 14, 18, 19, 24, 25, 35, 85, 171 Drug Combinations, 6, 172 Drug Design, 11, 122, 123, 172 Drug Interactions, 122, 172 Drug Tolerance, 172, 217 Duct, 18, 172, 210 Duodenum, 159, 172, 187, 214 Dura mater, 172, 191, 198 Dysphagia, 114, 172 Dysplasia, 133, 172 Dystrophy, 132, 172 E Eclampsia, 63, 172 Effector, 9, 19, 21, 27, 53, 151, 155, 166, 172, 188, 196, 200 Effector cell, 27, 155, 172, 188, 196 Efferent, 18, 172, 176 Efficacy, 29, 36, 53, 172, 219 Effusion, 172, 216 Elastic, 12, 22, 172, 213 Elasticity, 157, 172 Elastin, 88, 165, 167, 172, 176 Elective, 24, 172 Electrocoagulation, 165, 173 Electrolysis, 162, 173 Electrolyte, 28, 153, 168, 173, 192, 202, 213 Electrons, 158, 162, 173, 187, 206 Emboli, 4, 173, 213
Embolism, 76, 173 Embolus, 173, 185 Embryo, 163, 173, 185 Emphysema, 45, 173 Empiric, 38, 173 Encephalitis, 81, 173 Encephalitis, Viral, 173 Encephalomyelitis, 32, 173 Encephalopathy, 29, 173 Endocarditis, 9, 46, 83, 173, 175 Endocardium, 173 Endocytosis, 11, 173 Endophthalmitis, 174, 221 Endothelial cell, 11, 16, 19, 20, 23, 26, 28, 29, 32, 34, 35, 37, 48, 53, 73, 100, 101, 160, 173, 174, 187 Endothelium, 11, 19, 30, 32, 33, 100, 101, 174, 196 Endothelium, Lymphatic, 174 Endothelium, Vascular, 174 Endothelium-derived, 11, 174, 196 Endotoxin, 100, 101, 174, 219 End-stage renal, 164, 174, 201 Environmental Exposure, 14, 19, 25, 174, 197 Environmental Health, 7, 78, 128, 130, 174 Enzymatic, 161, 162, 166, 174, 182, 201, 208 Enzyme, 105 Enzyme-Linked Immunosorbent Assay, 62, 174 Eosinophilic, 42, 51, 54, 174 Eosinophils, 24, 174, 180, 188 Epidemiological, 7, 174, 176 Epidermal, 174, 188, 191 Epidermis, 174, 187, 188, 203, 206 Epinephrine, 152, 171, 175 Episcleritis, 175, 210 Epithelial, 26, 56, 59, 106, 151, 159, 175, 188 Epithelial carcinoma, 106, 175 Epithelial Cells, 26, 159, 175, 188 Epithelium, 158, 174, 175, 208, 222 Epitopes, 7, 9, 31, 33, 175 Epoprostenol, 175, 184 Erysipeloid, 24, 175, 209 Erythema, 24, 54, 55, 69, 175, 220 Erythrocytes, 154, 160, 175, 207 Esophagitis, 26, 175 Esophagus, 26, 175, 200, 207, 214 Essential Tremor, 132, 175 Estrogens, 175, 179 Ethanol, 28, 175
228
Vasculitis
Ethnic Groups, 24, 27, 175 Eukaryotic Cells, 175, 185, 197 Evoke, 175, 214 Excitatory, 176, 179 Excrete, 176, 207 Exogenous, 161, 176, 200 Exon, 24, 176 Extracellular, 32, 39, 157, 167, 173, 176, 177, 186, 191, 195, 212 Extracellular Matrix, 32, 39, 167, 176, 177, 186, 191 Extracellular Matrix Proteins, 176, 191 Extracellular Space, 176 Extravasation, 32, 176 Extremity, 176, 188, 198 Eye Manifestations, 139, 176 F Facial, 46, 176, 191, 197 Facial Nerve, 46, 176 Family Planning, 129, 176 Family Practice, 25, 176 Fat, 152, 156, 159, 160, 162, 168, 173, 176, 189, 209, 215 Fatal Outcome, 176, 206 Fatigue, 113, 118, 164, 176 Fatty acids, 153, 176, 204, 217 Feasibility Studies, 35, 177 Febrile, 41, 86, 177 Fetus, 177, 184, 220 Fibrin, 102, 160, 177, 199, 217 Fibrinogen, 102, 177, 200, 217 Fibroblasts, 24, 167, 177, 187 Fibroid, 177, 188 Fibrosis, 8, 12, 30, 133, 177, 209, 210 Flatus, 177, 178 Fluorescence, 9, 28, 177 Fluorouracil, 171, 177 Fluoxetine, 57, 177 Fold, 14, 177, 192 Follicles, 7, 10, 177 Fungi, 174, 177, 192, 222 Fungus, 168, 177 G Gallbladder, 58, 60, 151, 177 Ganglia, 151, 158, 177, 195, 199 Ganglion, 177, 197, 222 Gangrene, 83, 178 Gas, 28, 161, 170, 177, 178, 183, 196, 221 Gastric, 65, 178, 182 Gastric Bypass, 65, 178 Gastrin, 178, 182
Gastrointestinal, 18, 58, 59, 76, 79, 82, 86, 160, 175, 177, 178, 188, 189, 211, 215, 219 Gastrointestinal Hemorrhage, 79, 178 Gastrointestinal tract, 18, 76, 82, 175, 177, 178, 188, 189, 211, 219 Gene, 11, 14, 16, 18, 19, 20, 27, 28, 32, 37, 41, 106, 110, 133, 134 Gene Expression, 14, 16, 27, 28, 133, 178 Gene Expression Profiling, 27, 178 Genetic Code, 178, 197 Genetic Engineering, 160, 165, 178 Genetic testing, 178, 201 Genetics, 10, 16, 34, 36, 101, 178, 184 Genital, 114, 165, 178 Genomics, 16, 178 Genotype, 34, 178, 200 Geriatric, 4, 178 Germfree, 17, 178 Germinal Center, 10, 178 Giant Cells, 57, 178, 210 Gland, 114, 152, 168, 179, 182, 190, 198, 200, 204, 211, 214, 217 Gliosis, 29, 179 Glomerular, 7, 11, 13, 18, 19, 20, 29, 34, 60, 109, 179, 207 Glomeruli, 29, 179 Glomerulonephritis, 7, 8, 9, 11, 12, 14, 18, 19, 30, 33, 39, 40, 41, 109 Glomerulus, 11, 179, 195 Glucocorticoid, 32, 179, 202 Glucose, 132, 170, 179, 181, 210 Glucose Intolerance, 170, 179 Glucuronic Acid, 179, 181 Glutamate, 179 Glutamic Acid, 103, 179, 203 Glyburide, 69, 179 Glycine, 159, 179, 211 Glycoprotein, 100, 101, 177, 178, 179, 188, 219 Glycosylation, 28, 31, 179 Gonadal, 179, 214 Gonadotropin, 81, 179 Governing Board, 180, 202 Grade, 180 Grading, 34, 180 Graft, 21, 180, 182, 185, 194 Gram-positive, 180, 216 Gram-Positive Bacteria, 180, 216 Granule, 19, 102, 180, 209 Granulocytes, 180, 188, 194, 212, 221 Granuloma, 33, 60, 66, 180 Granuloma Annulare, 66, 180
229
Growth, 132 Growth factors, 117, 180 Guanylate Cyclase, 180, 196 Guinea Pigs, 94, 95, 180 H Haematoma, 180 Haemorrhage, 23, 58, 79, 180 Half-Life, 162, 180, 184 Haptens, 152, 180, 206, 211 Headache, 32, 42, 139, 181, 186 Headache Disorders, 181 Heart attack, 162, 181 Heart Transplantation, 54, 181 Hematopoietic growth factors, 117, 181 Hemoglobin, 154, 175, 181 Hemoglobinuria, 132, 181 Hemolytic, 102, 181 Hemorrhage, 20, 74, 75, 82, 168, 170, 173, 181, 194, 206, 214 Hemostasis, 181, 186, 211 Heparin, 102, 181, 201 Hepatic, 10, 18, 153, 181 Hepatitis, 4, 9, 10, 17, 46, 61, 64, 66, 70, 71, 81, 95, 115, 117, 181, 182 Hepatitis A, 18, 181 Hepatitis C, 10, 61, 181, 182 Hepatitis E, 17, 182 Hepatocellular, 18, 182 Hepatocellular carcinoma, 18, 182 Hepatocyte, 18, 182 Hepatomegaly, 18, 182 Hepatovirus, 181, 182 Hereditary, 132, 167, 182, 208 Heredity, 178, 182 Heterodimers, 182, 186 Heterogeneity, 27, 152, 182 Heterozygote, 24, 182 Hidradenitis, 67, 73, 182 Histamine, 154, 171, 182 Histology, 32, 116, 182 Homeostasis, 102, 182 Homologous, 153, 182, 215 Hormonal, 158, 168, 182 Hormone, 81, 152, 153, 168, 170, 175, 178, 182, 203, 209, 212, 217 Hormone therapy, 152, 182 Horseradish Peroxidase, 174, 182 Host, 8, 12, 20, 21, 22, 23, 27, 40, 63, 158, 169, 182, 184, 185, 188, 220, 221 Humoral, 19, 20, 33, 37, 106, 183 Humour, 183 Hyaluronidase, 103, 183
Hybrid, 183 Hybridization, 26, 183 Hydralazine, 75, 87, 117, 183 Hydrogen, 13, 158, 161, 170, 176, 183, 193, 196, 197, 205 Hydrogen Peroxide, 13, 183 Hydrolysis, 102, 151, 159, 183, 200, 202, 205 Hydroxylysine, 165, 183 Hydroxyproline, 165, 183 Hypercapnia, 29, 183 Hyperplasia, 18, 183 Hypersensitivity, 5, 41, 42, 46, 58, 63, 88, 104, 153, 170, 183, 188, 209 Hypertension, 4, 7, 157, 162, 181, 183, 195, 202, 203 Hypertrophy, 183 Hypesthesia, 183, 195 I Id, 91, 97, 132, 140, 146, 148, 183 Idiopathic, 55, 59, 64, 70, 73, 77, 87, 117, 182, 183, 210 Ileostomy, 183, 195 Iloprost, 82, 184 Imidazole, 161, 182, 184 Immune function, 34, 184, 185 Immune response, 3, 6, 7, 21, 22, 37, 104 Immune Sera, 184 Immune system, 6, 8, 16, 19, 22, 156, 158, 159, 172, 184, 185, 189, 190, 220, 221 Immune Tolerance, 27, 184 Immunity, 19, 20, 24, 169, 184, 218 Immunization, 18, 68, 152, 184, 185 Immunoassay, 174, 184 Immunochemistry, 33, 184 Immunocompromised, 12, 184 Immunodeficiency, 86, 105, 106, 132, 184 Immunogenetics, 24, 184 Immunogenic, 18, 184, 206 Immunoglobulin, 18, 66, 105, 155, 184, 193 Immunohistochemistry, 26, 28, 32, 184 Immunologic, 7, 17, 87, 90, 100, 101, 152, 164, 184 Immunology, 7, 9, 12, 22, 59, 64, 65, 76, 82, 87, 88, 89, 90, 94, 100, 152, 182, 184, 213 Immunosuppressant, 151, 153, 177, 184, 192 Immunosuppressive, 5, 61, 65, 77, 87, 88, 94, 111, 169, 179, 185, 210 Immunosuppressive Agents, 185, 210 Immunosuppressive therapy, 5, 87, 88, 94, 111, 185
230
Vasculitis
Immunotherapy, 152, 159, 170, 185 Impairment, 29, 157, 159, 185, 191 In situ, 26, 185 In Situ Hybridization, 26, 185 In vitro, 7, 9, 11, 16, 18, 19, 26, 32, 34, 185, 201, 209 In vivo, 10, 11, 12, 16, 18, 19, 21, 28, 30, 32, 35, 36, 106, 181, 185, 217 Incision, 185, 187, 188 Incontinence, 185, 194 Indicative, 102, 110, 185, 198, 220 Indocyanine Green, 86, 185 Induction, 7, 8, 9, 12, 18, 19, 20, 22, 32, 88, 100, 101, 111, 154, 185 Induction therapy, 111, 185 Infantile, 185, 189 Infarction, 15, 23, 47, 62, 185, 201, 207, 217 Infection, 4, 6, 10, 12, 16, 18, 20, 22, 45, 47, 48, 51, 58, 60, 61, 64, 71, 72, 74, 81, 83, 86, 89, 109, 116, 139, 159, 163, 164, 168, 173, 175, 184, 185, 186, 190, 195, 206, 209, 214, 220, 221, 222 Infiltration, 64, 81, 179, 186, 203, 222 Inflammatory bowel disease, 6, 25, 105, 186 Influenza, 65, 68, 77, 117, 186 Ingestion, 20, 186, 201 Inhalation, 86, 186, 201 Initiation, 3, 9, 43, 186, 218 Inner ear, 162, 186, 220 Innervation, 171, 176, 186, 197 Insight, 8, 13, 28, 34, 186 Integrins, 21, 39, 186 Intensive Care, 74, 75, 186 Interferon, 22, 63, 66, 81, 117, 186 Interferon-alpha, 63, 66, 186 Interleukin-1, 100, 101, 186 Interleukin-2, 89, 186, 187 Interleukin-8, 28, 187 Intermittent, 111, 187 Interstitial, 17, 21, 32, 52, 69, 114, 176, 187, 195, 207 Intestinal, 58, 139, 153, 162, 187, 190 Intestine, 159, 160, 187, 207, 212 Intracellular, 20, 21, 28, 185, 186, 187, 196, 202, 204, 209, 212 Intraocular, 174, 187, 221 Intraperitoneal, 94, 95, 187 Intravascular, 23, 187 Intravenous, 15, 33, 66, 87, 111, 139, 187 Intrinsic, 152, 158, 187 Invasive, 32, 55, 184, 187, 190
Involuntary, 158, 175, 187, 194 Ionizing, 153, 174, 187 Ions, 158, 171, 173, 183, 187, 205 Ischemia, 12, 15, 23, 26, 30, 102, 158, 187, 194, 207 J Jejunum, 178, 187 Joint, 8, 42, 139, 157, 187, 197, 201, 215, 216 K Kallidin, 160, 187 Kb, 128, 187 Keratin, 187, 188 Keratinocytes, 26, 187, 188 Keratitis, 17, 188 Kidney Disease, 52, 56, 75, 78, 128, 133, 188 Killer Cells, 19, 188 Kinetic, 16, 187, 188, 200 L Labile, 166, 188 Lacrimal, 176, 188 Laminin, 20, 159, 176, 188 Laparotomy, 48, 188 Latency, 12, 22, 188 Latent, 22, 188, 202 Left ventricular assist device, 54, 188 Leg Ulcer, 44, 65, 188 Leiomyoma, 64, 177, 188 Lesion, 16, 34, 42, 67, 102, 179, 180, 188, 189, 210, 219 Leucocyte, 153, 188 Leukemia, 63, 83, 90, 100, 101, 132, 151, 188, 194 Leukocyte Count, 111, 188 Leukocytes, 34, 69, 100, 101, 159, 160, 164, 174, 180, 186, 188, 219 Leukotrienes, 156, 188 Library Services, 146, 189 Life cycle, 27, 177, 189 Ligament, 189, 204 Ligands, 16, 26, 32, 163, 186, 189 Ligation, 20, 106, 189 Linkages, 25, 181, 189 Lipid, 157, 161, 164, 189 Lipodystrophy, 45, 189 Litter, 34, 189 Livedo, 66, 189 Liver, 18, 113 Liver scan, 189, 210 Localization, 11, 184, 189
231
Localized, 23, 24, 64, 70, 76, 139, 151, 154, 175, 180, 185, 188, 189, 194, 200, 210, 219, 220 Longitudinal Studies, 39, 189 Loop, 178, 183, 189 Lucida, 188, 189 Lumen, 5, 174, 189 Lupus, 8, 15, 23, 33, 34, 87, 105, 110, 117, 118, 136, 137, 138, 139 Lupus Nephritis, 34, 43, 189 Lyme Disease, 29, 47, 189 Lymph, 15, 154, 164, 174, 183, 190, 210, 211 Lymph node, 164, 190, 210 Lymphadenopathy, 15, 190, 211 Lymphatic, 174, 185, 190, 213, 214, 217 Lymphatic system, 190, 213, 214, 217 Lymphocyte, 11, 16, 76, 155, 156, 188, 190, 191 Lymphocytic, 42, 190 Lymphoid, 10, 64, 81, 155, 178, 188, 190 Lymphoma, 12, 50, 63, 82, 83, 90, 94, 132, 190 Lymphoproliferative, 12, 59, 190 Lyssavirus, 190, 206 Lytic, 190, 211 M Macrophage, 10, 11, 21, 27, 34, 39, 60, 155, 186, 190 Magnetic Resonance Imaging, 190, 210 Malabsorption, 132, 190 Malignancy, 4, 190 Malignant, 132, 151, 156, 157, 190, 193, 195, 210, 216 Malignant tumor, 190, 193 Malnutrition, 153, 158, 190, 193 Mammogram, 161, 190, 192 Matrix metalloproteinase, 28, 70, 190 Meat, 175, 191 Meatus, 191, 213 Medial, 157, 191, 209, 213 Mediate, 34, 40, 163, 171, 188, 191 Mediator, 19, 187, 191, 201, 211 Medical Records, 191, 209 Medical Staff, 171, 191 MEDLINE, 129, 131, 133, 191 Melanocytes, 191 Melanoma, 132, 191 Membrane, 20, 29 Memory, 170, 178, 191 Meninges, 162, 163, 168, 172, 191 Meningitis, 23, 70, 191
Menopause, 191, 203 Mental, iv, 6, 128, 130, 134, 164, 167, 170, 171, 176, 191, 205, 210, 219 Mental Disorders, 191, 205 Mercaptopurine, 6, 191 Mercuric Chloride, 87, 191 Mesenteric, 34, 53, 87, 192 Mesentery, 192, 199 Metabolite, 192, 203, 206 Metastasis, 35, 163, 191, 192 Metastatic, 100, 101, 192, 211 Methimazole, 161, 192 Methotrexate, 6, 111, 118, 192 MI, 73, 139, 149, 192 Microbe, 192, 218 Microbiology, 7, 9, 12, 94, 158, 192 Microcalcifications, 161, 192 Micromanipulation, 10, 192 Micromanipulators, 192 Microorganism, 165, 192, 198, 221 Micro-organism, 178, 192 Microscopy, 13, 159, 182, 192 Migration, 32, 39, 192, 195 Mineralocorticoids, 152, 168, 192 Mitochondrial Swelling, 192, 194 Mitosis, 156, 193 Mobility, 28, 193 Modeling, 172, 193 Modification, 34, 178, 193, 206 Monitor, 18, 28, 168, 193, 196 Monoclonal, 9, 10, 18, 37, 100, 193, 206, 209 Monocyte, 11, 16, 19, 29, 43, 60, 71, 155, 193 Mononuclear, 21, 36, 180, 193, 219 Morphological, 18, 73, 173, 177, 191, 193 Motility, 26, 40, 193, 211 Mucociliary, 193, 212 Mucosa, 189, 193, 194 Mucus, 193, 219 Multiple Myeloma, 69, 193 Muscle Fibers, 193 Muscular Atrophy, 132, 193 Muscular Dystrophies, 172, 193 Musculoskeletal Diseases, 25, 193 Myalgia, 24, 186, 193 Myelitis, 86, 193 Myelodysplasia, 76, 194 Myelofibrosis, 102, 194 Myelogenous, 151, 194 Myeloid Cells, 20, 37, 194 Myeloproliferative Disorders, 159, 194
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Vasculitis
Myocardial infarction, 15, 23, 56, 72, 159, 168, 192, 194 Myocardial Reperfusion, 194, 208 Myocardial Reperfusion Injury, 194, 208 Myocarditis, 104, 194 Myocardium, 192, 194 Myopathy, 117, 194 Myositis, 57, 117, 194 Myotonic Dystrophy, 132, 194 N Nasal Cavity, 194, 198, 213 Nasal Mucosa, 186, 194 Natural killer cells, 19, 194 Necrosis, 3, 5, 33, 34, 51, 100, 101, 104, 117, 156, 174, 185, 192, 194, 207, 208, 210 Necrotizing Enterocolitis, 59, 195 Need, 3, 5, 32, 39, 109, 111, 113, 117, 118, 122, 123, 136, 137, 138, 141 Neoplasia, 132, 195 Neoplasm, 195, 210 Neoplastic, 6, 190, 195 Nephritis, 20, 30, 34, 52, 60, 66, 69, 110, 114, 195 Nephrologist, 14, 195 Nephron, 179, 195 Nephropathy, 110, 188, 195 Nerve, 89, 90, 139 Nervous System, 23, 88, 111, 132 Networks, 27, 39, 195 Neural, 103, 152, 183, 195, 208 Neuritis, 74, 195 Neuroglia, 179, 195 Neurologic, 4, 89, 114, 195 Neurologic Manifestations, 89, 195 Neuromuscular, 151, 195, 197 Neuromuscular Junction, 151, 195, 197 Neuronal, 26, 195 Neurons, 165, 170, 176, 177, 195, 196, 206, 215 Neuropathy, 26, 43, 78, 195, 199 Neuropsychology, 24, 196 Neuroretinitis, 55, 64, 70, 77, 196 Neurotransmitters, 171, 196, 203 Neutrons, 153, 196, 206 Neutropenia, 95, 196 Neutrophil, 7, 8, 16, 18, 19, 20, 31, 33, 34, 35, 36, 38, 40, 62, 65, 72, 74, 89, 196 Neutrophil Activation, 18, 37, 196 Nicotine, 26, 196 Nifedipine, 102, 196 Nitric Oxide, 54, 103, 196 Nitrogen, 153, 154, 169, 176, 196, 219
Nuclear, 28, 51, 73, 158, 173, 175, 178, 194, 196 Nuclei, 153, 173, 178, 190, 193, 196, 197, 201, 205 Nucleic acid, 6, 151, 178, 183, 185, 196, 206, 209 Nucleic Acid Hybridization, 183, 197 Nucleus, 156, 158, 159, 164, 169, 170, 174, 175, 193, 196, 197, 205, 214, 216 O Occult, 87, 197 Ocular, 74, 80, 176, 197 Odds Ratio, 14, 197 Oncogene, 12, 132, 197 Oncogenic, 186, 197 Opacity, 170, 197 Ophthalmic, 197, 208 Ophthalmic Artery, 197, 208 Ophthalmoplegia, 62, 197 Opsin, 197, 208 Optic Nerve, 196, 197, 198, 208, 210 Optic nerve head, 196, 197 Organelles, 169, 191, 197 Osteoarthritis, 25, 197 Ovaries, 197, 216 Ovum, 189, 197, 203 P Pachymeningitis, 191, 198 Paediatric, 54, 57, 72, 198 Palliative, 198, 216 Palsies, 90, 198 Palsy, 46, 198 Pancreas, 151, 159, 198, 219 Pancreatic, 132, 198 Pancreatic cancer, 132, 198 Panniculitis, 51, 198 Paralysis, 26, 197, 198 Paranasal Sinuses, 198, 212, 213 Parenchyma, 23, 198 Paresis, 195, 198 Paresthesias, 195, 198 Paroxysmal, 132, 181, 198 Partial remission, 198, 207 Particle, 198, 213, 218 Patch, 26, 167, 189, 198 Pathogen, 16, 20, 22, 24, 27, 198 Pathogenesis, 5, 7, 10, 12, 16, 19, 20, 22, 25, 26, 27, 33, 34, 41, 102 Pathologic, 12, 18, 34, 35, 39, 156, 159, 168, 183, 198, 220 Pathologic Processes, 35, 156, 198 Pathologies, 30, 34, 199
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Pathophysiology, 29, 33, 38, 199 Patient Advocacy, 39, 199 Patient Education, 6, 138, 144, 146, 149, 199 Pelvic, 199, 204, 209 Peptide, 33, 187, 199, 202, 204, 205 Perforation, 67, 199 Perfusion, 64, 199 Pericarditis, 17, 24, 199 Pericardium, 199, 216 Peripheral blood, 186, 199 Peripheral Nervous System, 78, 198, 199, 203, 215 Peripheral Neuropathy, 66, 199 Peritoneal, 24, 59, 187, 199 Peritoneal Cavity, 187, 199 Peritoneum, 192, 199, 208 Peritonitis, 24, 199 Perivascular, 53, 199 Peroxide, 13, 199 Petechiae, 180, 199 Phagocytosis, 20, 199 Pharmacokinetics, 172, 200 Pharmacologic, 13, 154, 180, 200, 218 Pharynx, 186, 194, 200 Phenotype, 17, 21, 32, 37, 200 Phosphodiesterase, 103, 200 Phospholipases, 200, 212 Phosphorus, 161, 200 Photocoagulation, 58, 165, 200 Physical Examination, 4, 5, 139, 200 Physical Fitness, 200, 214 Physiologic, 20, 35, 100, 101, 152, 160, 180, 200, 204, 207, 219 Pigment, 191, 200, 208 Pituitary Gland, 168, 200 Plants, 153, 161, 164, 165, 169, 179, 200, 210, 218, 219 Plaque, 15, 200 Plasma, 27, 39, 53, 153, 155, 159, 160, 174, 177, 179, 181, 192, 193, 200, 201, 205, 207, 211 Plasma cells, 27, 155, 193, 200 Plasma protein, 153, 174, 200, 205 Plasmapheresis, 47, 75, 139, 201 Platelet Activation, 11, 102, 201, 212 Platelet Aggregation, 102, 154, 175, 184, 196, 201, 217 Platelet Factor 4, 53, 187, 201 Platelets, 20, 102, 159, 196, 201, 217 Pleomorphic, 90, 201 Pneumonitis, 77, 201
Poisoning, 201, 211 Polyarteritis Nodosa, 4, 16, 50, 62, 79, 88, 137, 201 Polycystic, 133, 201 Polymerase, 16, 201 Polymerase Chain Reaction, 16, 201 Polymorphism, 66, 68, 201 Polymyalgia Rheumatica, 5, 27, 105, 136, 201 Polypeptide, 153, 165, 177, 183, 202 Polyposis, 151, 202 Polysaccharide, 156, 202, 205 Port, 26, 105, 202 Port-a-cath, 202 Posterior, 157, 198, 202, 209, 210, 213 Postsynaptic, 202, 212, 215 Potassium, 153, 192, 202 Potentiates, 186, 202 Potentiation, 202, 212 Practicability, 177, 202, 219 Practice Guidelines, 130, 202 Precursor, 156, 164, 169, 171, 172, 174, 202, 203, 205, 219 Predisposition, 36, 202 Prednisolone, 202 Prednisone, 32, 118, 137, 139, 202 Pre-Eclampsia, 159, 202 Pre-eclamptic, 172, 203 Premenopausal, 15, 203 Presynaptic, 171, 203, 215 Presynaptic Terminals, 171, 203 Prevalence, 15, 24, 114, 197, 203 Prickle, 188, 203 Probe, 102, 203 Procainamide, 117, 203 Procaine, 203 Prodrug, 203, 206 Progesterone, 203, 214 Prognostic factor, 77, 203 Progression, 12, 13, 14, 15, 16, 18, 23, 30, 43, 111, 118, 155, 169, 203 Progressive, 5, 18, 26, 30, 41, 112 Progressive disease, 112, 203 Projection, 30, 169, 197, 203, 207 Proline, 165, 183, 203 Promoter, 11, 18, 203 Promyelocytic leukemia, 83, 203 Prone, 19, 34, 203 Prophylaxis, 203, 220 Proportional, 174, 204 Prospective Studies, 111, 204 Prospective study, 43, 204
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Vasculitis
Prostaglandin, 41, 88, 104, 175, 204, 217 Prostaglandins A, 204 Prostaglandins B, 105, 204 Prostaglandins F, 204 Prostate, 132, 159, 204, 219 Protease, 21, 31, 32, 204 Protein C, 153, 154, 158, 187, 204, 211 Protein S, 6, 133, 160, 178, 205, 209 Proteinuria, 20, 34, 193, 202, 205 Proteoglycan, 201, 205 Proteolytic, 153, 166, 177, 205 Prothrombin, 62, 205, 217 Protons, 153, 183, 187, 205, 206 Protozoa, 192, 205 Proximal, 59, 171, 178, 194, 201, 203, 205 Psychiatric, 23, 191, 205 Psychiatry, 24, 29, 49, 82, 205 Psychic, 191, 205, 211 Psychology, 171, 196, 205 Psychophysiology, 196, 205 Public Policy, 129, 205 Publishing, 40, 139, 205 Pulmonary, 51, 54, 71, 73, 74, 75, 76, 79, 80, 90, 112, 160, 167, 174, 175, 189, 205, 221 Pulmonary Artery, 73, 160, 205, 221 Pulmonary hypertension, 75, 175, 205 Pulse, 33, 118, 193, 205 Purines, 206, 211 Purpura, 4, 47, 58, 95, 137, 180, 206 Putrefaction, 178, 206 Q Quality of Life, 6, 36, 66, 206 R Rabies, 26, 190, 206 Rabies Virus, 26, 190, 206 Race, 192, 206 Radiation, 104, 152, 174, 177, 184, 187, 206, 210, 222 Radiation therapy, 152, 206 Radioactive, 160, 180, 183, 189, 196, 197, 206, 210 Radioimmunoassay, 159, 206 Ramipril, 49, 206 Randomized, 32, 172, 206 Reactivation, 12, 206 Reactive Oxygen Species, 13, 206 Receptor, 9, 10, 11, 20, 30, 32, 33, 37, 156, 171, 206, 207, 211, 212 Recombinant, 18, 63, 77, 101, 117, 207, 220 Rectum, 156, 166, 177, 178, 185, 186, 204, 207
Red blood cells, 175, 181, 207, 210 Red Nucleus, 157, 207 Reductase, 192, 207 Refer, 1, 161, 166, 177, 189, 196, 207 Reflux, 110, 207 Refraction, 207, 213 Refractory, 78, 173, 207 Regimen, 172, 207 Regurgitation, 52, 207 Relapse, 7, 14, 19, 31, 77, 207 Remission, 14, 19, 60, 65, 78, 89, 151, 207 Renal failure, 4, 207 Renal tubular, 110, 207 Renin, 161, 207 Renin-Angiotensin System, 161, 207 Reperfusion, 12, 17, 30, 100, 101, 194, 207, 208 Reperfusion Injury, 12, 30, 100, 101, 207, 208 Respiration, 161, 193, 208 Respiratory distress syndrome, 74, 208 Restoration, 194, 206, 207, 208, 221 Retina, 62, 64, 163, 167, 170, 195, 196, 197, 208, 209, 220, 221 Retinal, 46, 53, 55, 57, 58, 63, 64, 66, 70, 74, 77, 80, 81, 87, 89, 170, 197, 208, 221 Retinal Artery, 81, 208 Retinal Artery Occlusion, 81, 208 Retinal Detachment, 170, 208, 221 Retinal Neovascularization, 81, 208 Retinal Vein, 208 Retinoblastoma, 132, 208 Retinol, 208 Retroperitoneal, 76, 152, 208, 209 Retroperitoneal Fibrosis, 76, 209 Retroperitoneal Space, 209 Retrospective, 75, 89, 209 Retrospective study, 75, 89, 209 Rheumatic Diseases, 25, 111, 113, 117, 118 Rheumatism, 43, 49, 51, 53, 61, 65, 66, 68, 74, 209 Rheumatoid, 9, 10, 17, 40, 89, 90, 105, 113, 116, 117, 137 Rheumatoid arthritis, 9, 17, 46, 50, 75, 89, 90, 105, 113, 116, 117, 165, 209 Rhinitis, 112, 209 Rhusiopathiae, 175, 209 Ribavirin, 66, 81, 115, 209 Ribose, 151, 209 Ribosome, 209, 218 Rickettsiae, 209 Risk factor, 4, 14, 15, 17, 23, 36, 204, 209
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Ristocetin, 209, 220 Rituximab, 63, 78, 209 Rod, 158, 165, 209 Rural Population, 25, 209 S Sagittal, 29, 209 Saline, 28, 210 Saliva, 206, 210 Salivary, 114, 176, 198, 210 Salivary glands, 176, 210 Saponins, 210, 214 Sarcoid, 42, 210 Sarcoidosis, 210 Sarcoma, 22, 35, 210 Scans, 29, 210 Schizophrenia, 89, 210 Sclera, 167, 175, 210, 220 Scleritis, 17, 210 Scleroderma, 8, 114, 157, 210 Sclerosis, 61, 132, 133, 157, 165, 210 Screening, 165, 210 Secondary tumor, 192, 211 Secretion, 24, 168, 182, 183, 192, 193, 211, 220 Segmentation, 30, 211 Seizures, 198, 211 Semen, 204, 211 Sensibility, 154, 211 Sensory loss, 194, 211, 216 Septicemia, 56, 211 Sequencing, 26, 201, 211 Serine, 31, 211 Serologic, 17, 23, 184, 211 Serotonin, 177, 211, 219 Serous, 174, 211 Serum, 5, 8, 18, 28, 34, 39, 104, 105 Serum Sickness, 104, 105, 211 Sex Determination, 133, 211 Shock, 211, 219 Side effect, 105, 121, 123, 152, 159, 169, 212, 218 Signal Transduction, 32, 37, 212 Signs and Symptoms, 4, 104, 195, 201, 207, 212 Sinusitis, 77, 112, 212 Skeletal, 59, 70, 154, 165, 193, 212 Skeleton, 151, 187, 204, 212 Skin Manifestations, 24, 212 Skull, 168, 212, 216 Small intestine, 172, 182, 187, 212 Smooth muscle, 22, 100, 154, 167, 177, 182, 188, 204, 207, 212, 215
Social Environment, 206, 212 Social Support, 36, 212 Sodium, 153, 175, 192, 212, 215 Solid tumor, 155, 213 Solvent, 175, 213 Soma, 213 Somatic, 7, 22, 183, 193, 199, 213 Somatic cells, 22, 193, 213 Somatic mutations, 7, 213 Sound wave, 167, 213 Specialist, 140, 171, 213 Species, 12, 13, 153, 168, 171, 175, 180, 183, 192, 193, 206, 213, 215, 219, 221, 222 Species Specificity, 12, 213 Specificity, 7, 9, 10, 12, 21, 33, 87, 152, 213 Spectrum, 31, 35, 213, 215 Sperm, 154, 164, 213, 216 Sphenoid, 45, 198, 213 Sphenoid Sinus, 45, 213 Sphenoid Sinusitis, 45, 213 Spinal cord, 83, 157, 163, 164, 165, 172, 173, 178, 191, 193, 195, 198, 199, 213, 214 Spinal Cord Vascular Diseases, 194, 213 Spinal Nerves, 199, 214 Spinous, 174, 188, 214 Spirochete, 189, 214, 216 Spleen, 154, 190, 210, 214 Spondylitis, 105, 214 Sporadic, 208, 214 Sports Medicine, 113, 144, 214 Staging, 210, 214 Stasis, 4, 214 Steel, 165, 214 Sterile, 55, 214 Sterility, 169, 214 Steroid, 32, 159, 168, 210, 214 Stimulus, 10, 16, 172, 186, 187, 188, 198, 214, 217 Stomach, 151, 175, 178, 182, 199, 200, 207, 212, 214 Stool, 166, 185, 214 Strand, 201, 214 Stress, 6, 39, 66, 158, 202, 209, 214, 220 Stroke, 23, 57, 72, 88, 102, 128, 138, 162, 214 Stroma, 198, 214 Subacute, 185, 212, 214 Subarachnoid, 78, 181, 214 Subclinical, 15, 79, 185, 211, 214 Subcutaneous, 163, 188, 189, 198, 215 Subspecies, 213, 215 Substance P, 192, 209, 211, 215
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Vasculitis
Substrate, 174, 215 Sulbactam, 41, 215 Superoxide, 86, 93, 215 Suppression, 41, 90, 168, 215 Suppurative, 163, 174, 215 Sweat, 182, 215 Symphysis, 164, 204, 215 Symptomatology, 4, 215 Synapse, 21, 152, 195, 203, 215, 218 Synaptic, 196, 212, 215 Synaptic Transmission, 196, 215 Syncytium, 179, 215 Synergistic, 10, 18, 215 Synovial, 9, 24, 215, 216 Synovial Fluid, 9, 215, 216 Synovial Membrane, 215, 216 Synovitis, 114, 216 Syphilis, 29, 77, 216 Systemic, 3, 4, 5, 6, 8, 9, 10, 15, 16, 18, 19, 21, 23, 26, 36, 38, 41, 45, 46, 49, 50, 51, 52, 53, 55, 56, 59, 60, 61, 63, 64, 65, 66, 67, 69, 70, 74, 75, 77, 78, 79, 80, 83, 84, 86, 87, 88, 89, 90, 94, 96, 105, 110, 114, 115, 118, 139, 154, 156, 160, 165, 175, 185, 189, 202, 206, 210, 211, 216, 218 Systemic disease, 88, 211, 216 Systemic lupus erythematosus, 4, 15, 16, 23, 114 Systolic, 183, 216 T Teicoplanin, 60, 216 Telangiectasia, 132, 216 Telencephalon, 158, 216 Temporal, 4, 27, 32, 79, 90, 105, 110, 117, 138, 139, 181, 191, 202, 216 Teratoma, 55, 216 Testicles, 216 Testicular, 44, 67, 216 Testis, 216 Thalamic, 157, 216 Thalamic Diseases, 157, 216 Therapeutics, 37, 122, 216 Thermal, 171, 196, 201, 216 Thorax, 80, 151, 216 Threonine, 211, 217 Threshold, 183, 217 Thrombin, 177, 201, 204, 205, 217 Thrombocytes, 102, 201, 217 Thrombocytopenia, 10, 59, 217 Thrombosis, 10, 15, 23, 47, 80, 102, 159, 186, 205, 214, 217 Thromboxanes, 156, 217
Thrombus, 168, 185, 194, 201, 217, 221 Thymus, 184, 190, 217 Thyroid, 7, 192, 217 Thyroid Gland, 217 Thyroiditis, 7, 55, 217 Ticks, 189, 217 Ticlopidine, 44, 217 Tin, 199, 217 Tolerance, 9, 27, 34, 151, 179, 217 Tomography, 55, 57, 80, 136, 166, 167, 217 Tone, 13, 217 Tonus, 217 Topical, 175, 183, 192, 218 Torsion, 185, 218 Toxic, iv, 6, 36, 38, 94, 110, 153, 169, 173, 174, 184, 191, 195, 196, 200, 218, 220 Toxicity, 6, 26, 172, 209, 218 Toxicology, 130, 218 Toxins, 104, 156, 173, 179, 185, 211, 218 Trachea, 161, 200, 217, 218 Traction, 165, 218 Transcriptase, 16, 218 Transcription Factors, 32, 218 Transduction, 32, 37, 41, 212, 218 Transfection, 32, 160, 218 Transfer Factor, 184, 218 Transferases, 179, 218 Transfusion, 81, 181, 218 Transgenes, 18, 218 Translation, 7, 218 Translational, 38, 218 Transmitter, 151, 157, 171, 191, 195, 218 Transplantation, 16, 53, 58, 60, 61, 65, 67, 69, 71, 75, 77, 94, 165, 184, 218 Trauma, 104, 175, 194, 219 Treatment Outcome, 48, 219 Tremor, 132, 219 Tricyclic, 171, 219 Tropism, 22, 219 Tryptophan, 165, 211, 219 Tuberculosis, 54, 167, 189, 219 Tuberous Sclerosis, 133, 219 Tumor marker, 159, 219 Tumor Necrosis Factor, 44, 100, 101, 219 TYPHI, 41, 219 Typhoid fever, 219 U Ulcer, 163, 188, 219, 220 Ulcerative colitis, 47, 69, 186, 219 Unconscious, 169, 183, 219 Uremia, 207, 219 Ureters, 209, 219, 220
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Urethra, 204, 220 Urinary, 110, 162, 185, 220 Urinary tract, 110, 162, 220 Urinary tract infection, 110, 220 Urine, 18, 32, 53, 160, 168, 181, 185, 205, 219, 220 Urticaria, 25, 81, 94, 118, 211, 220 Uterus, 164, 177, 188, 197, 203, 220 Uvea, 174, 220 Uveitis, 66, 114, 220 V Vaccination, 65, 68, 77, 220 Vaccine, 152, 220 Vaccines, 117, 220, 221 Vacuoles, 173, 197, 220 Vagina, 164, 170, 220 Vancomycin, 60, 220 Varicose, 188, 220 Vasa Vasorum, 27, 57, 220 Vasodilatation, 13, 187, 220 Vasodilation, 184, 220 Vasodilator, 160, 171, 182, 183, 194, 196, 220 Vector, 218, 220 Vein, 28, 102, 154, 157, 187, 196, 208, 220, 221 Venereal, 216, 220 Venous, 4, 96, 102, 114, 157, 159, 188, 205, 217, 220, 221 Venous blood, 188, 221 Venous Thrombosis, 102, 159, 217, 221 Ventricle, 205, 216, 221 Ventricular, 194, 221
Venules, 160, 161, 174, 221 Verapamil, 102, 221 Vertebrae, 213, 214, 221 Veterinary Medicine, 22, 129, 221 Viral, 4, 22, 63, 173, 178, 186, 197, 206, 218, 221 Virulence, 18, 158, 218, 221 Virus, 10, 22, 89 Viscera, 192, 213, 221 Viscosity, 183, 221 Visual Acuity, 210, 221 Visual field, 208, 221 Vitrectomy, 58, 221 Vitreous Body, 208, 221 Vitro, 7, 9, 11, 13, 16, 18, 19, 22, 26, 32, 35, 181, 221 Vivo, 10, 11, 12, 16, 18, 19, 21, 28, 30, 32, 35, 36, 106, 221 W White blood cell, 155, 188, 190, 193, 194, 196, 200, 221 Windpipe, 200, 217, 221 Wound Healing, 35, 163, 186, 191, 221 X Xenograft, 155, 222 X-ray, 30, 155, 157, 162, 166, 177, 190, 196, 206, 210, 222 Y Yeasts, 177, 200, 222 Z Zoonoses, 206, 222 Zoster, 62, 82, 222
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240
Vasculitis
