MYOCARDITIS 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., 1960Myocarditis: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-497-00740-1 1. Myocarditis-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 myocarditis. 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 MYOCARDITIS ........................................................................................... 3 Overview........................................................................................................................................ 3 Federally Funded Research on Myocarditis ................................................................................... 3 E-Journals: PubMed Central ....................................................................................................... 36 The National Library of Medicine: PubMed ................................................................................ 38 CHAPTER 2. NUTRITION AND MYOCARDITIS ................................................................................. 85 Overview...................................................................................................................................... 85 Finding Nutrition Studies on Myocarditis.................................................................................. 85 Federal Resources on Nutrition ................................................................................................... 88 Additional Web Resources ........................................................................................................... 88 CHAPTER 3. ALTERNATIVE MEDICINE AND MYOCARDITIS ........................................................... 89 Overview...................................................................................................................................... 89 National Center for Complementary and Alternative Medicine.................................................. 89 Additional Web Resources ........................................................................................................... 92 General References ....................................................................................................................... 93 CHAPTER 4. DISSERTATIONS ON MYOCARDITIS ............................................................................. 95 Overview...................................................................................................................................... 95 Dissertations on Myocarditis....................................................................................................... 95 Keeping Current .......................................................................................................................... 96 CHAPTER 5. PATENTS ON MYOCARDITIS ........................................................................................ 97 Overview...................................................................................................................................... 97 Patents on Myocarditis ................................................................................................................ 97 Patent Applications on Myocarditis .......................................................................................... 102 Keeping Current ........................................................................................................................ 104 CHAPTER 6. BOOKS ON MYOCARDITIS ......................................................................................... 107 Overview.................................................................................................................................... 107 Book Summaries: Online Booksellers......................................................................................... 107 CHAPTER 7. PERIODICALS AND NEWS ON MYOCARDITIS............................................................ 109 Overview.................................................................................................................................... 109 News Services and Press Releases.............................................................................................. 109 Academic Periodicals covering Myocarditis .............................................................................. 111 CHAPTER 8. RESEARCHING MEDICATIONS .................................................................................. 113 Overview.................................................................................................................................... 113 U.S. Pharmacopeia..................................................................................................................... 113 Commercial Databases ............................................................................................................... 115 Researching Orphan Drugs ....................................................................................................... 115 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 119 Overview.................................................................................................................................... 119 NIH Guidelines.......................................................................................................................... 119 NIH Databases........................................................................................................................... 121 Other Commercial Databases..................................................................................................... 123 APPENDIX B. PATIENT RESOURCES ............................................................................................... 125 Overview.................................................................................................................................... 125 Patient Guideline Sources.......................................................................................................... 125 Finding Associations.................................................................................................................. 127 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 129 Overview.................................................................................................................................... 129 Preparation................................................................................................................................. 129 Finding a Local Medical Library................................................................................................ 129 Medical Libraries in the U.S. and Canada ................................................................................. 129
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ONLINE GLOSSARIES................................................................................................................ 135 Online Dictionary Directories ................................................................................................... 138 MYOCARDITIS DICTIONARY ................................................................................................. 139 INDEX .............................................................................................................................................. 199
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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 myocarditis 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 myocarditis, 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 myocarditis, 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 myocarditis. 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 myocarditis, 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 myocarditis. 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 MYOCARDITIS Overview In this chapter, we will show you how to locate peer-reviewed references and studies on myocarditis.
Federally Funded Research on Myocarditis The U.S. Government supports a variety of research studies relating to myocarditis. 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 myocarditis. 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 myocarditis. The following is typical of the type of information found when searching the CRISP database for myocarditis: •
Project Title: ABNORMALITIES MYOCARDITIS
OF
MITOCHONDRIA
IN
CHAGASIC
Principal Investigator & Institution: Garg, Nisha; Microbiology and Immunology; University of Texas Medical Br Galveston 301 University Blvd Galveston, Tx 77555 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 29-SEP-2004
2
Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
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Myocarditis
Summary: (provided by applicant): Chagas disease, caused by Trypanosoma cruzi, the most common cause of congestive heart failure-related mortality and morbidity of humans, is endemic in Latin America. Continuous immigration from endemic areas of South and Central America has increased the risk of exposure of the U.S. population to chagas disease as well. The precise mechanisms leading to ventricular dilation and myocardial hypertrophy, observed in chagasic patients, are not well understood. The present studies are aimed at understanding the role of host gene regulation in the pathogenesis of chagasic cardiomyopathy. Our preliminary studies have suggested that the progression of chagasic myocarditis is associated with aberrations in the expression of cardiac contractile proteins and an imbalance in the mitochondrial energy metabolism proteins. In this project, we propose to investigate the molecular events that might affect the host mitochondrial function and initiate the imbalance of cytoskeletal proteins during the progression of chagas disease. Our hypothesis is that the inflammatory mechanisms elicited to control the pathogen might adversely affect the host mitochondria at the DNA, RNA or protein levels, resulting in a feedback cycle of progressively greater levels of reactive oxidant production and mitochondrial dysfunction. It is possible that reactive oxygen provides a stimuli for initiation of cardiac hypertrophy, and might be the critical determinant in reformatting of myocytes and loss of contractile function observed in chagasic patients. The proposed studies will determine the pathophysiological contribution of host mitochondrial abnormalities in the progression of chagas disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ANTIGEN IMMUNOSUPPRESSION BY KILLER LANGERHANS CELLS Principal Investigator & Institution: Takashima, Akira; Professor; Dermatology; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2002; Project Start 01-JUN-2000; Project End 31-MAY-2005 Summary: Langerhans cells (LC) ordinarily deliver activation signals to T cells. We hypothesized that LC genetically modified to over-express CD95L (Fas ligand) termed "killer" LC, would deliver apoptotic signals to T cells upon antigen-specific interaction. To test this, we introduced CD95L cDNA into our LC line XS106 (derived from A/J mice) and selected a stable clone (XS 10-6-CD95L) that expressed abundant surface CD95L. This killer LC clone, when pulsed with ovalbumin (OVA), triggered apoptosis of OVA-reactive CD4+ T cells in vitro by an antigen-specific and CD95L-dependent mechanism. OVA-pulsed killer LC, when injected into A/J mice before or after sensitization, suppressed ear swelling responses to DNFB. Importantly, OVA-pulsed killer LC suppressed OVA responses, but not responses to the irrelevant antigen HEL, whereas HEL- pulsed killer LC inhibited only the HEL responses, establishing antigenspecificity. We will define mechanisms, under the new hypothesis that killer LC suppress diverse immunological responses by triggering apoptosis of putative effector T cells that recognize respective antigens. Specifically, we will study the impact of killer LC using five-established animal models: 1) Delayed type hypersensitivity: We will inject OVA- pulsed killer LC before or after sensitization to study the impact of CD4+ effect T cells and memory T cells, the fate of effector cells (adoptive transfer of OVAreactive, naive CD4+ T cells from the D011.10 transgenic mice), and the critical timing for cytotoxic interaction of killer LC with T cells (drug-inducible suicide system). 2) Contact hypersensitivity. We will inject DNFB-pulsed killer LC before or after sensitization to study the impact of CD8+ effector T cells and on Th2-like regulatory T cells, killer LC interaction with CD8+ T cells and antigen- specificity. 3) Th2-biased
Studies
5
immune responses. Mice will be sensitized epicutaneously with an OVA-absorbed "patch" to produce OVA-specific IgE and IgG1 antibodies and atopic dermatitis-like skin lesions. We will inject OVA-pulsed killer LC to study the impact on Th2-biased effector and helper T cells and "therapeutic" efficacy for skin lesions. 4) Experimental autoimmune myocarditis. Mice will be sensitized with cardiac myosin (CM) to produce autoimmune myocarditis. We will inject CM-pulsed killer LC to study the impact on CD4+ pathogenic T cells that recognize tissue-specific autoantigen, the fate of pathogenic T cells, and therapeutic efficacy and safety. 5) Skin graft rejection. We will study the impact of killer LC and "killer LC hybrids" on allo-reactive CD4+ and CD8+ T cells, which are ordinary activated via "direct" and "indirect" pathways. These studies will form the framework for establishing an entirely new immunosuppressive therapy for inflammatory skin diseases, the therapy designed to eliminate selectively the effector T cells that recognize pathogenic antigens (e.g., haptens, allergens, autoantigens, and alloantigens). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: APOPTOTIC SIGNALING IN VIRAL MYOCARDITIS Principal Investigator & Institution: Debiasi, Roberta L.; Pediatrics; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, Co 800450508 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-MAY-2007 Summary: (provided by applicant): This proposal describes a 5-year training program for the development of an independent academic career in Laboratory Medicine and Infectious Diseases. The program will promote the command of genomic and proteomic approaches applied to the study of viral pathogenesis. Kenneth L. Tyler will mentor the P.I.'s scientific development. Dr. Tyler is a recognized leader in the field of viral pathogenesis. As Professor of Neurology, Microbiology, Immunology, and Medicine, he has trained numerous postdoctoral fellows and graduate students. To enhance the training, the program will enlist the expertise of a multidisciplinary board of senior scientists, who will provide scientific and career advice. The University of Colorado provides an ideal setting for training physician-scientists by integrating expertise from diverse resources into customized programs. This environment maximizes the potential for the PI to establish a scientific niche from which a successful academic career can be constructed. Research will focus on delineating and targeting apoptotic signaling pathways in viral myocarditis. Dr.Tyler's laboratory has used reoviruses to study viral and cellular mechanisms of apoptotic cell death, both in vitro and in well-characterized murine models of viral encephalitis and myocarditis. Specific aims of this project are (1) to identify the importance of apoptosis as a critical determinant of virus-induced myocarditis, (2) to characterize virus-induced myocarditic signaling pathways in vitro and vivo at the transcriptional and translational levels, and (3) to target critical identified pathways in vivo, as a novel therapeutic strategy for viral myocarditis. Proposed experiments involve detailed analysis of infected murine cardiac myocytes and tissues, using myocarditic and non-myocarditic viruses. Virologic, histologic, immunohistochemical, genomic and proteomic approaches will be employed. Identified pathways will be targeted using specific inhibitors and mice with genetic mutations in pertinent signaling pathways. These studies are designed to identify specific cellular mechanisms of virus-induced apoptosis in the pathogenesis of viral myocarditis. Identification of these pathways is critical for the development of novel therapies for viral myocarditis and other diseases involving apoptotic tissue damage. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Myocarditis
Project Title: AUTOIMMUNE DETERMINANTS OF HUMAN CARDIAC MYOSIN Principal Investigator & Institution: Cunningham, Madeleine W.; George Lynn Cross Research Professor; Microbiology and Immunology; University of Oklahoma Hlth Sciences Ctr Health Sciences Center Oklahoma City, Ok 73126 Timing: Fiscal Year 2002; Project Start 01-AUG-1997; Project End 30-JUN-2007 Summary: (provided by applicant): Myocarditis and rheumatic carditis are sequelae of viral and bacterial infections, respectively, and occur in humans and animal models following coxsackievirus infection, group A streptococcal infection, or immunization with cardiac myosin. The pathogenesis of these diseases may be due to molecular mimicry between the infectious pathogen and the host autoantigen cardiac myosin. Although cardiac myosin can induce myocarditis in animals, the molecular pathogenesis of the disease in humans is unclear. In addition, there are few studies in humans, which define the immunological parameters of disease. The goal of the proposed work is to define the parameters of the autoimmune response to human cardiac myosin in humans and in a cardiac myosin-induced rat model of myocarditis and valvulitis. We will test the hypothesis that molecular mimicry and the influence of the cytokine environment leads to development of disease. We plan: 1)To produce and investigate human T cell clones from myocarditis patients which are crossreactive with human cardiac myosin, streptococcal M protein and coxsackievirus and their peptides; to determine cytokine responses of human T cell clones as well as HLA class I and II restriction of responses and cell surface antigens by FACS analysis 2)To evaluate expression of genes by crossreactive CD4+/- and CD8+ T cell clones and by normal and myocarditis patient peripheral blood CD4+ and CD8+ lymphocytes in response to stimulation with myosin, M protein and coxsackievirus or their peptides by DNA array analysis, cytokine production, and to study the cell surface markers on T lymphocytes by FACS analysis 3) To investigate a Lewis rat cardiac S2 peptide-induced model of severe myocarditis for parameters of inflammatory heart disease including the role of molecular mimicry and cytokines in susceptible, resistant, and tolerized rat strains (Lewis and BB/DR), to determine the epitope specificity of the heart specific infiltrating T cells from hearts in the Lewis rat model and to determine cytokine expression in hearts using the RNase protection assay for TH1/TH2 cytokines and expression of a large group of genes using DNA arrays. We will establish a tolerance model to investigate the downregulation of myosin specific I cells, antibodies and cytokines in disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: CAR FUNCTION IN VIRUS TROPISM AND CELL-CELL CONTACT Principal Investigator & Institution: Bergelson, Jeffrey M.; Assistant Professor; Children's Hospital of Philadelphia 34Th St and Civic Ctr Blvd Philadelphia, Pa 191044399 Timing: Fiscal Year 2002; Project Start 20-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): Coxsackie B viruses (CBV) and Adenoviruses (Ads) are the major causes of viral myocarditis, and CBV are implicated in the pancreatitis and diabetes. All CBV and many Ads initiate infection by attachment to the coxsackievirus and adenovirus receptor (CAR), a cell surface glycoprotein whose physiologic function has not been defined. This proposal concerns both CAR's role in virus tropism and its physiologic function. We recently found that CAR is a functional component of the epithelial cell tight junction, a specialized intercellular contact that serves as a barrier to the paracellular solute movement. On polarized epithelial cells, CAR is sequestered in
Studies
7
tight junctions; consequently, epithelial monolayers resist infection by both CBV and Ads. Some CBV also attach to a second receptor, DAF, a molecule whose role in infection has remained poorly understood. Preliminary data indicate that while DAF may alter the route by which virus enters a cell, it does not trigger conformational changes in the virion essential that are essential for infection. However, DAF is targeted to the apical surface of polarized cells, and a DAF-binding CBV variant efficiently infects epithelial monolayers; we propose that interaction with DAF provides a mechanism for virus infection at epithelial and mucosal surfaces. In the first series of proposed experiments, we will determine the functions of CAR and DAF during infection, define the route of virus entry for CAR-binding viruses and DAF-binding variants, and test the hypothesis that attachment to DAF permits CBV to cross epithelial surfaces In a second series of experiments we will define CAR's function in CBV pathogenesis in an in vivo model. In human tissues, CAR mRNA is most highly expressed in the heart and pancreas, the major CBV target organs both in humans and in animal models of infection. We will use a conditional gene targeting strategy to determine whether tissuespecific CAR expression is essential for CBV infection, and for virus-induced pathology in the heart and pancreas. In a final group of experiments we will explore CAR's physiologic functions. We have found that CAR is both a structural and functional component of the tight junction, that CAR interacts with the major junctional protein ZO-1, and that homotypic interactions between CAR extracellular domains mediate cell adhesion and contribute to junctional integrity. We will determine the structures involved in CAR-mediated homotypic adhesion, and define CAR' s interactions with other proteins important for junction formation and function. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CAR PROTEIN AND AUTO IMMUNITY Principal Investigator & Institution: Finberg, Robert W.; Professor; Medicine; Univ of Massachusetts Med Sch Worcester Office of Research Funding Worcester, Ma 01655 Timing: Fiscal Year 2002; Project Start 30-SEP-1999; Project End 28-FEB-2003 Summary: Many auto-immune diseases are thought to be triggered by viral infections. In particular auto-immune diabetes and myocarditis are said to follow infections with enteroviruses. Histopathologic studies indicate that mumps and adenoviruses are viruses associated with myocarditis. In addition the Group B Coxsackie viruses have been isolated from patients who subsequently develop diabetes or myocarditis. Studies of humans with acute myocarditis and diabetes indicate the infiltrating T cells have a restricted usage of T-cell receptor genes suggesting that they may be directed at a particular antigen. Animal models indicate that both auto-immune diabetes and myocarditis can be initiated by Coxsackie B viruses. In addition to evidence that T cells can transfer the disease, a role of cytokines has been postulated for auto-immune diabetes and myocarditis. Studies in knock-out mice indicate a role for chemokines in the initiation of the inflammatory process that leads to Coxsackie B virus induced myocarditis. Hypotheses concerning the pathogenesis of auto-immune responses have generally focused on either a viral epitope mimicking a cellular protein (e.g. the GAD protein and a Coxsackie B4 protein), or suggested that the inflammatory response stimulated by the infectious event might damage the cell causing inflammatory changes that subsequently result in the generation of an immune response to host tissues. Whether the inflammation stimulates T cells that recognize host proteins or there is persistence of viral proteins has been hard to define in most model systems. In addition it is unclear how the type of auto- immune response relates to the tropism of the viral agent. We have recently defined a host cell surface protein that serves as the receptor for
8
Myocarditis
all group B Coxsackie viruses, the fiber binding protein of most adenoviruses, and a major determinant in mumps infection. The distribution of this protein suggests that its expression correlates with the ability of these viruses to induce auto-immune diseases. We plan to define the role of this protein in the induction of auto-immune disease and use transgenic and knock-out mice to define the mechanisms by which viruses stimulate autoimmune responses. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CARDIAC SOCS PROTEINS: A ROLE IN ENTEROVIRUS INFECTION Principal Investigator & Institution: Knowlton, Kirk U.; Associate Professor; Medicine; University of California San Diego La Jolla, Ca 920930934 Timing: Fiscal Year 2004; Project Start 05-DEC-1998; Project End 30-APR-2008 Summary: (provided by applicant): Coxsackieviral infection of the heart is an important cause of cardiomyopathy in children and adults. However, little is known of the innate signaling mechanisms within the cardiac myocytes that control viral infection. A better understanding of these mechanisms may allow design of novel therapeutic strategies for viral heart disease. Recently, we have shown that inhibition of Janus kinase (JAK)signaling transducer and activator of transcription (STAT) in the cardiac myocyte by expression of SOCS 1 has a marked effect on viral replication and viral-mediated cytopathic effects. Disruption of interferon alpha/beta receptors had no effect and disruption of interferon-gamma receptors had minimal effect on early viral replication in the heart. We, therefore, hypothesize that other, non-interferon mediated innate immune mechanisms are important within the cardiac myocyte to combat viral infection. These could include signaling through the glycoprotein (gp) 130 that also activates JAK-STAT signaling. We, therefore, propose the following specific aims: 1) Determine in CVB3 infected mice whether gp130, IFN-gamma signaling, or both are important for a) the induction of JAK-STAT-SOCS signaling in the heart and b) the innate immune defense against viral infection. 2) Identify mechanisms related to viral infection and replication by which forced expression of SOCS1 in the cardiac myocyte induces a marked cytopathic effect following CVB3 infection and determine whether transgenic SOCS3 expression will also affect the innate immune response in a manner similar to that observed in SOCS1 transgenic mice. 3) Determine the effect of cardiacspecific knockout of SOCS1 and SOCS3 on JAK-STAT signaling in cardiac myocytes and the cardiomyopathy associated with CVB3 infection. These aims will provide a novel insight into the mechanisms by which JAK-STAT-SOCS activation within the cardiac myocyte regulates the innate anti-viral response. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: CARDIAC-RELATED ANTIPSYCHOTICS
MORTALITY
WITH
ATYPICAL
Principal Investigator & Institution: Kelly, Deanna L.; Psychiatry; University of Maryland Balt Prof School Baltimore, Md 21201 Timing: Fiscal Year 2004; Project Start 01-DEC-2003; Project End 30-NOV-2005 Summary: (provided by applicant): The increased mortality rate of persons with schizophrenia has been of concern for several decades and is known to be 2-3 times higher than the general population. Death from cardiovascular-related events are believed to occur more frequently in this population and may be rising annually possibly due to newer second-generation antipsychotic (SGA) medications. Since their
Studies
9
introduction, the more tolerable SGAs have moved fairly quickly into first-line treatment. However, along with the increased use of the SGAs, much literature on weight gain and related consequences has emerged. These include metabolic changes such as glucose dysregulation and hyperlipidemia. Additionally, with clozapine, cardiomyopathy, cardiac arrhythmias, and myocarditis are known to occur. In order for policy makers and clinicians to continue to advocate and prescribe these medications and for patients to continue to take these expensive medications the long-term treatment associated with SGAs should be beneficial, cost-effective and most importantly, safe. This proposed study will identify deaths from a group of 4,436 patients who have been treated with either dsperidone or clozapine in the State of Maryland and included in the Clozapine Authorization and Monitoring Program Database or the Maryland Antipsychotic Database. Death certificates for all who have died, identified by the Social Secudty Death Index, will be collected from the Maryland Division of Vital Records. Cardiac-related deaths are hypothesized to occur more frequently in patients who have been treated with clozapine as weight gain, glucose dysregulation and myocarditis occur more frequently with clozapine than risperidone. Risk factors for cardiac-related mortality associated with both medications will also be determined. Additionally, this preliminary study will provide a necessary foundation to set up a mechanism to collect autopsy reports and additional important clinical information such as cardiac and diabetes history on a case-cohort of patients. Other future plans include longer term follow-up and the comparison of all marketed SGAs. This study will provide needed information on the relative risk of cardiac-related mortality from antipsychotics, specifically those treated with risperidone and clozapine. This study is important as data on long-term health outcomes with atypical antipsychotics is lacking from the literature. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CARDIOMYOPATHY:PRO-OXIDANT ROLE OF AZT & MGDEFICIENCY Principal Investigator & Institution: Weglicki, William B.; Professor and Chair; Medicine; George Washington University 2121 I St Nw Washington, Dc 20052 Timing: Fiscal Year 2002; Project Start 01-MAY-2000; Project End 31-MAR-2004 Summary: (Abstract): The pathogenesis of HIV-related cardiomyopathy remains unclear and most likely may have multifactorial causes. Clinical data have revealed that both the virus and myocarditis are present, but often in separate areas, suggesting that HIV may play an indirect cytotoxic role. Both the HIV infection and drug therapy (AZT, pentamidine) may contribute to oxidative stress and Mg wasting. Clinical studies have indicated that HIV/AIDS patients may be deficient in Mg. In our studies, we have documented that Mg-deficiency triggers oxidative cardiomyopathic inflammation. We hypothesize that the drug therapy with AZT may synergize with pentamidine and Mgdeficiency to initiate neurogenic inflammatory events leading to oxidative stress and eventual cardiomyopathy. To test this hypothesis, we propose to use a rat model and cultured cardiovascular cells to determine the prooxidant effects of AZT (Aim 1) or with co-existing Mg-deficiency to induce cardiomyopathy, and cardiac dysfunction with imposed ischemia/reperfusion (I/R) stress (Aim 2). We will assess the therapeutic interventions by NMDA and NK-1 receptor blockade and by vitamin E (Aim 3). In collaboration with Dr. A. Basile of NIH, we will also employ the murine AIDS (MAIDS) model to assess the synergistic contributions of the virus and Mg-deficiency to the oxidative pathogenesis and possible interventional therapy (Aim 4). We will employ sensitive immunochemical techniques to quantify neuropeptides and cytokines, and in collaboration with Dr. Haudenschild of the American Red Cross Holland Laboratory, to
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Myocarditis
characterize histopathological progression in cardiac and skeletal muscles. Oxidative stress will be determined by measuring tissue glutathione and thiol status, accumulation of lipid peroxidation and nitric oxide products, and by free radical production and injury to isolated perfused I/R hearts. We anticipate that the information from these in vivo animal, tissue, and cellular studies may lead to potential diagnostic criteria and therapy for patients at risk of developing cardiomyopathy due to HIV disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CDI AND GAMMA DELTA+ IN VIRAL MYOCARDITIS Principal Investigator & Institution: Huber, Sally A.; Professor; Pathology; University of Vermont & St Agric College 340 Waterman Building Burlington, Vt 05405 Timing: Fiscal Year 2002; Project Start 01-APR-1998; Project End 30-JUN-2006 Summary: (provided by applicant): Coxsackievirus B3 (CVB3) infection causes myocarditis and dilated cardiomyopathy. The pathogenic mechanisms of the disease are complex. Myocarditis susceptibility correlates with activation of T cells expressing the Vgamma4 T cell receptor (TCR), CD4+ Thi (IFNgamma+) and CD8+alphabeta TCR+ autoimmune cytolytic T cells (CTL). Myocarditis resistance correlates to activation of Vgamma1+ and CD4+Th2 (IL4+) cells, and the absence of autoimmune CD8+alphabeta TCR+ effectors. Vgamma4+ cells kill both CVB3-infected myocytes and CD4+Th2 cells in vitro, and comprise up to 50% of the inflammatory T cells in the heart. CD8+alphabeta TCR+ autoimmune CTL kill uninfected but not virus-infected myocytes, and are the second most populous inflammatory cells in myocarditis. Since both Vgamma4+ and CD8+alphabeta TCR+ cells are cytolytic to cardiac myocytes in vitro, either or both populations might contribute to cardiac injury in vivo. Vgamma4+ cells recognize CD1, a major histocompatibility complex (MHC) class I-like molecule which normally presents hydrophobic lipid or peptide antigens. The autoimmune CD8+alphabeta TCR+ cells recognize antigen presented by classical MHC class I molecules. The overall goal of this application is to define the relative contributions of Vgamma4+ and CD8+alphabeta TCR+ cells to myocarditis in vivo, and determine whether Vgamma4+ cells facilitate CD8+alphabeta TCR+ cell activation by promoting CD4+ Th1 cell responses. The Specific Aims are to: 1) determine the relative importance of Vgamma4+ cell mediated killing of myocytes or modulation of CD4+ cell phenotype and activation of CD8+alphabeta TCR+ CTL in myocarditis; 2) determine CD1d expression in pathogenic versus non-pathogenic CVB3 infections and the role for lipid or peptide antigens in the CD1d-restricted Vgamma4+ T cell response; and 3) determine whether Vgamma4+ cells kill CD4+Th2 cells through CD1 -restricted responses. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: COCAINE AND CARDIOVASCULAR DYSFUNCTION IN MURINE AIDS Principal Investigator & Institution: Bauer, John A.; Associate Professor; Children's Research Institute 700 Children's Dr Columbus, Oh 432052664 Timing: Fiscal Year 2002; Project Start 07-JUL-1999; Project End 30-JUN-2004 Summary: The combination of cocaine abuse and HIV infection is an emerging problem and unique challenge for clinicians and researchers. Both are associated with cardiovascular complications alone, including acute events (angina, arrhythmias, myocardial infarction) and chronic conditions (myocarditis, vasculopathy, cardiomyopathy, congestive heart failure), but the mechanisms involved are undefined and and therapeutic strategies have not been optimized. Since they often coexist, it is
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reasonable to evaluate the pathophysiologic consequences of their combination. In this proposal our primary objectives are to define the mechanisms of cocaine induced cardiovascular dysfunction, and to determine the interactions of cocaine during retroviral infection, using an established and relevant animal model (murine AIDS, LPBM5 infection). Our collaborative studies are designed to provide new and integrated information at the functional, biochemical, cellular, and molecular levels. Our SPECIFIC AIMS are: 1. Test the hypothesis that dysregulation of NO is a key mechanism of cocaine-induced cardiovascular toxicity. -In vivo echocardiography and isolated vascular function will be related to tissue lipid peroxidation, protein nitration, NOS isoforms, and antioxidant enzymes. Transgenic mice will be employed. 2. Define cardiac responses to cocaine induced injury. -Tissue responses to injury will be evaluated, including immune cell infiltration, morphology, and apoptosis. Isolated myocyte electrophysiology, contractile protein function, and myosin isoform expression will also be examined. 3. Test the hypothesis that cardiac and vascular dysfunction is enhanced following cocaine and murine AIDS in combination. -Cardiovascular function, cellular, biochemical, and molecular parameters will be evaluated. 4. Corroborate the findings from our mouse studies using human autopsy tissues. -Cardiac specimens from HIV/AIDS patients will be examined. These studies will yield new information regarding mechanisms of cocaine- and retrovirus-induced complications and provide important insights regarding immune and cardiovascular system interactions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: COXSACKIE MYOCARDITIS AND VIRAL PERSISTENCE IN THE HEART Principal Investigator & Institution: Whitton, J Lindsay.; Professor; Scripps Research Institute Tpc7 La Jolla, Ca 92037 Timing: Fiscal Year 2002; Project Start 01-JAN-1998; Project End 31-DEC-2002 Summary: Coxsackieviruses, members of the picornavirus family, are important human pathogens. Coxsackievirus B3 (CVB3), is a common associated factor in human subacute, acute, and chronic myocarditis. In young adults CVB3 infections may cause cardiac arrhythmias and acute heart failure; and chronic disease may supervene, leading to dilated cardiomyopathy, requiring transplantation, or to death. To better understand the pathogenesis of this disease, several mouse model systems have been established, which appear to parallel many aspects of the human disease process. We have begun to investigate the mechanisms underlying CVB myocarditis. The goals of this proposal are: 1. To further investigate the immune determinants of CVB3 myocarditis. What viral proteins do CD4+ and CD8+ T cells recognize, and how do these cells interact? Is the Fas pathway involved in disease? 2. To investigate the roles of antibodies and T cells in control of CVB3 infection and disease. Which virus proteins can protect against CVB? Is priming of CD8+ T-cell immunity beneficial or harmful? 3. To determine the cells infected during acute and persistent CVB3 infection. Does CVB interact with B cells early in infection? What other cells are infected? What cells are infected during virus persistence? 4. To begin evaluation of the nature of persistent CVB3. We have developed a system in which persistently-infected mice contain high levels of infectious virus. Does this persisting virus differ from the original? 5. To evaluate treatments for persistent CVB3 infection. Antibody- deficient humans often suffer from chronic picornavirus infections, which are frequently refractory to treatment. Our mouse model of persistence in the absence of B cells will be used for testing different treatment regimens. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: COXSACKIEVIRUS 3B PERSISTENCE AND REACTIVATION IN VIVO Principal Investigator & Institution: Feuer, Ralph; Scripps Research Institute Tpc7 La Jolla, Ca 92037 Timing: Fiscal Year 2002; Project Start 01-MAR-2002 Summary: Coxsackieviruses have been implicated in a number of different human diseases, including acute and chronic myocarditis, viral-induced insulin-dependent diabetes mellitus (IDDM), pancreatitis, chronic inflammatory myopathy, and chronic fatigue syndrome. The proposed research will examine the mechanisms of persistence in Coxsackievirus B3 (CVB3) infected mice, using a recombinant virus expressing the enhanced green fluorescent protein (eGFP). Our laboratory has established a solid foundation of molecular and immunological techniques and reagents from previous studies of CVB3 persistence and pathogenesis. Preliminary studies with recombinant eGFP-CVB3 indicate that a certain population of Hela RW cells in culture cannot support a productive infection, including quiescent cells (G0) and cells blocked at the G2/M phase of the cell cycle. The following experiments will test the hypothesis that persistence of CVB3 in mice may rely on infection of quiescent cells incapable of supporting viral replication; and that a subsequent change in the cell-cycle status may lead to virus reactivation and further viral/immune mediated pathology (including myocarditis) in the host. SPECIFIC AIMS: 1. To examine the stability of persistent or latent CVB3 RNA. Quiescent cells infected with eGFP-CVB3 and maintained in serum free media without passage will be monitored at multiple time points for viral replication (plaque assay) and for stability of viral RNA (RT-PCR). Virus rescue will be observed (GFP, RT-PCR, and plaque assay) after cell stimulation with 10 % FBS. 2. To investigate what factors or stimuli may be involved in reactivation of CVB3. Transgenic mice expressing SV40 T antigen in cardiac tissues will be characterized for greater pathogenesis following infection with eGFP-CVB3 by histology and GFP fluorescence. Stimulated PBLs from persistently infected mice will be examined for CVB3 reactivation by GFP expression. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CYTOKINES CARDIOMYOPATHY
AND
LV
RECOVERY
IN
RECENT
ONSET
Principal Investigator & Institution: Mcnamara, Dennis M.; Director, Heart Failure Research Program; Medicine; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2002; Project Start 01-MAY-2002; Project End 31-MAR-2007 Summary: (provided by applicant): For patients presenting with the recent onset of primary dilated cardiomyopathy, the presence of myocardial inflammation may suggest a potentially self limited and reversible process, and patients with acute "myocarditis" may actually have a better probability of left ventricular recovery than those with more chronic disease. The poor sensitivity of endomyocardial biopsy has limited its clinical utility, and circulating plasma cytokines are potentially more sensitive indicators of a reversible myocardial inflammatory process. This proposal will investigate the hypothesis that the assessment of plasma cytokines in recent onset dilated cardiomyopathy, can help to prospectively delineate patients with greater likelihood of myocardial recovery. Specific Aim 1 will assess the correlation of baseline plasma cytokine levels (TNFa, TNF receptors, and IL-6) with echocardiographic measures of left ventricular systolic and diastolic function. The study will enroll 120 patients with recent
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onset idiopathic dilated cardiomyopathy or myocarditis with an LVEF less than or equal to 0.40. This will evaluate the hypothesis that plasma cytokines in recent onset cardiomyopathy are markers of cardiac inflammation and will correlate with more profound perturbations of myocardial function. Specific Aim 2 will evaluate the hypothesis that patients with more active myocardial inflammation (higher plasma TNFa) upon presentation, are more likely to have significant recovery of left ventricular systolic function at 12 month follow up. Echocardiographic assessment will be repeated at 6 and 12 months after entry. In addition we will evaluate the hypothesis that patients with higher plasma IL-6 levels will have a poorer event free survival during subsequent follow up. Specific Aim 3 will explore the hypothesis that polymorphisms of cytokine genes, in particular those in the TNFa and IL-6 promoters, will effect levels of their respective mediators, and will subsequently influence clinical outcomes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ENTEROVIRUS PERSISTENCE IN MYOCARDITIS Principal Investigator & Institution: Chapman, Nora M.; Pathology and Microbiology; University of Nebraska Medical Center Omaha, Ne 681987835 Timing: Fiscal Year 2002; Project Start 17-SEP-2002; Project End 16-SEP-2004 Summary: (provided by applicant): 20-40% of patients diagnosed with myocarditis or idiopathic dilated cardiomyopathy have been shown to have enteroviral RNA in their heart muscle, most likely resulting from infection with a coxsackievirus of the B (CVB) group. Studies of the murine model for myocarditis has also indicated that infection with cardiovirulent CVB3 results in persistence of viral RNA beyond the time at which infectious virus can be isolated. An investigation into the form of this persisting genomic RNA demonstrated that the enteroviral RNA has deletions of the extreme 5' end of the genome, a form which may have a more limited extent of replication than the wild type. This persisting virus can replicate in cell culture and can be passed but does not generate the classic cytopathic effect seen in cell culture of the wild type virus. This virus population displays interference with the replication of wild type CVBs. The hypothesis of this proposal is that deleted coxsackieviruses are generated in infection of the heart that limit replication and translation of this virus and interfere with remaining wild type virus so that virus persists. This persisting viral infection contributes to chronic inflammation and cardiomyopathy in later stage enterovirus-related inflammatory heart disease. The specific aims of this proposal are to analyze the replication in cell culture of five deleted genomes that we have detected, and their ability to interfere with replication of wild type CVBs and to assay for similar deleted genomes in enterovirus-positive human heart biopsies and in murine heart tissue from mice infected with different CVB serotypes. The careful analysis of how these defective genomes replicate is likely to lead to an antiviral treatment which may provide means of halting the progression to cardiomyopathy and preventing the necessity for heart transplantation in perhaps a quarter of candidates for this radical treatment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ENTEROVIRUS RNA TRANSLATION AND REPLICATION Principal Investigator & Institution: Barton, David J.; Assistant Professor; Microbiology; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, Co 800450508 Timing: Fiscal Year 2004; Project Start 01-JUL-1998; Project End 30-JUN-2009
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Myocarditis
Summary: (provided by applicant): Enteroviruses cause a diverse spectrum of human diseases including conjunctivitis, myocarditis, aseptic meningitis, acute flaccid paralysis, and fatal systemic infections of neonates. Poliovirus, the prototypic enterovirus, is well characterized at the molecular level and still serves as the most appropriate virus for detailed studies of RNA translation and RNA replication. In this proposal, poliovirus mRNA translation and RNA replication will be studied in cell-free reactions capable of supporting sequential translation and replication of poliovirus RNA. These reactions are advantageous because they support authentic translation and replication of poliovirus RNA while providing numerous technical advantages including the ability to synchronize viral mRNA translation and viral RNA replication. Using these reactions, we discovered that a cis-active RNA structure at the 5' terminus of poliovirus RNA interacts with seemingly distal cis-active structures in the viral open reading frame and the 3' nontranslated region to coordinately regulate the efficient translation and replication of poliovirus RNA. Partially characterized temporally dynamic ribonucleoproteins containing these cis-active RNA structures mediate and regulate the sequential steps of poliovirus mRNA translation and RNA replication. The experiments described in this proposal will characterize these ribonucleoproten complexes more thoroughly. Experiments will be performed to: 1) determine how the 5' cloverleaf RNA structure of poliovirus potentiates viral mRNA translation, 2) determine how translating ribosomes regulate, in part, the switch from viral mRNA translation to RNA replication, 3) identify the seemingly distal cis-active RNA structures that interact to regulate sequential steps of viral RNA replication, and 4) determine how protein 2C ATPase mediates interactions between seemingly distal cis-active ribonucleoprotein complexes. These studies will contribute substantial new information to support the popular new paradigm of 5'-3' RNA interactions in messenger ribonucleoprotein complexes and RNA replication complexes. The experiments directly test a hypothesis concerning the mechanism by which RNA replication machinery avoids ribosomereplicase collisions. The experiments also test a new, theoretically appealing hypothesis that clearly explains the mechanisms controlling asymmetric RNA replication. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ETHANOL & AIDS CARDIOMYOPATHY--MITOCHONDRIAL CONNECTION Principal Investigator & Institution: Wallace, Douglas C.; Professor; Ecology and Evolutionary Biol; University of California Irvine Irvine, Ca 926977600 Timing: Fiscal Year 2002; Project Start 03-JUL-1999; Project End 30-JUN-2004 Summary: Chronic ethanol (EtOH) exposure and AIDS exposure are known to cause cardiomyopathy, and to act synergistically when combined. Moreover, both ethanol and AIDS exposure have been observed to inhibit mitochondrial function, alter mitochondrial structure, and increase oxidative stress. Inhibition of mitochondrial oxidative phosphorylation reduces mitochondrial energy production and increases mitochondrial reactive oxygen species (ROS) generation, which have been linked to hypertrophic cardiomyopathy and dilated cardiomyopathy, respectively. Therefore, we hypothesize that both ethanol and AIDS exposure induce cardiomyopathy by reducing mitochondrial energy production through the direct disruption of OXPHOS and the indirect inhibition of OXPHOS by mitochondrial ROS. To test this hypothesis, we propose to challenge mice harboring various genetic defects in mitochondrial energy production and ROS detoxification to chronic ethanol, murine AIDS (MAIDS), and ethanol plus MAIDS exposure. The four strains will include (1) wildtype mice, (2) mice deficient (-/-) in the mitochondrial heart-muscle isoform of the adenine nucleotide
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translocator (ANT1), (3) mice partially deficient (+/-) in the mitochondrial Mn superoxide dismutase (MnSOD), and (4) mice deficient (-/-)in the glutathione peroxidase (GPx). The ANTI-defect reduces mitochondrial ATP availability to the heart and predisposes to hypertrophic cardiomyopathy. The MnSOD-defect increases mitochondrial ROS production and leads to dilated cardiomyopathy. The GPx1 -defect increases cardiac cytosolic hydrogen peroxide levels and increases the potential for viral myocarditis. Control, ethanol, MAIDS, and ethanol + MAIDS exposed mice will then be analyzed for cardiac pathology, changes in cardiac mitochondrial OXPHOS, increased cardiac oxidative damage, and alterations in the expression of mitochondrial and oxidative stress gene expression. If the ANT -/- animals develop a more severe hypertrophic cardiomyopathy and an increased predilection to dilated cardiomyopathy an ethanol and MAIDS exposure then this will indicate that mitochondrial energy deficiency is important in cardiomyopathy. If the MnSOD +/- animals have an increased frequency of dilated cardiomyopathy, then this will implicate mitochondrial ROS toxicity. If the GPx1 -/- animals have an increased incidence of myocarditis, then this will indicate that cytosolic oxidative stress is important in induced cardiomyopathy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GAMMA DELTA T CELL REGULATION OF MHC IE DEPENDENT TH2 CELL Principal Investigator & Institution: Newell, M. Karen.; Associate Professor; University of Vermont & St Agric College 340 Waterman Building Burlington, Vt 05405 Timing: Fiscal Year 2002 Summary: CD4+ T cells, activated in response to antigens presented by MHC class II molecules, differentiate from a common, naive precursor into Th1 or Th2 subtypes. These subtypes are distinguished by the cytokines they produce. Th1 cells make interferon gamma and IL-2, while Th2 cells make IL-4, IL-5 and IL-6. At least three mechanisms determine Th subset bias during immune response. The most widely studies mechanism involves conditions present during initial antigen stimulation and differentiation of the Th0 cell precursor. Thus, Th0 cell activation in the presence of IL12, IFNgamma, low antigen load, and possibly specific accessory molecules such as B71, results in preferential differentiation of Th0 cells to the Th1 phenotype. Once differentiated, Th1 cells are more susceptible to antigen driven activation induced cell death (AICD) than Th2 cells. Th1 cell populations may be more susceptible to AICD because these cells may undergo a form of autocrine cell death. AICD might lead to ultimate dominance of Th2 cells subsequent to antigenic stimuli unless there is a counterbalancing mechanism for selective elimination of Th2 cells. Using a murine model of coxsackievirus B3 (CVB3)-induced myocarditis, we have uniquely shown that T cells expressing the gamma-delta T cell receptor selectively kill differentiated Th2 cells but spare Th1 cells. Our studies indicate that expression of MHC class II IE molecules is necessary for gammadelta+ T cell regulation of Th2 cell response. These molecules may positively select unique populations of gammadelta+ T cells (Vgamma/Vdelta) during T cell ontogeny. Alternatively, gammadelta+ T cells capable of killing Th2 cells may require interaction with IE for activation or target cell recognition. The purpose of this application is to establish a link between the presence of IE and the activation of gammadelta T cells that regulate cytokine bias by death of Th2 cells. We propose that a specific type of gammadelta T cell dominating in IE+ mice kills Th2 cells leaving a Th1 dominant response. The following specific aims will test this model: 1) To determine if unique gammadelta subsets promote Th1 cell responses; 2) To determine how IE
16
Myocarditis
influences gammadelta T cell dependent death of Th2 cells and consequent Th1 bias; and 3) To determine the mechanism of gammadelta T cell dependent Th2 cell death. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENDER-BASED REGULATION OF AUTOIMMUNE MEMORY Principal Investigator & Institution: Tuohy, Vincent K.; Associate Staff; Cleveland Clinic Foundation 9500 Euclid Ave Cleveland, Oh 44195 Timing: Fiscal Year 2002; Project Start 01-JUN-2002; Project End 31-MAY-2006 Summary: (provided by applicant): Gender differences in the immune response are particularly evident in autoimmunity where females show increased susceptibility for developing autoimmune disease but males are predisposed to a poorer prognosis. This sex-based divergence in both disease susceptibility and disease outcome is not well understood yet is clearly evident in several diseases having prominent autoimmune features, including multiple sclerosis (MS), systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Graves' disease, and DCM. The experiments proposed in the current application are designed to address the basis for the differential prognosis of males versus females with autoimmune disease. To this end we have developed a murine EAMC model in which male SWXJ mice show prolonged maintenance of cardiac self- recognition and develop a high incidence of DCM, whereas female mice show aborted maintenance of T cell autoimmune memory and significant protection from the development of DCM. Thus, we hypothesize that the poor prognosis in males with autoimmune disease is due to their enhanced ability to maintain autoimmune T cell memory and persistence of inflammatory self-recognition. In Specific Aim 1, we will determine the mechanism by which differential gender- based maintenance of selfrecognition occurs in male versus female SWXJ mice with EAMC. In Specific Aim 2, we will determine how the patterns of autoimmune memory may be altered by immune and non-immune manipulations. In addition, we will determine whether persistence of memory causes DCM and whether the gender-based differential development of autoimmune memory may be therapeutically manipulated to alter disease outcome. We believe that our proposed studies will lead to a better understanding of how autoimmune memory is maintained or aborted by gender-defined conditions. Such information may ultimately serve as a basis for therapeutic intervention during the development of autoimmune disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GENETIC ANALYSIS OF PICORNAVIRUS RNA REPLICATION IN VIVO Principal Investigator & Institution: Flanegan, James B.; Professor; Biochem and Molecular Biology; University of Florida Gainesville, Fl 32611 Timing: Fiscal Year 2002; Project Start 01-JAN-1992; Project End 30-APR-2007 Summary: (provided by applicant): Poliovirus has served as the prototype virus for studying the replication mechanisms of picornaviruses and other (+) strand RNA viruses. The Picornaviridae family of small RNA viruses includes a large number of important pathogens. Some of the diseases associated with these viruses include meningitis, encephalitis, poliomyelitis, myocarditis, respiratory infections and hepatitis. In this study, we are using molecular genetic techniques to study poliovirus RNA replication in vitro and in vivo. We have developed new experimental methods that can be used in combination with classic viral genetic procedures in virus-infected cells. Using HeLa S10 in vitro translation-RNA replication reactions and preinitiation RNA
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replication complexes, we are investigating the viral replication cycle in vitro including viral protein synthesis, the cre(2C)-dependent synthesis of VPgpUpU, the synthesis of () and (+) strand RNA and the formation of infectious virus. Genetic complementation and RNA recombination assays are powerful methods to study the activities associated with trans-acting viral proteins and the cis-acting sequences and structures in the viral RNA. Since all of the viral replication proteins can be provided in trans in cell-free reactions, we are using genetic complementation assays to identify specific viral proteins and viral protein precursors that are required for the assembly of functional RNA replication complexes. We are also using complementation assays to identify and characterize cis-acting RNA sequences that are required for the initiation of (-) and (+) strand RNA synthesis. During the course of our recent studies, we have developed an in vitro recombination assay and methods to specifically assay for (-) and (+) strand RNA synthesis. Our basic experimental plan is to use these methods to answer questions of fundamental importance regarding the replication of poliovirus and other picornaviruses. In this renewal application, we are requesting funding that will include the following specific aims. (1) Identify and characterize the cis-acting replication elements in poliovirus genomic RNA. (2) Use a genetic complementation analysis to characterize the viral replication proteins and their precursors regarding their role in viral RNA replication. (3) Investigate the mechanisms involved in viral RNA recombination using an in vitro recombination assay. (4) Characterize the role of the 3' NTR and associated poly(A) tail in viral RNA replication. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HIV TAT EFFECT ON ENDOTHELIAL CELL FUNCTION Principal Investigator & Institution: Terada, Lance S.; Professor of Medicine; Internal Medicine; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2002; Project Start 30-SEP-1998; Project End 31-JUL-2003 Summary: Infection of patients with Human Immunodeficiency Virus 1 (HIV) is associated with diverse alterations in endothelial function. These include syndromes marked by inappropriate endothelial cell (EC hyperplasia (primary pulmonary hypertension), incomplete differentiation (Kaposi's sarcoma), and acute inflammation (pneumonitis, myocarditis, encephalitis, pericarditis). Although these perturbations in EC function can be diffuse, direct infection of EC by HIV is unusual, may be restricted to certain vascular beds, and is generally abortive. Such endothelial alterations are therefore more likely to be the result of HIV-related circulating mediators, rather than of direct endothelial infection by retrovirus. We hypothesize that the secreted HIV transcription factor Tat acts to modify EC proliferation, differentiation, apoptosis, and expression of inflammatory molecules, and additionally, that these effects are modulated by the cytokines TNF alpha, IL-1 beta, and IFN gamma. We further hypothesize that the diverse and sometimes opposing effects of Tat are mediated by the oxidant-dependent differential activation of the various MAP Kinase signaling cassettes. Our preliminary data confirm that exposure of human EC to Tat acutely increases intracellular oxidant levels concomitant with activation of c-Jun amino terminal kinase (JNK). Further, Tat alters the TNF-alpha- mediated activation of JNK and the DNAbinding affinity of the transcription factor AP-1, a potential target of JNK. Our general objectives are to correlate oxidase assembly, oxidant production, MAPK activation, and DNA binding and promoter activation of transcription factors, with cell phenotype (proliferation, differentiation, apoptosis, inflammatory molecule expression, and leukocyte adhesion) in human EC exposed to Tat and cytokines, using a variety of interventions designed to dissect different signaling pathways. The significance of this
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Myocarditis
work is to provide further insight into the cause of various AIDS-related vascular syndromes, as well as to understand the basis for fundamental EC functions in normal individuals. This may lead to specific treatments for HIV-infected patients, and may also suggest novel strategies for treatment of non-HIV related diseases through modulation of endothelial cell function. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INHIBITION PHAGOCYTOPHILA
OF
NADPH
OXIDASE
BY
ANAPLASMA
Principal Investigator & Institution: Carlyon, Jason A.; Internal Medicine; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2003; Project Start 15-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): Human granulocytic ehrlichiosis (HGE) is an emerging infection of the blood that results in leukopenia and thrombocytopenia. If left untreated, the disease can manifest itself as severe neutropenia, hypotension, shock, and may potentially be fatal due to myocarditis, pancarditis, or to opportunistic infections resulting from impaired host defense mechanisms. Recent evidence suggests that kidney and pancreas transplant recipients are at risk for contracting HGE. A. phagocytophila, the etiologic agent of HGE, persists within its mammalian host by colonizing neutrophils. Neutrophils are primary effector cells involved in phagocytosing and killing bacterial invaders. This bactericidal activity is partially dependent on the superoxide anion produced by the rapidly activatable, multi-component enzyme, NADPH oxidase. A. phagocytophila, however, utilizes multiple strategies to prevent superoxide anion production. It is established that the bacterium inhibits the mRNA expression of gp91phox, a component of NADPH oxidase. Preliminary data presented here demonstrates that A. phagocytophila also prevents transcription of rac2, the key factor of NADPH oxidase. Aims 1 and 2 seek to define the mechanisms responsible for the inhibition of rac2 transcription. Evidence suggests that, prior to preventing rac2 and gp91phox mRNA expression once inside the host cell, A. phagocytophila initially inhibits activation of preformed NADPH oxidase components during invasion. Activation of Rac2 represents the initial, integral step of NADPH oxidase assembly. Therefore, Aim 3 will investigate whether A. phagocytophila inhibits Rac2 activation during invasion. Collectively, these studies will decipher the complex means by which A. phagocytophila prevents the neutrophil respiratory burst. In addition, these studies will lead to a more thorough understanding of neutrophil biology, specifically he factors that regulate rac2 mRNA expression and NADPH oxidase activation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MATERNAL AUTOANTIBODIES--PATHOGENESIS OF NEONATAL LUPUS Principal Investigator & Institution: Buyon, Jill P.; Professor; Hospital for Joint Diseases Ortho Inst Orthopaedic Institute New York, Ny 10003 Timing: Fiscal Year 2002; Project Start 01-FEB-1994; Project End 15-JUN-2003 Summary: (Adapted from the Applicant's Abstract): Congenital heart block (CHB) is associated with transplacental passage of maternal autoantibodies to the ribonucleoproteins (RNP), 48kD SSB/La, and 52kD and 60kD SSA/Ro. The affected mothers might have SLE, or Sjogren's syndrome or might be asymptomatic. Why the developing fetal heart is specially vulnerable to such autoantibodies and why CHB occurs in the children of only a fraction of mothers with the autoantibodies, are not
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known. Moreover, the putative autoantigens are intracellular RNP particles, therefore it is not clear how they cause damage to the fetal cardiocytes. In Aim 1, the applicants propose to identify proteins that interact with the Ro and La RNP complexes and are selectively expressed in the human fetal heart. Novel autoantigens unique to fetal heart that are recognized by antisera from mothers of children with CHB might be discovered and a better understanding of the biological function of the Ro and La autoantigens may result from these studies. In Aim 2, the applicants will determine if the candidate autoantigens associated with autoimmune-CHB come to the surface membrane of cardiocytes during apoptosis thus being accessible to the maternally transmitted autoantibodies. In Aim 3, the applicants will develop a mouse model of CHB to understand the pathogenesis of the human disease in depth. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MECHANISMS OF COCAINE INDUCED EXACCERBATION OF VIRAL MYO Principal Investigator & Institution: Morgan, James P.; Herman Dana Prof. of Medicine; Beth Israel Deaconess Medical Center St 1005 Boston, Ma 02215 Timing: Fiscal Year 2002; Project Start 15-JUL-1999; Project End 31-MAY-2004 Summary: Clinical evidence suggests that cocaine abusers have an increased incidence of Human Immunodeficiency Virus (HIV) infection and HIV-related myocarditis. These data indicate a causal relationship between cocaine use and myocarditic viral pathogenicity, which we plan to investigate in this proposal by studying a readily reproducible murine model of viral myocarditis using Encephalomyocarditis (EMC) Virus as a surrogate for HIV. Our central, unifying hypothesis is that cocaine-induced exacerbation of viral myocarditis is an indirect effect mediated by drug-induced enhancement of catecholamine concentrations in the heart. When catecholamines from the systemic circulation and local release at cardiac sympathetic nerve endings reach toxic concentrations, they may compromise cellular integrity and specific cellular and humoral body defenses, making the myocardium more susceptible to infection. We will test this hypothesis by means of seven specific aims that employ techniques currently available in the laboratories of the collaborating Investigators. I. We will determine whether chronic cocaine treatment alone can induce myocarditis, necrosis or apoptosis. II. We will test the hypothesis that exposure to cocaine can enhance the susceptibility of mice to myocarditis after virus exposure. III. We will determine whether cocaine can enhance persistence of the viral genome. IV. We will determine whether cocaine can impair specific body defenses against viral infection by measuring T cell function and IgM levels. V. We will determine whether the adrenergic or local anesthetic properties of cocaine are responsible for increased viral myocarditic pathogenicity. VI. We will test the hypothesis that catecholamine-mediated stimulation of the adrenergic receptors on myocytes is responsible for increased viral myocarditic pathogenicity by use of sympatholytic agents. VII. We will demonstrate that the enhancement of viral myocarditic pathogenicity produced by cocaine is synergistic with other drugs, foods and activities that increase catecholamine levels. Taken together, these results will provide new mechanistic information about the etiology of viral myocarditis in cocaine abusers, should allow us to identify distinct risk factors for developing myocarditis in the general population, and may provide a rational basis for predicting who may place themselves at increased additional risk by the use of cocaine, particularly among the HIV-exposed population. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: INTERACTION
MOLECULAR
CHARACTERIZATION
OF
MCLI
PCNA
Principal Investigator & Institution: Fujise, Kenichi; None; University of Texas Hlth Sci Ctr Houston Box 20036 Houston, Tx 77225 Timing: Fiscal Year 2002; Project Start 01-JUL-1999; Project End 30-JUN-2004 Summary: Dr. Fujise's long-term objectives is to serve as a molecular biologist and cardiologist, whose main focus is prevention and treatment of cardiovascular diseases using molecular biological approach. Under the guidance and direction of Dr. Edward T.H. Yeh, Dr. Fujise has performed the research in the field of apoptosis regulation. In the process of characterizing MCL1(ML1 myeloid cell leukemia), a Bcl-2 homologue, Dr. Fujise discovered a novel interaction between MCL1 and PCNA (Proliferating cell nuclear antigen). PCNA is a 29kDa nuclear protein involved in DNA repair and replication and cell proliferation and differentiation. The role of PCNA has been implicated in pathogenesis of SLE (Systemic lupus erythematosis), restenosis after angioplasty and others. Apoptosis as well as the lack of it play critical roles in many human diseases including cancer, AIDS, myocarditis, atherosclerosis and myocardial infarction. The MCL1-PCNA interaction may be an important molecular link between anti-apoptotic proteins and cell cycle proteins. Based on the hypothesis that MCL1 plays a role in DNA repair and replication and cell proliferation and differentiation through its interaction with PCNA, Dr. Fujise here proposes to characterize the MCL1-PCNA interaction over the five years of the Award. First, Dr. Fujise will further characterize biochemical aspects of MCL1-PCNA interaction, using yeast two hybrid system. Second, Dr. Fujise will investigate the functional significance of the MCL1-PCNA interaction, including the effect of MCL1 over- expression on cell proliferation and the effect of MCL1 on DNA polymerase delta, DNA methylase, and DNA repair enzymes in the presence of PCNA. Finally, the impact of cell cycle phases, phosphorylation and DNA damage on MCL1-PCNA interaction and MCL1's subcellular localization will be evaluated. With Dr. Yeh as his Mentor, Dr. Fujise will perform his research at Research Center for Cardiovascular Diseases within the Institute of Molecular Medicine for Prevention of Human Diseases, devoting 80 percent of his professional time to the research. The Research Center and Institute will provide Dr. Fujise with a highly interactive and productive environment as well as with all the equipment needed for his research. The Scientific Advisory Committee, consisting of three senior scientists including the mentor will guide Dr. Fujise's scientific progress. At the completion of this Award, Dr. Fujise will be an independent, highly productive investigator with a high likelihood of making critical contributions in the fieled of apoptosis regulations and in prevention and treatment of cardiac diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOLECULAR MECHANISMS IN T. CRUZI CARDIOMYOPATHY IN AIDS Principal Investigator & Institution: Tanowitz, Herbert B.; Professor; Pathology; Yeshiva University 500 W 185Th St New York, Ny 10033 Timing: Fiscal Year 2004; Project Start 01-JAN-2004; Project End 31-DEC-2008 Summary: (provided by applicant): Chagas' disease is caused by the protozoan parasite T. cruzi and is now recognized as an emerging HIV/AIDS-related, opportunistic infection. Subsequent to immunosuppression there is reactivation of dormant organisms leading to myocarditis and necrotizing encephalitis. Since HIV-infected patients receiving HAART live for many years there is the likelihood that there will be repeated
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episodes of reactivation as their immune status waxes and wanes. Hence, progressive myocarditis and cardiovascular remodeling and chronic cardiomyopathy will likely develop in a more rapid fashion. In this application we have defined ventricular remodeling as changes in structure and function following myocardial damage together with characteristic molecular changes. These changes are the result of inflammation and/or necrosis. T. cruzi infection of the myocardium results in a dilated cardiomyopathy. Our overall objective is to examine some of the important signaling pathways involved in cardiac remodeling as a consequence of the T. cruzi infection. We plan to examine the consequences of T. cruzi-infection on cyclins in vitro, Our investigations clearly indicate that T. cruzi-induced ERK activation modulates the expression and/or activity of cyclins, which function as mediators of cellular proliferation and differentiation. Cyclins are responsible for remodeling in the cardiovascular system. Therefore, the kinetics of the expression of cyclins in infected cultured cells and co-culture systems. Since we have demonstrated that T. cruzi induces expression of cyclin D1, we will determine the molecular mechanisms involved in regulation of cyclin D 1 promoter activation in cardiac fibroblasts employing transient transfection/promoter assays. We plan to determine the consequence of T. cruzi infection on cyclins in mouse models of chagasic heart disease on. During acute T. cruzi infection there is activation of ERK, transcription factors AP-1 and NF-kB and increased expression of cyclin D 1 in the myocardium. Therefore, in the mouse model of Chagas' disease the kinetics of expression of cell cycle regulatory proteins in the cells of the myocardium of T. cruzi-infected mice will be determined and correlated with progression of cardiomyopathy. The mechanisms underlying the alterations in these proteins in the myocardium will be investigated by a variety of techniques including immune complex assays and cell proliferation experiments. The contribution of cyclin D 1 in cardiovascular remodeling will be investigated utilizing mouse models including cyclin D1 null mice and mice in which NF-r.d3 and ET-1 have been selectively deleted from cardiac myocytes. These studies will lead to a better understanding of cardiac remodeling in chagasic cardiomyopathy, an emerging opportunistic infection in AIDS. In addition, it will provide potential targets of adjunctive therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOLECULAR MECHANISMS OF AUTOIMMUNE HEART DISEASE Principal Investigator & Institution: Lipes, Myra A.; Joslin Diabetes Center Boston, Ma 02215 Timing: Fiscal Year 2004; Project Start 15-JUL-2004; Project End 31-MAY-2008 Summary: (provided by applicant): Autoimmune myocarditis is a major cause of sudden death in children and young adults. Although widely thought to be of infectious etiology, in the majority of cases the cause of disease is unknown. We have discovered that expression of the human HLA class II molecule, HLA-DQ8, in nonobese diabetic mice that lack endogenous murine class II genes results in the spontaneous development of autoimmune myocarditis. Disease was characterized by premature death due to heart failure, destructive lymphocytic infiltrates in the myocardium, and circulating IgG autantibodies against cardiac myosin heavy chain, similar to human myocarditis. Analysis of CD4 T cell clones isolated directly from the heart lesions reveals that, in contrast to the autoantibodies that cross-react with skeletal and cardiac myosin, the CD4 T cells recognize only cardiac myosin, consistent with the cardiac-specificity of this autoimmune disease process. These clones produce large amounts of interferon-gamma, but not IL-4, consistent with a pathogenic Th1 phenotype. The specific aims of this project are: 1) to use the T cell clones a functional probes to identify the epitopes of the
22
Myocarditis
myosin 3rotein that are reponsible for the loss of self-tolerance to cardiac myocytes, 2) to identify the primary cellular mediators involved in the pathogenesis of disease and to use congenic strains to determine whether type 1 diabetes and autoimmune myocarditis are controlled by common 'autoimmunity genes', 3) to investigate whether myocarditis in humans is an organ-specific autoimmune disease associated with HLA-DQ8 and whether it can be detected with a combination of HLA typing and immunological testing. These translational studies will involve a collaboration between the PI and Dr. Kenneth Baughman, Director of the Advanced Heart Disease Division at Brigham and Women's Hospital and a leader in the field of myocarditis. The results of these studies could open a new window into the etiology of human myocarditis and lead to improved methods to diagnose and treat this serious disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOLECULAR MECHANISMS OF TH1/TH2 DEVELOPMENT Principal Investigator & Institution: Budd, Ralph C.; Director, Immunobiology Program; Medicine; University of Vermont & St Agric College 340 Waterman Building Burlington, Vt 05405 Timing: Fiscal Year 2002; Project Start 30-SEP-1999; Project End 31-AUG-2003 Summary: This Multi-Project Program investigates the regulation of Th1 and Th2 cells at two specific levels, control by gammadelta T cells and by transcription. The first two projects study the model the gammadelta T cells promote a Th1 environment by selectively killing Th2 cells. This model evolved from work in two laboratories. Dr. Sally Huber showed that susceptibility to murine Coxsackievirus (CVB3)-induced autoimmune myocarditis correlated with a Th1 response and resulted from gammadelta T cell-mediated death of Th2 cells. Dr. Ralph Budd showed that gammadelta T cells selectively kill differentiated Th2 cells, but spare Th1 cells during the pathogenesis of Borrelia Burgdorferi- induced Lyme arthritis. In the Coxsackievirus system, depletion of gammadelta T cells alleviated the myocarditis and left a Th2 response whereas adoptive transfer of gammadelta T cells enhanced disease and a Th1 response. Drs. Karen Newell and Huber have extended these results showing that expression of MHC class II IE in resistant C57BL/6 mice renders them susceptible to CVB3 myocarditis. This susceptibility is alleviated by the removal of gammadelta T cells which results in a Th2 response. Project 1 uses in vivo murine systems in Drs. Newell and Huber s laboratories, and in vitro murine systems with Dr. Susan Swain s group, to establish a link between expression of MHC class II IE molecules and the activation of gammadelta T cells that kill Th2 cells during the course of Coxsackieviral infection. Project 2 uses human synovial Vdelta1 T cell clones to determine if gammadelta T cells bias the Cd4+ immune response in vitro by selectively lysing Th2 cells in a Fas (CD95)-dependent manner. These two projects are complementary and will provide a basis for comparison between Coxsackievirus and Borrelia Burgdorferi- induced autoimmune diseases. Surviving antigen-specific T cells provide long lived specific memory. Little is known of the regulatory mechanisms that control the balance between naive, effector Th1 and Th2, and ultimately memory T cell responses to antigens. Dr. Mercedes Rincon s group has shown that Th2 effector cells manifest considerably more NFAT and AP-1 transcriptional activity than Th1 cells. In Project 3 Dr. Rincon will extend these findings to determine a) mechanisms that regulate NFAT transcriptional activity in naive, effector Th1 and Th2, and memory CD4+ T cells, and b) the role of specific NFAT family members in the activation, differentiation, and survival of these CD4+ T cell populations. These studies will provide information about the cellular regulation of effector Th1 and Th2 cells (Projects 1 and 2) as well as the molecular regulation of
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cytokine differentiation during the transition from naive to become memory T cells (Project 3). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOLECULAR PATHOGENESIS OF CARDIAC DYSFUNCTION Principal Investigator & Institution: Giroir, Brett P.; Associate Professor; Pediatrics; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2002; Project Start 01-APR-2000; Project End 31-MAR-2004 Summary: The goal of this proposal is to determine the molecular mechanisms of cardiac dysfunction that occurs during septic shock and following thermal trauma. Previous work has demonstrated that cardiac dysfunction is mediated by the cytokine tumor necrosis factor-alpha (TNF), which is produced locally in the myocardium by cardiac myocytes. This proposal utilizes novel molecular and genetic strategies to investigate the mechanisms of TNF's detrimental effects and to develop therapeutic approaches for TNF-related cardiac contributions. First, we will study transgenic mice in which TNF is constitutively expressed only by cardiac myocytes. These mice develop profound cardiac dysfunction, cardiomyopathy, myocarditis, and cardiac failure which mimics cardiac contractile dysfunction in humans. By breeding these transgenic animals to mice which have undergone targeted disruption of iNOS (inducible nitric oxide synthase), IRAK (IL-1 receptor associated kinase), and ICAM-1 / P-selectin, as well as by pharmacological inhibition of specific pathways, we will quantitatively determine the involvement of iNOS, IL-1, and transmigrated leukocytes in the pathogenesis of myocardial failure. Cardiac phenotype will be characterized primarily by in vitro Langendorff perfusion of isolated mouse hearts; confirmatory longitudinal analysis of function will be accomplished in vivo by ECG-gated MRI imaging. Physiologic findings will be correlated with survival, post-mortem histology, and the pattern of cardiac gene expression. Next, we will optimize the transgenic animal model by developing a binary transgene system which is cardiac specific, and regulatable by dietary tetracycline. Through this system, we will determine if the effects of TNF are related to dose and duration of expression. We will describe the cascade of secondary cytokines induced by TNF. We will also determine whether low-level, transient expression of TNF may be evolutionary adaptive, and serve a protective role against subsequent cardiac insults. By understanding the molecular mechanisms by which TNF impedes myocardial performance, it will be possible to develop specific, targeted therapeutic strategies for the treatment of sepsis, burn trauma, and other TNF-related cardiac conditions such as cardiomyopathy, myocarditis, and ischemic heart disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NOVEL SIGNALING PATHWAYS FOR ANGIOTENSIN II IN THE HEART Principal Investigator & Institution: Baker, Kenneth M.; Professor; None; Texas A&M University Health Science Ctr College Station, Tx 778433578 Timing: Fiscal Year 2002; Project Start 01-JUL-1999; Project End 30-JUN-2004 Summary: (Adapted from Investigator's Abstract): Angiotensin II, the effector peptide of the renin-angiotensin system, regulates volume and electrolyte homeostasis and is involved in cardiac and vascular cellular growth in humans and other species. This system, which has been conserved throughout evolution, plays an important role in cardiac and vascular pathology associated with hypertension, coronary heart disease, myocarditis and congestive heart failure. These critical actions of angiotensin II are
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Myocarditis
mediated primarily through the AT1, G-protein (guanylyl nucleotide binding protein) coupled receptor. In addition to coupling to conventional G-protein signal transduction pathways, the AT1 receptor was recently shown to increase the tyrosine phosphorylation of several intracellular substrates, including the STAT (Signal Transducers and Activators of Transcription) family of novel transcription factors, in rat cardiac fibroblasts, myocytes and vascular smooth muscle cells, and AT1A receptor transfected Chinese Hamster Ovary (CHO) cells. It is likely that this pathway has a role in angiotensin II mediated gene regulation, cardiac and vascular cellular growth and inflammatory responses. The AT1 receptor, which lacks intrinsic tyrosine kinase activity, has been shown in rat vascular smooth muscle cells and cardiomyocytes, to associate with Jak2, a member of the Janus family of kinases (JAK), implicated in the tyrosine phosphorylation of the STATs. These findings, as originally described for cytokines (interleukins and interferon gamma), suggest that the AT1 receptor may contain a docking site for Jak2. Analysis of the amino acid sequence of the AT1 receptor, also suggests potential binding motifs for Src kinase, Stat3, and SH-PTP1D (a tyrosine phosphatase), all of which are components of the JAK-STAT pathway. However, for Gprotein receptors, the proximal mechanisms for coupling and activation of these novel signal transduction pathways, remain to be elucidated. Utilizing molecular, biochemical and cellular approaches, the PI will determine the structural regions of the AT1 receptor responsible for the interaction of signaling proteins and cytosolic tyrosine kinases and define the role of G-proteins in the recruitment and activation of the JAK-STAT components. These studies are important for elucidating angiotensin II mediated actions in target cells and for a more complete understanding of the molecular signaling of the heptahelical superfamily of receptors. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PEPTIDE MYOCARDITIS
VACCINE
FOR
EXPERIMENTAL
AUTOIMMUNE
Principal Investigator & Institution: Zimmerman, Daniel H.; Cel-Sci Corporation 8229 Boone Blvd, Ste 802 Vienna, Va 22182 Timing: Fiscal Year 2003; Project Start 01-MAY-2003; Project End 31-OCT-2004 Summary: (provided by the applicant): In A/J Mice Experimental Autoimmune Myocarditis (EAM) can be induced by infection with coxsackie virus B 3 or by immunization with murine or porcine cardiac myosin or a cardiogenic peptide from the murine cardiac myosin (My-l). In all these three cases the mice develop autoantibodies to cardiac myosin, and the disease is characterized by a Th2 phenotype. Previously one of us has shown that the EAM disease process can be blocked by: (1) cobra venom factor (CVF), which depletes complement; or by (2) monoclonal antibodies to the complement receptors involved with the innate immune system; or by (3) antibodies to IL-4 or by (4) Interferon-gamma, which inhibit the Th2 pathway of the inductive immune system. Furthermore, anti-IFN-gamma, treatment exacerbated the EAM. More recently one of our (NRR) studies has demonstrated that IL-10 has a disease inhibiting effect during the later effector phase (after day 10) and not in the early inductor phase (before day 10) using a revised the model which eliminates the Pertussis toxin and results in a slower milder form of disease. Other recent reports also have show a role for IL-10 in disease control in EAM, including use of pentoxifylline which was reported as being used in the human condition. In preliminary studies we have found that pretreatment with a peptide conjugate of the cardiogenic peptide My-l, J-My-l, which is designed to promote a Th1 response against the My-1 antigen, has significantly reduced disease severity. In this study, we intend to examine in more detail and define the role and the effect this
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conjugate has using the slower progressing EAM model by eliminating the Pertussis toxin. While from a commercialization point the ultimate goal is a product that can be used after disease is diagnosed in this phase I SBIR we will determine whether administration of J-My-1 is beneficial if performed before (1) induction of disease, or (2) during either the induction or (3) effector phases. The specific aims are three Specific Aim 1 To evaluate and compare efficacy of the My-1 L.E.A.P.S. construct, J-My-l, as either an immunotherapeutic vaccine and/or prophylactic treatment for My-1 induced EAM in A/J mice. Specific Aim 2 To evaluate the TH1 and TH2 cytokine(s) profiles and apoptosis markers in spleen lymphocytes obtained from individual NJ mice immunized with J-My-1 to define some aspects of disease induction by the My-1 and the mode of action of J-My-land elucidate the cell population associated with the Thl, Th2 cytokines. The effects of J-My-1 administration on the presence and frequency of this cell type will be evaluated. Our goal is to demonstrate that the severity of EAM can be reduced by JMy-1 administration in animals with EAM. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PEROXYNITRITE AND NITROTYROSINE IN HEART DISEASE Principal Investigator & Institution: Beckman, Joseph S.; Professor & Director; None; Oregon State University Corvallis, or 973391086 Timing: Fiscal Year 2002; Project Start 01-JAN-1998; Project End 31-DEC-2002 Summary: Peroxynitrite (ONOO-) formed by the diffusion-limited reaction of superoxide with nitric oxide is a major mechanism of oxidative damage in the heart. Isolated heart muscle exposed to micromolar concentrations of peroxynitrite for only a few minutes exhibit many of the pathological changes characteristic of clinical heart disease, including injury to mitochondria, loss of contractile function and irreversible increases in diastolic stiffness. One of the major consequences of peroxynitrite attack is the selective nitration of tyrosine residues in specific proteins. Myocytes in rat heart become nitrated quickly during ischemia/reperfusion and inhibition of nitric oxide production both preserves myocardial function and reduces tyrosine nitration. In the human heart, similar patterns of myocyte nitration occur after ischemia, sepsis and myocarditis. Quantitative HPLC analysis revealed 1-7% of protein-bound tyrosines are nitrated in septic patients, showing nitration is a significant pathological process in humans. Western blots demonstrate that a surprisingly limited number of proteins are vulnerable to tyrosine nitration by peroxynitrite. The principal investigator has shown that manganese superoxide dismutase, actin and intermediate filaments are nitrated in human autopsy material and that the function of these proteins is markedly diminished by peroxynitrite in vitro. Electrospray mass spectrometry has revealed that peroxynitrite preferentially nitrates certain tyrosine motifs in hydrophilic regions common to many structural proteins. The principal investigator hypothesizes that tyrosine nitration of structural proteins by peroxynitrite contributes to myocardial injury. His first aim is to quantitatively assess the magnitude of tyrosine nitrosation in ischemic rat heart and to directly measure peroxynitrite using a novel probe they have developed. The second aim is to identify which specific proteins are nitrated in rat and human heart and determine by tandem mass spectrometry which tyrosines in these proteins are nitrated. The third aim is to characterize how nitration affects the function of actin and then other structural proteins to assess how nitration can affect myocontractile proteins. These studies are a new and novel approach to understanding the specific mechanisms by which biologically generated oxidants injure the heart and allow us to identify major targets for peroxynitrite attack in vivo. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Myocarditis
Project Title: POXVIRUS ADVERSE EFFECTS ON CARDIAC CELLS AND THE HEART Principal Investigator & Institution: Sherry, Barbara A.; Professor; Molecular Biomedical Sciences; North Carolina State University Raleigh 2230 Stinson Drive Raleigh, Nc 27695 Timing: Fiscal Year 2004; Project Start 01-APR-2004; Project End 31-MAR-2006 Summary: (provided by applicant): In response to concerns that bioterrorists may release smallpox virus in the United States, the government has implemented a multistage vaccination program. However, the observation of cardiac adverse events following vaccination has resulted in the Centers for Disease Control recommending that people at risk for heart disease should be excluded from the vaccination program. Notably, myocarditis has been diagnosed in 18 recent smallpox vaccinees in the USA. Despite this recent temporal association between myocarditis and smallpox vaccination as well as a similar historic association, there have been no studies of the effects of poxviruses on cardiac cells, or the development of any animal models to study poxvirus-induced myocarditis. For other viruses, myocarditis can reflect a direct cytopathogenic effect of the virus on cardiac myocytes, or can be mediated by immune cells, cytokines, or other soluble factors. Poxviruses can be directly cytopathogenic, but also encode a number of modulators of cytokine responses. Cowpox virus contains the full complement of known orthopoxvirus accessory genes that affect immune responses, while DryVax (the current vaccine strain of vaccinia virus) encodes fewer accessory genes, and modified vaccinia Ankara virus (MVA, which is replication-defective in human cells) contains even fewer accessory genes. Our preliminary data demonstrate that cowpox virus and DryVax replicate in murine primary cardiac myocyte cultures (PCMCs) whereas MVA does not. Moreover, cowpox, DryVax, and MVA are each cytopathogenic to these cultures, though the type of cytopathogenicity is virus strainspecific. We hypothesize that poxviruses have virus strain-specific adverse effects on cardiac cells, either directly or indirectly, resulting in damage to cardiac myocytes and the heart. In Specific Aim 1, we will determine the effect of these three poxviruses (cowpox, DryVax, and MVA) on murine primary cardiac myocyte cultures (PCMCs) and control cultures, analyzing viral infection and gene expression, and induction of cytopathogenicity. In Specific Aim 2, we will determine the association between cytokines and poxvirus infection on cytopathogenicity to PCMCs and control cultures. In Specific Aim 3, we will determine whether these poxviruses induce myocarditis in a variety of mouse strains. Studies proposed in this R21 application will provide the foundation for future in-depth studies with the goal of improving current and future smallpox vaccines. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RECEPTOR DIVERSITY IN RECOGNITION OF INFLUENZA HA Principal Investigator & Institution: Caton, Andrew J.; Associate Professor; Wistar Institute Philadelphia, Pa 191044268 Timing: Fiscal Year 2002; Project Start 01-APR-1987; Project End 28-FEB-2007 Summary: (provided by applicant): The objective is to analyze factors governing tolerance and autoreactivity among murine CD4+ T and B cells in transgenic mice that express the influenza virus PR8 hemagglutinin (HA) as a well-characterized neo-self antigen (HA Tg mice). In particular, how the distinct specificities of separate populations of CD4+ T and B cells affect their negative selection by the neo-self HA, and processes that can lead to the activation of autoreactive lymphocytes in HA Tg mice will be examined. Aim 1 will examine the selection and functional potential of autoreactive
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CD4+ T cells that have low avidities for a self-peptide in TCRxHA Tg mice. Whether activation increases the sensitivity of low avidity T cells to the extent that they become responsive to a self-peptide will be determined. In addition, how TCR specificity and/or virus infection contributes to the ability of CD4+ T cells to mediate autoimmune myocarditis in HA Tg mice expressing the HA in cardiac tissue will be assessed. Aim 2 will examine factors governing the phenotypic potentials of B cells that express characteristic variable region clonotypes, that are representative of primary versus memory responses to the HA in virus-immunized BALB/c mice, and that differ in their sensitivity to negative selection in HA Tg mice. Whether selection into different B cell subsets and/or affinity for the HA determines the distinct phenotypic potentials of B cells expressing these clonotypes will be evaluated. In addition, whether autoreactive CD4+ T cells rescue primary response B cells from deletion and/or promote memory B cell formation in response to the neo-self HA will be assessed. Aim 3 will examine the processes that lead to the development of organ-specific autoimmunity. An autoimmune syndrome resembling rheumatoid arthritis develops in TCRxHACII mice in which the HA is expressed on antigen presenting cells, and the cellular interactions that lead to its development will be assessed. Whether virus infection provokes autoimmunity in TCRxHACII mice expressing low affinity CD4+ T cells and/or CD4+ T cells directed to a cryptic self-peptide will also be examined. These studies will provide fundamental insights into the mechanisms of immune tolerance, and will have direct relevance to understanding the processes that lead to the development of autoimmune disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATING MYOCARDIUM
NOS2
IN
ISCHEMIC
&
POST-ISCHEMIC
Principal Investigator & Institution: Lowenstein, Charles J.; Assistant Professor; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002 Summary: Nitric oxide (NO) plays a major role in inflammatory diseases of the myocardium. NO is produced during viral myocarditis, transplant rejection, and postischemic inflammation in the heart. The major source of NO in the heart is normally endothelial nitric oxide synthase (eNOS or NOS3), which is present in endothelial cells, cardiac myocytes, and platelets. However, cytokines produced during ischemia or inflammation of the heart can induce expression of the inducible NOS (iNOS or NOS2) in a variety of cells, including cardiac myocytes and macrophages. Since NOS2 produces large amounts of NO continuously, in contrast to eNOS producing smaller amounts of NO transiently, the expression of NOS2 changes the concentration and location of NO in the heart. Alterations in NO production can have profound implications for cardiac physiology, since NO has a variety of effects upon the heart, including relaxation of coronary arterial smooth muscle, inhibition of cardiac myocyte contractility, reduction of platelet and leukocyte adhesion to the coronary artery wall, inhibition of glycolysis and oxidative phosphorylation, and regulation of apoptotic pathways. Because NO derived from NOS2 can affect a diversity of cardiac systems, the regulation of NOS2 is of critical importance. Although transcription was thought to be the primary mechanism by which NOS2 is regulated, other mechanisms regulate NOS2 expression as well. Our preliminary data show that novel proteins regulate the stability of NOS2 mRNA and regulate the activity of NOS2 protein. We propose to study transcriptional, posttranscriptional, and also post-translational mechanisms of NOS2 regulation. We then will examine the physiological relevance of NOS2 regulation in a post-ischemic model of
28
Myocarditis
myocardial infarction. These studies will characterize novel mechanisms which regulate radical production in ischemic myocardium. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: RNA DEPENDENT RNA POLYMERASE MECHANISM Principal Investigator & Institution: Cameron, Craig E.; Associate Professor; Biochem and Molecular Biology; Pennsylvania State University-Univ Park 110 Technology Center University Park, Pa 16802 Timing: Fiscal Year 2002; Project Start 01-JUL-1999; Project End 30-JUN-2004 Summary: (adapted from applicant's abstract) Positive-strand RNA viruses represent an existing and emerging threat to the US public health. These viruses cause diseases ranging from the common cold and summer flu to hepatitis and myocarditis. Currently, there is no effective treatment for positive-strand RNA virus infection. At the heart of replication of these viruses is the RNA-dependent RNA polymerase (RdRP). This enzyme represents a very attractive target for the design of antiviral agents as RdRP activity is only found in virus-infected cells. However, a large gap exists in our understanding of the biochemical mechanism of the RdRP relative to that of cellular, DNA-dependent DNA and RNA polymerases. A better understanding of the RdRP should permit this enzyme to be distinguished from cellular polymerases, thus facilitating the design of specific inhibitors for treatment of RNA virus infection. The primary goal of this proposal is to elucidate the thermodynamic, kinetic and structural basis for correct and incorrect nucleotide incorporation catalyzed by the RdRP from poliovirus. Studies with poliovirus polymerase (3Dpol) are proposed to exploit the wealth of existing information available for this system as a result of decades of effort by many laboratories that has culminated in the discovery of most, if not all, of the virusencoded replication proteins and the solution of the poliovirus polymerase crystal structure. The specific aims are as follows: (1) to characterize the substrate and cofactor specificity of 3Dpol by using steady state kinetic and steady-state fluorescence approaches; (2) to elaborate the minimal kinetic mechanism for correct and incorrect nucleotide incorporation catalyzed by 3Dpol by using pre-steady-state kinetic methods (chemical quench-flow and stopped-flow fluorescence); and (3) to evaluate the function of amino acid residues implicated in catalysis and/or binding of nucleic acid and nucleotide substrates by using kinetic analysis of site-directed mutants of 3Dpol. Successful completion of these studies will represent a systematic, quantitative characterization of an animal virus RdRP and should provide information which will facilitate the development and evaluation of inhibitors of this enzyme. Moreover, the availability of a minimal kinetic mechanism will also provide a framework in which to evaluate the effect, if any, of viral and host proteins on RdRP-catalyzed nucleotide incorporation. The identification of host and viral factors which modulate RdRP function will not only expand our understanding of the molecular mechanism of RNA virus genome replication but also suggest additional targets for chemotherapeutic intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ROLE OF AUTOIMMUNITY IN TRANSPLANT REJECTION Principal Investigator & Institution: Benichou, Gilles A.; Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-MAY-2008
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Summary: (provided by applicant): The exact role of graft tissue specific antigens in transplant rejection is unknown. Recently, we have detected CD4+ T cell- and B cellmediated autoimmunity to cardiac myosin (CM) in murine, porcine, and human recipients of heart transplants. CM is known to initiate autoimmune myocarditis, an autoimmune disease causing cardiac tissue damage and heart failure. Most importantly, we have shown that: 1) pre-transplant sensitization of recipients to CM causes accelerated allograft rejection, 2) induced anti-CM responses are sufficient to trigger rejection of syngeneic heart grafts and 3) modulation of anti-CM responses in recipients results in long-term survival of transplanted hearts. Based on these results, we hypothesize that, in heart-transplanted individuals, the CD4 pathway of alloresponse contributes to acute and/or chronic heart graft rejection by triggering autoimmune responses to CM thereby causing cardiac tissue damages in a fashion similar to that observed in autoimmune myocarditis. To test this hypothesis, the specific aims of the present proposal are to: 1) identify CM determinants and characterize T cells mediating CM autoimmunity post-heart transplantation and, 2) investigate the mechanism(s) by which alloresponse causes autoimmunity to CM in heart-transplanted mice and, and 3) to elucidate the mechanisms by which modulation of anti-CM response can impact the rejection of heart allografts. We anticipate that this knowledge will provide new insights into the mechanisms governing the immune rejection of allotransplants and set the path for the development of new diagnostic tools and selective immune therapies to alleviate graft rejection in clinical transplantation. This award will enhance my career development by allowing me to devote my primary research effort to new transgenic and chimeric mice and a tissue-specific peptide approach for modulation in vivo of antigraft immunity. This will directly complement my previous training in heart transplantation and enhance my career interest in learning new ways of preventing antidonor immune reactivity and inducing tissue graft specific tolerance in human clinical organ transplantation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF INNATE IMMUNITY IN AUTOIMMUNE MYOCARDITIS Principal Investigator & Institution: Rose, Noel R.; Professor; Pathology; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-AUG-2006 Summary: (provided by applicant): Myocarditis is an important cause of heart failure among adolescents and young adults. While about 33% of myocarditis patients recover, the remainder may develop chronic dilated cardiomyopathy which accounts for 25% of all heart failures in North America. Coxsackievirus B3 (CB3) infections have been implicated in around 40% of myocarditis cases. Antiviral drugs and immunosuppressive therapies have given mixed results, requiring further research in order to develop effective therapies. Studies of CB3-induced myocarditis in mice have provided valuable information about the role of the adaptive, acquired immune response to CB3 in the development of autoimmune myocarditis. Although the adaptive T cell response to CB3 is known to play a role in the development of myocarditis, little is understood on how the early, innate immune response to CB3 infection effects the development of autoimmune disease. The aim of this proposal is to characterize the innate immune response to CB3 infection in order to determine the factors that lead to autoimmune disease. We hypothesize that the early innate immune response to CB3 infection determines the later adaptive immune response leading to the development of autoimmune myocarditis. To investigate this hypothesis, we propose three specific aims: (i) to examine the role of early innate immune cytokines, (ii) the role
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of early innate immune cells, and (iii) the role of complement in the development of autoimmune myocarditis. The findings generated by these studies will aid in understanding the development of autoimmune disease initiated by infection. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF RELB IN HIV-1 TAT-MEDIATED IMMUNE RESPONSES Principal Investigator & Institution: Cota-Gomez, Adela; Instructor; None; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, Co 800450508 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2007 Summary: (Applicant's abstract) Infection with human immunodeficiency virus-1 (HIV1) leads to complications such as myocarditis, alveolitis and pulmonary hypertension that cannot be attributed to viral or bacterial pathogens, resulting in cardiopulmonary dysfunction, morbidity and mortality. The HIV- 1 Tat protein, a viral transcriptional regulator essential for viral replication, is secreted from infected cells, taken up by uninfected cells and acts as a cellular transcription activator. Dr. Flores found that soluble Tat induces oxidative stress via inhibition of antioxidant enzymes and activates proinflammatory molecules. Upon joining Dr. Flores' group 1 discovered that Tat upregulates expression of the NF-kB family member, RelB. RelB regulates immune responses including antigen presentation and inflammation. This proposal is based on the premise that higher levels of RelB in essence reset the threshold for inflammation resulting in a "primed" immune system that is increasingly sensitive to further inflammatory stimuli. The research plan addresses the mechanisms of Tat-mediated RelB activation and whether Tat affects RelB expression in vivo. Using an in vitro tissue culture system, the following specific questions will be addressed: 1) What are the mechanisms of Tat-mediated RelB up-regulation? 2) What are the downstream effects of Tat-activated RelB? A transgenic mouse model with targeted expression of Tat in the lungs, engineered by Dr. Flores, will be used to address the following specific question: 1) Is there evidence of inflammation in the lungs of Tat-transgenic mice? 2) Is RelB upregulated in transgenic mouse lung tissues or in alveolar macrophages? 3) Does Tat enhance endotoxin-mediated Relb overexpression in lungs? The proposed research plan should provide new insights into the mechanisms of dysregulated inflammation in AIDS. As part of the career development of the candidate, there will be an advisory committee composed of the co-members as well as three additional members with expertise in various areas relevant to the project. The candidate will be in frequent communication with the committee and will meet at least once a year to assess progress. The candidate will enroll in formal course work on material relevant to the research and will obtain further experience on the technique of in vivo radiolabeling in Dr. Granger's laboratory at LSU Medical Center. The plan is designed to shape the candidate into an independent and investigator. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SIV CARDIOMYOPATHY: PATHOGENESIS AND PREVENTION Principal Investigator & Institution: Shannon, Richard P.; Professor of Medicine; Primate Research Center; Harvard University (Medical School) Medical School Campus Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 30-JUN-2008 Summary: (provided by applicant): HIV associated cardiac pathology is being recognized increasingly as patients with chronic HIV infection who survive to live productive lives. HIV associated cardiomyopathy is among the most common cardiac
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specific manifestation of chronic HIV infection and was observed in between 6-12% of patients that succumb to AIDS. However, cardiovascular involvement has emerged as more than a pathologic curiosity, but rather as a significant cause of morbidity as individuals live longer, more productive lives with HIV. Increased use of HAART therapy has served to unmask HIV associated predispositions to cardiac involvement. Despite the increased recognition, the risks factors for, the pathogenesis of, and the specific treatments required in HIV associated cardiac disease remain unknown. The nonhuman primate model of SIV infection in rhesus macaques affords an unparalleled opportunity to study these critical features. Prior work from our laboratory has characterized the time course, the role of CIM counts, and the pleomoprhic cardiac manifestations in simian AIDS. The work has demonstrated the need to consider both viral and host factors in identifying those at increased risk and to create a consistent, reproducible model of cardiac involvement for further investigation. We have determined that macrophage-tropic strains of SIV are most commonly associated with lymphocytic myocarditis. SIV is localized to the myocardium in approximately one third of cases of cardiac involvement, and when present, always co-localizes to cells of the macrophage lineage, either tissue macrophages or cardiac dendritic cells. TNFalpha, produced by activated macrophages, mediates both up-regulation of NOS2 in cardiac myocytes and the expression of Fas (CD95) receptors leading to cardiac myocyte apoptosis. As such, we have shown that cytokines play a central mechanistic role in both reversible LV dysfunction (increased NF-kappaB NOS2 expression) and irreversible myocardial injury (Fas-FasL mediated apoptosis). In addition, lymphocytic infiltrates are frequently perivascular and associated with coronary vascular lesions characterized by endothelial activation, smooth muscle proliferation, and thrombotic occlusions, leading to acute ischemic injury. These pathological features are mirrored in the lung where lymphocytic interstitial pneumonia and pulmonary vasculopathy are observed and contribute to increased right ventricular dysfunction. We plan to explore both host and viral factors that lead to SIV transmission into the myocardium (SIV cardiotropism) and SIV mediated injury (cardiovirulence). The identified mechanisms will serve as a prerequisite for exploring specific strategies to prevent cardiac involvement in chronic SIV infection. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: T CELL COSTIMULATION AND REGULATION IN MYOCARDITIS Principal Investigator & Institution: Lichtman, Andrew H.; Associate Professor; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 30-JUN-2007 Summary: (provided by applicant): Auotimmune myocarditis, which can occur after viral infection, underlies many cases of dilated cardiomyopathy. CD8+ cytolytic T lymphocytes mediate much of the damage in myocarditis, but the mechanisms by which naive CD8+ T cell tolerance is broken, and the regulation of autoreactive effector CD8+ T cells are incompletely understood. In this proposal, a newly developed transgenic model of myocarditis will be used to study the regulation of heart antigenspecific CD8+ T cells and to determine how several T cell costimulatory and inhibitory pathways influence disease. Mice that express the model antigen ovalbumin (cMymOva) will be used in conjunction with ovalbumin peptide-specific CD8+ T cells from the OT-1 TCR transgenic mouse. Adoptive transfer of activated OT-1 cells, or naive OT-I cells followed by infections with ovalbumin-expressing virus, causes myocarditis in cMy-mOva-ova mice. Disease can be assessed by histology, serum troponin levels, ultrasonography, and mortality. There are three Specific Aims in this proposal. Specific
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Aim 1. Determine the role of CTLA-4 in regulation of heart-antigen specific CD+ T cells. CTLA-4 is a negative regulator of T cell activation, but little is known, about the role of this molecule in inhibiting autoreactive CD8+ T cells. In this Aim, the pathogenic potential and in vivo fate of CTLA-4+/+ and CTLA-4 OT-I cells in alpha MHC-ova mice will be compared. Specific Aim 2. Determine the role of the PD-1:PD-L 1/2 pathway in CD8+ T cell-mediated myocarditis PD-1, a newly identified member of the CD28 family, inhibits effector functions of T cells when it binds its ligands PD-L1 and PD-L2. The role of this pathway in negatively regulating heart-antigen specific CD8+ T cells in vivo will be explored using PD-L1/L2 -/- cMy-mOva mice as recipients of OT-I cells. Specific Aim 3. Determine the role of ICOS in CD8+ T cell-mediated myocarditis. ICOS, a member of the CD28 family of costimulatory molecules, may have particular importance in sustaining activation of effector T cells. In this Aim, the pathogenic potential, effector functions, and in vivo fate of ICOS -/- and ICOS +/+ OT-I cells will be compared in the cMy-mOva mouse model of myocarditis. This project will provide new information about the regulation of autoreactive CD8+ T cells, and will clarify how CD8+ T cell responses against myocardial antigens are controlled. The focus is on newly characterized T cell regulatory pathways, which are potential targets for immunotherapy of myocarditis and other autoimmune diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THE CYTOSKELETON IN HAART-INDUCED CARDIOMYOPATHY Principal Investigator & Institution: Bowles, Neil E.; Instructor; Pediatrics; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2007 Summary: (provided by applicant): One of the consequences of the development of improved therapies for the treatment of HIV infection and the acquired immunodeficiency syndrome, and the associated longer survival of infected patients, has been the emergence of diseases such as myocarditis and/or dilated cardiomyopathy (DCM). A number of etiological agents have been proposed to be responsible for the initiation of the pathologic processes leading to the development of myocarditis and DCM in HIV-infected patients. These have included infection of myocytes with HIV or cardiotropic viruses, or cardiotoxicity resulting from drugs commonly used by AIDS patients, such as AZT. Monotherapy with AZT is uncommon today because highly active antiretroviral therapy (HAART) is a formidable clinical combination. However, AZT has been reported to cause a mitochondrial skeletal myopathy, similar to inherited skeletal myopathies, as well as myopathies secondary to inherited cardiomyopathies. Dystrophin was identified as the gene responsible for cardiomyopathy in patients with X-linked cardiomyopathy (XLCM). Dystrophin is thought to provide structural support for the myocyte and cardiomyocyte membrane. Mutations in dystrophin or dystrophin associated protein subcomplexes result in a wide spectrum of skeletal myopathy and/or cardiomyopathy in humans and animal models such as the mouse or hamster. We have recently shown in patients with DCM or ischemic cardiomyopathy that dystrophin remodeling is a useful indicator of left ventricular function. It has been reported that the 2A protease of Coxsackievirus B3, a major etiologic agent of acquired DCM, is capable of cleaving dystrophin, resulting in sarcolemmal disruption in infected mouse hearts. Further, in murine models of DCM defects in the integrity of dystrophin and/or other components of the cytoskeleton may be important in disease pathogenesis in these models. In order to further delineate the role of cytoskeletal disruption in models of acquired DCM we are proposing the following specific aims: Specific Aim 1: Delineation of the events leading to disruption of the cytoskeleton in transgenic mice. Specific Aim
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2: Characterization of the cytoskeleton in HAART-treated transgenic mice. Specific Aim 3: Role of extrinsic stimuli in the development of HAART-induced cardiomyopathy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THE INFLUENCE OF NUTRITION ON INFLUENZA VIRUS INFECTION Principal Investigator & Institution: Beck, Melinda A.; Associate Professor; Pediatrics; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 Timing: Fiscal Year 2002; Project Start 01-JUL-2001; Project End 31-MAY-2005 Summary: Infection with influenza virus causes a great deal of morbidity and mortality worldwide every year. Influenza virus is notorious for changing its genome, thus continually introducing new strains of influenza virus into the population. Because of the genomic changes, infection with an influenza strain from the previous year does not guarantee immune protection from a new strain. Thus, influenza researchers attempt each year to predict the new strain of influenza that may arise in order to produce a vaccine. Our previous work with coxsackievirus, an RNA virus, demonstrated that the nutritional status of the host could influence the genome of the virus. We were able to show that mice fed a nutritionally adequate diet did not develop myocarditis when infected with an avirulent strain of coxsackievirus B3 (CVB3/0). However, when the mice were fed a diet deficient in either selenium (Se) or vitamin E, they now developed myocarditis following infection with the normally benign CVB3/0. This change in virulence was found to be due to mutations that occurred in the virus that repliated in the Se- deficient animals. We found 6 nucleotides had changed in the virus isolated from the Se-deficient mice. No changes occurred in virus which replicated in the Se-adequate mice. These changes were all associated with virulent strains of the virus. This was the first demonstration of a specific nutritional deficiency causing changes in a viral genome, changing an avirulent virus to a virulent one. This proposal is designed to extend our study with coxsackievirus to another RNA virus, namely influenza virus. Preliminary results demonstrate that influenza virus, like coxsackievirus, mutates to a more virulent genotype when replicating in a Se-deficient host. Once these mutations occurred in the Se-deficient animals, even mice with normal Se status are susceptible to the increase virulence of the newly mutated influenza virus. This proposal is designed to determine the underlying mechanism(s) involved in inducing the influenza virus to mutate. This work will lead to a further understanding of how the nutritional status of the host can not only affect the host itself, but also the viral pathogen as well. By extending our observations with coxsackievirus to a new viral system, we can demonstrate that our findings are not unique to coxsackievirus, but rather can occur in another RNA virus. These findings point to the importance of host nutritional status during an infection and demonstrate that the nutritional status of the host can also play a role in emerging infectious diseases by having a direct effect on the genome of a virus, a previously unknown phenomenon. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TISSUE ENGINEERING OF A CARDIAC PATCH Principal Investigator & Institution: Terracio, Louis; Associate Dean for Resarch; Basic Science and Craniofacial Biology; New York University 15 Washington Place New York, Ny 10003 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2005
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Summary: (provided by applicant): Despite a dramatic decline over the past 15 years, cardiovascular disease remains the leading cause of death and disability in the Western world. The adult onset disease processes that compromise cardiac function include, infarction, ischemic heart disease, myocarditis, and a variety of idiopathic cardiomyopathies. The focal loss of muscular tissue, as a result of a congenital defect or a disease process, alters the unique architectural arrangement of the heart and impairs its function. An engineered segment of artificial myocardium (cardiac patch) potentially offers a nearly unlimited source of material for reconstructive surgery. In preliminary experiments from our lab we have successfully constructed small, multilayered cultures of fetal and neonatal cardiac myocytes that exhibit a tissue-like pattern of organization. These multilayered cultures are composed of myocytes that have an elongated, rod-like cell shape, but require further development before they would be suitable for transplantation. This proposal takes advantage of the Pl's experience in cardiac development, in vitro cultivation of cardiac myocytes on various ECM components, in vitro mechanical stimulation of cells in culture, morphological characterization of tissues, proof of concept studies, and established collaborations with bioengineering colleagues. The Specific Aims of this proposal are: 1) To use specially fabricated collagen substrates and a series of bioreactors to produce histotypic cultures of cardiac cells suitable for transplantation. 2) Characterize and compare the artificial myocardium to the intact heart by morphometric, biochemical and molecular techniques. 3) Transplant the artificial myocardium to in vivo locations that will allow vascularization of the tissue. The transplanted cultures will be compared by morphometric, biochemical, and molecular techniques to the structure and function of the intact heart. Data from these studies will identify the mechanical and chemical parameters necessary to produce the three-dimensional organization of the heart patches. These cultures will provide a potential source of biological material for repairing focal damage to the myocardium. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TRANSGENIC MOUSE MODEL FOR ECHOVIRUS PATHOGENESIS Principal Investigator & Institution: Racaniello, Vincent R.; Professor; Microbiology; Columbia University Health Sciences Po Box 49 New York, Ny 10032 Timing: Fiscal Year 2002; Project Start 01-JUN-2001; Project End 30-APR-2005 Summary: (provided by applicant): Animal viruses initiate their replicative cycles by attaching to a cellular membrane receptor, followed by entry into the cell. Identification of the poliovirus receptor, Pvr, was essential for the establishment of a transgenic mouse model for poliomyelitis. Although a great deal is known about the pathogenesis of poliovirus infection, relatively little is understood about how echoviruses cause disease. Echoviruses are important human pathogens and are responsible for aseptic meningitis, neonatal sepsis, myocarditis, exanthemas, respiratory illness and gastrointestinal disease. Because most echovirus strains only replicate in humans, a mouse model has not been available for studying echovirus pathogenesis. The object of work in this proposal is to isolate transgenic mice that express human cell receptors for echovirus, to establish a new animal model for studying echovirus pathogenesis. We propose to isolate transgenic mice that express VLA-2, a heterodimeric integrin consisting of alpha2 and beta1 subunits, which is known to be the cell receptor for echovirus types 1 and 8. Three specific aims are planned. First, human cDNA encoding the alpha2 and beta1 subunits of VLA-2 will be placed under the transcriptional control of the human betaactin promoter, and used to establish transgenic mice that express both proteins. Second, tissues and organs of VLA-2 transgenic mice will be examined by Northern and Western blot analysis and immunohistochemistry for expression of VLA-2 RNA and protein.
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Third, the susceptibility of VLA-2 transgenic mice to echovirus type 1 infection by different routes, as well as the location of virus replication after inoculation, will be determined. In addition, the ability of echovirus to spread from muscle and intestine to the central nervous system by axonal transport will be determined. Fourth, experiments will be done to determine if an immune response is mounted during echovirus 1 infection of VLA-2 transgenic mice. Knock-out mice will be used to study the role of the immune response in limiting or exacerbating echovirus pathogenesis. Transgenic animal models would enable studies on the sites of echovirus replication, the mechanisms of viral spread, and the basis of echovirus tissue tropism. Establishment of a small animal model may yield information about echovirus pathogenesis that could stimulate development of echovirus vaccines or antiviral drugs. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TRANSLATION-INHIBITION OF HEPATITIS C AND POLIO VIRUSES Principal Investigator & Institution: Dasgupta, Asim; Professor; Microbiol, Imm & Molec Genetics; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2002; Project Start 01-SEP-1999; Project End 30-JUN-2004 Summary: Picorna and Flaviviruses encompass a large variety of medically important human viruses which include those inducing poliomyelitis (poliovirus), infectious (Hep. A) and chronic hepatitis (hepatitis C), common cold (rhinovirus), and myocarditis and encephalitis (coxsackie) among others. A common feature of these viruses is the strategy they employ for synthesis of viral proteins. While cellular mRNAs are translated by capdependent "scanning" mechanism, the viral RNAs are translated by a distinct mechanism involving internal entry of ribosomes within the 5' untranslated region (5' UTR) of viral RNA (IRES-mediated translation). Two inhibitors (a small RNA, IRNA and a small peptide, LAP) which efficiently block hepatitis C and poliovirus IRESmediated translation (but not cellular translation) both in vivo and in vitro, will be studied. Both biochemical and genetic approaches will be used to determine the mechanism by which IRNA and LAP preferentially inhibit translation of HCV and PV RNAs over cellular mRNAs. Cellular proteins involved in IRES-mediated translation will be purified and their roles in HCV RNA translation will be determined. Structurefunction analysis of IRNA will be performed. The mechanism of entry of LAP into hepatocytes will be determined. Identity and normal function of IRNA in the yeast S. cerevisiae will be addressed by cloning and characterizing the IRNA gene. IRNA gene knockout will be performed to better understand the role of IRNA in yeast. We will examine whether IRNA-binding proteins in yeast play any role in IRES-mediated translation (in yeast). Finally, we will develop transgenic mice expressing IRNA and LAP to determine the long term expression of IRNA in animals as well as efficacy of IRNA in blocking virus infections in transgenic animals. It is hoped that the studies proposed here will not only further our understanding of the mechanism of internal initiation of translation in eukaryotic cells, but also provide novel strategies to develop antivirals effective against hepatitis C. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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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 “myocarditis” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for myocarditis in the PubMed Central database: •
Active Lymphocytic Myocarditis Treated with Murine OKT3 Monoclonal Antibody in a Patient Presenting with Intractable Ventricular Tachycardia. by Bilinska ZT, Grzybowski J, Szajewski T, Stepinska J, Michalak E, Walczak E, Wagner T, Kwiatkowska B, Ruzyllo W.; 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=116737
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Alterations in major histocompatibility complex association of myocarditis induced by coxsackievirus B3 mutants selected with monoclonal antibodies to group A streptococci. by Huber SA, Moraska A, Cunningham M.; 1994 Jun 7; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=44032
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Antipsychotic clozapine (Clozaril): myocarditis and cardiovascular toxicity. by Wooltorton E.; 2002 Apr 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=102361
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Assessment of cell-mediated immunity against coxsackievirus B3-induced myocarditis in a primate model (Papio papio). by Paque RE, Gauntt CJ, Nealon TJ.; 1981 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=351806
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Assessment of Coxsackievirus B3 ts Mutants for Induction of Myocarditis in a Murine Model. by Trousdale MD, Paque RE, Nealon T, Gauntt CJ.; 1979 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=414191
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Autoimmune myocarditis induced in mice by cardiac C-protein. Cloning of complementary DNA encoding murine cardiac C-protein and partial characterization of the antigenic peptides. by Kasahara H, Itoh M, Sugiyama T, Kido N, Hayashi H, Saito H, Tsukita S, Kato N.; 1994 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=295155
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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Depletion of T-cell subpopulations results in exacerbation of myocarditis and parasitism in experimental Chagas' disease. by Tarleton RL, Sun J, Zhang L, Postan M.; 1994 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=186416
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Enhanced Production of Macrophage Inflammatory Protein 2 (MIP-2) by In Vitro and In Vivo Infections with Encephalomyocarditis Virus and Modulation of Myocarditis with an Antibody against MIP-2. by Kishimoto C, Kawamata H, Sakai S, Shinohara H, Ochiai H.; 2001 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=114035
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Expression of intercellular adhesion molecule-1 in murine hearts with acute myocarditis caused by coxsackievirus B3. by Seko Y, Matsuda H, Kato K, Hashimoto Y, Yagita H, Okumura K, Yazaki Y.; 1993 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=288103
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Fatal Myocarditis Associated with Acute Parvovirus B19 and Human Herpesvirus 6 Coinfection. by Rohayem J, Dinger J, Fischer R, Klingel K, Kandolf R, Rethwilm A.; 2001 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=88596
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Ganciclovir and Cidofovir Treatment of Cytomegalovirus-Induced Myocarditis in Mice. by Lenzo JC, Shellam GR, Lawson CM.; 2001 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=90486
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HIV-Associated Myocarditis Treated with Zidovudine (AZT). by Wilkins CE, Sexton DJ, McAllister HA.; 1989; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=324842
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Hormonal Regulation of CD4 + T-Cell Responses in Coxsackievirus B3-Induced Myocarditis in Mice. by Huber SA, Kupperman J, Newell MK.; 1999 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=112510
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Mycophenolate mofetil inhibits the development of Coxsackie B3-virus-induced myocarditis in mice. by Padalko E, Verbeken E, Matthys P, Aerts JL, De Clercq E, Neyts J.; 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=317291
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Ongoing enterovirus-induced myocarditis is associated with persistent heart muscle infection: quantitative analysis of virus replication, tissue damage, and inflammation. by Klingel K, Hohenadl C, Canu A, Albrecht M, Seemann M, Mall G, Kandolf R.; 1992 Jan 1; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=48227
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Polyomyositis and myocarditis associated with acquired toxoplasmosis in an immunocompetent girl. by Paspalaki PK, Mihailidou EP, Bitsori M, Tsagkaraki D, Mantzouranis E.; 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=65052
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Reovirus Induction of and Sensitivity to Beta Interferon in Cardiac Myocyte Cultures Correlate with Induction of Myocarditis and Are Determined by Viral Core Proteins. by Sherry B, Torres J, Blum MA.; 1998 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=124610
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Reovirus-induced acute myocarditis in mice correlates with viral RNA synthesis rather than generation of infectious virus in cardiac myocytes. by Sherry B, Baty CJ, Blum MA.; 1996 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=190713
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Restricted usage of T cell receptor V alpha-V beta genes in infiltrating cells in the hearts of patients with acute myocarditis and dilated cardiomyopathy. by Seko Y, Ishiyama S, Nishikawa T, Kasajima T, Hiroe M, Kagawa N, Osada K, Suzuki S, Yagita H, Okumura K, et al.; 1995 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=286383
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The development of fatal myocarditis and polymyositis in mice heterozygous for IFN-[gamma] and lacking the SOCS-1 gene. by Metcalf D, Di Rago L, Mifsud S, Hartley L, Alexander WS.; 2000 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=16841
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The Role of Myocarditis in End-Stage Dilated Cardiomyopathy. by O'Connell JB.; 1987 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=324736
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Transgenic mouse model for echovirus myocarditis and paralysis. by Hughes SA, Thaker HM, Racaniello VR.; 2003 Dec 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=307666
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Treatment of Coxsackievirus A9 myocarditis in mice with WIN 54954. by See DM, Tilles JG.; 1992 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=188451
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V[gamma]4 + T Cells Promote Autoimmune CD8 + Cytolytic T-Lymphocyte Activation in Coxsackievirus B3-Induced Myocarditis in Mice: Role for CD4 + Th1 Cells. by Huber SA, Sartini D, Exley M.; 2002 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=136647
The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with myocarditis, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “myocarditis” (or 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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synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for myocarditis (hyperlinks lead to article summaries): •
A case report of giant cell myocarditis and myositis observed during the clinical course of invasive thymoma associated with myasthenia gravis. Author(s): Tanahashi N, Sato H, Nogawa S, Satoh T, Kawamura M, Shimoda M. Source: The Keio Journal of Medicine. 2004 March; 53(1): 30-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15096726
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A clinical and histopathologic comparison of cardiac sarcoidosis and idiopathic giant cell myocarditis. Author(s): Okura Y, Dec GW, Hare JM, Kodama M, Berry GJ, Tazelaar HD, Bailey KR, Cooper LT. Source: Journal of the American College of Cardiology. 2003 January 15; 41(2): 322-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12535829
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A formidable challenge: the diagnosis and treatment of viral myocarditis in children. Author(s): Wheeler DS, Kooy NW. Source: Critical Care Clinics. 2003 July; 19(3): 365-91. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12848311
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A spontaneous model for autoimmune myocarditis using the human MHC molecule HLA-DQ8. Author(s): Taylor JA, Havari E, McInerney MF, Bronson R, Wucherpfennig KW, Lipes MA. Source: Journal of Immunology (Baltimore, Md. : 1950). 2004 February 15; 172(4): 2651-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14764740
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Activation of dendritic cells through the interleukin 1 receptor 1 is critical for the induction of autoimmune myocarditis. Author(s): Eriksson U, Kurrer MO, Sonderegger I, Iezzi G, Tafuri A, Hunziker L, Suzuki S, Bachmaier K, Bingisser RM, Penninger JM, Kopf M. Source: The Journal of Experimental Medicine. 2003 February 3; 197(3): 323-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12566416
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Acute fatal toxic myocarditis after black widow spider envenomation. Author(s): Pneumatikos IA, Galiatsou E, Goe D, Kitsakos A, Nakos G, Vougiouklakis TG. Source: Annals of Emergency Medicine. 2003 January; 41(1): 158. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12526131
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Acute myocarditis associated with adenoviral infection in a patient with scleroderma. Author(s): Dziadzio M, Giovagnoni A, Pomponio G, Recanatini A, della Costanza OP, Manzin A, Casagrande W, Gabrielli A. Source: Clinical Rheumatology. 2003 December; 22(6): 487-90. Epub 2003 November 08. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14677036
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Acute myocarditis associated with tetanus vaccination. Author(s): Dilber E, Karagoz T, Aytemir K, Ozer S, Alehan D, Oto A, Celiker A. Source: Mayo Clinic Proceedings. 2003 November; 78(11): 1431-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14601707
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Acute necrotizing eosinophilic myocarditis successfully treated by high dose methylprednisolone. Author(s): Watanabe N, Nakagawa S, Fukunaga T, Fukuoka S, Hatakeyama K, Hayashi T. Source: Japanese Circulation Journal. 2001 October; 65(10): 923-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11665801
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Acute parvovirus B19 infection associated with myocarditis in an immunocompetent adult. Author(s): Lamparter S, Schoppet M, Pankuweit S, Maisch B. Source: Human Pathology. 2003 July; 34(7): 725-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12874772
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Acute renal failure and myocarditis associated with intravenous immunoglobulin therapy. Author(s): Akhtar I, Bastani B. Source: Annals of Internal Medicine. 2003 August 19; 139(4): W65. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12966002
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Acute viral myocarditis in the ED pediatric patient: three case presentations. Author(s): Mecham N. Source: Journal of Emergency Nursing: Jen : Official Publication of the Emergency Department Nurses Association. 2004 April; 30(2): 179-82. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15039679
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Adenovirus-mediated gene transfer of ICOSIg fusion protein ameliorates ongoing experimental autoimmune myocarditis. Author(s): Matsui Y, Okamoto H, Inobe M, Jia N, Shimizu T, Akino M, Sugawara T, Tezuka K, Nakayama Y, Morimoto J, Kimura C, Kon S, Miyazaki T, Kitabatake A, Uede T. Source: Human Gene Therapy. 2003 April 10; 14(6): 521-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12718763
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Advances in the understanding of myocarditis. Author(s): Liu PP, Mason JW. Source: Circulation. 2001 August 28; 104(9): 1076-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11524405
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An autopsy case of sudden death in a patient with giant cell myocarditis. Author(s): Singh AM, Debnath K, Devi SS, Devi PG, Konjengbam R, Nabachandra H. Source: Indian J Chest Dis Allied Sci. 2003 July-September; 45(3): 195-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12866637
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Analysis of the coxsackievirus B-adenovirus receptor gene in patients with myocarditis or dilated cardiomyopathy. Author(s): Bowles NE, Javier Fuentes-Garcia F, Makar KA, Li H, Gibson J, Soto F, Schwimmbeck PL, Schultheiss HP, Pauschinger M. Source: Molecular Genetics and Metabolism. 2002 November; 77(3): 257-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12409275
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Angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists in experimental myocarditis. Author(s): Godsel LM, Leon JS, Engman DM. Source: Current Pharmaceutical Design. 2003; 9(9): 723-35. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12570790
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Antiinflammatory therapy in myocarditis. Author(s): Vallejo J, Mann DL. Source: Current Opinion in Cardiology. 2003 May; 18(3): 189-93. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12826819
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Apoptosis in myocarditis and dilated cardiomyopathy: does enterovirus genome persistence protect from apoptosis? An endomyocardial biopsy study. Author(s): Alter P, Jobmann M, Meyer E, Pankuweit S, Maisch B. Source: Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology. 2001 September-October; 10(5): 229-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11673061
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Assessment of myocardial recovery in a patient with acute myocarditis supported with a left ventricular assist device: a case report. Author(s): Maybaum S, Stockwell P, Naka Y, Catanese K, Flannery M, Fisher P, Oz M, Mancini D. Source: The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation. 2003 February; 22(2): 202-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12581771
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Basement membrane thickening in small intramyocardial vessels in eosinophilic myocarditis. Author(s): Rossi M, Marin-Neto J, Uchida E, Ramos S. Source: Acta Cardiol. 1996; 51(3): 271-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8817010
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Biopsy diagnosis of myocarditis. Author(s): Marboe CC, Fenoglio JJ Jr. Source: Cardiovasc Clin. 1988; 18(2): 137-54. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3275410
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Biopsy evidence of atrial myocarditis in an athlete developing transient sinoatrial disease. Author(s): Frustaci A, Cameli S, Zeppilli P. Source: Chest. 1995 November; 108(5): 1460-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7587462
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Blood dyscrasias and myocarditis in infectious mononucleosis. Author(s): Das RK, Seidelin R. Source: British Medical Journal. 1972 January 29; 1(795): 289. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5008481
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Borderline myocarditis on initial endomyocardial biopsy: no-man's-land no more? Author(s): Factor SM. Source: Journal of the American College of Cardiology. 1990 February; 15(2): 290-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2299070
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Brain natriuretic peptide can be a useful biochemical marker for myocarditis in patients with Kawasaki disease. Author(s): Kawamura T, Wago M. Source: Cardiology in the Young. 2002 March; 12(2): 153-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12018720
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Bridge to recovery with a left ventricular assist device for fulminant acute myocarditis. Author(s): Ueno T, Bergin P, Richardson M, Esmore DS. Source: The Annals of Thoracic Surgery. 2000 January; 69(1): 284-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10654540
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Bridge-to-recovery from acute myocarditis in a 12-year-old child. Author(s): Hotz H, Linneweber J, Dohmen PM, Vargas O, Braun J, Konertz W. Source: Artificial Organs. 2004 June; 28(6): 587-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15153152
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Brief report: healed myocarditis as a cause of ventricular repolarization abnormalities in athlete's heart. Author(s): Zeppilli P, Santini C, Cameli S, Dello Russo A, Picani C, Giordano A, Frustaci A. Source: International Journal of Sports Medicine. 1997 April; 18(3): 213-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9187977
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Brief report: recognition of acute myocarditis masquerading as acute myocardial infarction. Author(s): Narula J, Khaw BA, Dec GW Jr, Palacios IF, Southern JF, Fallon JT, Strauss HW, Haber E, Yasuda T. Source: The New England Journal of Medicine. 1993 January 14; 328(2): 100-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8416421
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Bullous pemphigoid associated with acute myocarditis. Author(s): Bachmeyer C, Seoud J, Carlotti A, Bernard P, Batteux F, Weill B, Roujeau JC. Source: Dermatology (Basel, Switzerland). 2002; 204(2): 161-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11937752
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Cardiac troponin T: its role in the diagnosis of clinically suspected acute myocarditis and chronic dilated cardiomyopathy in children. Author(s): Soongswang J, Durongpisitkul K, Ratanarapee S, Leowattana W, Nana A, Laohaprasitiporn D, Akaniroj S, Limpimwong N, Kangkagate C. Source: Pediatric Cardiology. 2002 September-October; 23(5): 531-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12211203
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Cardiovascular imaging in clinical and experimental acute infectious myocarditis. Author(s): Shirani J, Ilercil A, Chandra M, Jelicks LA, Tanowitz HB. Source: Frontiers in Bioscience : a Journal and Virtual Library. 2003 May 1; 8: E323-36. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12700067
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Cases from the aerospace medicine residents' teaching file. Case report of an aviator with focal myocarditis mimicking myocardial infarction with normal coronaries. Author(s): Huff LA, Kruyer WB. Source: Aviation, Space, and Environmental Medicine. 2002 December; 73(12): 1235-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12498555
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Catecholaminergic polymorphic ventricular tachycardia in a 3-year-old with occult myocarditis. Author(s): Bryant RM, Redfearn SP, Marangi D, Davenport JP, Kuntz ST, Schowengerdt KO. Source: Pacing and Clinical Electrophysiology : Pace. 2002 October; 25(10): 1520-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12418752
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CD83+ dendritic cells in inflammatory infiltrates of Churg-Strauss myocarditis. Author(s): Schoppet M, Pankuweit S, Maisch B. Source: Archives of Pathology & Laboratory Medicine. 2003 January; 127(1): 98-101. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12521377
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Celiac disease associated with autoimmune myocarditis. Author(s): Frustaci A, Cuoco L, Chimenti C, Pieroni M, Fioravanti G, Gentiloni N, Maseri A, Gasbarrini G. Source: Circulation. 2002 June 4; 105(22): 2611-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12045166
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Changes in the peripheral eosinophil count in patients with acute eosinophilic myocarditis. Author(s): Morimoto S, Kubo N, Hiramitsu S, Uemura A, Ohtsuki M, Kato S, Kato Y, Sugiura A, Miyagishima K, Mori N, Yoshida Y, Hishida H. Source: Heart and Vessels. 2003 September; 18(4): 193-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14520487
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Churg-Strauss syndrome with myocarditis manifesting as acute myocardial infarction with cardiogenic shock: case report and review of the literature. Author(s): Shanks M, Ignaszewski AP, Chan SY, Allard MF. Source: The Canadian Journal of Cardiology. 2003 September; 19(10): 1184-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14532945
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Circulating cardiac autoantibodies in dilated cardiomyopathy and myocarditis: pathogenetic and clinical significance. Author(s): Caforio AL, Mahon NJ, Tona F, McKenna WJ. Source: European Journal of Heart Failure : Journal of the Working Group on Heart Failure of the European Society of Cardiology. 2002 August; 4(4): 411-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12167378
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Circulatory support for fulminant myocarditis: consideration for implantation, weaning and explantation. Author(s): Leprince P, Combes A, Bonnet N, Ouattara A, Luyt CE, Theodore P, Leger P, Pavie A. Source: European Journal of Cardio-Thoracic Surgery : Official Journal of the European Association for Cardio-Thoracic Surgery. 2003 September; 24(3): 399-403. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12965311
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Commentary on: Dettmeyer R, Kandolf R, Baasner A, Banaschak S, Eis-hubinger AM, Madea B. Fatal parvovirus B19 myocarditis in an 8-year-old boy. J Forensic Sci 2003;48(1): 183-186. Author(s): Arya SC, Agarwal N. Source: J Forensic Sci. 2003 September; 48(5): 1204; Author Reply 1205. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14535705
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Complete atrioventricular block following myocarditis in children. Author(s): Wang JN, Tsai YC, Lee WL, Lin CS, Wu JM. Source: Pediatric Cardiology. 2002 September-October; 23(5): 518-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12189408
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Completely inverse images in dual-isotope SPECT with Tl-201 and I-123 MIBG in a patient with myocarditis. Author(s): Nakahara T, Hashimoto J, Suzuki T, Fujii H, Kubo A. Source: Ann Nucl Med. 2001 June; 15(3): 277-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11545202
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Coronary artery disease obscuring giant cell myocarditis--a case report. Author(s): Kwok OH, Chau EM, Wang EP, Chow WH. Source: Angiology. 2002 September-October; 53(5): 599-603. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12365870
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Coxsackie B3 myocarditis in 4 cases of suspected sudden infant death syndrome: diagnosis by immunohistochemical and molecular-pathologic investigations. Author(s): Dettmeyer R, Baasner A, Schlamann M, Haag C, Madea B. Source: Pathology, Research and Practice. 2002; 198(10): 689-96. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12498225
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Coxsackievirus B3 induces apoptosis in the early phase of murine myocarditis: a comparative analysis of cardiovirulent and noncardiovirulent strains. Author(s): Joo CH, Hong HN, Kim EO, Im JO, Yoon SY, Ye JS, Moon MS, Kim D, Lee H, Kim YK. Source: Intervirology. 2003; 46(3): 135-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12867750
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Coxsackievirus B3 sequences in the blood of a neonate with congenital myocarditis, plus serological evidence of maternal infection. Author(s): Bendig JW, Franklin OM, Hebden AK, Backhouse PJ, Clewley JP, Goldman AP, Piggott N. Source: Journal of Medical Virology. 2003 August; 70(4): 606-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12794724
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Cryptic epitope identified in rat and human cardiac myosin S2 region induces myocarditis in the Lewis rat. Author(s): Li Y, Heuser JS, Kosanke SD, Hemric M, Cunningham MW. Source: Journal of Immunology (Baltimore, Md. : 1950). 2004 March 1; 172(5): 3225-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14978130
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Current role of endomyocardial biopsy in the management of dilated cardiomyopathy and myocarditis. Author(s): Wu LA, Lapeyre AC 3rd, Cooper LT. Source: Mayo Clinic Proceedings. 2001 October; 76(10): 1030-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11605687
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Cytokines that regulate autoimmune myocarditis. Author(s): Kurrer MO, Kopf M, Penninger JM, Eriksson U. Source: Swiss Medical Weekly : Official Journal of the Swiss Society of Infectious Diseases, the Swiss Society of Internal Medicine, the Swiss Society of Pneumology. 2002 July 27; 132(29-30): 408-13. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12428186
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Definition of inflammatory cardiomyopathy (myocarditis): on the way to consensus. A status report. Author(s): Maisch B, Portig I, Ristic A, Hufnagel G, Pankuweit S. Source: Herz. 2000 May; 25(3): 200-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10904839
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Detection of acute myocarditis using nuclear magnetic resonance imaging. Author(s): Lie JT. Source: The American Journal of Medicine. 1988 August; 85(2): 282-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3400714
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Detection of Coxsackie B2 virus myocarditis in a neonate using Tl-201 and I-123 BMIPP myocardial imaging. Author(s): Sawada T, Kohno Y, Ikegami H, Tsujii H, Ikuta H, Okabe H, Sugihara H. Source: Clinical Nuclear Medicine. 2000 January; 25(1): 77-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10634546
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Detection of enterovirus capsid protein VP1 in myocardium from cases of myocarditis or dilated cardiomyopathy by immunohistochemistry: further evidence of enterovirus persistence in myocytes. Author(s): Zhang H, Li Y, McClean DR, Richardson PJ, Florio R, Sheppard M, Morrison K, Latif N, Dunn MJ, Archard LC. Source: Medical Microbiology and Immunology. 2004 May; 193(2-3): 109-14. Epub 2003 November 22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14634804
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Detection of enterovirus RNA in myocardial biopsies from patients with myocarditis and cardiomyopathy using gene amplification by polymerase chain reaction. Author(s): Jin O, Sole MJ, Butany JW, Chia WK, McLaughlin PR, Liu P, Liew CC. Source: Circulation. 1990 July; 82(1): 8-16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2163780
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Detection of eosinophilic myocarditis using contrast-enhanced magnetic resonance imaging: case report. Author(s): Takahashi N, Murakami Y, Shimada T, Kashima Y, Nakamura K, Inoue S, Sugamori T, Katoh H, Ishibashi Y, Maruyama R. Source: Canadian Association of Radiologists Journal = Journal L'association Canadienne Des Radiologistes. 2001 February; 52(1): 20-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11247259
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Detection of viruses in myocardial tissues by polymerase chain reaction. evidence of adenovirus as a common cause of myocarditis in children and adults. Author(s): Bowles NE, Ni J, Kearney DL, Pauschinger M, Schultheiss HP, McCarthy R, Hare J, Bricker JT, Bowles KR, Towbin JA. Source: Journal of the American College of Cardiology. 2003 August 6; 42(3): 466-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12906974
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Diagnosis and management of myocarditis in athletes. Author(s): Brennan FH Jr, Stenzler B, Oriscello R. Source: Curr Sports Med Rep. 2003 April; 2(2): 65-71. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12831661
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Diagnosis and management of pediatric myocarditis. Author(s): Bohn D, Benson L. Source: Paediatric Drugs. 2002; 4(3): 171-81. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11909009
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Diagnosis and treatment of pediatric viral myocarditis. Author(s): Levi D, Alejos J. Source: Current Opinion in Cardiology. 2001 March; 16(2): 77-83. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11224637
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Diagnosis of myocarditis by endomyocardial biopsy. Author(s): Aretz HT. Source: The Medical Clinics of North America. 1986 November; 70(6): 1215-26. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3784689
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Diagnostic accuracy of antimyosin scintigraphy in suspected myocarditis. Author(s): Narula J, Khaw BA, Dec GW, Palacios IF, Newell JB, Southern JF, Fallon JT, Strauss HW, Haber E, Yasuda T. Source: Journal of Nuclear Cardiology : Official Publication of the American Society of Nuclear Cardiology. 1996 September-October; 3(5): 371-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8902668
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Diagnostic endomyocardial biopsy pathology--general biopsy considerations, and its use for myocarditis and cardiomyopathy: a review. Author(s): Veinot JP. Source: The Canadian Journal of Cardiology. 2002 January; 18(1): 55-65. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11826329
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Dilated cardiomyopathy, myocarditis, and the bioptome. Author(s): Lowry PJ, Gammage MD, Littler WA. Source: British Medical Journal (Clinical Research Ed.). 1986 August 9; 293(6543): 392. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3015326
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Dilated cardiomyopathy, myocarditis, and the bioptome. Author(s): Olsen EG. Source: British Medical Journal (Clinical Research Ed.). 1986 July 12; 293(6539): 90-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3089431
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Diphtheritic myocarditis: clinical and laboratory parameters of prognosis and fatal outcome. Author(s): Havaldar PV, Sankpal MN, Doddannavar RP. Source: Annals of Tropical Paediatrics. 2000 September; 20(3): 209-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11064774
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Does rheumatic myocarditis really exists? Systematic study with echocardiography and cardiac troponin I blood levels. Author(s): Kamblock J, Payot L, Iung B, Costes P, Gillet T, Le Goanvic C, Lionet P, Pagis B, Pasche J, Roy C, Vahanian A, Papouin G. Source: European Heart Journal. 2003 May; 24(9): 855-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12727153
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Dor's endoaneurysmorrhaphy in severe heart failure due to giant cell myocarditis. Author(s): Oomman A, Ramachandran P, Rao PV, Girinath MR. Source: The Annals of Thoracic Surgery. 2001 June; 71(6): 2036-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11426798
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Drug-induced toxic myocarditis. Author(s): Ansari A, Maron BJ, Berntson DG. Source: Texas Heart Institute Journal / from the Texas Heart Institute of St. Luke's Episcopal Hospital, Texas Children's Hospital. 2003; 30(1): 76-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12638679
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Dystrophin disruption in enterovirus-induced myocarditis and dilated cardiomyopathy: from bench to bedside. Author(s): Badorff C, Knowlton KU. Source: Medical Microbiology and Immunology. 2004 May; 193(2-3): 121-6. Epub 2003 August 12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12920582
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Early and long-term mortality of the clinical subtypes of myocarditis. Author(s): Kodama M, Oda H, Okabe M, Aizawa Y, Izumi T. Source: Japanese Circulation Journal. 2001 November; 65(11): 961-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11716247
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Echocardiographic findings in myocarditis. Author(s): Pinamonti B, Alberti E, Cigalotto A, Dreas L, Salvi A, Silvestri F, Camerini F. Source: The American Journal of Cardiology. 1988 August 1; 62(4): 285-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3400607
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Effect of suplatast tosilate, an antiallergic selective Th2 cytokine inhibitor, on acute eosinophilic myocarditis: a case report. Author(s): Umemoto S, Itagaki K, Kimura M, Itoh S, Tanaka M, Haraguchi M, Matsuzaki M. Source: Heart and Vessels. 2003 May; 18(2): 100-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12756607
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Efficacy of steroid therapy for pacing failure in a patient with chronic myocarditis. Author(s): Mitsuya N, Kishi R, Suzuki N, Tamura M, Imai Y, Tanaka O, Takagi A, Nakazawa K, Miyake F, Nobuoka S, Koike J. Source: Intern Med. 2004 March; 43(3): 213-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15098603
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Encephalitis and myocarditis in a child with acute lymphoblastic leukemia: role of coxsackievirus B5? Author(s): Moschovi M, Sterpi P, Youroukos S, Tzortzatou-Stathopoulou F, Moscjovi MA. Source: Pediatric Hematology and Oncology. 2002 April-May; 19(3): 205-10. Erratum In: Pediatr Hematol Oncol. 2002 September; 19(6): 449. Moscjovi Maria a [corrected to Moschovi Mary]. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11936734
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Endomyocardial biopsy findings in 50 patients with idiopathic atrioventricular block: presence of myocarditis. Author(s): Uemura A, Morimoto S, Hiramitsu S, Hishida H. Source: Japanese Heart Journal. 2001 November; 42(6): 691-700. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11933919
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Enhanced ERK-1/2 activation in mice susceptible to coxsackievirus-induced myocarditis. Author(s): Opavsky MA, Martino T, Rabinovitch M, Penninger J, Richardson C, Petric M, Trinidad C, Butcher L, Chan J, Liu PP. Source: The Journal of Clinical Investigation. 2002 June; 109(12): 1561-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12070303
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Eosinophilia-myalgia syndrome and giant cell myocarditis: a case report and therapeutic approach. Author(s): Amidon TM, Baldwin JL, George E. Source: Heart Disease. 1999 May-June; 1(2): 66-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11720607
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Eosinophilic myocarditis in patients awaiting heart transplantation. Author(s): Takkenberg JJ, Czer LS, Fishbein MC, Luthringer DJ, Quartel AW, Mirocha J, Queral CA, Blanche C, Trento A. Source: Critical Care Medicine. 2004 March; 32(3): 714-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15090952
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Eosinophilic myocarditis in the explanted hearts of cardiac transplant recipients: Interesting pathologic finding or pathophysiologic entity of clinical significance? Author(s): Johnson MR. Source: Critical Care Medicine. 2004 March; 32(3): 888-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15090985
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Eosinophilic-lymphocytic myocarditis after smallpox vaccination. Author(s): Murphy JG, Wright RS, Bruce GK, Baddour LM, Farrell MA, Edwards WD, Kita H, Cooper LT. Source: Lancet. 2003 October 25; 362(9393): 1378-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14585641
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Eradication of viral myocarditis: is there hope? Author(s): Baboonian C, McKenna W. Source: Journal of the American College of Cardiology. 2003 August 6; 42(3): 473-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12906975
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Essential role of HIV type 1-infected and cyclooxygenase 2-activated macrophages and T cells in HIV type 1 myocarditis. Author(s): Liu QN, Reddy S, Sayre JW, Pop V, Graves MC, Fiala M. Source: Aids Research and Human Retroviruses. 2001 October 10; 17(15): 1423-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11679155
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Etiology of Chagas disease myocarditis: autoimmunity, parasite persistence, or both? Author(s): Girones N, Fresno M. Source: Trends in Parasitology. 2003 January; 19(1): 19-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12488221
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Evaluation of the usefulness of the ELISA method for detection of enterovirus antibodies in serum samples of patients with myocarditis. Author(s): Wielkopolska A, Gut W, Binduga-Gajewska I, Jarzabek Z. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2002 January; 8(1): Mt10-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11782682
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Expansion of specific alphabeta+ T-cell subsets in the myocardium of patients with myocarditis and idiopathic dilated cardiomyopathy associated with Coxsackievirus B infection. Author(s): Luppi P, Rudert W, Licata A, Riboni S, Betters D, Cotrufo M, Frati G, Condorelli G, Trucco M. Source: Human Immunology. 2003 February; 64(2): 194-210. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12559622
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Experimental chronic Chagas' disease myocarditis is an autoimmune disease preventable by induction of immunological tolerance to myocardial antigens. Author(s): Pontes-de-Carvalho L, Santana CC, Soares MB, Oliveira GG, Cunha-Neto E, Ribeiro-dos-Santos R. Source: Journal of Autoimmunity. 2002 March; 18(2): 131-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11908945
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Expression of Toll-like receptor 4 is associated with enteroviral replication in human myocarditis. Author(s): Satoh M, Nakamura M, Akatsu T, Iwasaka J, Shimoda Y, Segawa I, Hiramori K. Source: Clinical Science (London, England : 1979). 2003 June; 104(6): 577-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12589705
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Expression of tumor necrosis factor ligand superfamily costimulatory molecules CD27L, CD30L, OX40L and 4-1BBL in the heart of patients with acute myocarditis and dilated cardiomyopathy. Author(s): Seko Y, Ishiyama S, Nishikawa T, Kasajima T, Hiroe M, Suzuki S, Ishiwata S, Kawai S, Tanaka Y, Azuma M, Kobata T, Yagita H, Okumura K, Nagai R. Source: Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology. 2002 May-June; 11(3): 166-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12031769
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Extracorporeal membrane oxygenation in fulminant myocarditis complicating systemic lupus erythematosus. Author(s): Leung MC, Harper RW, Boxall J. Source: The Medical Journal of Australia. 2002 April 15; 176(8): 374-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12041632
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Fatal acute myocarditis in an infant with human herpesvirus 6 infection. Author(s): Yoshikawa T, Ihira M, Suzuki K, Suga S, Kito H, Iwasaki T, Kurata T, Tanaka T, Saito Y, Asano Y. Source: Journal of Clinical Pathology. 2001 October; 54(10): 792-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11577130
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Fatal Aspergillus myocarditis following short-term corticosteroid therapy for chronic obstructive pulmonary disease. Author(s): Carrascosa Porras M, Herreras Martinez R, Corral Mones J, Ares Ares M, Zabaleta Murguiondo M, Ruchel R. Source: Scandinavian Journal of Infectious Diseases. 2002; 34(3): 224-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12035764
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Fatal catecholamine myocarditis in a child with severe scalding injury. Author(s): Riedel T, Sojcic SG, Pfenninger J. Source: Intensive Care Medicine. 2002 November; 28(11): 1687-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12583384
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Fatal haemorrhagic myocarditis secondary to cyclophosphamide therapy. Author(s): Birchall IW, Lalani Z, Venner P, Hugh J. Source: The British Journal of Radiology. 2000 October; 73(874): 1112-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11271907
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Fatal myocarditis associated with acute parvovirus B19 and human herpesvirus 6 coinfection. Author(s): Rohayem J, Dinger J, Fischer R, Klingel K, Kandolf R, Rethwilm A. Source: Journal of Clinical Microbiology. 2001 December; 39(12): 4585-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11724892
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Fatal parvovirus B19 myocarditis in an 8-year-old boy. Author(s): Dettmeyer R, Kandolf R, Baasner A, Banaschak S, Eis-Hubinger AM, Madea B. Source: J Forensic Sci. 2003 January; 48(1): 183-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12570225
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Fatal parvovirus B19-associated myocarditis clinically mimicking ischemic heart disease: an endothelial cell-mediated disease. Author(s): Bultmann BD, Klingel K, Sotlar K, Bock CT, Baba HA, Sauter M, Kandolf R. Source: Human Pathology. 2003 January; 34(1): 92-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12605372
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Fatal parvovirus myocarditis in a 5-year-old girl. Author(s): Murry CE, Jerome KR, Reichenbach DD. Source: Human Pathology. 2001 March; 32(3): 342-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11274646
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Fatal, rotavirus-associated myocarditis and pneumonitis in a 2-year-old boy. Author(s): Grech V, Calvagna V, Falzon A, Mifsud A. Source: Annals of Tropical Paediatrics. 2001 June; 21(2): 147-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11471258
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Fc receptor-mediated inhibitory effect of immunoglobulin therapy on autoimmune giant cell myocarditis: concomitant suppression of the expression of dendritic cells. Author(s): Shioji K, Kishimoto C, Sasayama S. Source: Circulation Research. 2001 September 14; 89(6): 540-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11557742
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First successful bridge to recovery with the Impella Recover 100 left ventricular assist device for fulminant acute myocarditis. Author(s): Colombo T, Garatti A, Bruschi G, Lanfranconi M, Russo C, Milazzo F, Catena E, Frigerio M, Vitali E. Source: Ital Heart J. 2003 September; 4(9): 642-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14635384
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Focal lymphocytic myocarditis in acquired immunodeficiency syndrome (AIDS): a correlative morphologic and clinical study in 26 consecutive fatal cases. Author(s): Baroldi G, Corallo S, Moroni M, Repossini A, Mutinelli MR, Lazzarin A, Antonacci CM, Cristina S, Negri C. Source: Journal of the American College of Cardiology. 1988 August; 12(2): 463-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3392340
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Focal parvovirus B19 myocarditis in a patient with Brugada syndrome. Author(s): Buob A, Siaplaouras S, Janzen I, Schwaab B, Hammer B, Schneider G, Kandolf R, Bohm M, Jung J. Source: Cardiology in Review. 2003 January-February; 11(1): 45-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12493136
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Four cases of acute chagasic myocarditis in French Guiana. Author(s): Carme B, Aune I, Nguyen G, Aznar C, Beaudet B. Source: The American Journal of Tropical Medicine and Hygiene. 2001 March-April; 64(3-4): 162-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11442212
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FR167653 suppresses the progression of experimental autoimmune myocarditis. Author(s): Maruyama S, Kato K, Kodama M, Okura Y, Hirono S, Fuse K, Hanawa H, Nakagawa O, Nakazawa M, Miida T, Yaoita E, Yamamoto T, Inoue I, Aizawa Y. Source: Molecular and Cellular Biochemistry. 2003 April; 246(1-2): 39-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12841341
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Frequency and quantity of the parvovirus B19 genome in endomyocardial biopsies from patients with suspected myocarditis or idiopathic left ventricular dysfunction. Author(s): Klein RM, Jiang H, Niederacher D, Adams O, Du M, Horlitz M, Schley P, Marx R, Lankisch MR, Brehm MU, Strauer BE, Gabbert HE, Scheffold T, Gulker H. Source: Zeitschrift Fur Kardiologie. 2004 April; 93(4): 300-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15085375
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Fulminant acute myocarditis with intractable shock. Author(s): Mokhobo KP, Khatib FK, Tshabalala AK. Source: South African Medical Journal. Suid-Afrikaanse Tydskrif Vir Geneeskunde. 1988 August 6; 74(3): 139-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3399996
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Fulminant coxsackieviral myocarditis. Author(s): Seong IW, Choe SC, Jeon ES. Source: The New England Journal of Medicine. 2001 August 2; 345(5): 379. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11484710
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Fulminant myocarditis in polymyositis. Author(s): Yukiiri K, Mizushige K, Ueda T, Nanba T, Tanimoto K, Wada Y, Takagi Y, Ohmori K, Kohno M. Source: Japanese Circulation Journal. 2001 November; 65(11): 991-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11716253
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Fungal myocarditis. Author(s): Nosanchuk JD. Source: Frontiers in Bioscience : a Journal and Virtual Library. 2002 June 1; 7: D1423-38. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12045009
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Giant cell myocarditis as a manifestation of drug hypersensitivity. Author(s): Daniels PR, Berry GJ, Tazelaar HD, Cooper LT. Source: Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology. 2000 September-October; 9(5): 287-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11064276
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Giant cell myocarditis due to coxsackie B2 virus infection. Author(s): Meyer T, Grumbach IM, Kreuzer H, Morguet AJ. Source: Cardiology. 1997 May-June; 88(3): 296-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9129853
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Giant cell myocarditis in a 12-year-old girl with common variable immunodeficiency. Author(s): Laufs H, Nigrovic PA, Schneider LC, Oettgen H, Del NP, Moskowitz IP, Blume E, Perez-Atayde AR. Source: Mayo Clinic Proceedings. 2002 January; 77(1): 92-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11795251
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Giant cell myocarditis in a young man responsive to T-lymphocyte cytolytic therapy. Author(s): Pinderski LJ, Fonarow GC, Hamilton M, Fishbein MC, Marelli D, Moriguchi J, Cohen B, Kobashigawa JA. Source: The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation. 2002 July; 21(7): 818-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12100910
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Giant cell myocarditis presenting as rapidly progressive congestive heart failure complicated by ventricular arrhythmias. Author(s): Greer RW, Taggart MW, Sartin BW, Angelica NJ, Johnson GM, Pappas ND, Newman WP 3rd, Glancy DL. Source: J La State Med Soc. 2003 July-August; 155(4): 198-202; Quiz 202. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14506826
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Giant cell myocarditis responding to immunosuppressive therapy. Author(s): Frustaci A, Chimenti C, Pieroni M, Gentiloni N. Source: Chest. 2000 March; 117(3): 905-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10713027
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Giant Cell Myocarditis Study Group. Author(s): Cooper LT Jr, Shabetai R. Source: American Heart Journal. 1995 December; 130(6): 1312. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7484795
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Giant cell myocarditis study group. Author(s): Cooper LT Jr, Shabetai R. Source: Journal of the American College of Cardiology. 1995 July; 26(1): 301. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7797768
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Giant cell myocarditis, in a patient with Crohn's disease, treated with etanercept--a tumour necrosis factor-alpha antagonist. Author(s): Nash CL, Panaccione R, Sutherland LR, Meddings JB. Source: Canadian Journal of Gastroenterology = Journal Canadien De Gastroenterologie. 2001 September; 15(9): 607-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11573104
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Giant cell myocarditis. Author(s): Cooper LT Jr, Berry GJ, Rizeq M, Schroeder JS. Source: The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation. 1995 March-April; 14(2): 394-401. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7779862
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Giant cell myocarditis: a fatal cause of dyspnea in pregnancy. Author(s): van Haelst PL, van Rossem M, Valentijn RM, Beijer GJ. Source: European Journal of Obstetrics, Gynecology, and Reproductive Biology. 2001 December 10; 100(1): 105-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11728670
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Giant cell myocarditis: an entity distinct from sarcoidosis characterized by multiphasic myocyte destruction by cytotoxic T cells and histiocytic giant cells. Author(s): Litovsky SH, Burke AP, Virmani R. Source: Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc. 1996 December; 9(12): 1126-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8972471
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Giant cell myocarditis: clinical presentation, bridge to transplantation with mechanical circulatory support, and long-term outcome. Author(s): Davies RA, Veinot JP, Smith S, Struthers C, Hendry P, Masters R. Source: The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation. 2002 June; 21(6): 674-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12057701
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Giant cell myocarditis: diagnosis and treatment. Author(s): Cooper LT Jr. Source: Herz. 2000 May; 25(3): 291-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10904855
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Giant cell myocarditis: monocytic immunophenotype of giant cells in a case associated with ulcerative colitis. Author(s): Ariza A, Lopez MD, Mate JL, Curos A, Villagrasa M, Navas-Palacios JJ. Source: Human Pathology. 1995 January; 26(1): 121-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7821909
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Giant cell myocarditis: most fatal of autoimmune diseases. Author(s): Rosenstein ED, Zucker MJ, Kramer N. Source: Seminars in Arthritis and Rheumatism. 2000 August; 30(1): 1-16. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10966208
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Giant cell myocarditis--a case report. Author(s): Lazar A, Frasik W, Garlicki M, Wierzbicki K, Stachura J, Dziatkowiak A. Source: Pol J Pathol. 2001; 52(4): 221-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11915185
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Global biventricular dysfunction in patients with asymptomatic coronary artery disease may be caused by myocarditis. Author(s): Frustaci A, Chimenti C, Maseri A. Source: Circulation. 1999 March 16; 99(10): 1295-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10077512
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Group B coxsackievirus myocarditis and pancreatitis: connection between viral virulence phenotypes in mice. Author(s): Tracy S, Hofling K, Pirruccello S, Lane PH, Reyna SM, Gauntt CJ. Source: Journal of Medical Virology. 2000 September; 62(1): 70-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10935991
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Growth hormone interferes with the progression of myocarditis in rats. Author(s): Zong ZP, Matsui S, Li AL, Yamaguchi N, Katsuda S, Hayase M, Fu ML. Source: European Journal of Pharmacology. 2001 March 9; 415(1): 51-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11245852
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Healing of acute myocarditis with left ventricular assist device: morphological recovery and evolution to the aspecific features of dilated cardiomyopathy. Author(s): Arbustini E, Grasso M, Porcu E, Bellini O, Magrini G, Campana C, Rinaldi M, Pagani F, Vigano M, Tavazzi L. Source: Ital Heart J. 2001 January; 2(1): 55-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11214703
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Heart transplantation for giant cell myocarditis. Author(s): Cooper DK, Schlesinger RG, Shrago S, Zuhdi N. Source: The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation. 1994 May-June; 13(3): 555. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8061036
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Heart transplantation in dilated heart muscle disease and myocarditis. Author(s): O'Connell JB, Breen TJ, Hosenpud JD. Source: European Heart Journal. 1995 December; 16 Suppl O: 137-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8682081
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Hepatitis C virus from the hearts of patients with myocarditis and cardiomyopathy. Author(s): Matsumori A, Yutani C, Ikeda Y, Kawai S, Sasayama S. Source: Laboratory Investigation; a Journal of Technical Methods and Pathology. 2000 July; 80(7): 1137-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10908160
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Hepatitis C virus infection and chronic active myocarditis. Author(s): Kao JH, Hwang JJ. Source: Circulation. 1998 September 8; 98(10): 1044-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9737529
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Human parvovirus B19 infection in infancy associated with acute and chronic lymphocytic myocarditis and high cytokine levels: report of 3 cases and review. Author(s): Nigro G, Bastianon V, Colloridi V, Ventriglia F, Gallo P, D'Amati G, Koch WC, Adler SP. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 2000 July; 31(1): 65-9. Epub 2000 July 14. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10913398
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Hydrops due to myocarditis in a fetus. Author(s): Benirschke K, Swartz WH, Leopold G, Sahn D. Source: Am J Cardiovasc Pathol. 1987 January; 1(1): 131-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2843206
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Identification and characterization of a novel mouse gene encoding a Ras-associated guanine nucleotide exchange factor: expression in macrophages and myocarditis elicited by Trypanosoma cruzi parasites. Author(s): Ferreira LR, Abrantes EF, Rodrigues CV, Caetano B, Cerqueira GC, Salim AC, Reis LF, Gazzinelli RT. Source: Journal of Leukocyte Biology. 2002 December; 72(6): 1215-27. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12488504
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Idiopathic giant cell myocarditis--a case report and review of literature. Author(s): Konapur PG, Dhaded AV, Udayakumar M. Source: Indian J Pathol Microbiol. 2003 April; 46(2): 241-3. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15022927
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Images in cardiovascular medicine. Diagnosis of myocarditis by cardiac tissue velocity imaging in an olympic athlete. Author(s): Urhausen A, Kindermann M, Bohm M, Kindermann W. Source: Circulation. 2003 July 29; 108(4): E21-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12885735
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Images in cardiovascular medicine. Echocardiographic description of recurrent idiopathic giant-cell myocarditis in cardiac allograft. Author(s): Palka P, Lange A, Clarke B, Duhig E, Galbraith A. Source: Circulation. 2003 July 8; 108(1): E1-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12847057
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Increase in serum free fatty acids, phospholipids and reduction in total cholesterol in acute myocarditis produced by scorpion (Buthus tamulus) venom injection in dogs. Author(s): Murthy RK, Medh JD. Source: Indian Heart J. 1986 September-October; 38(5): 369-72. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3570321
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Indium-111 monoclonal antimyosin cardiac scintigraphy in suspected acute myocarditis: evolution and diagnostic impact. Author(s): Margari ZJ, Anastasiou-Nana MI, Terrovitis J, Toumanidis S, Agapitos EV, Lekakis JP, Nanas JN. Source: International Journal of Cardiology. 2003 August; 90(2-3): 239-45. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12957757
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Induction of myocarditis and valvulitis in lewis rats by different epitopes of cardiac myosin and its implications in rheumatic carditis. Author(s): Galvin JE, Hemric ME, Kosanke SD, Factor SM, Quinn A, Cunningham MW. Source: American Journal of Pathology. 2002 January; 160(1): 297-306. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11786423
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Inotropic response in CHF: myocarditis vs dilated cardiomyopathy. Author(s): Meyer W, Neumann J, Nose M, Schmitz W, Scholz H, Scholz J, Starbatty J, Steinkraus V, Doring V, Kalmar P, et al. Source: American Heart Journal. 1988 June; 115(6): 1346-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3376865
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Interacting nutritional and infectious etiologies of Keshan disease. Insights from coxsackie virus B-induced myocarditis in mice deficient in selenium or vitamin E. Author(s): Levander OA, Beck MA. Source: Biological Trace Element Research. 1997 January; 56(1): 5-21. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9152508
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Intractable ventricular tachycardia in a patient with giant cell myocarditis, thymoma and myasthenia gravis. Author(s): de Jongste MJ, Oosterhuis HJ, Lie KI. Source: International Journal of Cardiology. 1986 December; 13(3): 374-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3793292
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Intravenous cyclophosphamide improves cardiac dysfunction in lupus myocarditis. Author(s): Chan YK, Li EK, Tam LS, Chow LT, Ng HK. Source: Scandinavian Journal of Rheumatology. 2003; 32(5): 306-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14690145
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Intravenous gamma-globulin therapy in myocarditis complicated with complete heart block: Report of one case. Author(s): Tsai YG, Ou TY, Wang CC, Tsai MC, Yuh YS, Hwang B. Source: Acta Paediatr Taiwan. 2001 September-October; 42(5): 311-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11729711
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Late persistent expressions of ICAM-1 and VCAM-1 on myocardial tissue in children with lymphocytic myocarditis. Author(s): Ino T, Kishiro M, Okubo M, Akimoto K, Nishimoto K, Yabuta K, Okada R. Source: Cardiovascular Research. 1997 May; 34(2): 323-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9205546
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Lethal hypersensitivity myocarditis associated with the use of intravenous gammaglobulin for Guillain-Barre syndrome, in combination with phenytoin. Author(s): Koehler PJ, Koudstaal J. Source: Journal of Neurology. 1996 April; 243(4): 366-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8965113
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Level of left ventricular dysfunction in endomyocardial biopsy-proven myocarditis. Author(s): Zivkov-Saponja D, Stojsic-Milosavljevic A, Stojsic D, Vuckovic D. Source: Med Pregl. 1999 November-December; 52(11-12): 429-36. English, Croatian. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10748763
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Levels of soluble Fas in patients with myocarditis, heart failure of unknown origin, and in healthy volunteers. Author(s): Toyozaki T, Hiroe M, Saito T, Iijima Y, Takano H, Hiroshima K, Kohno H, Ishiyama S, Marumo F, Masuda Y, Ohwada H. Source: The American Journal of Cardiology. 1998 March 15; 81(6): 798-800. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9527100
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Levels of soluble Fas ligand in myocarditis. Author(s): Toyozaki T, Hiroe M, Tanaka M, Nagata S, Ohwada H, Marumo F. Source: The American Journal of Cardiology. 1998 July 15; 82(2): 246-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9678301
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Life-threatening parvovirus B19-associated myocarditis and cardiac transplantation as possible therapy: two case reports. Author(s): Enders G, Dotsch J, Bauer J, Nutzenadel W, Hengel H, Haffner D, Schalasta G, Searle K, Brown KE. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1998 February; 26(2): 355-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9502455
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Local expression of interleukin-1 receptor antagonist by plasmid DNA improves mortality and decreases myocardial inflammation in experimental coxsackieviral myocarditis. Author(s): Lim BK, Choe SC, Shin JO, Ho SH, Kim JM, Yu SS, Kim S, Jeon ES. Source: Circulation. 2002 March 19; 105(11): 1278-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11901035
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Localization of porcine cardiac myosin epitopes that induce experimental autoimmune myocarditis. Author(s): Inomata T, Hanawa H, Miyanishi T, Yajima E, Nakayama S, Maita T, Kodama M, Izumi T, Shibata A, Abo T. Source: Circulation Research. 1995 May; 76(5): 726-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7537184
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Lone hepatitis C virus myocarditis responsive to immunosuppressive therapy. Author(s): Frustaci A, Calabrese F, Chimenti C, Pieroni M, Thiene G, Maseri A. Source: Chest. 2002 October; 122(4): 1348-56. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12377863
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Long-term follow-up of patients paragraph sign with acute myocarditis by magnetic paragraph sign resonance imaging. Author(s): Wagner A, Schulz-Menger J, Dietz R, Friedrich MG. Source: Magma (New York, N.Y.). 2003 February; 16(1): 17-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12695882
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Long-term outcome of acute myocarditis is independent of cardiac enzyme release. Author(s): Ammann P, Naegeli B, Schuiki E, Straumann E, Frielingsdorf J, Rickli H, Bertel O. Source: International Journal of Cardiology. 2003 June; 89(2-3): 217-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12767545
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Long-term outcome of patients with biopsy-proved myocarditis: comparison with idiopathic dilated cardiomyopathy. Author(s): Grogan M, Redfield MM, Bailey KR, Reeder GS, Gersh BJ, Edwards WD, Rodeheffer RJ. Source: Journal of the American College of Cardiology. 1995 July; 26(1): 80-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7797779
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Low prevalence of hepatitis C virus antibodies and RNA in patients with myocarditis and dilated cardiomyopathy. Author(s): Grumbach IM, Heermann K, Figulla HR. Source: Cardiology. 1998 October; 90(2): 75-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9778541
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Lupus myocarditis in children. Author(s): Gupta A, Singh S, Minz RW, Radotra BD, Ahluwalia J, Grover A. Source: Annals of the Rheumatic Diseases. 2004 June; 63(6): 745-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15140786
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Lyme myocarditis presenting as fascicular tachycardia with underlying complete heart block. Author(s): Greenberg YJ, Brennan JJ, Rosenfeld LE. Source: Journal of Cardiovascular Electrophysiology. 1997 March; 8(3): 323-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9083882
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Lympho-monocytic enteroviral myocarditis: traditional, immunohistological and molecularpathological methods for diagnosis in a case of suspected sudden infant death syndrome (SIDS). Author(s): Dettmeyer R, Kandolf R, Schmidt P, Schlamann M, Madea B. Source: Forensic Science International. 2001 June 1; 119(1): 141-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11348811
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Magnetic resonance imaging in acute myocarditis: a case report and a review of literature. Author(s): Geluk CA, Otterspoor IC, de Boeck B, Gevers RM, Velthuis BK, Cramer MJ. Source: The Netherlands Journal of Medicine. 2002 June; 60(5): 223-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12365479
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Mechanical circulatory support for myocarditis: how much recovery should occur before device removal? Author(s): Davies JE, Kirklin JK, Pearce FB, Rayburn BK, Winokur TS, Holman WL. Source: The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation. 2002 November; 21(11): 1246-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12431502
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Mechanical circulatory support for the treatment of children with acute fulminant myocarditis. Author(s): Duncan BW, Bohn DJ, Atz AM, French JW, Laussen PC, Wessel DL. Source: The Journal of Thoracic and Cardiovascular Surgery. 2001 September; 122(3): 440-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11547292
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Meningoencephalitis, myocarditis and disseminated intravascular coagulation in a patient with scrub typhus. Author(s): Ben RJ, Feng NH, Ku CS. Source: J Microbiol Immunol Infect. 1999 March; 32(1): 57-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11561571
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Molecular diagnosis of myocarditis and dilated cardiomyopathy in children: clinicopathologic features and prognostic implications. Author(s): Calabrese F, Rigo E, Milanesi O, Boffa GM, Angelini A, Valente M, Thiene G. Source: Diagnostic Molecular Pathology : the American Journal of Surgical Pathology, Part B. 2002 December; 11(4): 212-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12459637
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Mortality in primary and secondary myocarditis. Author(s): Pulerwitz TC, Cappola TP, Felker GM, Hare JM, Baughman KL, Kasper EK. Source: American Heart Journal. 2004 April; 147(4): 746-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15077094
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MRI of acute myocarditis: a comprehensive approach based on various imaging sequences. Author(s): Laissy JP, Messin B, Varenne O, Iung B, Karila-Cohen D, Schouman-Claeys E, Steg PG. Source: Chest. 2002 November; 122(5): 1638-48. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12426265
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Multimedia article. Cardiovascular magnetic resonance assessment of human myocarditis: a comparison to histology and molecular pathology. Author(s): Mahrholdt H, Goedecke C, Wagner A, Meinhardt G, Athanasiadis A, Vogelsberg H, Fritz P, Klingel K, Kandolf R, Sechtem U. Source: Circulation. 2004 March 16; 109(10): 1250-8. Epub 2004 Mar 01. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14993139
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Mycophenolate mofetil inhibits the development of Coxsackie B3-virus-induced myocarditis in mice. Author(s): Padalko E, Verbeken E, Matthys P, Aerts JL, De Clercq E, Neyts J. Source: Bmc Microbiology [electronic Resource]. 2003 December 21; 3(1): 25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14687413
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Myocarditis after smallpox vaccination: a case report. Author(s): Saurina G, Shirazi S, Lane JM, Daniel B, DiEugenia L. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 2003 July 1; 37(1): 145-6. Epub 2003 June 20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12830420
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Myocarditis and dilated cardiomyopathy: an inflammatory link. Author(s): Mason JW. Source: Cardiovascular Research. 2003 October 15; 60(1): 5-10. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14522402
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Myocarditis and inflammatory cardiomyopathy: microbiological and molecular biological aspects. Author(s): Calabrese F, Thiene G. Source: Cardiovascular Research. 2003 October 15; 60(1): 11-25. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14522403
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Myocarditis associated with Hashimoto's disease: a case report. Author(s): Lorin De La Grandmaison G, Izembart M, Fornes P, Paraire F. Source: International Journal of Legal Medicine. 2003 December; 117(6): 361-4. Epub 2003 October 01. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14520579
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Myocarditis associated with reovirus infection. Author(s): Terheggen F, Benedikz E, Frissen PH, Brinkman K. Source: European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology. 2003 March; 22(3): 197-8. Epub 2003 March 01. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12649721
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Myocarditis associated with visceral larva migrans due to Toxocara canis. Author(s): Abe K, Shimokawa H, Kubota T, Nawa Y, Takeshita A. Source: Intern Med. 2002 September; 41(9): 706-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12322796
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Myocarditis in systemic lupus erythematosus. Author(s): Wijetunga M, Rockson S. Source: The American Journal of Medicine. 2002 October 1; 113(5): 419-23. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12401537
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Myocarditis related to Campylobacter jejuni infection: a case report. Author(s): Cunningham C, Lee CH. Source: Bmc Infectious Diseases [electronic Resource]. 2003 July 17; 3(1): 16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12869210
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Myocarditis. Author(s): Kingman A, Van Bakel AB. Source: J S C Med Assoc. 2001 October; 97(10): 421-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11688311
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Myocarditis: an expected health hazard associated with water resources contaminated with Coxsackie viruses type B. Author(s): Ali MA, Abdel-Dayem TM. Source: International Journal of Environmental Health Research. 2003 September; 13(3): 261-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12909557
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Myocarditis: the unexpected return of smallpox vaccine adverse events. Author(s): Chen RT, Lane JM. Source: Lancet. 2003 October 25; 362(9393): 1345-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14585633
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N-acetylcysteine infusion in viral myocarditis: a case report. Author(s): Rowbotham DS, Wendon JA, Harrison PM. Source: International Journal of Cardiology. 1997 August 8; 60(3): 315-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9261645
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Narrowing of the left ventricular cavity associated with transient ventricular wall thickening reduces stroke volume in patients with acute myocarditis. Author(s): Morimoto S, Kato S, Hiramitsu S, Uemura A, Ohtsuki M, Kato Y, Sugiura A, Miyagishima K, Iwase M, Ito T, Hishida H. Source: Circulation Journal : Official Journal of the Japanese Circulation Society. 2003 June; 67(6): 490-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12808264
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National survey of fulminant myocarditis in Japan: therapeutic guidelines and longterm prognosis of using percutaneous cardiopulmonary support for fulminant myocarditis (special report from a scientific committee). Author(s): Aoyama N, Izumi T, Hiramori K, Isobe M, Kawana M, Hiroe M, Hishida H, Kitaura Y, Imaizumi T; Japanese Investigators of Fulminant Myocarditis. Source: Circulation Journal : Official Journal of the Japanese Circulation Society. 2002 February; 66(2): 133-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11999637
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Natural and lectin-dependent cytotoxicity in virus-induced human myocarditis. Author(s): Tchorzewski H, Goch JH, Baj Z, Tkaczewski W. Source: Arch Immunol Ther Exp (Warsz). 1987; 35(4): 405-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2830855
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Natural evolution of antimyosin scan and cardiac function in patients with acute myocarditis. Author(s): Lekakis J, Nanas J, Prassopoulos V, Kostamis P, Moulopoulos S. Source: International Journal of Cardiology. 1995 November 10; 52(1): 53-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8707437
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Necropsy diagnosis of myocarditis: a retrospective study using CD45RO immunohistochemistry. Author(s): Feeley KM, Harris J, Suvarna SK. Source: Journal of Clinical Pathology. 2000 February; 53(2): 147-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10767832
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Neonatal lupus: fetal myocarditis progressing to atrioventricular block in triplets. Author(s): Fesslova V, Mannarino S, Salice P, Boschetto C, Trespidi L, Acaia B, Mosca F, Cimaz R, Meroni PL. Source: Lupus. 2003; 12(10): 775-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14596427
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Neonatal myocarditis presenting as an apparent life threatening event. Author(s): Khan MA, Das B, Lohe A, Sharma J. Source: Clinical Pediatrics. 2003 September; 42(7): 649-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14552526
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Newer aspects of pathogenesis of heart failure: hepatitis C virus infection in myocarditis and cardiomyopathy. Author(s): Matsumori A, Sasayama S. Source: Journal of Cardiac Failure. 1996 December; 2(4 Suppl): S187-94. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8951578
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Nitric oxide donors inhibit the coxsackievirus B3 proteinases 2A and 3C in vitro, virus production in cells, and signs of myocarditis in virus-infected mice. Author(s): Zell R, Markgraf R, Schmidtke M, Gorlach M, Stelzner A, Henke A, Sigusch HH, Gluck B. Source: Medical Microbiology and Immunology. 2004 May; 193(2-3): 91-100. Epub 2003 September 26. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14513374
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Non-invasive detection of myocyte necrosis in myocarditis and dilated cardiomyopathy with radiolabelled antimyosin. Author(s): Khaw BA, Narula J. Source: European Heart Journal. 1995 December; 16 Suppl O: 119-23. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8682077
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Notes from a recent visitor to Berlin: on myocarditis, effect of coronary angiography on thyroid function, and Virchow's inflammatory theory of atherosclerosis. Author(s): Cheng TO. Source: The American Journal of Cardiology. 2002 April 15; 89(8): 1011-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11950453
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Novel associations of giant cell myocarditis: two case reports and a review of the literature. Author(s): Shariff S, Straatman L, Allard M, Ignaszewski A. Source: The Canadian Journal of Cardiology. 2004 April; 20(5): 557-61. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15100760
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Of molecules and myocardium. PCR diagnosis of viral myocarditis in cardiac biopsies. Author(s): Ross RS, Chien KR. Source: Circulation. 1990 July; 82(1): 294-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2364515
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Orbital myositis and giant cell myocarditis. Author(s): Klein BR, Hedges TR 3rd, Dayal Y, Adelman LS. Source: Neurology. 1989 July; 39(7): 988-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2739928
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Orbital myositis, vitiligo, and giant cell myocarditis. Author(s): Stevens AW, Grossman ME, Barr ML. Source: Journal of the American Academy of Dermatology. 1996 August; 35(2 Pt 2): 3102. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8698913
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Orbital polymyositis and giant cell myocarditis. Author(s): Leib ML, Odel JG, Cooney MJ. Source: Ophthalmology. 1994 May; 101(5): 950-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8190486
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Organisms in myocarditis/endocarditis viruses. Author(s): Grist NR, Reid D. Source: The Journal of Infection. 1997 March; 34(2): 155. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9138141
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Overexpression of interleukin-6 aggravates viral myocarditis: impaired increase in tumor necrosis factor-alpha. Author(s): Tanaka T, Kanda T, McManus BM, Kanai H, Akiyama H, Sekiguchi K, Yokoyama T, Kurabayashi M. Source: Journal of Molecular and Cellular Cardiology. 2001 September; 33(9): 1627-35. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11549342
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Overexpression of neural cell adhesion molecule in Chagas' myocarditis. Author(s): Soler AP, Gilliard G, Xiong Y, Knudsen KA, Martin JL, De Suarez CB, Mota Gamboa JD, Mosca W, Zoppi LB. Source: Human Pathology. 2001 February; 32(2): 149-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11230701
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Overwhelming myocarditis due to Cryptococcus neoformans in an AIDS patient. Author(s): Lafont A, Wolff M, Marche C, Clair B, Regnier B. Source: Lancet. 1987 November 14; 2(8568): 1145-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2890037
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Overwhelming myocarditis due to Fusarium oxysporum following bone marrow transplantation. Author(s): Mohammedi I, Gachot B, Grossin M, Marche C, Wolff M, Vachon F. Source: Scandinavian Journal of Infectious Diseases. 1995; 27(6): 643-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8685650
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Oxidative stress in patients with acute coxsackie virus myocarditis. Author(s): Xie B, Zhou JF, Lu Q, Li CJ, Chen P. Source: Biomed Environ Sci. 2002 March; 15(1): 48-57. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12046548
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Pathology of Toxoplasma myocarditis in acquired immunodeficiency syndrome. Author(s): Sahasrabudhe NS, Jadhav MV, Deshmukh SD, Holla VV. Source: Indian J Pathol Microbiol. 2003 October; 46(4): 649-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025367
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Pathophysiology of viral myocarditis: the role of humoral immune response. Author(s): Maisch B, Ristic AD, Hufnagel G, Pankuweit S. Source: Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology. 2002 March-April; 11(2): 112-22. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11934603
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Pediatric viral myocarditis. Author(s): Snyder M. Source: Air Medical Journal. 2003 July-August; 22(4): 6-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12847456
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Phaeochromocytoma-induced myocarditis mimicking acute myocardial infarction. Author(s): Dinckal MH, Davutoglu V, Soydinc S, Kirilmaz A. Source: Int J Clin Pract. 2003 November; 57(9): 842-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14686578
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PKR's protective role in viral myocarditis. Author(s): Stewart MJ, Blum MA, Sherry B. Source: Virology. 2003 September 15; 314(1): 92-100. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14517063
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Polyclonal proliferation of lymphocytes containing the epstein-barr virus genome in a patient dying of myocarditis in chronic active Epstein-Barr virus infection. Author(s): Fujiwara M, Shimozono H, Ono H, Fujita N, Nishimura S, Ueda K, Kaneko M. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 January; 25(1): 85-8. Erratum In: J Pediatr Hematol Oncol. 2003 May; 25(5): 428. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12544781
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Presence of poorly stained myocytes in acute myocarditis predicts improvement in cardiac function. Author(s): Sakai A, Fukunami M, Nagareda T, Ohmori M, Kumagai K, Umemoto K, Yamada T, Kondoh N, Minamino T, Kotoh K, Hoki N. Source: J Cardiol. 1996 October; 28(4): 213-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8934337
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Prevalence of viral myocarditis. Author(s): Cheng TO. Source: Archives of Internal Medicine. 2003 July 28; 163(14): 1742. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12885693
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Pulmonary hypertension and risk of death in cardiomyopathy: patients with myocarditis are at higher risk. Author(s): Cappola TP, Felker GM, Kao WH, Hare JM, Baughman KL, Kasper EK. Source: Circulation. 2002 April 9; 105(14): 1663-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11940544
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Q wave and non-Q wave myocarditis with special reference to clinical significance. Author(s): Nakashima H, Katayama T, Ishizaki M, Takeno M, Honda Y, Yano K. Source: Japanese Heart Journal. 1998 November; 39(6): 763-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10089938
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QS pattern in the right precordial leads of a child with extensive myocardial fibrosis following myocarditis. Author(s): Onouchi Z, Tamiya H, Mizuno S, Sakakibara Y, Ando M, Fujimoto T. Source: Pediatric Cardiology. 1988; 9(3): 167-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3263629
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Quantitation of leukocytes in endomyocardial tissue from 100 normal human hearts at autopsy. Implications for diagnosis of myocarditis from biopsy specimens of living patients. Author(s): Foley DA, Edwards WD. Source: Am J Cardiovasc Pathol. 1988; 2(2): 145-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3207496
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Quantitative texture analysis in echocardiography: application to the diagnosis of myocarditis. Author(s): Ferdeghini EM, Pinamonti B, Picano E, Lattanzi F, Bussani R, Slavich G, Benassi A, Camerini F, Landini L, L'Abbate A. Source: Journal of Clinical Ultrasound : Jcu. 1991 June; 19(5): 263-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1651341
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Rapidly fatal acute bacterial myocarditis in a nonneutropenic child with acute lymphoblastic leukemia in remission. Author(s): Scothorn DJ, Winick NJ, Timmons CF, Aquino VM. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2002 November; 24(8): 662-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12439040
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Recognition and optimum management of myocarditis. Author(s): Caforio AL, McKenna WJ. Source: Drugs. 1996 October; 52(4): 515-25. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8891464
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Recurrent fulminant viral myocarditis with a short clinical course. Author(s): Takehana H, Inomata T, Kuwao S, Nakahata J, Sasaki T, Nishii M, Kurokawa S, Izumi T. Source: Circulation Journal : Official Journal of the Japanese Circulation Society. 2003 July; 67(7): 646-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12845193
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Recurrent, life-threatening atrioventricular dissociation associated with toxoplasma myocarditis. Author(s): Duffield JS, Jacob AJ, Miller HC. Source: Heart (British Cardiac Society). 1996 November; 76(5): 453-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8944597
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Resolved hypersensitivity myocarditis after ventricular circulatory assist. Author(s): Grabellus F, Hoffmeier A, Schmitz KJ, Kandolf R, Bultmann BD, Scheld HH, Baba HA. Source: The Annals of Thoracic Surgery. 2003 December; 76(6): 2102-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14667660
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Reversible infra-Hisian atrioventricular block in acute myocarditis. Author(s): Yu TH, Guo GF, Chen MC, Yang CH. Source: Chang Gung Med J. 2001 October; 24(10): 651-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11771189
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Reversible myocarditis in a patient receiving clozapine. Author(s): Kirpekar VC, Deshpande SM, Joshi PP. Source: Indian Heart J. 2001 November-December; 53(6): 779-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11838936
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Risks versus benefits of NSAIDs including aspirin in myocarditis: a review of the evidence from animal studies. Author(s): Meune C, Spaulding C, Mahe I, Lebon P, Bergmann JF. Source: Drug Safety : an International Journal of Medical Toxicology and Drug Experience. 2003; 26(13): 975-81. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14583071
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Role of cytokines in autoimmune myocarditis and cardiomyopathy. Author(s): Furukawa Y, Kobuke K, Matsumori A. Source: Autoimmunity. 2001; 34(3): 165-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11908773
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Role of noninvasive antimyosin imaging in infants and children with clinically suspected myocarditis. Author(s): Martin ME, Moya-Mur JL, Casanova M, Crespo-Diez A, Asin-Cardiel E, Castro-Beiras JM, Diez-Jimenez L, Ballester M, Carrio I, Narula J. Source: Journal of Nuclear Medicine : Official Publication, Society of Nuclear Medicine. 2004 March; 45(3): 429-37. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15001683
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Serum levels of eosinophil cationic protein in patients with eosinophilic myocarditis. Author(s): Arima M, Kanoh T, Kawano Y, Oigawa T, Yamagami S, Matsuda S. Source: International Journal of Cardiology. 2002 July; 84(1): 97-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12104073
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Specific stimulation of peripheral blood mononuclear cells from patients with acute myocarditis by peptide-bound flavin adenine dinucleotide (FAD), a naturally occurring autologous hapten. Author(s): Cicek G, Schiltz E, Staiger J, Neumann FJ, Melchers I, Brandsch R. Source: Clinical and Experimental Immunology. 2003 May; 132(2): 366-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12699430
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Successful explantation of a ventricular assist device following fulminant influenza type A-associated myocarditis. Author(s): McGovern PC, Chambers S, Blumberg EA, Acker MA, Tiwari S, Taubenberger JK, Carboni A, Twomey C, Loh E. Source: The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation. 2002 February; 21(2): 290-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11834359
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Successful immunoglobulin treatment for fulminant myocarditis and serial analysis of serum thioredoxin: a case report. Author(s): Shioji K, Matsuura Y, Iwase T, Kitaguchi S, Nakamura H, Yodoi J, Hashimoto T, Kawai C, Kishimoto C. Source: Circulation Journal : Official Journal of the Japanese Circulation Society. 2002 October; 66(10): 977-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12381097
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Successful LVAS and RVAS-ECMO support in a patient with fulminant myocarditis who failed to recover from ventricular fibrillation with PCPS and IABP. Author(s): Gojo S, Kyo S, Sato H, Nishimura M, Asakura T, Ito H, Koyama K. Source: The Journal of Thoracic and Cardiovascular Surgery. 2003 September; 126(3): 885-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14502181
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Successful treatment of Candida glabrata myocarditis with voriconazole. Author(s): Einarsdottir HM, Danielsen R, Gottfredsson M. Source: Scandinavian Journal of Infectious Diseases. 2002; 34(10): 778-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12477337
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Successful treatment of enterovirus-induced myocarditis with interferon-alpha. Author(s): Daliento L, Calabrese F, Tona F, Caforio AL, Tarsia G, Angelini A, Thiene G. Source: The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation. 2003 February; 22(2): 214-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12581773
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Sudden death due to granulomatous myocarditis: a case of sarcoidosis? Author(s): Loh AH, Wee KP. Source: Ann Acad Med Singapore. 2002 November; 31(6): 805-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12520839
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Support with the BVS 5000 assist device during treatment of acute giant-cell myocarditis. Author(s): Marelli D, Kermani R, Bresson J, Fishbein MC, Hamilton M, Moriguchi J, Fonarow GC, Cohen B, Kobashigawa J, Laks H. Source: Texas Heart Institute Journal / from the Texas Heart Institute of St. Luke's Episcopal Hospital, Texas Children's Hospital. 2003; 30(1): 50-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12638672
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Surgical management of localized left ventricular aneurysm associated with acute myocarditis. Author(s): Miura M, Fukuju T, Shibata M, Katahira Y. Source: Jpn J Thorac Cardiovasc Surg. 2003 June; 51(6): 249-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12831240
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The clinical course of acquired complete heart block in children with acute myocarditis. Author(s): Batra AS, Epstein D, Silka MJ. Source: Pediatric Cardiology. 2003 September-October; 24(5): 495-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14627323
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The current status of immune modulating therapy for myocarditis: a case of acute parvovirus myocarditis treated with intravenous immunoglobulin. Author(s): Stouffer GA, Sheahan RG, Lenihan DJ, Patel P, Lenihan DJ. Source: The American Journal of the Medical Sciences. 2003 December; 326(6): 369-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14671501
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The prevalence of myocarditis and skeletal muscle injury during acute viral infection in adults: measurement of cardiac troponins I and T in 152 patients with acute influenza infection. Author(s): Greaves K, Oxford JS, Price CP, Clarke GH, Crake T. Source: Archives of Internal Medicine. 2003 January 27; 163(2): 165-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12546606
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Therapeutic role of pericardiocentesis for acute necrotizing eosinophilic myocarditis with cardiac tamponade. Author(s): Kazama R, Okura Y, Hoyano M, Toba K, Ochiai Y, Ishihara N, Kuroha T, Yoshida T, Namura O, Sogawa M, Nakamura Y, Yoshimura N, Nishikura K, Kato K, Hanawa H, Tamura Y, Morimoto S, Kodama M, Aizawa Y. Source: Mayo Clinic Proceedings. 2003 July; 78(7): 901-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12839087
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Three cases of myocarditis in childhood associated with human parvovirus (B19 virus). Author(s): Munro K, Croxson MC, Thomas S, Wilson NJ. Source: Pediatric Cardiology. 2003 September-October; 24(5): 473-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14627316
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Torsade de pointes tachycardia as a rare manifestation of acute enteroviral myocarditis. Author(s): Badorff C, Zeiher AM, Hohnloser SH. Source: Heart (British Cardiac Society). 2001 November; 86(5): 489-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11602535
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Transformation of myocarditis and inflammatory cardiomyopathy to idiopathic dilated cardiomyopathy: facts and fiction. Author(s): Figulla HR. Source: Medical Microbiology and Immunology. 2004 May; 193(2-3): 61-4. Epub 2003 November 01. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14595559
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Transgenic mouse model for echovirus myocarditis and paralysis. Author(s): Hughes SA, Thaker HM, Racaniello VR. Source: Proceedings of the National Academy of Sciences of the United States of America. 2003 December 23; 100(26): 15906-11. Epub 2003 Dec 12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14673080
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Transient ventricular wall thickening in acute myocarditis: a serial echocardiographic and histopathologic study. Author(s): Hiramitsu S, Morimoto S, Kato S, Uemura A, Kubo N, Kimura K, Sugiura A, Itoh T, Hishida H. Source: Japanese Circulation Journal. 2001 October; 65(10): 863-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11665789
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Trypanosoma cruzi-elicited CD8+ T cell-mediated myocarditis: chemokine receptors and adhesion molecules as potential therapeutic targets to control chronic inflammation? Author(s): Lannes-Vieira J. Source: Memorias Do Instituto Oswaldo Cruz. 2003 April; 98(3): 299-304. Epub 2003 July 18. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12886406
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Ultrasonic tissue characterization in acute myocarditis: a case report. Author(s): Omi W, Nagai H, Takata S, Yuasa T, Sakagami S, Kobayashi K. Source: Circulation Journal : Official Journal of the Japanese Circulation Society. 2002 April; 66(4): 416-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11954960
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Ultrastructural aspect of myocarditis: its relevance for the diagnosis. Author(s): Milin J, Stojsic D, Vuckovic D, Benc D, Hadzic M, Stojsic A, Zivkov-Saponja D. Source: Ultrastructural Pathology. 1995 November-December; 19(6): 463-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8597200
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Unexpected eosinophilic myocarditis in a young woman with rapidly progressive dilated cardiomyopathy. Author(s): Bilinska ZT, Bilinska M, Grzybowski J, Przyluski J, Michalak E, Walczak E, Wagner T, Ruzyllo W. Source: International Journal of Cardiology. 2002 December; 86(2-3): 295-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12419569
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Unexpected hazard of illegal immigration: Outbreak of viral myocarditis exacerbated by confinement and deprivation in a shipboard cargo container. Author(s): Li MK, Beck MA, Shi Q, Harruff RC. Source: The American Journal of Forensic Medicine and Pathology : Official Publication of the National Association of Medical Examiners. 2004 June; 25(2): 117-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15166761
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Unusual complications of varicella infection: myocarditis, incessant ventricular tachycardia and transverse myelitis. Author(s): Dwivedi S, Suresh K. Source: J Assoc Physicians India. 1998 September; 46(9): 831. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11229263
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Upregulation of redox-regulating protein, thioredoxin, in endomyocardial biopsy samples of patients with myocarditis and cardiomyopathies. Author(s): Nimata M, Kishimoto C, Shioji K, Ishizaki K, Kitaguchi S, Hashimoto T, Nagata N, Kawai C. Source: Molecular and Cellular Biochemistry. 2003 June; 248(1-2): 193-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12870673
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Use of OKT3 for acute myocarditis in infants and children. Author(s): Ahdoot J, Galindo A, Alejos JC, George B, Burch C, Marelli D, Sadeghi A, Laks H. Source: The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation. 2000 November; 19(11): 1118-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11077231
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Use of percutaneous cardiopulmonary support of patients with fulminant myocarditis and cardiogenic shock for improving prognosis. Author(s): Kato S, Morimoto S, Hiramitsu S, Nomura M, Ito T, Hishida H. Source: The American Journal of Cardiology. 1999 February 15; 83(4): 623-5, A10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10073879
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Usefulness of antimyosin antibody imaging for the detection of active rheumatic myocarditis. Author(s): Narula J, Malhotra A, Yasuda T, Talwar KK, Reddy KS, Chopra P, Southern JF, Vasan RS, Tandon R, Bhatia ML, Khaw BA, Strauss HW. Source: The American Journal of Cardiology. 1999 October 15; 84(8): 946-50, A7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10532521
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Usefulness of extracorporeal membrane oxygenation for treatment of fulminant myocarditis and circulatory collapse. Author(s): Kawahito K, Murata S, Yasu T, Adachi H, Ino T, Saito M, Misawa Y, Fuse K, Shimada K. Source: The American Journal of Cardiology. 1998 October 1; 82(7): 910-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9781978
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Valsalva maneuver in chagasic patients with documented past medical history of acute chagasic myocarditis. Author(s): Odreman RO, Davila DF, Donis JH, Torres A, Ferrer J, Inglessis I. Source: International Journal of Cardiology. 2004 February; 93(2-3): 163-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14975542
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Varicella myocarditis producing congestive cardiomyopathy. Author(s): Thandroyen FT, Asmal AC, Armstrong TG. Source: Postgraduate Medical Journal. 1981 March; 57(665): 199-201. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7329890
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Ventricular assist surprise: giant cell myocarditis or sarcoidosis? Author(s): Stoica SC, Goddard M, Tsui S, Dunning J, McNeil K, Parameshwar J, Large SR. Source: The Journal of Thoracic and Cardiovascular Surgery. 2003 December; 126(6): 2072-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14688728
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Ventricular expression of atrial natriuretic peptide in chronic chagasic cardiomyopathy is not induced by myocarditis. Author(s): Benvenuti LA, Aiello VD, Palomino SA, Higuchi Mde L. Source: International Journal of Cardiology. 2003 March; 88(1): 57-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12659985
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Viral latency: a link between myocarditis and dilated cardiomyopathy? Author(s): Mason JW. Source: Journal of Molecular and Cellular Cardiology. 2002 July; 34(7): 695-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12099707
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Viral myocarditis. Author(s): Leonard EG. Source: The Pediatric Infectious Disease Journal. 2004 July; 23(7): 665-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15247607
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Viral myocarditis. A review. Author(s): Woodruff JF. Source: American Journal of Pathology. 1980 November; 101(2): 425-84. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6254364
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Viral myocarditis. Clinical, electrocardiographic and evolutive diversity. Author(s): Olinic N, Vida Simiti L, Valeanu S, Bedeleanu D, Vlaicu R, Petrescu M, Olteanu L, Sovrea D. Source: Med Interne. 1981 April-June; 19(2): 147-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7268280
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Viral myocarditis. Clinical, electrocardiographic and evolutive diversity. Author(s): Olinic N, Vida-Simiti L, Valeanu S, Bedeleanu D, Vlaicu R, Petrescu M, Olteanu L, Sovrea D. Source: Med Interne. 1981 April-June; 19(2): 147-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7052972
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Viral myocarditis: balance between viral infection and immune response. Author(s): Liu P, Martino T, Opavsky MA, Penninger J. Source: The Canadian Journal of Cardiology. 1996 October; 12(10): 935-43. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9191484
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West Nile virus encephalitis and myocarditis in wolf and dog. Author(s): Lichtensteiger CA, Heinz-Taheny K, Osborne TS, Novak RJ, Lewis BA, Firth ML. Source: Emerging Infectious Diseases. 2003 October; 9(10): 1303-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14609468
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Wolff Parkinson White syndrome in a case of myocarditis in infancy. Author(s): Ward OC, Denham B. Source: Ir J Med Sci. 1986 July; 155(7): 232-3. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3744748
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Yet another report of anesthetic death due to unsuspected myocarditis. Author(s): Critchley LA. Source: Journal of Clinical Anesthesia. 1997 December; 9(8): 676-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9438900
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CHAPTER 2. NUTRITION AND MYOCARDITIS Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and myocarditis.
Finding Nutrition Studies on Myocarditis 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 “myocarditis” (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 “myocarditis” (or a synonym): •
An autopsy case of giant cell myocarditis probably due to a non-steroidal antiinflammatory drug. Author(s): First Department of Pathology, Kansai Medical University, Osaka, Japan. Source: Adachi, Y Yasumizu, R Hashimoto, F Otsuka, Y Okamura, A Kato, Y Oyaizu, H Ikebukuro, K Fukuhara, S Nakai, Y Ikehara, S Pathol-Int. 2001 February; 51(2): 113-7 1320-5463
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Anti-mitochondrial flavoprotein autoantibodies of patients with myocarditis and dilated cardiomyopathy (anti-M7): interaction with flavin-carrying proteins, effect of vitamin B2 and epitope mapping. Author(s): Institute of Biochemistry and Molecular Biology, University of Freiburg, Germany. Source: Stahle, I Brizzio, C Barile, M Brandsch, R Clin-Exp-Immunol. 1999 March; 115(3): 404-8 0009-9104
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Clinical and immunologic status of viral myocarditis and its treatment. Source: Yu, G R Chen, S X Mei, S W Zheng, Y Chen, L Zhou, G Y Lu, P H Chin-Med-J(Engl). 1988 March; 101(3): 191-6 0366-6999
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Effect of Astragalus membranaceus on electrophysiological activities of acute experimental Coxsackie B-3 viral myocarditis in mice. Author(s): Affiliated Hospital of Zhenjiang Medical College. Source: Rui, T Yang, Y Zhou, T Zhang, J Yang, X Chen, H Chin-Med-Sci-J. 1993 December; 8(4): 203-6 1001-9294
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Effect of indomethacin in the late phase of coxsackievirus myocarditis in a murine model. Author(s): Department of Internal Medicine, Harper Hospital, Detroit, MI 48201. Source: Rezkalla, S Khatib, R Khatib, G Smith, F Walsh, M Sowers, J Kloner, R J-LabClin-Med. 1988 July; 112(1): 118-21 0022-2143
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Hypersensitivity myocarditis associated with ephedra use. Author(s): Rush Presbyterian St. Luke's Medical Center, Chicago, Illinois 60612, USA. Source: Zaacks, S M Klein, L Tan, C D Rodriguez, E R Leikin, J B J-Toxicol-Clin-Toxicol. 1999; 37(4): 485-9 0731-3810
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Immunohistochemical staining of lymphocytes for the reliable diagnosis of myocarditis in endomyocardial biopsies. Author(s): Cardiopsis, Hospital Fernandez, Instituto de Estudios Oncologicos, Buenos Aires, Argentina. Source: Milei, J Bortman, G Fernandez Alonso, G Grancelli, H Beigelman, R Cardiology. 1990; 77(2): 77-85 0008-6312
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In vivo administration of serum thymic factor (FTS) prevents EMC-D virus-induced diabetes and myocarditis in BALB/cAJcl mice. Author(s): Department of Molecular Immunology, University of Tokyo, Japan. Source: Mizutani, M El Fotoh, M Mori, M Ono, K Doi, K Awaya, A Matsumoto, Y Matsumoto, Y Onodera, T Arch-Virol. 1996; 141(1): 73-83 0304-8608
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Interacting nutritional and infectious etiologies of Keshan disease: insights from Coxsackie virus B-induced myocarditis in mice deficient in selenium or vitamin E. Source: Levander, O.A. Beck, M.A. Biol-trace-elem-res. Totowa, N.J. : Humana Press. January 1997. volume 56 (1) page 5-21. 0163-4984
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Massive myocardial calcification of right and left ventricles following acute myocarditis complicated with rhabdomyolysis-induced acute renal failure. Author(s): Second Department of Internal Medicine, Sapporo Medical College, Japan. Source: Wada, A Nakata, T Tsuchihashi, K Aoyama, S Nanba, M Murakami, H Shimamoto, K Iimura, O Jpn-Circ-J. 1993 June; 57(6): 567-72 0047-1828
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Nitric oxide synthase in experimental autoimmune myocarditis dysfunction. Author(s): Centro de Estudios Farmacologicos y Botanicos (CEFYBO) and Catedra de Farmacologia de la Facultad de Odontologia de la Universidad de Buenos Aires, Consejo Nacional de Investigaciones Cientificas y Tecnicas (CONICET), Argentina. Source: Goren, N Leiros, C P Sterin Borda, L Borda, E J-Mol-Cell-Cardiol. 1998 November; 30(11): 2467-74 0022-2828
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Reactivation of Chagas' myocarditis during therapy of Hodgkin's disease. Author(s): Department of Pathology, Medical School, State University of Campinas, Brazil. Source: Metze, K Lorand Metze, I De Almeida, E A De Moraes, S L Trop-Geogr-Med. 1991 Jan-April; 43(1-2): 228-30 0041-3232
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Recurrence of myocarditis presenting as pacing and sensing failure after implantation of a permanent pacemaker at first onset. Author(s): Department of Internal Medicine, Juntendo Urayasu Hospital, Juntendo University School of Medicine, Chiba, Japan. Source: Arima, M Kanoh, T Kawano, Y Okazaki, S Oigawa, T Yamagami, S Matsuda, S Jpn-Circ-J. 2001 April; 65(4): 345-8 0047-1828
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Temocapril treatment ameliorates autoimmune myocarditis associated with enhanced cardiomyocyte thioredoxin expression. Author(s): Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, 54 Kawaracho, Shogoin, Sakyo-ku, Kyoto, 606-8507, Japan. Source: Yuan, Z Kishimoto, C Shioji, K Nakamura, H Yodoi, J Sasayama, S CardiovascRes. 2002 August 1; 55(2): 320-8 0008-6363
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The protective effect of selenium against viral myocarditis in mice. Source: Ge, K.Y. Bai, J. Deng, X.J. Wu, S.Q. Wang, S.Q. Xue, A.N. Su, C.Q. Selenium in biology and medicine : proceedings of the Third International Symposium on Selenium in Biology and Medicine, held May 27-June 1, 1984, Xiangshan (Fragrance Hills) Hotel Beijing, People's Republic of China. New York : Van Nostrand Reinhold, c1987. page 761-768. ISBN: 0442221088
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Treatment of experimental Coxsackie B-3 viral myocarditis with Astragalus membranaceus in mice. Author(s): Shanghai Institute of Cardiovascular Disease, Zhongshan Hospital, Shanghai Medical University. Source: Yang, Y Z Jin, P Y Guo, Q Wu, W Z Pu, S Y Chen, H Z Yang, J H Wang, K Q Shi, J Y Gong, Z X et al. Chin-Med-J-(Engl). 1990 January; 103(1): 14-8 0366-6999
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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 MYOCARDITIS Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to myocarditis. 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 myocarditis 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 “myocarditis” (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 myocarditis: •
A case of giant cell myocarditis. Author(s): Sundstrom C. Source: Upsala Journal of Medical Sciences. 1973; 78(2): 83-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4748147
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Effect of Astragalus membranaceus on electrophysiological activities of acute experimental Coxsackie B-3 viral myocarditis in mice. Author(s): Rui T, Yang Y, Zhou T, Zhang J, Yang X, Chen H. Source: Chinese Medical Sciences Journal = Chung-Kuo I Hsueh K'o Hsueh Tsa Chih / Chinese Academy of Medical Sciences. 1993 December; 8(4): 203-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8032064
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Effect of Astragulas membranaceus on natural killer cell activity and induction of alpha- and gamma-interferon in patients with Coxsackie B viral myocarditis.
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Author(s): Yang YZ, Jin PY, Guo Q, Wang QD, Li ZS, Ye YC, Shan YF, Zhao HY, Zhu JR, Pu SY, et al. Source: Chinese Medical Journal. 1990 April; 103(4): 304-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2167822 •
Ephedra causes myocarditis. Author(s): Leikin JB, Klein L. Source: Journal of Toxicology. Clinical Toxicology. 2000; 38(3): 353-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10866341
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Fatal cardiac arrhythmia in a patient with interstitial myocarditis related to chronic arsenic poisoning. Author(s): Hall JC, Harruff R. Source: Southern Medical Journal. 1989 December; 82(12): 1557-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2595426
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Herbal medicines for viral myocarditis. Author(s): Liu J, Yang M, Du X. Source: Cochrane Database Syst Rev. 2004; 3: Cd003711. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15266498
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Hypersensitivity myocarditis associated with ephedra use. Author(s): Zaacks SM, Klein L, Tan CD, Rodriguez ER, Leikin JB. Source: Journal of Toxicology. Clinical Toxicology. 1999; 37(4): 485-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10465246
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Hypersensitivity myocarditis with ephedra use. Author(s): Kurt TL. Source: Journal of Toxicology. Clinical Toxicology. 2000; 38(3): 351. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10866340
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Interferon and thymic hormones in the therapy of human myocarditis and idiopathic dilated cardiomyopathy. Author(s): Miric M, Miskovic A, Vasiljevic JD, Keserovic N, Pesic M. Source: European Heart Journal. 1995 December; 16 Suppl O: 150-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8682086
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Long-term follow-up of patients with myocarditis and idiopathic cardiomyopathy after immunomodulatory therapy. Author(s): Miric M, Miskovic A, Brkic S, Vasiljevic J, Keserovic N, Pesic M.
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Source: Fems Immunology and Medical Microbiology. 1994 November; 10(1): 65-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7874080 •
Prof. Cao Hongxin's experience in treating viral myocarditis with xuefu zhuyu tang. Author(s): Deng W, Yang Z. Source: J Tradit Chin Med. 2003 March; 23(1): 14-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12747189
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Protective effects of Mu-Fang-Ji-Tang against myocardial injury in a murine model of congestive heart failure induced by viral myocarditis. Author(s): Wang WZ, Matsumori A, Matoba Y, Matsui S, Sato Y, Hirozane T, Shioi T, Sasayama S. Source: Life Sciences. 1998; 62(13): 1139-46. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9519794
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Reactivation of Chagas' myocarditis during therapy of Hodgkin's disease. Author(s): Metze K, Lorand-Metze I, De Almeida EA, De Moraes SL. Source: Trop Geogr Med. 1991 January-April; 43(1-2): 228-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1750119
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Reversible myocarditis due to chronic lead poisoning in childhood. Author(s): FREEMAN R. Source: Archives of Disease in Childhood. 1965 August; 40: 389-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14329255
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Sjogren's syndrome with myocarditis. Report of a case. Author(s): Wang YX. Source: Chinese Medical Journal. 1981 January; 94(1): 45-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6785023
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Successful treatment of complete left bundle branch block complicating acute viral myocarditis employing Chinese herbs. Author(s): Kuo C. Source: The American Journal of Chinese Medicine. 1986; 14(3-4): 124-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3799528
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Treatment of experimental Coxsackie B-3 viral myocarditis with Astragalus membranaceus in mice. Author(s): Yang YZ, Jin PY, Guo Q, Wu WZ, Pu SY, Chen HZ, Yang JH, Wang KQ, Shi JY, Gong ZX, et al.
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Source: Chinese Medical Journal. 1990 January; 103(1): 14-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2161724
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 myocarditis; 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 Serum Sickness Source: Integrative Medicine Communications; www.drkoop.com Shock Source: Integrative Medicine Communications; www.drkoop.com
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Herbs and Supplements Astragalus Mem Alternative names: Huang-Qi; Astragalus membranaceus Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
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Thymus Extracts Source: Healthnotes, Inc.; www.healthnotes.com
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 4. DISSERTATIONS ON MYOCARDITIS Overview In this chapter, we will give you a bibliography on recent dissertations relating to myocarditis. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “myocarditis” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on myocarditis, we have not necessarily excluded nonmedical dissertations in this bibliography.
Dissertations on Myocarditis ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to myocarditis. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •
Identification of a novel diagnostic marker for viral myocarditis using cDNA microarrays by Cerullo, Dante, MSc from UNIVERSITY OF TORONTO (CANADA), 2003, 132 pages http://wwwlib.umi.com/dissertations/fullcit/MQ84427
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Pathogenesis of coxsackievirus B3 induced myocarditis and systemic disease: Viral localization, direct injury and activation of host cell death machinery by Carthy, Christopher Michael, PhD from THE UNIVERSITY OF BRITISH COLUMBIA (CANADA), 2003, 245 pages http://wwwlib.umi.com/dissertations/fullcit/NQ79206
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Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.
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CHAPTER 5. PATENTS ON MYOCARDITIS 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 “myocarditis” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on myocarditis, we have not necessarily excluded nonmedical patents in this bibliography.
Patents on Myocarditis By performing a patent search focusing on myocarditis, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We will tell you how to obtain this information later in the chapter. The following is an 8Adapted
from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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example of the type of information that you can expect to obtain from a patent search on myocarditis: •
Diagnosing and treating subacute cardiac dysfunction Inventor(s): Lerner; Albert M. (660 Woodland, Birmingham, MI 48009) Assignee(s): none reported Patent Number: 5,464,020 Date filed: April 4, 1994 Abstract: A method for diagnosing subacute cardiac dysfunction is performed by electrocardiographically monitoring an ambulatory patient who has persistent unexplainable fatigue and determining the frequency when the T-wave of the ambulatory patient is not positive to determine that subacute myocarditis or a cardiomyopathy is present. This monitoring is preferably performed by a portable monitor and the data is magnetically stored so as to permit subsequent analysis. A treatment is prescribed, preferably restricting activity and refraining from the intake of alcohol as well as antiviral chemotherapy and immunomodulators, when there is an excessively high frequency of the T-wave not being positive. Recovery is determined by further electrocardiographic monitoring of the ambulatory patient and noting when the normally positive T-waves are present all, or at least almost all, of the time. Excerpt(s): This invention relates to a method for diagnosing and treating a previously unrecognizable subacute cardiac dysfunction by electrocardiographic monitoring. The medical community now recognizes a condition of unknown cause that is referred to as chronic fatigue syndrome. The role of cardiac dysfunction in this syndrome, the diagnosis and preferred treatment have not been heretofore understood or explainable. A competent diagnosis for fatigue will conventionally include a complete medical history, a physical examination and appropriate laboratory studies in order to determine whether the fatigue can be explained by other diagnoses such as arteriosclerosis or other coronary artery disease, heart muscle damage from. coronary thrombosis or other acute heart disease, or heart damage such as pericarditis, etc. Other recognizable infections or other diverse maladies may, of course, cause chronic fatigue; but, as mentioned above, this chronic fatigue syndrome has not been heretofore understood or diagnosable. Also, while some consider chronic fatigue syndrome to exist only when it persists for six months or longer, others consider this syndrome to be present when there is an unexplainable fatigue for much shorter periods of time such as one or two months. Conventional diagnosis for heart disease includes electrocardiographic monitoring which has been done for many years such as disclosed, for example, by U.S. Pat. Nos.: 3,267,934 Thornton; 3,572,321 Bloomfield et al; 3,829,766 Herz; and 4,275,742 Faisandier. Most electrocardiographic monitorings are performed on a sedentary patient; however, it is also conventional to electrocardiographically monitor an ambulatory patient such as disclosed by U.S. Pat. Nos.: 4,183,354 Sibly et al; 4,457,315 Bennish; 4,546,776 Bellin et al; 4,583,553 Shah et al; and 4,883,065 Kelen. Web site: http://www.delphion.com/details?pn=US05464020__
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Method for testing cardiac myocarditis or cardiomyopathy Inventor(s): Matsumori; Akira (Osaka, JP) Assignee(s): Toray Industries, Inc. (JP) Patent Number: 6,214,535 Date filed: April 16, 1997 Abstract: The present invention relates to a method for the treatment of cardiac disease resulting from a viral infection of the cardiac tissue with human hepatitis C virus or EMC virus comprising administering an antiviral agent to a subject. The antiviral agent is useful in the treatment of myocarditis and cardiomyopathy. Excerpt(s): The present invention relates to a therapeutic agent for a cardiac disease in which the cardiac muscle tissue is infected with human hepatitis C virus and a method for testing a cardiac disease. Myocarditis is a disease caused by infection, allergy, poisoning or the like which will lead to inflammatory myocardial disorders and most of myocarditis is believed to be viral. As causative viruses, a number of enteroviruses are considered. In particular, Coxsackie B virus is believed to cause viral myocarditis most frequently. However, as viruses associated with cardiac diseases, various viruses such as influenza virus, Coxsackie A virus, cytomegalovirus, parainfluenza virus are reported in addition to Coxsackie B virus, and the major causative virus has not been ascertained yet (Akira Matsumori, Circular System Now No. 6: Cardiomyopathy/Myocarditis, Nanko-Do Co., p. 36, 1994). The search for a causative virus has been performed mainly by an indirect method in which a virus antibody is detected in a serum. There has been almost no direct proof from the cardiac muscle. One of the reasons for this is that, since a virus which has invaded the cardiac muscle disappears in several days, it is almost impossible to identify a causative virus in the cardiac muscle, particularly in a clinical scene. Web site: http://www.delphion.com/details?pn=US06214535__
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Method for treating heart failure using tetrapyrroles and metallotetrapyrroles Inventor(s): Danziger; Robert S. (New York, NY) Assignee(s): The Trustees of Columbia University in the City of New York (New York, NY) Patent Number: 5,948,771 Date filed: June 6, 1996 Abstract: A method to improve the contractile function of the heart in myocarditis and other forms of heart failure is disclosed. The method consists essentially of administering a tetrapyrrole or metallotetrapyrrole which inhibits or reduces the endogenous guanylyl cyclase activity in cardiac myocyte of the patient. Excerpt(s): Heart or cardiac failure is defined as the pathological "state in which an abnormality of cardiac function is responsible for failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues. and is frequently caused by a defect (decrease) in myocardial contraction." (Hurst, Willis J. (ed) 1990 The Heart, McGraw Hill Inc., New York, 388-440). Heart failure is characterized by decreased cardiac contractility, i.e., inotropy. The causes are well known in the art. The mechanism is generally considered to be a reduction in the the force of contraction and may be directly attributed to a decreased contractile response of cardiac myocytes.
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Changes in cardiac myocytes from failing hearts include: increased oxygen consumption, decreased mitochondrial mass, oxidative phosphorylation, reduced intracellular calcium, sarcomere "overstretching", decreased myosin and myofibrillar ATPase activity, changes in myosin isoforms, and reduced.alpha.,.beta.-adrenoreceptors and.alpha.,.beta.-adrenergic signalling (Braunwald, E., Textbook of Cardiovascular Disease, W. B. Saunders Co., Philadelphia, Pa. (1994)). Approaches to the treatment of heart failure have included: reducing the workload of the heart, reducing salt intake, diuretics, inotropic agents such as digitalis, and vasodilators. Web site: http://www.delphion.com/details?pn=US05948771__ •
Reduction of porcine circovirus-2 viral load with inactivated PCV-2 Inventor(s): Audonnet; Jean-Christophe Francis (Lyons, FR), Chappuis; Gilles Emile (Lyons, FR), Charreyre; Catherine Elisabeth (Saint-Laurent de Mure, FR), Clark; Edward (Saskatoon, CA), Ellis; John Albert (Saskatoon, CA), Haines; Deborah (Saskatoon, CA), Harding; John (Humboldt, CA), Hassard; Lori (Saskatoon, CA), Krakowka; George Steve (Columbus, OH), McNeilly; Francis (Newtownards, GB), Meehan; Brian (Belfast, GB), Moore; Gordon Allan (Belfast, GB) Assignee(s): Merial (Lyons, FR), The Queen's University of Belfast (Belfast, GB), University of Saskatchewan (Saskatoon, CA) Patent Number: 6,517,843 Date filed: May 31, 2000 Abstract: Porcine circovirus-2 (PCV-2) is a recently identified agent wherein the potential spectrum of PCV-2-associated disease has been expanded by evidence of vertical and sexual transmission and associated reproductive failure in swine populations. PCV-2 was isolated from a litter of aborted piglets from a farm experiencing late term abortions and stillbirths. Severe, diffuse myocarditis was present in one piglet associated with extensive immunohistochemical staining for PCV-2 antigen. Variable amounts of PCV-2 antigen were also present in liver, lung and kidney of multiple fetuses. Inoculation of female pigs with a composition including an immunogen from PCV-2 or an epitope of interest from such an immunogen or with a vector expressing such an immunogen or epitope of interest prior to breeding, such as within the first five weeks of life, or prior to the perinatal period, or repeatedly over a lifetime, or during pregnancy, such as between the 6.sup.th and 8.sup.th and/or the 10.sup.th and 13.sup.th weeks of gestation, can prevent myocarditis, abortion and intrauterine infection associated with porcine circovirus-2. In addition, innoculation of male and/or female pigs with the aforementioned compositions can be carried out to prevent transmission of PCV-2 from male to female (or vice versa) during mating. Thus, the invention involves methods and compositions for preventing myocarditis, abortion and intrauterine infection associated with porcine circovirus-2. Excerpt(s): The invention relates to methods and/or compositions for the prevention and/or treatment of PCV-2-caused myocarditis, and/or abortion and/or intrauterine infection, as well as pathologic sequelae including but not limited to post-weaning multisystemic wasting syndrome; and, to methods for preparing such compositions and kits for preparing such compositions or for performing such methods, inter alia. Various documents are cited in this text. Citations in the text can be by way of a citation to a document in the reference list, e.g., by way of an author(s) and document year citation to a document listed in the reference list, or by full citation in the text to a document that may or may not also be listed in the reference list. There is no admission that any of the
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various documents cited in this text are prior art as to the present invention. Any document having as an author or inventor person or persons named as an inventor herein is a document that is not by another as to the inventive entity herein. All documents cited in this text ("herein cited documents") and all documents cited or referenced in herein cited documents are hereby incorporated herein by reference. Web site: http://www.delphion.com/details?pn=US06517843__ •
Treatment of arthritis disorders, rheumatoid arthritis and manifestations associated with rheumatoid disorders Inventor(s): Murray; James (Dorfet, GB), Snorrason; Ernir (Stigahlid 80, 105 Reykjavik, IS) Assignee(s): Snorrason; Ernir (Reykjavik, IS) Patent Number: 6,358,941 Date filed: May 3, 1999 Abstract: The present invention relates to the use of pharmaceutically acceptable cholinesterase inhibitors for the preparation of a pharmaceutical composition for the treatment or prophylaxis of arthritic disorders, including osteoarthritis, rheumatoid arthritis and other rheumatoid diseases such as Juvenile Arthritis, Systemic Lupus Erythematosis, Sjogren's Syndrome, Progressive Systemic Sclerosis, Polymyositis, Dermatomyositis, Ankylosing Spondilitis, Reiter's Syndrome, Psoriatic Arthritis, Relapsing Polychondritis, Relapsing Panniculitis, Crohn's Disease, Ulcerative Colitis, Heredity Complement Deficiencies, Collagen Vascular Diseases, Felty's Syndrome, rheumatological manifestations associated with bacterial and viral endocarditis or myocarditis and other rheumatological manifestations such as anaemia of chronic disorders. The invention also relates to a novel method of treatment or prophylaxis of such diseases and manifestations. Preferably, the cholinesterase inhibitors are selected from a group of nicotinic acetylcholinesterase inhibitors such as galantamine (the name of this drug was previously spelled galanthamine). Excerpt(s): The present invention relates to the use of pharmaceutically acceptable cholinesterase inhibitors of the preparation of a pharmaceutical composition for the treatment or prophylaxis of arthritic disorders, including osteoarthritis, rheumatoid arthritis and other rheumatoid diseases such as Juvenile Arthritis, Systemic Lupus Erythematosis, Sjogren's Syndrome, Progressive Systemic Sclerosis, Polymyositis, Dermatomyositis, Ankylosing Spondilitis, Reiter's Syndrome, Psoriatic Arthritis, Relapsing Polychondritis, Relapsing Panniculitis, Crohn's Disease, Ulcerative Colitis, Hereditary Complement Deficiencies, Collagen Vascular Diseases, Felty's Syndrome, rheumatological manifestations associated with bacterial and viral endocarditis or myocarditis and other rheumatological manifestations such as anaemia of chronic disorders. The invention also relates to a novel method of treatment or prophylaxis of such diseases and manifestations. Preferably, the cholinesterase inhibitors are selected from a group of nicotinic acetylcholinesterase inhibitors such as galantamine (The name of this drug was previously spelled galanthamine). In the present description and claims, the term "rheumatoid" covers any of a variety of disorders marked by degeneration or metabolic derangement of the connective tissue structures of the body, especially the joints and related structures, including muscles, bursae (snyovial membranes), tendons and fibrous tissue. They are attended by pain, stiffness, or limitation of motion of these parts. Rheumatoid Arthritis is a chronic, recurrent systemic inflammatory disease primarily of the joints, usually polyarticular, marked by
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inflammatory changes in the snyovial membranes and articular structures and by atrophy and rarefaction of the bones. In late stages deformity and ankylosis develop. Extra-articular manifestations include vasculitis, atrophy of the skin and muscle, subcutaneous nodules, lymphadenopathy, splenomegaly, leukopaenia and often chronic anaemia. Web site: http://www.delphion.com/details?pn=US06358941__
Patent Applications on Myocarditis 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 myocarditis: •
Gene therapy composition for treating viral myocarditis Inventor(s): Jeon, Eun-Seok; (Seoul, KR), Kim, Jong-Mook; (Seoul, KR), Kim, Sunyoung; (Seoul, KR), Lim, Byung-Kwan; (Seoul, KR) Correspondence: David A. Einhorn, ESQ.; Anderson Kill & Olick, P.C.; 1251 Avenue OF The Americas; New York; NY; 10020; US Patent Application Number: 20030139367 Date filed: January 17, 2003 Abstract: An intracardiac injection composition for treating viral myocarditis in a mammal, which comprises a DNA encoding interleukin-1 receptor antagonist (IL-1Ra) and a pharmaceutically acceptable carrier Excerpt(s): The present invention relates to an intracardiac injection composition for treating viral myocarditis, which comprises a DNA encoding interleukin-1 receptor antagonist (IL-1Ra); and a method for treating viral myocarditis by injecting same into the myocardium of a subject. Among the etiological viruses of viral myocarditis, enteroviruses, in particular coxsackievirus B, are the most common (Feldman A. and McNamara D., N Engl J Med, 343:1388-1398(2000); I. -W. Seong, et al., N Engl J Med, 345:379(2001); Woodruff J. F., Am J Pathol, 101:425-483(1980); and Li Y. et al., Circulation, 101:231-234(2000)). In viral myocarditis, virus proliferation in myocytes can induce direct cytotoxicity, independent of an immune response, and some coxsackieviral proteins can cause direct myocyte damage (Badorff C. et al., Nat Med, 5:320-326(1999)). The immune responses may induce tissue damage by: 1) the protective host response to remove virus-infected myocytes, and/or, 2) inappropriate cardiac injury caused by sensitized T-lymphocytes (Huber S. A. and Pfaeffle B., J Virol, 68:51265132(1994)). This immune response should be specific, attacking only infected cells, but such an imbalance in the immune response may lead to either an overwhelming virusinduced myocardial injury or predominantly immune-mediated tissue damage (Knowlton K. U. and Badorff C., Circ Res, 85:559-561(1999)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
9
This has been a common practice outside the United States prior to December 2000.
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PICORNAVIRUSES, VACCINES AND DIAGNOSTIC KITS Inventor(s): NIKLASSON, BO; (STOCKHOLM, SE) Correspondence: James F. Haley, JR., ESQ.; C/o Fish & Neave; 1251 Avenue OF The Americas - 50th Floor; New York; NY; 10020; US Patent Application Number: 20030044960 Date filed: March 11, 1999 Abstract: A new group of picornaviruses is disclosed. The picornaviruses of the invention comprise in the non-coding region of their viral genome a nucleotide sequence which corresponds to cDNA sequence (I) or homologous sequences having at least 75% homology to the SEQ ID NO:1, and they cause mammalian disease. Further aspects of the invention comprise a protein corresponding to a protein of the picornaviruses, antiserum or antibody directed against a protein of the picornaviruses, antigen comprising a protein of the picornaviruses, diagnostic kits, vaccines, use of the picornaviruses in medicaments, particularly for the treatment or prevention of Myocarditis, Cardiomyopathia, Guillain Barr Syndrome, and Diabetes Mellitus, Multiple Sclerosis, Chronic Fatique Syndrome, Myasthenia Gravis, Amyothrophic Lateral Sclerosis, Dermatomyositis, Polymyositis, Spontaneous Abortion, and Sudden Infant Death Syndrome, and methods of treatment of diseases caused by the picornaviruses. 1 SEQ ID NO: 1 (Ljungan 87-012) AGTCTAGTCT TATCTTGTAT GTGTCCTGCA CTGAACTTGT 50 TTCTGTCTCT GGAGTGCTCT ACACTTCAGT AGGGGCTGTA CCCGGGCGGT 100 CCCACTCTTC ACAGGAATCT GCACAGGTGG CTTTCACCTC TGGACAGTGC 150 (I) ATTCCACACC CGCTCCACGG TAGAAGATGA TGTGTGTCTT TGCTTGTGAA 200 AAGCTTGTGA AAATCGTGTG TAGGCGTAGC GGCTACTTGA GTGCCAGCGG 250 ATTACCCCTA GTGGTAACAC TAGC Excerpt(s): The present invention relates to new picornaviruses, proteins expressed by the viruses, antisera and antibodies directed against said viruses, antigens comprising structural proteins of said viruses, diagnostic kits, vaccines, use of said viruses, antisera or antibodies and antigens in medicaments, and methods of treating or preventing diseases caused by said viruses, such as Myocarditis, Cardiomyopathia, Guillain Barr Syndrome, and Diabetes Mellitus, Multiple Sclerosis, Chronic Fatigue Syndrome, Myasthenia Gravis, Amyothrophic Lateral Sclerosis, Dermatomyositis, Polymyositis, Spontaneous Abortion, and Sudden Infant Death Syndrome. Recently, a sudden death syndrome among Swedish orienteers has been observed. Of approximately 200 elite orienteers six died in myocarditis during 1989-1992 (1). Orienteering, aiming to find the fastest/shortest way between several checkpoints and often in forested areas, is exceptional with respect to environmental exposure. Thus it has been speculated, that the sudden deaths syndrome among orienteers is caused by a vector borne (rodent or arthropod) infectious agent. It has now been shown in an epidemiological study that the incidence of deaths in myocarditis in northern Sweden tracked the 3-4 year population fluctuations (cycles) of bank voles (Clethrionomys glareolus) with one year time lag. Previously, it has been shown that cardioviruses, with rodents as their natural reservoir, can cause Guillain Barr Syndrome (GBS) in man, Diabetes Mellitus (DM) in mice and myocarditis in several species including non-human primates. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Predicting, detecting and monitoring treatment of cardiomyopathies and myocarditis Inventor(s): De Bold, Adolfo J.; (Ottawa, CA) Correspondence: Fish & Richardson PC; 225 Franklin ST; Boston; MA; 02110; US Patent Application Number: 20040132013 Date filed: November 13, 2003 Abstract: The present invention provides a method of diagnosing or detecting cardiomyopathies or myocarditis in a patient following an infection. The method comprises obtaining a sample of a biological fluid from the patient, and determining the level of a brain natriuretic peptide (BNP) or a fragment thereof, atrial natriuretic factor (ANF) or a fragment thereof, or both, within the sample of body fluid. The current invention also relates to the monitoring of treatment of cardiomyopathies or myocarditis as a result of an infection, by determining the levels of BNP or a fragment thereof, ANF or a fragment thereof, or both, at one or more than period prior to and optionally subsequent to, treatment. The step of determining the concentration of BNP or ANF involves an assay comprising at least one antibody exhibiting affinity for the BNP or a fragment thereof, ANF or a fragment thereof, and the biological fluid comprises plasma, urine or cerebrospinal fluid. Furthermore, the antibody used within the method may comprise a polyclonal antibody, a monoclonal antibody, or a combination thereof. The method described herein may also involves obtaining at least two samples of body fluid from the patient over a period of time and comparing the BNP, ANF, or both BNP and ANF levels, with a significant decrease of BNP, ANF or both BNP and ANF being indicative of a positive effect of treatment. Excerpt(s): This application claims priority to U.S. Provisional Application Serial No. 60/426,986, filed Nov. 15, 2002, which is incorporated by reference herein. The present invention relates to a method for the prediction and diagnosis of heart dysfunction and the monitoring of treatment thereof. More specifically, the present invention relates to a method for the prediction and diagnosis of cardiomyopathies and myocarditis following an infection, and the monitoring of treatment thereof. The cardiac natriuretic peptides (NP) atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) are polypeptide hormones synthesized, stored and released by cardiac muscle cells (cardiocytes). In many ways, the endocrine heart is a modulator of systems such as the sympathetic nervous system, the renin-angiotensin-aldosterone system and other determinants of vascular tone, extracellular fluid volume and renal function. 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 myocarditis, 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 “myocarditis” (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 myocarditis.
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You can also use this procedure to view pending patent applications concerning myocarditis. 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 6. BOOKS ON MYOCARDITIS Overview This chapter provides bibliographic book references relating to myocarditis. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on myocarditis 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: 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 “myocarditis” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “myocarditis” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “myocarditis” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •
Cardiomyopathies, Myocarditis and Pericardial Disease: Slide Atlas (Atlas of Heart Diseases) by Eugene Braunwald; ISBN: 187813289X; http://www.amazon.com/exec/obidos/ASIN/187813289X/icongroupinterna
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Drug Therapy in Dilated Cardiomyopathy and Myocarditis (Basic and Clinical Cardiology Series, Vol 11) by Richard S. Engelmeier, John B. O'Connell; ISBN: 082477843X; http://www.amazon.com/exec/obidos/ASIN/082477843X/icongroupinterna
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Pathogenesis of Myocarditis and Cardiomyopathy: Recent Experimental and Clinical Studies (Cardiomyopathy Update 1) by Chuichi Kawai, Walter H. Abelmann; ISBN: 0860084191; http://www.amazon.com/exec/obidos/ASIN/0860084191/icongroupinterna
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Pathogenesis of myocarditis and cardiomyopathy: Recent experimental and clinical studies (Cardiomyopathy update); ISBN: 413068129X; http://www.amazon.com/exec/obidos/ASIN/413068129X/icongroupinterna
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Prognosis and treatment of cardiomyopathies and myocarditis (Cardiomyopathy update); ISBN: 4130681567; http://www.amazon.com/exec/obidos/ASIN/4130681567/icongroupinterna
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Prognosis and Treatment of Cardiomyopathies and Myocarditis (Cardiomyopathy Update, 5) by Morie Sekiguchi, Peter J. Richardson; ISBN: 0860085112; http://www.amazon.com/exec/obidos/ASIN/0860085112/icongroupinterna
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CHAPTER 7. PERIODICALS AND NEWS ON MYOCARDITIS Overview In this chapter, we suggest a number of news sources and present various periodicals that cover myocarditis.
News Services and Press Releases One of the simplest ways of tracking press releases on myocarditis 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 “myocarditis” (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 myocarditis. 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 “myocarditis” (or synonyms). The following was recently listed in this archive for myocarditis: •
Therapeutic target for enterovirus-induced myocarditis identified Source: Reuters Industry Breifing Date: February 24, 2003
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Pulmonary hypertension in myocarditis increases mortality Source: Reuters Medical News Date: March 18, 2002
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Complement important for induction of autoimmune myocarditis in mice Source: Reuters Medical News Date: July 27, 2001
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T-cell receptor-based immunotherapy effective for myocarditis in rats Source: Reuters Medical News Date: March 08, 2000
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Increased risk of myocarditis likely in pediatric HIV infection Source: Reuters Medical News Date: September 03, 1999
•
Acute myocarditis in young Finnish men usually mimics myocardial infarction Source: Reuters Medical News Date: August 24, 1999
•
Natural History Of Idiopathic Giant-Cell Myocarditis And Treatment Described Source: Reuters Medical News Date: June 26, 1997 The NIH
Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine. Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name. Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “myocarditis” (or synonyms) into the search box, and click on “Search News.” As this service is technology oriented, you may wish to use it when searching for press releases covering diagnostic procedures or tests. Search Engines Medical news is also available in the news sections of commercial Internet search engines. See the health news page at Yahoo (http://dir.yahoo.com/Health/News_and_Media/), or
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you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “myocarditis” (or synonyms). If you know the name of a company that is relevant to myocarditis, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for the company name there. News items across various news sources are reported on indicated hyperlinks. Google offers a similar service at http://news.google.com/. BBC Covering news from a more European perspective, the British Broadcasting Corporation (BBC) allows the public free access to their news archive located at http://www.bbc.co.uk/. Search by “myocarditis” (or synonyms).
Academic Periodicals covering Myocarditis Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to myocarditis. In addition to these sources, you can search for articles covering myocarditis that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”
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CHAPTER 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 myocarditis. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a nonprofit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI Advice for the Patient can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with myocarditis. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.). The
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following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to myocarditis: Amphotericin B •
Systemic - U.S. Brands: Amphocin; Fungizone Intravenous http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202032.html
•
Topical - U.S. Brands: Not commercially available http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202033.html
Anticoagulants •
Systemic - U.S. Brands: Coumadin; Miradon http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202050.html
Cyclophosphamide •
Systemic - U.S. Brands: Cytoxan; Neosar http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202174.html
Cyclosporine •
Systemic - U.S. Brands: Neoral; Sandimmune; SangCya http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202176.html
Doxorubicin •
Systemic - U.S. Brands: Adriamycin PFS; Adriamycin RDF; Rubex http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202209.html
Isoniazid •
Systemic - U.S. Brands: Laniazid; Nydrazid http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202307.html
Lithium •
Systemic - U.S. Brands: Cibalith-S; Eskalith; Eskalith CR; Lithane; Lithobid; Lithonate; Lithotabs http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202330.html
Methyldopa •
Systemic - U.S. Brands: Aldomet http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202359.html
Phenothiazines •
Systemic - U.S. Brands: Chlorpromazine Hydrochloride Intensol; Compazine; Compazine Spansule; Mellaril; Mellaril Concentrate; Mellaril-S; Permitil; Permitil Concentrate; Prolixin; Prolixin Concentrate; Prolixin Decanoate; Prolixin Enanthate; Serentil; Serentil Concentrate; Stelazine; Stelazine Concentrate; Thorazine; Thorazine Spansule; Trilafon; Trilafon Concentrate; Vesprin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202457.html
Quinidine •
Systemic - U.S. Brands: Cardioquin; Quinaglute Dura-tabs; Quinidex Extentabs; Quin-Release
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http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202498.html Sulfonamides •
Ophthalmic - U.S. Brands: Ak-Sulf; Bleph-10; Cetamide; Gantrisin; IsoptoCetamide; I-Sulfacet; Ocu-Sul-10; Ocu-Sul-15; Ocu-Sul-30; Ocusulf-10; Ophthacet; Sodium Sulamyd; Spectro-Sulf; Steri-Units Sulfacetamide; Sulf-10; Sulfair; Sulfair 10; Sulfair 15; Sulfair Forte; Sulfamide; Sulten-10 http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202539.html
•
Systemic - U.S. Brands: Gantanol; Gantrisin; Thiosulfil Forte; Urobak http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202540.html
•
Vaginal - U.S. Brands: AVC; Sultrin; Trysul http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202541.html
Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.
Mosby’s Drug Consult Mosby’s Drug Consult database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/. PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html. Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee.
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 myocarditis by using the database managed by the
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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 “myocarditis” (or synonyms) into the search box, and click “Submit Query.” When you receive your results, note that not all of the drugs may be relevant, as some may have been withdrawn from orphan status. Write down or print out the name of each drug and the relevant contact information. From there, visit the Pharmacopeia Web site and type the name of each orphan drug into the search box at http://www.nlm.nih.gov/medlineplus/druginformation.html. You may need to contact the sponsor or NORD for further information. NORD conducts “early access programs for investigational new drugs (IND) under the Food and Drug Administration’s (FDA’s) approval ‘Treatment INDs’ programs which allow for a limited number of individuals to receive investigational drugs before FDA marketing approval.” If the orphan product about which you are seeking information is approved for marketing, information on side effects can be found on the product’s label. If the product is not approved, you may need to contact the sponsor. The following is a list of orphan drugs currently listed in the NORD Orphan Drug Designation Database for myocarditis: •
Immune globulin intravenous (human) (trade name: Immune Globulin Intravenous (human) Immuno, Iveega) http://www.rarediseases.org/nord/search/nodd_full?code=53
•
Indium In 111 murine monoclonal antibody FAB to my (trade name: Myoscint) http://www.rarediseases.org/nord/search/nodd_full?code=64
If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.
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APPENDICES
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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute10: •
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
•
National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
•
National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
•
National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
•
National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
•
National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
•
National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
•
National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
10
These publications are typically written by one or more of the various NIH Institutes.
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•
National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
•
National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
•
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
•
National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
•
National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
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National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
•
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
•
National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
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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
•
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
•
Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
•
National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
•
National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
•
Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
•
Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.11 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:12 •
Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html
•
HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
•
NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
•
Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
•
Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
•
Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
•
Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
•
Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
•
Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
•
Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
•
MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
11
Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 12 See http://www.nlm.nih.gov/databases/databases.html.
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•
Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html
•
Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html
The NLM Gateway13 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.14 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “myocarditis” (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 10658 60 33 51 190 10992
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 “myocarditis” (or synonyms) at the following Web site: http://text.nlm.nih.gov.
13
Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.
14
The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH). 15 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 16 17
The HSTAT URL is http://hstat.nlm.nih.gov/.
Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations.
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Coffee Break: Tutorials for Biologists18 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.19 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.20 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.
Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •
CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.
•
Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.
18 Adapted 19
from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html.
The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 20 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process.
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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on myocarditis 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 myocarditis. 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 myocarditis. 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 “myocarditis”:
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Arrhythmia http://www.nlm.nih.gov/medlineplus/arrhythmia.html Cardiomyopathy http://www.nlm.nih.gov/medlineplus/cardiomyopathy.html Heart Attack http://www.nlm.nih.gov/medlineplus/heartattack.html Heart Diseases http://www.nlm.nih.gov/medlineplus/heartdiseases.html Heart Failure http://www.nlm.nih.gov/medlineplus/heartfailure.html Heart Transplantation http://www.nlm.nih.gov/medlineplus/hearttransplantation.html Lupus http://www.nlm.nih.gov/medlineplus/lupus.html Vasculitis http://www.nlm.nih.gov/medlineplus/vasculitis.html You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the search box and click “Search.” This utility is similar to the NIH search utility, with the exception that it only includes materials that are linked within the MEDLINEplus system (mostly patient-oriented information). It also has the disadvantage of generating unstructured results. We recommend, therefore, that you use this method only if you have a very targeted search. The 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 myocarditis. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
•
Family Village: http://www.familyvillage.wisc.edu/specific.htm
•
Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
Patient Resources
•
Med Help International: http://www.medhelp.org/HealthTopics/A.html
•
Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
•
Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
•
WebMDHealth: http://my.webmd.com/health_topics
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Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to myocarditis. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with myocarditis. 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 myocarditis. 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 “myocarditis” (or a synonym), and you will receive information on all relevant organizations listed in the database. Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given the option to search by keyword or by browsing the subject list. When you have received your search results, click on the name of the organization for its description and contact information. The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “myocarditis”. 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
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publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “myocarditis” (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 “myocarditis” (or a synonym) into the search box, and click “Submit Query.”
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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.
Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.21
Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.
Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of
21
Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.
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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)22: •
Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/
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Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)
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Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
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California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
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California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
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California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html
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California: Gateway Health Library (Sutter Gould Medical Foundation)
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California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
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California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
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California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
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California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
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California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
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California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
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California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
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California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
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Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
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Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
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Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
22
Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
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Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
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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/
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Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
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New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
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New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
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New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
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New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
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New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
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New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html
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New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
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Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
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Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp
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Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/
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Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/
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Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml
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Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html
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Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html
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Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml
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Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
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Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
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Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/
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South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp
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Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/
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Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/
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Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72
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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
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MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
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Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
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Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
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On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
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Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
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Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm
Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a). The NIH suggests the following Web sites in the ADAM Medical Encyclopedia when searching for information on myocarditis: •
Basic Guidelines for Myocarditis Echinococcus Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000676.htm Myocarditis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000149.htm
•
Signs & Symptoms for Myocarditis Chest pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003079.htm Difficulty breathing Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003075.htm Edema Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003103.htm
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Fever Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003090.htm Hepatomegaly Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003275.htm Joint pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003261.htm Palpitations Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003081.htm Peripheral edema Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003104.htm Rapid heartbeat Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003081.htm Swelling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003103.htm Tachycardia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003077.htm Urine output, decreased Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003147.htm •
Diagnostics and Tests for Myocarditis ALT Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003473.htm Antibody titer Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003333.htm Anticoagulants Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003804.htm AST Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003472.htm Biopsy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003416.htm Biopsy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003873.htm Blood culture Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003744.htm BUN Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003474.htm
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Cardiac catheterization Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003419.htm CBC Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003642.htm Chest X-ray Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003804.htm CK Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003503.htm ECG Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003868.htm Echocardiogram Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003804.htm Echocardiogram Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003869.htm Eosinophils Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003649.htm ESR Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003638.htm Heart attack Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003804.htm LDH Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003471.htm Lyme disease antibody Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003554.htm Myocardial biopsy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003873.htm Syncope Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003804.htm X-ray Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003337.htm •
Surgery and Procedures for Myocarditis Heart transplant Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003003.htm
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Background Topics for Myocarditis Acute Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002215.htm Analgesics Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002123.htm Physical examination Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002274.htm Systemic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002294.htm Toxins Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002331.htm
Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •
Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical
•
MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html
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Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/
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Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
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MYOCARDITIS DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 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] Abortion: 1. The premature expulsion from the uterus of the products of conception - of the embryo, or of a nonviable fetus. The four classic symptoms, usually present in each type of abortion, are uterine contractions, uterine haemorrhage, softening and dilatation of the cervix, and presentation or expulsion of all or part of the products of conception. 2. Premature stoppage of a natural or a pathological process. [EU] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acetylcholinesterase: An enzyme that catalyzes the hydrolysis of acetylcholine to choline and acetate. In the CNS, this enzyme plays a role in the function of peripheral neuromuscular junctions. EC 3.1.1.7. [NIH] Acetylcysteine: The N-acetyl derivative of cysteine. It is used as a mucolytic agent to reduce the viscosity of mucous secretions. It has also been shown to have antiviral effects in patients with HIV due to inhibition of viral stimulation by reactive oxygen intermediates. [NIH] Acquired Immunodeficiency Syndrome: An acquired defect of cellular immunity associated with infection by the human immunodeficiency virus (HIV), a CD4-positive Tlymphocyte count under 200 cells/microliter or less than 14% of total lymphocytes, and increased susceptibility to opportunistic infections and malignant neoplasms. Clinical manifestations also include emaciation (wasting) and dementia. These elements reflect criteria for AIDS as defined by the CDC in 1993. [NIH] Actin: Essential component of the cell skeleton. [NIH] Actinin: A protein factor that regulates the length of R-actin. It is chemically similar, but immunochemically distinguishable from actin. [NIH] Acute lymphoblastic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphocytic leukemia. [NIH] Acute lymphocytic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphoblastic 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]
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Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adenine: A purine base and a fundamental unit of adenine nucleotides. [NIH] Adenovirus: A group of viruses that cause respiratory tract and eye infections. Adenoviruses used in gene therapy are altered to carry a specific tumor-fighting gene. [NIH] Adjunctive Therapy: Another treatment used together with the primary treatment. Its purpose is to assist the primary treatment. [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 Medulla: The inner part of the adrenal gland; it synthesizes, stores and releases catecholamines. [NIH] Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Aerospace Medicine: A specialty which is concerned with the health and medical problems of man in aviation (aviation medicine) and space (space medicine). [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]
Akathisia: 1. A condition of motor restlessness in which there is a feeling of muscular quivering, an urge to move about constantly, and an inability to sit still, a common extrapyramidal side effect of neuroleptic drugs. 2. An inability to sit down because of intense anxiety at the thought of doing so. [EU] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin,
Dictionary 141
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] Allergen: An antigenic substance capable of producing immediate-type hypersensitivity (allergy). [EU] Allo: A female hormone. [NIH] 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] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Alveolitis: Inflammation of an alveolus. Called also odontobothritis. [EU] Amino acid: Any organic compound containing an amino (-NH2 and a carboxyl (- COOH) group. The 20 a-amino acids listed in the accompanying table are the amino acids from which proteins are synthesized by formation of peptide bonds during ribosomal translation of messenger RNA; all except glycine, which is not optically active, have the L configuration. Other amino acids occurring in proteins, such as hydroxyproline in collagen, are formed by posttranslational enzymatic modification of amino acids residues in polypeptide chains. There are also several important amino acids, such as the neurotransmitter y-aminobutyric acid, that have no relation to proteins. Abbreviated AA. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] 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] Anaemia: A reduction below normal in the number of erythrocytes per cu. mm., in the quantity of haemoglobin, or in the volume of packed red cells per 100 ml. of blood which occurs when the equilibrium between blood loss (through bleeding or destruction) and blood production is disturbed. [EU] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU]
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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] 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] Aneurysm: A sac formed by the dilatation of the wall of an artery, a vein, or the heart. [NIH] Angina: Chest pain that originates in the heart. [NIH] Angiotensinogen: An alpha-globulin of which a fragment of 14 amino acids is converted by renin to angiotensin I, the inactive precursor of angiotensin II. It is a member of the serpin superfamily. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Ankylosis: Fixation and immobility of a joint. [NIH] Annealing: The spontaneous alignment of two single DNA strands to form a double helix. [NIH]
Anorexia: Lack or loss of appetite for food. Appetite is psychologic, dependent on memory and associations. Anorexia can be brought about by unattractive food, surroundings, or company. [NIH] Antagonism: Interference with, or inhibition of, the growth of a living organism by another living organism, due either to creation of unfavorable conditions (e. g. exhaustion of food supplies) or to production of a specific antibiotic substance (e. g. penicillin). [NIH] 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]
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Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Anticonvulsant: An agent that prevents or relieves convulsions. [EU] Antiemetic: An agent that prevents or alleviates nausea and vomiting. Also antinauseant. [EU]
Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Antigen-presenting cell: APC. A cell that shows antigen on its surface to other cells of the immune system. This is an important part of an immune response. [NIH] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antipsychotic: Effective in the treatment of psychosis. Antipsychotic drugs (called also neuroleptic drugs and major tranquilizers) are a chemically diverse (including phenothiazines, thioxanthenes, butyrophenones, dibenzoxazepines, dibenzodiazepines, and diphenylbutylpiperidines) but pharmacologically similar class of drugs used to treat schizophrenic, paranoid, schizoaffective, and other psychotic disorders; acute delirium and dementia, and manic episodes (during induction of lithium therapy); to control the movement disorders associated with Huntington's chorea, Gilles de la Tourette's syndrome, and ballismus; and to treat intractable hiccups and severe nausea and vomiting. Antipsychotic agents bind to dopamine, histamine, muscarinic cholinergic, a-adrenergic, and serotonin receptors. Blockade of dopaminergic transmission in various areas is thought to be responsible for their major effects : antipsychotic action by blockade in the mesolimbic and mesocortical areas; extrapyramidal side effects (dystonia, akathisia, parkinsonism, and tardive dyskinesia) by blockade in the basal ganglia; and antiemetic effects by blockade in the chemoreceptor trigger zone of the medulla. Sedation and autonomic side effects (orthostatic hypotension, blurred vision, dry mouth, nasal congestion and constipation) are caused by blockade of histamine, cholinergic, and adrenergic receptors. [EU] Antiserum: The blood serum obtained from an animal after it has been immunized with a particular antigen. It will contain antibodies which are specific for that antigen as well as antibodies specific for any other antigen with which the animal has previously been immunized. [NIH] Antiviral: Destroying viruses or suppressing their replication. [EU] Antiviral Agents: Agents used in the prophylaxis or therapy of virus diseases. Some of the
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ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly. [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] 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] 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] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Articular: Of or pertaining to a joint. [EU] Aseptic: Free from infection or septic material; sterile. [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] Asymptomatic: Having no signs or symptoms of disease. [NIH] Ataxia: Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharnyx, larnyx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or peripheral nerve diseases. Motor ataxia may be associated with cerebellar diseases; cerebral cortex diseases; thalamic diseases; basal ganglia diseases; injury to the red nucleus; and other conditions. [NIH] Atopic: Pertaining to an atopen or to atopy; allergic. [EU] Atrial: Pertaining to an atrium. [EU]
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Atrial Natriuretic Factor: A potent natriuretic and vasodilatory peptide or mixture of different-sized low molecular weight peptides derived from a common precursor and secreted by the heart atria. All these peptides share a sequence of about 20 amino acids. [NIH] Atrioventricular: Pertaining to an atrium of the heart and to a ventricle. [EU] Atrium: A chamber; used in anatomical nomenclature to designate a chamber affording entrance to another structure or organ. Usually used alone to designate an atrium of the heart. [EU] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Attenuated: Strain with weakened or reduced virulence. [NIH] Attenuation: Reduction of transmitted sound energy or its electrical equivalent. [NIH] Atypical: Irregular; not conformable to the type; in microbiology, applied specifically to strains of unusual type. [EU] Autoantibodies: Antibodies that react with self-antigens (autoantigens) of the organism that produced them. [NIH] Autoantigens: Endogenous tissue constituents that have the ability to interact with autoantibodies and cause an immune response. [NIH] Autodigestion: Autolysis; a condition found in disease of the stomach: the stomach wall is digested by the gastric juice. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autoimmunity: Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by autoimmune diseases. [NIH] Autologous: Taken from an individual's own tissues, cells, or DNA. [NIH] Autonomic: Self-controlling; functionally independent. [EU] Autonomic Nervous System: The enteric, parasympathetic, and sympathetic nervous systems taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the central nervous system, especially the hypothalamus and the solitary nucleus, which receive information relayed from visceral afferents; these and related central and sensory structures are sometimes (but not here) considered to be part of the autonomic nervous system itself. [NIH] Autopsy: Postmortem examination of the body. [NIH] Avidity: The strength of the interaction of an antiserum with a multivalent antigen. [NIH] Axonal: Condition associated with metabolic derangement of the entire neuron and is manifest by degeneration of the distal portion of the nerve fiber. [NIH] 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
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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] 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]
Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [NIH] Biliary Tract: The gallbladder and its ducts. [NIH] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biochemical reactions: In living cells, chemical reactions that help sustain life and allow cells to grow. [NIH] Bioengineering: The application of engineering principles to the solution of biological problems, for example, remote-handling devices, life-support systems, controls, and displays. [NIH] Biological Transport: The movement of materials (including biochemical substances and drugs) across cell membranes and epithelial layers, usually by passive diffusion. [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] Bioreactors: Tools or devices for generating products using the synthetic or chemical conversion capacity of a biological system. They can be classical fermentors, cell culture perfusion systems, or enzyme bioreactors. For production of proteins or enzymes, recombinant microorganisms such as bacteria, mammalian cells, or insect or plant cells are usually chosen. [NIH] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Black Widow Spider: A venomous New World spider with an hourglass-shaped red mark on the abdomen. [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 Glucose: Glucose in blood. [NIH]
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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] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [NIH]
Body Burden: The total amount of a chemical, metal or radioactive substance present at any time after absorption in the body of man or animal. [NIH] 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 Transplantation: The transference of bone marrow from one human or animal to another. [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] Breeding: The science or art of changing the constitution of a population of plants or animals through sexual reproduction. [NIH] Broad-spectrum: Effective against a wide range of microorganisms; said of an antibiotic. [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] 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] Capsid: The outer protein protective shell of a virus, which protects the viral nucleic acid. [NIH]
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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] 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] Cardiogenic: Originating in the heart; caused by abnormal function of the heart. [EU] Cardiomyopathy: A general diagnostic term designating primary myocardial disease, often of obscure or unknown etiology. [EU] Cardiomyopathy, Congestive: A syndrome characterized by cardiac enlargement and congestive heart failure. It probably represents the end result of many forms of myocardial damage produced by a variety of toxic, metabolic, or infectious agents. [NIH] Cardiopulmonary: Having to do with the heart and lungs. [NIH] Cardiotonic: 1. Having a tonic effect on the heart. 2. An agent that has a tonic effect on the heart. [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] Cardiovascular System: The heart and the blood vessels by which blood is pumped and circulated through the body. [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] Catecholamine: A group of chemical substances manufactured by the adrenal medulla and secreted during physiological stress. [NIH] Catheterization: Use or insertion of a tubular device into a duct, blood vessel, hollow organ, or body cavity for injecting or withdrawing fluids for diagnostic or therapeutic purposes. It differs from intubation in that the tube here is used to restore or maintain patency in obstructions. [NIH] Causal: Pertaining to a cause; directed against a cause. [EU] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Cefaclor: Semisynthetic, broad-spectrum antibiotic derivative of cephalexin. [NIH]
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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 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 Cycle Proteins: Proteins that control the cell division cycle. This family of proteins includes a wide variety of classes, including cyclin-dependent kinases, mitogen-activated kinases, cyclins, and phosphoprotein phosphatases (phosphoprotein phosphatase) as well as their putative substrates such as chromatin-associated proteins, cytoskeletal proteins, and transcription factors. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Division: The fission of a cell. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Cephalexin: A semisynthetic cephalosporin antibiotic with antimicrobial activity similar to that of cephaloridine or cephalothin, but somewhat less potent. It is effective against both gram-positive and gram-negative organisms. [NIH] Cerebrospinal: Pertaining to the brain and spinal cord. [EU] Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cervix: The lower, narrow end of the uterus that forms a canal between the uterus and vagina. [NIH] Chagas Disease: A form of trypanosomiasis endemic in Central and South America, caused by Trypanosoma cruzi. It may follow either an acute or chronic course, the former commonly in children. [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] Chemoreceptor: A receptor adapted for excitation by chemical substances, e.g., olfactory and gustatory receptors, or a sense organ, as the carotid body or the aortic (supracardial) bodies, which is sensitive to chemical changes in the blood stream, especially reduced oxygen content, and reflexly increases both respiration and blood pressure. [EU] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or
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immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chemotherapy: Treatment with anticancer drugs. [NIH] Chicken Anemia Virus: The type species of Circovirus, a small, non-enveloped DNA virus originally isolated from contaminated vaccines in Japan. It causes chicken infectious anemia and may possibly play a key role in hemorrhagic anemia syndrome, anemia dermatitis, and blue wing disease. [NIH] Cholera: An acute diarrheal disease endemic in India and Southeast Asia whose causative agent is vibrio cholerae. This condition can lead to severe dehydration in a matter of hours unless quickly treated. [NIH] Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Choline: A basic constituent of lecithin that is found in many plants and animal organs. It is important as a precursor of acetylcholine, as a methyl donor in various metabolic processes, and in lipid metabolism. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] Cholinesterase Inhibitors: Drugs that inhibit cholinesterases. The neurotransmitter acetylcholine is rapidly hydrolyzed, and thereby inactivated, by cholinesterases. When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. Cholinesterase inhibitors are widely used clinically for their potentiation of cholinergic inputs to the gastrointestinal tract and urinary bladder, the eye, and skeletal muscles; they are also used for their effects on the heart and the central nervous system. [NIH] Chorea: Involuntary, forcible, rapid, jerky movements that may be subtle or become confluent, markedly altering normal patterns of movement. Hypotonia and pendular reflexes are often associated. Conditions which feature recurrent or persistent episodes of chorea as a primary manifestation of disease are referred to as choreatic disorders. Chorea is also a frequent manifestation of basal ganglia diseases. [NIH] 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 Disease: Disease or ailment of long duration. [NIH] Chronic Fatigue Syndrome: Fatigue caused by the combined effects of different types of prolonged fatigue. [NIH] Chronic Obstructive Pulmonary Disease: Collective term for chronic bronchitis and emphysema. [NIH] Circovirus: A genus of the family Circoviridae that infects fowl, swine, and psittacine birds. It is the only DNA virus affecting mammals which contains a single-stranded circular genome. The three species are chicken anemia virus causing transient anemia and immunosuppression in baby chicks; beak and feather disease virus causing a fatal disease in psittacine birds; and porcine circovirus, not yet associated with any disease. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public,
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interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [NIH]
Clinical study: A research study in which patients receive treatment in a clinic or other medical facility. Reports of clinical studies can contain results for single patients (case reports) or many patients (case series or clinical trials). [NIH] Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Clone: The term "clone" has acquired a new meaning. It is applied specifically to the bits of inserted foreign DNA in the hybrid molecules of the population. Each inserted segment originally resided in the DNA of a complex genome amid millions of other DNA segment. [NIH]
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] Clozapine: A tricylic dibenzodiazepine, classified as an atypical antipsychotic agent. It binds several types of central nervous system receptors, and displays a unique pharmacological profile. Clozapine is a serotonin antagonist, with strong binding to 5-HT 2A/2C receptor subtype. It also displays strong affinity to several dopaminergic receptors, but shows only weak antagonism at the dopamine D2 receptor, a receptor commonly thought to modulate neuroleptic activity. Agranulocytosis is a major adverse effect associated with administration of this agent. [NIH] 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] 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] 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] 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]
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Common Variable Immunodeficiency: Heterogeneous group of immunodeficiency syndromes characterized by hypogammaglobulinemia of most isotypes, variable B-cell defects, and the presence of recurrent bacterial infections. [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] Complementation: The production of a wild-type phenotype when two different mutations are combined in a diploid or a heterokaryon and tested in trans-configuration. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Concomitant: Accompanying; accessory; joined with another. [EU] Congestion: Excessive or abnormal accumulation of blood in a part. [EU] Congestive heart failure: Weakness of the heart muscle that leads to a buildup of fluid in body tissues. [NIH]
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Conjunctiva: The mucous membrane that lines the inner surface of the eyelids and the anterior part of the sclera. [NIH] Conjunctivitis: Inflammation of the conjunctiva, generally consisting of conjunctival hyperaemia associated with a discharge. [EU] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue Cells: A group of cells that includes fibroblasts, cartilage cells, adipocytes, smooth muscle cells, and bone cells. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Constipation: Infrequent or difficult evacuation of feces. [NIH] Constitutional: 1. Affecting the whole constitution of the body; not local. 2. Pertaining to the constitution. [EU] Constriction: The act of constricting. [NIH] Contamination: The soiling or pollution by inferior material, as by the introduction of organisms into a wound, or sewage into a stream. [EU] Contractile Proteins: Proteins which participate in contractile processes. They include muscle proteins as well as those found in other cells and tissues. In the latter, these proteins participate in localized contractile events in the cytoplasm, in motile activity, and in cell aggregation phenomena. [NIH] Contractility: Capacity for becoming short in response to a suitable stimulus. [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] Contrast medium: A substance that is introduced into or around a structure and, because of the difference in absorption of x-rays by the contrast medium and the surrounding tissues, allows radiographic visualization of the structure. [EU] 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 pathologic involvement of them. [EU] Coronary Angiography: Radiography of the vascular system of the heart muscle after injection of a contrast medium. [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]
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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] Cowpox: A mild, eruptive skin disease of milk cows caused by cowpox virus, with lesions occurring principally on the udder and teats. Human infection may occur while milking an infected animal. [NIH] Cowpox Virus: A species of orthopoxvirus that is the etiologic agent of cowpox. It is closely related to but antigenically different from vaccina virus. [NIH] Coxsackie virus: Group of viruses that is a common source of infection in kids. It is transmitted primarily by touch. The most common symptoms children experience are simply fever, feeling rundown, and a rash. [NIH] Coxsackieviruses: A heterogeneous group of the genus enterovirus found in association with various diseases in man and other animals. Two groups (A and B) have been identified with a number of serotypes in each. The name is derived from a village in New York State where the virus was first identified. [NIH] Coxsackieviruses A: One of the two groups of coxsackieviruses. Coxsackie A viruses are divided into 24 serotypes and are associated with or implicated in herpangina, aseptic meningitis, paralytic disease, encephalitis, ataxia, and cardiac diseases. Coxsackie A24 variant can cause acute hemorrhagic conjunctivitis. [NIH] Crossing-over: The exchange of corresponding segments between chromatids of homologous chromosomes during meiosia, forming a chiasma. [NIH] Cultured cells: Animal or human cells that are grown in the laboratory. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Cutaneous: Having to do with the skin. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cyclin: Molecule that regulates the cell cycle. [NIH] Cyclin-Dependent Kinases: Protein kinases that control cell cycle progression in all eukaryotes and require physical association with cyclins to achieve full enzymatic activity. Cyclin-dependent kinases are regulated by phosphorylation and dephosphorylation events. [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] Cysteine: A thiol-containing non-essential amino acid that is oxidized to form cystine. [NIH] Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom
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of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, . New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytochrome b: Cytochromes (electron-transporting proteins) with protoheme or a related heme as the prosthetic group. The prosthetic group is not covalently bound to the protein moiety. [NIH] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytomegalovirus: A genus of the family Herpesviridae, subfamily Betaherpesvirinae, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytoskeletal Proteins: Major constituent of the cytoskeleton found in the cytoplasm of eukaryotic cells. They form a flexible framework for the cell, provide attachment points for organelles and formed bodies, and make communication between parts of the cell possible. [NIH]
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] 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] Delirium: (DSM III-R) an acute, reversible organic mental disorder characterized by reduced ability to maintain attention to external stimuli and disorganized thinking as manifested by rambling, irrelevant, or incoherent speech; there are also a reduced level of consciousness, sensory misperceptions, disturbance of the sleep-wakefulness cycle and level of psychomotor activity, disorientation to time, place, or person, and memory impairment. Delirium may be caused by a large number of conditions resulting in derangement of cerebral metabolism, including systemic infection, poisoning, drug intoxication or withdrawal, seizures or head trauma, and metabolic disturbances such as hypoxia, hypoglycaemia, fluid, electrolyte, or acid-base imbalances, or hepatic or renal failure. Called also acute confusional state and acute brain syndrome. [EU] 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
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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] Depigmentation: Removal or loss of pigment, especially melanin. [EU] Deprivation: Loss or absence of parts, organs, powers, or things that are needed. [EU] Dermatitis: Any inflammation of the skin. [NIH] Dermis: A layer of vascular connective tissue underneath the epidermis. The surface of the dermis contains sensitive papillae. Embedded in or beneath the dermis are sweat glands, hair follicles, and sebaceous glands. [NIH] Desensitization: The prevention or reduction of immediate hypersensitivity reactions by administration of graded doses of allergen; called also hyposensitization and immunotherapy. [EU] Detoxification: Treatment designed to free an addict from his drug habit. [EU] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Device Removal: Removal of an implanted therapeutic or prosthetic device. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diarrhea: Passage of excessively liquid or excessively frequent stools. [NIH] Diastole: Period of relaxation of the heart, especially the ventricles. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Diffusion: The tendency of a gas or solute to pass from a point of higher pressure or concentration to a point of lower pressure or concentration and to distribute itself throughout the available space; a major mechanism of biological transport. [NIH] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digitalis: A genus of toxic herbaceous Eurasian plants of the Scrophulaceae which yield cardiotonic glycosides. The most useful are Digitalis lanata and D. purpurea. [NIH] Dilated cardiomyopathy: Heart muscle disease that leads to enlargement of the heart's chambers, robbing the heart of its pumping ability. [NIH] Dilation: A process by which the pupil is temporarily enlarged with special eye drops (mydriatic); allows the eye care specialist to better view the inside of the eye. [NIH] Diploid: Having two sets of chromosomes. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Discrete: Made up of separate parts or characterized by lesions which do not become blended; not running together; separate. [NIH]
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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] 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] Dissociative Disorders: Sudden temporary alterations in the normally integrative functions of consciousness. [NIH] 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] Dominance: In genetics, the full phenotypic expression of a gene in both heterozygotes and homozygotes. [EU] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate 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] Drug Hypersensitivity: Immunologically mediated adverse reactions to medicinal substances used legally or illegally. [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] Dura mater: The outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain and spinal cord; called also pachymeninx. [EU] Dyskinesia: Impairment of the power of voluntary movement, resulting in fragmentary or incomplete movements. [EU] Dyspnea: Difficult or labored breathing. [NIH] Dystrophin: A muscle protein localized in surface membranes which is the product of the Duchenne/Becker muscular dystrophy gene. Individuals with Duchenne muscular dystrophy usually lack dystrophin completely while those with Becker muscular dystrophy have dystrophin of an altered size. It shares features with other cytoskeletal proteins such as spectrin and alpha-actinin but the precise function of dystrophin is not clear. One possible
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role might be to preserve the integrity and alignment of the plasma membrane to the myofibrils during muscle contraction and relaxation. MW 400 kDa. [NIH] Dystrophy: Any disorder arising from defective or faulty nutrition, especially the muscular dystrophies. [EU] Echocardiography: Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic. [NIH] Echoviruses: A group of enteroviruses isolated from man and originally thought not to be associated with disease, whence the name ECHO (enteric cytopathic human orphan); however, several serotypes have been found to cause meningitis, diarrhea, and respiratory disease. [NIH] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Effector cell: A cell that performs a specific function in response to a stimulus; usually used to describe cells in the immune system. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Ehrlichiosis: A tick-borne disease characterized by fever, headache, myalgias, anorexia, and occasionally rash. In humans the disease is caused by Ehrlichia chaffeensis, in dogs it is caused by E. canis, and in horses, E. equi. [NIH] Elasticity: Resistance and recovery from distortion of shape. [NIH] Elastin: The protein that gives flexibility to tissues. [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] Electrophysiological: Pertaining to electrophysiology, that is a branch of physiology that is concerned with the electric phenomena associated with living bodies and involved in their functional activity. [EU] Emaciation: Clinical manifestation of excessive leanness usually caused by disease or a lack of nutrition. [NIH] Embolus: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Embryology: The study of the development of an organism during the embryonic and fetal stages of life. [NIH] Emphysema: A pathological accumulation of air in tissues or organs. [NIH] Encephalitis: Inflammation of the brain due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see encephalitis, viral) are a relatively frequent cause of
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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] Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] 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] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [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-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxins: Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells. [NIH] Enterovirus: A genus of the family Picornaviridae whose members preferentially inhabit the intestinal tract of a variety of hosts. The genus contains many species. Newly described members of human enteroviruses are assigned continuous numbers with the species designated "human enterovirus". [NIH] Environmental Exposure: The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]
Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. [NIH] Eosinophil: A polymorphonuclear leucocyte with large eosinophilic granules in its cytoplasm, which plays a role in hypersensitivity reactions. [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] Epidemics: A period of increased prevalence of a particular disease in a population. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU]
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Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Epitope: A molecule or portion of a molecule capable of binding to the combining site of an antibody. For every given antigenic determinant, the body can construct a variety of antibody-combining sites, some of which fit almost perfectly, and others which barely fit. [NIH]
Epitope Mapping: Methods used for studying the interactions of antibodies with specific regions of protein antigens. Important applications of epitope mapping are found within the area of immunochemistry. [NIH] Epstein-Barr virus: EBV. A common virus that remains dormant in most people. It has been associated with certain cancers, including Burkitt's lymphoma, immunoblastic lymphoma, and nasopharyngeal carcinoma. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [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] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Exocrine: Secreting outwardly, via a duct. [EU] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Extensor: A muscle whose contraction tends to straighten a limb; the antagonist of a flexor. [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] Extracorporeal: Situated or occurring outside the body. [EU] Extracorporeal Membrane Oxygenation: Application of a life support system that circulates the blood through an oxygenating system, which may consist of a pump, a membrane oxygenator, and a heat exchanger. Examples of its use are to assist victims of smoke inhalation injury, respiratory failure, and cardiac failure. [NIH] Extrapyramidal: Outside of the pyramidal tracts. [EU] Eye Infections: Infection, moderate to severe, caused by bacteria, fungi, or viruses, which occurs either on the external surface of the eye or intraocularly with probable inflammation, visual impairment, or blindness. [NIH]
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Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fat: Total lipids including phospholipids. [NIH] 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]
Fetal Heart: The heart of the fetus of any viviparous animal. It refers to the heart in the postembryonic period and is differentiated from the embryonic heart (heart/embryology) only on the basis of time. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrillation: A small, local, involuntary contraction of muscle, invisible under the skin, resulting from spontaneous activation of single muscle cells or muscle fibres. [EU] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Fixation: 1. The act or operation of holding, suturing, or fastening in a fixed position. 2. The condition of being held in a fixed position. 3. In psychiatry, a term with two related but distinct meanings : (1) arrest of development at a particular stage, which like regression (return to an earlier stage), if temporary is a normal reaction to setbacks and difficulties but if protracted or frequent is a cause of developmental failures and emotional problems, and (2) a close and suffocating attachment to another person, especially a childhood figure, such as one's mother or father. Both meanings are derived from psychoanalytic theory and refer to 'fixation' of libidinal energy either in a specific erogenous zone, hence fixation at the oral, anal, or phallic stage, or in a specific object, hence mother or father fixation. 4. The use of a fixative (q.v.) to preserve histological or cytological specimens. 5. In chemistry, the process whereby a substance is removed from the gaseous or solution phase and localized, as in carbon dioxide fixation or nitrogen fixation. 6. In ophthalmology, direction of the gaze so that the visual image of the object falls on the fovea centralis. 7. In film processing, the chemical removal of all undeveloped salts of the film emulsion, leaving only the developed silver to form a permanent image. [EU] Flaccid: Weak, lax and soft. [EU] 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] Free Radicals: Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated. [NIH] 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
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those that grow as multicelluar colonies (mushrooms and molds). [NIH] Galanthamine: A cholinesterase inhibitor. It has been used to reverse the muscular effects of gallamine and tubocurarine and has been studied as a treatment for Alzheimer's disease and other central nervous system disorders. [NIH] Gamma-interferon: Interferon produced by T-lymphocytes in response to various mitogens and antigens. Gamma interferon appears to have potent antineoplastic, immunoregulatory and antiviral activity. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Ganglion: 1. A knot, or knotlike mass. 2. A general term for a group of nerve cell bodies located outside the central nervous system; occasionally applied to certain nuclear groups within the brain or spinal cord, e.g. basal ganglia. 3. A benign cystic tumour occurring on a aponeurosis or tendon, as in the wrist or dorsum of the foot; it consists of a thin fibrous capsule enclosing a clear mucinous fluid. [EU] Gangrenous: A circumscribed, deep-seated, suppurative inflammation of the subcutaneous tissue of the eyelid discharging pus from several points. [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] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]
Gastroenteritis: An acute inflammation of the lining of the stomach and intestines, characterized by anorexia, nausea, diarrhoea, abdominal pain, and weakness, which has various causes, including food poisoning due to infection with such organisms as Escherichia coli, Staphylococcus aureus, and Salmonella species; consumption of irritating food or drink; or psychological factors such as anger, stress, and fear. Called also enterogastritis. [EU] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal 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 Amplification: A selective increase in the number of copies of a gene coding for a specific protein without a proportional increase in other genes. It occurs naturally via the excision of a copy of the repeating sequence from the chromosome and its extrachromosomal replication in a plasmid, or via the production of an RNA transcript of the entire repeating sequence of ribosomal RNA followed by the reverse transcription of the molecule to produce an additional copy of the original DNA sequence. Laboratory techniques have been introduced for inducing disproportional replication by unequal crossing over, uptake of DNA from lysed cells, or generation of extrachromosomal sequences from rolling circle replication. [NIH] Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Targeting: The integration of exogenous DNA into the genome of an organism at sites where its expression can be suitably controlled. This integration occurs as a result of homologous recombination. [NIH] Gene Therapy: The introduction of new genes into cells for the purpose of treating disease by restoring or adding gene expression. Techniques include insertion of retroviral vectors,
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transfection, homologous recombination, and injection of new genes into the nuclei of single cell embryos. The entire gene therapy process may consist of multiple steps. The new genes may be introduced into proliferating cells in vivo (e.g., bone marrow) or in vitro (e.g., fibroblast cultures) and the modified cells transferred to the site where the gene expression is required. Gene therapy may be particularly useful for treating enzyme deficiency diseases, hemoglobinopathies, and leukemias and may also prove useful in restoring drug sensitivity, particularly for leukemia. [NIH] 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 Techniques: Chromosomal, biochemical, intracellular, and other methods used in the study of genetics. [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] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Giant Cells: Multinucleated masses produced by the fusion of many cells; often associated with viral infections. In AIDS, they are induced when the envelope glycoprotein of the HIV virus binds to the CD4 antigen of uninfected neighboring T4 cells. The resulting syncytium leads to cell death and thus may account for the cytopathic effect of the virus. [NIH] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]
Glucocorticoids: A group of corticosteroids that affect carbohydrate metabolism (gluconeogenesis, liver glycogen deposition, elevation of blood sugar), inhibit corticotropin secretion, and possess pronounced anti-inflammatory activity. They also play a role in fat and protein metabolism, maintenance of arterial blood pressure, alteration of the connective tissue response to injury, reduction in the number of circulating lymphocytes, and functioning of the central nervous system. [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] 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] Glutathione Peroxidase: An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9. [NIH]
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Glycerol: A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent. [NIH]
Glycerophospholipids: Derivatives of phosphatidic acid in which the hydrophobic regions are composed of two fatty acids and a polar alcohol is joined to the C-3 position of glycerol through a phosphodiester bond. They are named according to their polar head groups, such as phosphatidylcholine and phosphatidylethanolamine. [NIH] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycolysis: The pathway by which glucose is catabolized into two molecules of pyruvic acid with the generation of ATP. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Gonadal: Pertaining to a gonad. [EU] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Graft Rejection: An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient. [NIH] Grafting: The operation of transfer of tissue from one site to another. [NIH] Granule: A small pill made from sucrose. [EU] Gravis: Eruption of watery blisters on the skin among those handling animals and animal products. [NIH] Guanine: One of the four DNA bases. [NIH] Guanylate Cyclase: An enzyme that catalyzes the conversion of GTP to 3',5'-cyclic GMP and pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC 4.6.1.2. [NIH] Habitat: An area considered in terms of its environment, particularly as this determines the type and quality of the vegetation the area can carry. [NIH] 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] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; craniocerebral trauma; central nervous system infections; intracranial hypertension; and other disorders. In general, recurrent headaches that are not associated with a primary disease process are referred to as headache disorders (e.g., migraine). [NIH] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Heart Transplantation: The transference of a heart from one human or animal to another. [NIH]
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Heartbeat: One complete contraction of the heart. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [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] Hepatocytes: The main structural component of the liver. They are specialized epithelial cells that are organized into interconnected plates called lobules. [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] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]
Heterozygotes: Having unlike alleles at one or more corresponding loci on homologous chromosomes. [NIH] Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] 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] Homotypic: Adhesion between neutrophils. [NIH] Homozygotes: An individual having a homozygous gene pair. [NIH] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Humoral: Of, relating to, proceeding from, or involving a bodily humour - now often used of endocrine factors as opposed to neural or somatic. [EU] Humour: 1. A normal functioning fluid or semifluid of the body (as the blood, lymph or bile) especially of vertebrates. 2. A secretion that is itself an excitant of activity (as certain hormones). [EU] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hybridomas: Cells artificially created by fusion of activated lymphocytes with neoplastic cells. The resulting hybrid cells are cloned and produce pure or "monoclonal" antibodies or T-cell products, identical to those produced by the immunologically competent parent, and continually grow and divide as the neoplastic parent. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H,
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atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hyperaemia: An excess of blood in a part; engorgement. [EU] Hyperlipidemia: An excess of lipids in the 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] Hyperreflexia: Exaggeration of reflexes. [EU] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypersensitivity, Immediate: Hypersensitivity reactions which occur within minutes of exposure to challenging antigen due to the release of histamine which follows the antigenantibody reaction and causes smooth muscle contraction and increased vascular permeability. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hypertrophic cardiomyopathy: Heart muscle disease that leads to thickening of the heart walls, interfering with the heart's ability to fill with and pump blood. [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] Hypogammaglobulinemia: The most common primary immunodeficiency in which antibody production is deficient. [NIH] Hypotension: Abnormally low blood pressure. [NIH] Idiopathic: Describes a disease of unknown cause. [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
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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] 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] 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] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunodeficiency syndrome: The inability of the body to produce an immune response. [NIH]
Immunofluorescence: A technique for identifying molecules present on the surfaces of cells or in tissues using a highly fluorescent substance coupled to a specific antibody. [NIH] Immunogen: A substance that is capable of causing antibody formation. [NIH] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunology: The study of the body's immune system. [NIH] Immunosuppression: Deliberate prevention or diminution of the host's immune response. It may be nonspecific as in the administration of immunosuppressive agents (drugs or radiation) or by lymphocyte depletion or may be specific as in desensitization or the simultaneous administration of antigen and immunosuppressive drugs. [NIH] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunosuppressive Agents: Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of suppressor T-cell populations or by inhibiting the activation of helper cells. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of interleukins and other cytokines are emerging. [NIH] Immunosuppressive therapy: Therapy used to decrease the body's immune response, such as drugs given to prevent transplant rejection. [NIH] 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] Implantation: The insertion or grafting into the body of biological, living, inert, or radioactive material. [EU] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incision: A cut made in the body during surgery. [NIH]
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Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] Incubation: The development of an infectious disease from the entrance of the pathogen to the appearance of clinical symptoms. [EU] Indomethacin: A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes. [NIH] Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Infancy: The period of complete dependency prior to the acquisition of competence in walking, talking, and self-feeding. [NIH] Infantile: Pertaining to an infant or to infancy. [EU] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]
Infectious Mononucleosis: A common, acute infection usually caused by the Epstein-Barr virus (Human herpesvirus 4). There is an increase in mononuclear white blood cells and other atypical lymphocytes, generalized lymphadenopathy, splenomegaly, and occasionally hepatomegaly with hepatitis. [NIH] Infiltration: The diffusion or accumulation in a tissue or cells of substances not normal to it or in amounts of the normal. Also, the material so accumulated. [EU] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Influenza: An acute viral infection involving the respiratory tract. It is marked by inflammation of the nasal mucosa, the pharynx, and conjunctiva, and by headache and severe, often generalized, myalgia. [NIH] Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH] Ingestion: Taking into the body by mouth [NIH] Inhalation: The drawing of air or other substances into the lungs. [EU] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Inotropic: Affecting the force or energy of muscular contractions. [EU] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH]
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Insulator: Material covering the metal conductor of the lead. It is usually polyurethane or silicone. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Intercellular Adhesion Molecule-1: A cell-surface ligand with a role in leukocyte adhesion and inflammation. Its production is induced by gamma-interferon and it is required for neutrophil migration into inflamed tissue. [NIH] Interferon: A biological response modifier (a substance that can improve the body's natural response to disease). Interferons interfere with the division of cancer cells and can slow tumor growth. There are several types of interferons, including interferon-alpha, -beta, and gamma. These substances are normally produced by the body. They are also made in the laboratory for use in treating cancer and other diseases. [NIH] Interferon-alpha: One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells when exposed to live or inactivated virus, double-stranded RNA, or bacterial products. It is the major interferon produced by virus-induced leukocyte cultures and, in addition to its pronounced antiviral activity, it causes activation of NK cells. [NIH] Interleukin-1: A soluble factor produced by monocytes, macrophages, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. IL-1 consists of two distinct forms, IL-1 alpha and IL-1 beta which perform the same functions but are distinct proteins. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. The factor is distinct from interleukin-2. [NIH] Interleukin-2: Chemical mediator produced by activated T lymphocytes and which regulates the proliferation of T cells, as well as playing a role in the regulation of NK cell activity. [NIH] Interleukin-6: Factor that stimulates the growth and differentiation of human B-cells and is also a growth factor for hybridomas and plasmacytomas. It is produced by many different cells including T-cells, monocytes, and fibroblasts. [NIH] Interleukins: Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli. [NIH] Intermediate Filaments: Cytoplasmic filaments intermediate in diameter (about 10 nanometers) between the microfilaments and the microtubules. They may be composed of any of a number of different proteins and form a ring around the cell nucleus. [NIH] 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] Intravascular: Within a vessel or vessels. [EU] Intravenous: IV. Into a vein. [NIH]
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Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Intubation: Introduction of a tube into a hollow organ to restore or maintain patency if obstructed. It is differentiated from catheterization in that the insertion of a catheter is usually performed for the introducing or withdrawing of fluids from the body. [NIH] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Involuntary: Reaction occurring without intention or volition. [NIH] 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] 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] Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Laceration: 1. The act of tearing. 2. A torn, ragged, mangled wound. [EU] Lag: The time elapsing between application of a stimulus and the resulting reaction. [NIH] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH] 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] Lead Poisoning: Disease caused by the gradual accumulation of a significant body burden of lead. [NIH] Lectin: A complex molecule that has both protein and sugars. Lectins are able to bind to the outside of a cell and cause biochemical changes in it. Lectins are made by both animals and plants. [NIH] Left ventricular assist device: A mechanical device used to increase the heart's pumping ability. [NIH] Leishmaniasis: A disease caused by any of a number of species of protozoa in the genus Leishmania. There are four major clinical types of this infection: cutaneous (Old and New World), diffuse cutaneous, mucocutaneous, and visceral leishmaniasis. [NIH] Lesion: An area of abnormal tissue change. [NIH] Lethal: Deadly, fatal. [EU] Leucocyte: All the white cells of the blood and their precursors (myeloid cell series, lymphoid cell series) but commonly used to indicate granulocytes exclusive of lymphocytes. [NIH]
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Leukemia: Cancer of blood-forming tissue. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Leukopenia: A condition in which the number of leukocytes (white blood cells) in the blood is reduced. [NIH] Ligaments: Shiny, flexible bands of fibrous tissue connecting together articular extremities of bones. They are pliant, tough, and inextensile. [NIH] Ligands: A RNA simulation method developed by the MIT. [NIH] Lipid: Fat. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] Lithium: An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight 6.94. Salts of lithium are used in treating manic-depressive disorders. [NIH]
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] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [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] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH] Lymph node: A rounded mass of lymphatic tissue that is surrounded by a capsule of connective tissue. Also known as a lymph gland. Lymph nodes are spread out along lymphatic vessels and contain many lymphocytes, which filter the lymphatic fluid (lymph). [NIH]
Lymphadenopathy: Disease or swelling of the lymph nodes. [NIH] Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphoblasts: Interferon produced predominantly by leucocyte cells. [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]
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Lymphocyte Count: A count of the number of lymphocytes in the blood. [NIH] Lymphocyte Depletion: Immunosuppression by reduction of circulating lymphocytes or by T-cell depletion of bone marrow. The former may be accomplished in vivo by thoracic duct drainage or administration of antilymphocyte serum. The latter is performed ex vivo on bone marrow before its transplantation. [NIH] 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] 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] Maculopapular: Both macular and papular, as an eruption consisting of both macules and papules; sometimes erroneously used to designate a papule that is only slightly elevated. [EU]
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] Major Histocompatibility Complex: The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) transplantation antigens, genes which control the structure of the immune responseassociated (Ia) antigens, the immune response (Ir) genes which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]
Mammogram: An x-ray of the breast. [NIH] Manic: Affected with mania. [EU] Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Mastitis: Inflammatory disease of the breast, or mammary gland. [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] Medical Records: Recording of pertinent information concerning patient's illness or illnesses. [NIH] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Melanin: The substance that gives the skin its color. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Membrane Lipids: Lipids, predominantly phospholipids, cholesterol and small amounts of glycolipids found in membranes including cellular and intracellular membranes. These lipids may be arranged in bilayers in the membranes with integral proteins between the
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layers and peripheral proteins attached to the outside. Membrane lipids are required for active transport, several enzymatic activities and membrane formation. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Meningitis: Inflammation of the meninges. When it affects the dura mater, the disease is termed pachymeningitis; when the arachnoid and pia mater are involved, it is called leptomeningitis, or meningitis proper. [EU] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Health: The state wherein the person is well adjusted. [NIH] Mental Processes: Conceptual functions or thinking in all its forms. [NIH] Mesolimbic: Inner brain region governing emotion and drives. [NIH] Methylprednisolone: (6 alpha,11 beta)-11,17,21-Trihydroxy-6-methylpregna-1,4-diene-3,2dione. A prednisolone derivative which has pharmacological actions similar to prednisolone. [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] Mice Minute Virus: The type species of parvovirus prevalent in mouse colonies and found as a contaminant of many transplanted tumors or leukemias. [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] Microfilaments: The smallest of the cytoskeletal filaments. They are composed chiefly of actin. [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] Microtubules: Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein tubulin. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] 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] Mitochondria: Parts of a cell where aerobic production (also known as cell respiration) takes place. [NIH] Mitochondrial Swelling: Increase in volume of mitochondria due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of
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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] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Modulator: A specific inductor that brings out characteristics peculiar to a definite region. [EU]
Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] Monoclonal antibodies: Laboratory-produced substances that can locate and bind to cancer cells wherever they are in the body. Many monoclonal antibodies are used in cancer detection or therapy; each one recognizes a different protein on certain cancer cells. Monoclonal antibodies can be used alone, or they can be used to deliver drugs, toxins, or radioactive material directly to a tumor. [NIH] Monocytes: Large, phagocytic mononuclear leukocytes produced in the vertebrate bone marrow and released into the blood; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles. [NIH] Mononuclear: A cell with one nucleus. [NIH] Morphological: Relating to the configuration or the structure of live organs. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Motility: The ability to move spontaneously. [EU] Mucolytic: Destroying or dissolving mucin; an agent that so acts : a mucopolysaccharide or glycoprotein, the chief constituent of mucus. [EU] Mucosa: A mucous membrane, or tunica mucosa. [EU] Mucus: The viscous secretion of mucous membranes. It contains mucin, white blood cells, water, inorganic salts, and exfoliated cells. [NIH] Multiple sclerosis: A disorder of the central nervous system marked by weakness, numbness, a loss of muscle coordination, and problems with vision, speech, and bladder control. Multiple sclerosis is thought to be an autoimmune disease in which the body's immune system destroys myelin. Myelin is a substance that contains both protein and fat (lipid) and serves as a nerve insulator and helps in the transmission of nerve signals. [NIH] Multivalent: Pertaining to a group of 5 or more homologous or partly homologous chromosomes during the zygotene stage of prophase to first metaphasis in meiosis. [NIH] Muscle Contraction: A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments. [NIH]
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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] Muscle Proteins: The protein constituents of muscle, the major ones being ACTINS and MYOSIN. More than a dozen accessary proteins exist including troponin, tropomyosin, and dystrophin. [NIH] Muscle relaxant: An agent that specifically aids in reducing muscle tension, as those acting at the polysynaptic neurons of motor nerves (e.g. meprobamate) or at the myoneural junction (curare and related compounds). [EU] Muscle Spindles: Mechanoreceptors found between skeletal muscle fibers. Muscle spindles are arranged in parallel with muscle fibers and respond to the passive stretch of the muscle, but cease to discharge if the muscle contracts isotonically, thus signaling muscle length. The muscle spindles are the receptors responsible for the stretch or myotactic reflex. [NIH] Mutate: To change the genetic material of a cell. Then changes (mutations) can be harmful, beneficial, or have no effect. [NIH] Myalgia: Pain in a muscle or muscles. [EU] Myasthenia: Muscular debility; any constitutional anomaly of muscle. [EU] Mydriatic: 1. Dilating the pupil. 2. Any drug that dilates the pupil. [EU] Myelin: The fatty substance that covers and protects nerves. [NIH] Myelitis: Inflammation of the spinal cord. Relatively common etiologies include infections; autoimmune diseases; spinal cord; and ischemia (see also spinal cord vascular diseases). Clinical features generally include weakness, sensory loss, localized pain, incontinence, and other signs of autonomic dysfunction. [NIH] Myocardial Contraction: Contractile activity of the heart. [NIH] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myofibrils: Highly organized bundles of actin, myosin, and other proteins in the cytoplasm of skeletal and cardiac muscle cells that contract by a sliding filament mechanism. [NIH] Myopathy: Any disease of a muscle. [EU] Myosin: Chief protein in muscle and the main constituent of the thick filaments of muscle fibers. In conjunction with actin, it is responsible for the contraction and relaxation of muscles. [NIH] Myositis: Inflammation of a voluntary muscle. [EU] Nasal Mucosa: The mucous membrane lining the nasal cavity. [NIH] Nausea: An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses. [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH]
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Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Neoplasm: A new growth of benign or malignant tissue. [NIH] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH] Nerve Endings: Specialized terminations of peripheral neurons. Nerve endings include neuroeffector junction(s) by which neurons activate target organs and sensory receptors which transduce information from the various sensory modalities and send it centrally in the nervous system. Presynaptic nerve endings are presynaptic terminals. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neuroeffector Junction: The synapse between a neuron (presynaptic) and an effector cell other than another neuron (postsynaptic). Neuroeffector junctions include synapses onto muscles and onto secretory cells. [NIH] Neuroleptic: A term coined to refer to the effects on cognition and behaviour of antipsychotic drugs, which produce a state of apathy, lack of initiative, and limited range of emotion and in psychotic patients cause a reduction in confusion and agitation and normalization of psychomotor activity. [EU] Neuromuscular: Pertaining to muscles and nerves. [EU] Neuromuscular Junction: The synapse between a neuron and a muscle. [NIH] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropeptides: Peptides released by neurons as intercellular messengers. Many neuropeptides are also hormones released by non-neuronal cells. [NIH] Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins, endorphins, and serotonin. [EU] Neutropenia: An abnormal decrease in the number of neutrophils, a type of white blood cell. [NIH] Neutrophil: A type of white blood cell. [NIH] Niche: The ultimate unit of the habitat, i. e. the specific spot occupied by an individual organism; by extension, the more or less specialized relationships existing between an organism, individual or synusia(e), and its environment. [NIH] Nitrates: Inorganic or organic salts and esters of nitric acid. These compounds contain the NO3- radical. [NIH] Nitric acid: A toxic, corrosive, colorless liquid used to make fertilizers, dyes, explosives, and other chemicals. [NIH]
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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] Nitrosamines: A class of compounds that contain a -NH2 and a -NO radical. Many members of this group have carcinogenic and mutagenic properties. [NIH] Nitrosation: Conversion into nitroso compounds. An example is the reaction of nitrites with amino compounds to form carcinogenic N-nitrosamines. [NIH] Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclear magnetic resonance imaging: NMRI. A procedure in which a magnet linked to a computer is used to create detailed pictures of areas inside the body. Also called magnetic resonance imaging (MRI). [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleolus: A small dense body (sub organelle) within the nucleus of eukaryotic cells, visible by phase contrast and interference microscopy in live cells throughout interphase. Contains RNA and protein and is the site of synthesis of ribosomal RNA. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nutritional Status: State of the body in relation to the consumption and utilization of nutrients. [NIH] Occult: Obscure; concealed from observation, difficult to understand. [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] Opportunistic Infections: An infection caused by an organism which becomes pathogenic
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under certain conditions, e.g., during immunosuppression. [NIH] Organ Culture: The growth in aseptic culture of plant organs such as roots or shoots, beginning with organ primordia or segments and maintaining the characteristics of the organ. [NIH] Organ Transplantation: Transference of an organ between individuals of the same species or between individuals of different species. [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] Orthostatic: Pertaining to or caused by standing erect. [EU] Osteoarthritis: A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans. [NIH] Ovalbumin: An albumin obtained from the white of eggs. It is a member of the serpin superfamily. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] Oxidants: Oxidizing agents or electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (oxidation-reduction). In vivo, it appears that phagocyte-generated oxidants function as tumor promoters or cocarcinogens rather than as complete carcinogens perhaps because of the high levels of endogenous antioxidant defenses. It is also thought that oxidative damage in joints may trigger the autoimmune response that characterizes the persistence of the rheumatoid disease process. [NIH]
Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]
Oxidation-Reduction: A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471). [NIH] Oxidative Phosphorylation: Electron transfer through the cytochrome system liberating free energy which is transformed into high-energy phosphate bonds. [NIH] Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] Oxygen Consumption: The oxygen consumption is determined by calculating the difference between the amount of oxygen inhaled and exhaled. [NIH] Oxygenation: The process of supplying, treating, or mixing with oxygen. No:1245 oxygenation the process of supplying, treating, or mixing with oxygen. [EU] Oxygenator: An apparatus by which oxygen is introduced into the blood during circulation outside the body, as during open heart surgery. [NIH]
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Pacemaker: An object or substance that influences the rate at which a certain phenomenon occurs; often used alone to indicate the natural cardiac pacemaker or an artificial cardiac pacemaker. In biochemistry, a substance whose rate of reaction sets the pace for a series of interrelated reactions. [EU] Pachymeningitis: Inflammation of the dura mater of the brain, the spinal cord or the optic nerve. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Pancreas Transplant: A surgical procedure that involves replacing the pancreas of a person who has diabetes with a healthy pancreas that can make insulin. The healthy pancreas comes from a donor who has just died or from a living relative. A person can donate half a pancreas and still live normally. [NIH] Pancreatic: Having to do with the pancreas. [NIH] Pancreatitis: Acute or chronic inflammation of the pancreas, which may be asymptomatic or symptomatic, and which is due to autodigestion of a pancreatic tissue by its own enzymes. It is caused most often by alcoholism or biliary tract disease; less commonly it may be associated with hyperlipaemia, hyperparathyroidism, abdominal trauma (accidental or operative injury), vasculitis, or uraemia. [EU] Papio: A genus of the subfamily Cercopithecinae, family Cercopithecidae, consisting of seven named species: P. ursinus (chacma baboon), P. cynocephalus (yellow baboon), P. papio (western or Guinea baboon), P. anubis (anubis or olive baboon), P. hamadryas (hamadryas or sacred baboon), P. sphinx (mandrill), and P. leucophaeus (drill). Some authors have recognized a separate genus for the drill and mandrill: Mandrillus. The Papio genus is geographically distributed throughout east and west Africa, Arabia, Egypt, and the Sudan. [NIH] Paralysis: Loss of ability to move all or part of the body. [NIH] Parasite: An animal or a plant that lives on or in an organism of another species and gets at least some of its nutrition from that other organism. [NIH] Parasitic: Having to do with or being a parasite. A parasite is an animal or a plant that lives on or in an organism of another species and gets at least some of its nutrients from it. [NIH] Parasitism: A) The mode of life of a parasite; b) The relationship between an organism (parasite) that derives benefits from, and at the expense of, another organism (host). [NIH] Parkinsonism: A group of neurological disorders characterized by hypokinesia, tremor, and muscular rigidity. [EU] Parotid: The space that contains the parotid gland, the facial nerve, the external carotid artery, and the retromandibular vein. [NIH] 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] Parvovirus: A genus of the family Parvoviridae, subfamily Parvovirinae, infecting a variety of vertebrates including humans. Parvoviruses are responsible for a number of important diseases but also can be non-pathogenic in certain hosts. The type species is mice minute virus. [NIH]
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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 tissues and organs. [NIH] Pentamidine: Antiprotozoal agent effective in trypanosomiasis, leishmaniasis, and some fungal infections; used in treatment of Pneumocystis carinii pneumonia in HIV-infected patients. It may cause diabetes mellitus, central nervous system damage, and other toxic effects. [NIH] Pentoxifylline: A methylxanthine derivative that inhibits phosphodiesterase and affects blood rheology. It improves blood flow by increasing erythrocyte and leukocyte flexibility. It also inhibits platelet aggregation. Pentoxifylline modulates immunologic activity by stimulating cytokine production. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Percutaneous: Performed through the skin, as injection of radiopacque material in radiological examination, or the removal of tissue for biopsy accomplished by a needle. [EU] Perfusion: Bathing an organ or tissue with a fluid. In regional perfusion, a specific area of the body (usually an arm or a leg) receives high doses of anticancer drugs through a blood vessel. Such a procedure is performed to treat cancer that has not spread. [NIH] Pericarditis: Inflammation of the pericardium. [EU] Perinatal: Pertaining to or occurring in the period shortly before and after birth; variously defined as beginning with completion of the twentieth to twenty-eighth week of gestation and ending 7 to 28 days after birth. [EU] Peripheral blood: Blood circulating throughout the body. [NIH] Perivascular: Situated around a vessel. [EU] Phagocyte: An immune system cell that can surround and kill microorganisms and remove dead cells. Phagocytes include macrophages. [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] Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phenytoin: An anticonvulsant that is used in a wide variety of seizures. It is also an antiarrhythmic and a muscle relaxant. The mechanism of therapeutic action is not clear, although several cellular actions have been described including effects on ion channels, active transport, and general membrane stabilization. The mechanism of its muscle relaxant effect appears to involve a reduction in the sensitivity of muscle spindles to stretch.
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Phenytoin has been proposed for several other therapeutic uses, but its use has been limited by its many adverse effects and interactions with other drugs. [NIH] Phosphodiesterase: Effector enzyme that regulates the levels of a second messenger, the cyclic GMP. [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Physical Examination: Systematic and thorough inspection of the patient for physical signs of disease or abnormality. [NIH] Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]
Physiology: The science that deals with the life processes and functions of organismus, their cells, tissues, and organs. [NIH] Picornavirus: Any of a group of tiny RNA-containing viruses including the enteroviruses and rhinoviruses. [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] Plaque Assay: Method for measuring viral infectivity and multiplication in cultured cells. Clear lysed areas or plaques develop as the viral particles are released from the infected cells during incubation. With some viruses, the cells are killed by a cytopathic effect; with others, the infected cells are not killed but can be detected by their hemadsorptive ability. Sometimes the plaque cells contain viral antigens which can be measured by immunofluorescence. [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] Plasmid: An autonomously replicating, extra-chromosomal DNA molecule found in many bacteria. Plasmids are widely used as carriers of cloned genes. [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]
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Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Pneumonia: Inflammation of the lungs. [NIH] 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] Poliomyelitis: An acute viral disease, occurring sporadically and in epidemics, and characterized clinically by fever, sore throat, headache, and vomiting, often with stiffness of the neck and back. In the minor illness these may be the only symptoms. The major illness, which may or may not be preceded by the minor illness, is characterized by involvement of the central nervous system, stiff neck, pleocytosis in the spinal fluid, and perhaps paralysis. There may be subsequent atrophy of groups of muscles, ending in contraction and permanent deformity. The major illness is called acute anterior p., infantile paralysis and Heine-Medin disease. The disease is now largely controlled by vaccines. [EU] Polymerase: An enzyme which catalyses the synthesis of DNA using a single DNA strand as a template. The polymerase copies the template in the 5'-3'direction provided that sufficient quantities of free nucleotides, dATP and dTTP are present. [NIH] Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships. [NIH] Polymorphic: Occurring in several or many forms; appearing in different forms at different stages of development. [EU] Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called tripeptides, tetrapeptides, etc. according to the number of amino acids contained. [EU] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] 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] Post-translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [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] 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
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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] Precordial: Pertaining to the precordium (= region over the heart and lower part of the thorax). [EU] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] 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] 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] 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] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Prostaglandins: A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes. [NIH] 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] 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 and VIIIa at the rate-limiting steps of thrombin formation. [NIH]
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Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. Quaternary protein structure describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain). [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] 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] 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] Protozoal: Having to do with the simplest organisms in the animal kingdom. Protozoa are single-cell organisms, such as ameba, and are different from bacteria, which are not members of the animal kingdom. Some protozoa can be seen without a microscope. [NIH] Protozoan: 1. Any individual of the protozoa; protozoon. 2. Of or pertaining to the protozoa; protozoal. [EU] Psychology: The science dealing with the study of mental processes and behavior in man and animals. [NIH] Psychosis: A mental disorder characterized by gross impairment in reality testing as evidenced by delusions, hallucinations, markedly incoherent speech, or disorganized and agitated behaviour without apparent awareness on the part of the patient of the incomprehensibility of his behaviour; the term is also used in a more general sense to refer to mental disorders in which mental functioning is sufficiently impaired as to interfere grossly with the patient's capacity to meet the ordinary demands of life. Historically, the term has been applied to many conditions, e.g. manic-depressive psychosis, that were first described in psychotic patients, although many patients with the disorder are not judged psychotic. [EU] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]
Pulmonary: Relating to the lungs. [NIH] Pulmonary 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
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pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Pupil: The aperture in the iris through which light passes. [NIH] Quiescent: Marked by a state of inactivity or repose. [EU] 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] Radioactive: Giving off radiation. [NIH] Radiological: Pertaining to radiodiagnostic and radiotherapeutic procedures, and interventional radiology or other planning and guiding medical radiology. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Rarefaction: The reduction of the density of a substance; the attenuation of a gas. [NIH] 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] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Refractory: Not readily yielding to treatment. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Relative risk: The ratio of the incidence rate of a disease among individuals exposed to a specific risk factor to the incidence rate among unexposed individuals; synonymous with risk ratio. Alternatively, the ratio of the cumulative incidence rate in the exposed to the cumulative incidence rate in the unexposed (cumulative incidence ratio). The term relative risk has also been used synonymously with odds ratio. This is because the odds ratio and relative risk approach each other if the disease is rare ( 5 percent of population) and the number of subjects is large. [NIH] Remission: A decrease in or disappearance of signs and symptoms of cancer. In partial remission, some, but not all, signs and symptoms of cancer have disappeared. In complete remission, all signs and symptoms of cancer have disappeared, although there still may be cancer in the body. [NIH] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and
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progressive renal glomerular tubular or interstitial disease. [NIH] Renin: An enzyme which is secreted by the kidney and is formed from prorenin in plasma and kidney. The enzyme cleaves the Leu-Leu bond in angiotensinogen to generate angiotensin I. EC 3.4.23.15. (Formerly EC 3.4.99.19). [NIH] Renin-Angiotensin System: A system consisting of renin, angiotensin-converting enzyme, and angiotensin II. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming angiotensin I. The converting enzyme contained in the lung acts on angiotensin I in the plasma converting it to angiotensin II, the most powerful directly pressor substance known. It causes contraction of the arteriolar smooth muscle and has other indirect actions mediated through the adrenal cortex. [NIH] Reperfusion: Restoration of blood supply to tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. It is primarily a procedure for treating infarction or other ischemia, by enabling viable ischemic tissue to recover, thus limiting further necrosis. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing reperfusion injury. [NIH] Reperfusion Injury: Functional, metabolic, or structural changes, including necrosis, in ischemic tissues thought to result from reperfusion to ischemic areas of the tissue. The most common instance is myocardial reperfusion injury. [NIH] 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 Burst: A large increase in oxygen uptake by neutrophils and most types of tissue macrophages through activation of an NADPH-cytochrome b-dependent oxidase that reduces oxygen to a superoxide. Individuals with an inherited defect in which the oxidase that reduces oxygen to superoxide is decreased or absent (granulomatous disease, chronic) often die as a result of recurrent bacterial infections. [NIH] Respiratory failure: Inability of the lungs to conduct gas exchange. [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] 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] Retrovirus: A member of a group of RNA viruses, the RNA of which is copied during viral replication into DNA by reverse transcriptase. The viral DNA is then able to be integrated into the host chromosomal DNA. [NIH] Rhabdomyolysis: Necrosis or disintegration of skeletal muscle often followed by myoglobinuria. [NIH] Rheology: The study of the deformation and flow of matter, usually liquids or fluids, and of the plastic flow of solids. The concept covers consistency, dilatancy, liquefaction, resistance to flow, shearing, thixotrophy, and viscosity. [NIH] 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]
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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] Rhinovirus: A genus of Picornaviridae inhabiting primarily the respiratory tract of mammalian hosts. It includes the human strains associated with common colds. [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] Risperidone: A selective blocker of dopamine D2 and serotonin-5-HT-2 receptors that acts as an atypical antipsychotic agent. It has been shown to improve both positive and negative symptoms in the treatment of schizophrenia. [NIH] Rod: A reception for vision, located in the retina. [NIH] Rotavirus: A genus of Reoviridae, causing acute gastroenteritis in birds and mammals, including humans. Transmission is horizontal and by environmental contamination. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] Sarcoidosis: An idiopathic systemic inflammatory granulomatous disorder comprised of epithelioid and multinucleated giant cells with little necrosis. It usually invades the lungs with fibrosis and may also involve lymph nodes, skin, liver, spleen, eyes, phalangeal bones, and parotid glands. [NIH] Sarcoma: A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant. [NIH] Sarcomere: The repeating structural unit of a striated muscle fiber. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [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] Scrub Typhus: An acute infectious disease caused by Orientia tsutsugamushi. It is limited to
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eastern and southeastern Asia, India, northern Australia, and the adjacent islands. Characteristics include the formation of a primary cutaneous lesion at the site of the bite of an infected mite, fever lasting about two weeks, and a maculopapular rash. [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] Sedentary: 1. Sitting habitually; of inactive habits. 2. Pertaining to a sitting posture. [EU] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Selenium: An element with the atomic symbol Se, atomic number 34, and atomic weight 78.96. It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of glutathione peroxidase. [NIH] Sensitization: 1. Administration of antigen to induce a primary immune response; priming; immunization. 2. Exposure to allergen that results in the development of hypersensitivity. 3. The coating of erythrocytes with antibody so that they are subject to lysis by complement in the presence of homologous antigen, the first stage of a complement fixation test. [EU] 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] Sepsis: The presence of bacteria in the bloodstream. [NIH] Septic: Produced by or due to decomposition by microorganisms; putrefactive. [EU] Septicaemia: A term originally used to denote a putrefactive process in the body, but now usually referring to infection with pyogenic micro-organisms; a genus of Diptera; the severe type of infection in which the blood stream is invaded by large numbers of the causal. [NIH] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [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] Serotypes: A cause of haemorrhagic septicaemia (in cattle, sheep and pigs), fowl cholera of birds, pasteurellosis of rabbits, and gangrenous mastitis of ewes. It is also commonly found in atrophic rhinitis of pigs. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock. [NIH]
Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the
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one sought to be benefited by its administration. [EU] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smallpox: A generalized virus infection with a vesicular rash. [NIH] Smoke Inhalation Injury: Pulmonary injury following the breathing in of toxic smoke from burning materials such as plastics, synthetics, building materials, etc. This injury is the most frequent cause of death in burn patients. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]
Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectrin: A high molecular weight (220-250 kDa) water-soluble protein which can be extracted from erythrocyte ghosts in low ionic strength buffers. The protein contains no lipids or carbohydrates, is the predominant species of peripheral erythrocyte membrane proteins, and exists as a fibrous coating on the inner, cytoplasmic surface of the membrane. [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]
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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] 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] Splenomegaly: Enlargement of the spleen. [NIH] Stabilization: The creation of a stable state. [EU] Steady state: Dynamic equilibrium. [EU] Sterile: Unable to produce children. [NIH] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Steroid therapy: Treatment with corticosteroid drugs to reduce swelling, pain, and other symptoms of inflammation. [NIH] Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [NIH] Streptococcal: Caused by infection due to any species of streptococcus. [NIH] Streptococci: A genus of spherical Gram-positive bacteria occurring in chains or pairs. They are widely distributed in nature, being important pathogens but often found as normal commensals in the mouth, skin, and intestine of humans and other animals. [NIH] Streptococcus: A genus of gram-positive, coccoid bacteria whose organisms occur in pairs or chains. No endospores are produced. Many species exist as commensals or parasites on man or animals with some being highly pathogenic. A few species are saprophytes and occur in the natural environment. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH]
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Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substrate: A substance upon which an enzyme acts. [EU] Sudden death: Cardiac arrest caused by an irregular heartbeat. The term "death" is somewhat misleading, because some patients survive. [NIH] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Superoxide Dismutase: An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC 1.15.1.1. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Sympathetic Nervous System: The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Synapse: The region where the processes of two neurons come into close contiguity, and the nervous impulse passes from one to the other; the fibers of the two are intermeshed, but, according to the general view, there is no direct contiguity. [NIH] 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] Systemic: Affecting the entire body. [NIH] Systemic disease: Disease that affects the whole body. [NIH] Systemic lupus erythematosus: SLE. A chronic inflammatory connective tissue disease marked by skin rashes, joint pain and swelling, inflammation of the kidneys, inflammation of the fibrous tissue surrounding the heart (i.e., the pericardium), as well as other problems. Not all affected individuals display all of these problems. May be referred to as lupus. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Tachycardia: Excessive rapidity in the action of the heart, usually with a heart rate above 100 beats per minute. [NIH] Tamponade: The inserting of a tampon; a dressing is inserted firmly into a wound or body cavity, as the nose, uterus or vagina, principally for stopping hemorrhage. [NIH] Tardive: Marked by lateness, late; said of a disease in which the characteristic lesion is late in appearing. [EU] 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] Tetani: Causal agent of tetanus. [NIH] Tetanic: Having the characteristics of, or relating to tetanus. [NIH] Tetanus: A disease caused by tetanospasmin, a powerful protein toxin produced by
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Clostridium tetani. Tetanus usually occurs after an acute injury, such as a puncture wound or laceration. Generalized tetanus, the most common form, is characterized by tetanic muscular contractions and hyperreflexia. Localized tetanus presents itself as a mild condition with manifestations restricted to muscles near the wound. It may progress to the generalized form. [NIH] Tetracycline: An antibiotic originally produced by Streptomyces viridifaciens, but used mostly in synthetic form. It is an inhibitor of aminoacyl-tRNA binding during protein synthesis. [NIH] 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] Thioredoxin: A hydrogen-carrying protein that participates in a variety of biochemical reactions including ribonucleotide reduction. Thioredoxin is oxidized from a dithiol to a disulfide during ribonucleotide reduction. The disulfide form is then reduced by NADPH in a reaction catalyzed by thioredoxin reductase. [NIH] Thorax: A part of the trunk between the neck and the abdomen; the chest. [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] Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation. [NIH]
Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] 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] Thymoma: A tumor of the thymus, an organ that is part of the lymphatic system and is located in the chest, behind the breastbone. [NIH] 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] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Culture: Maintaining or growing of tissue, organ primordia, or the whole or part of an organ in vitro so as to preserve its architecture and/or function (Dorland, 28th ed). Tissue culture includes both organ culture and cell culture. [NIH] 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]
Dictionary 193
Tone: 1. The normal degree of vigour and tension; in muscle, the resistance to passive elongation or stretch; tonus. 2. A particular quality of sound or of voice. 3. To make permanent, or to change, the colour of silver stain by chemical treatment, usually with a heavy metal. [EU] Tonus: A state of slight tension usually present in muscles even when they are not undergoing active contraction. [NIH] 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] Toxin: A poison; frequently used to refer specifically to a protein produced by some higher plants, certain animals, and pathogenic bacteria, which is highly toxic for other living organisms. Such substances are differentiated from the simple chemical poisons and the vegetable alkaloids by their high molecular weight and antigenicity. [EU] Toxoplasma: A genus of protozoa parasitic to birds and mammals. T. gondii is one of the most common infectious pathogenic animal parasites of man. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [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] Translating: Conversion from one language to another language. [NIH] Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Transplantation: Transference of a tissue or organ, alive or dead, within an individual, between individuals of the same species, or between individuals of different species. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH]
194
Myocarditis
Trigger zone: Dolorogenic zone (= producing or causing pain). [EU] Tropism: Directed movements and orientations found in plants, such as the turning of the sunflower to face the sun. [NIH] Tropomyosin: A protein found in the thin filaments of muscle fibers. It inhibits contraction of the muscle unless its position is modified by troponin. [NIH] Troponin: One of the minor protein components of skeletal muscle. Its function is to serve as the calcium-binding component in the troponin-tropomyosin B-actin-myosin complex by conferring calcium sensitivity to the cross-linked actin and myosin filaments. [NIH] Trypanosomiasis: Infection with protozoa of the genus Trypanosoma. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [NIH] Tubocurarine: A neuromuscular blocker and active ingredient in curare; plant based alkaloid of Menispermaceae. [NIH] Tumor Necrosis Factor: Serum glycoprotein produced by activated macrophages and other mammalian mononuclear leukocytes which has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. It mimics the action of endotoxin but differs from it. It has a molecular weight of less than 70,000 kDa. [NIH] Tumour: 1. Swelling, one of the cardinal signs of inflammations; morbid enlargement. 2. A new growth of tissue in which the multiplication of cells is uncontrolled and progressive; called also neoplasm. [EU] Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] 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] Ultrasonography: The visualization of deep structures of the body by recording the reflections of echoes of pulses of ultrasonic waves directed into the tissues. Use of ultrasound for imaging or diagnostic purposes employs frequencies ranging from 1.6 to 10 megahertz. [NIH] Uraemia: 1. An excess in the blood of urea, creatinine, and other nitrogenous end products of protein and amino acids metabolism; more correctly referred to as azotemia. 2. In current usage the entire constellation of signs and symptoms of chronic renal failure, including nausea, vomiting anorexia, a metallic taste in the mouth, a uraemic odour of the breath, pruritus, uraemic frost on the skin, neuromuscular disorders, pain and twitching in the muscles, hypertension, edema, mental confusion, and acid-base and electrolyte imbalances. [EU]
Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [NIH] 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] 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]
Dictionary 195
Uterine Contraction: Contraction of the uterine muscle. [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] Vaccination: Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis. [NIH] Vaccines: Suspensions of killed or attenuated microorganisms (bacteria, viruses, fungi, protozoa, or rickettsiae), antigenic proteins derived from them, or synthetic constructs, administered for the prevention, amelioration, or treatment of infectious and other diseases. [NIH]
Vaccinia: The cutaneous and occasional systemic reactions associated with vaccination using smallpox (variola) vaccine. [NIH] Vaccinia Virus: The type species of Orthopoxvirus, related to cowpox virus, but whose true origin is unknown. It has been used as a live vaccine against smallpox. It is also used as a vector for inserting foreign DNA into animals. Rabbitpox virus is a subspecies of vaccinia virus. [NIH] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Varicella: Chicken pox. [EU] Variola: A generalized virus infection with a vesicular rash. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasculitis: Inflammation of a blood vessel. [NIH] Vasodilators: Any nerve or agent which induces dilatation of the 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] Venom: That produced by the poison glands of the mouth and injected by the fangs of poisonous snakes. [NIH] Venous: Of or pertaining to the veins. [EU] 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] Ventricular Dysfunction: A condition in which the ventricles of the heart exhibit a decreased functionality. [NIH] Ventricular fibrillation: Rapid, irregular quivering of the heart's ventricles, with no effective heartbeat. [NIH] Ventricular Function: The hemodynamic and electrophysiological action of the ventricles. [NIH]
Ventricular Remodeling: The geometric and structural changes that the ventricle undergoes, usually following myocardial infarction. It comprises expansion of the infarct and dilatation of the healthy ventricle segments. While most prevalent in the left ventricle, it can also occur in the right ventricle. [NIH] Vesicular: 1. Composed of or relating to small, saclike bodies. 2. Pertaining to or made up of vesicles on the skin. [EU]
196
Myocarditis
Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Viral Load: The quantity of measurable virus in the blood. Change in viral load, measured in plasma, is used as a surrogate marker in HIV disease progression. [NIH] Viral Proteins: Proteins found in any species of virus. [NIH] Virion: The infective system of a virus, composed of the viral genome, a protein core, and a protein coat called a capsid, which may be naked or enclosed in a lipoprotein envelope called the peplos. [NIH] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virulent: A virus or bacteriophage capable only of lytic growth, as opposed to temperate phages establishing the lysogenic response. [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] Virus Diseases: A general term for diseases produced by viruses. [NIH] Virus Replication: The process of intracellular viral multiplication, consisting of the synthesis of proteins, nucleic acids, and sometimes lipids, and their assembly into a new infectious particle. [NIH] Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Visceral Larva Migrans: Infestation of the dermis by various larvae, characterized by bizarre red irregular lines which are broad at one end and fade at the other, produced by burrowing larvae. [NIH] Viscosity: A physical property of fluids that determines the internal resistance to shear forces. [EU] Vitiligo: A disorder consisting of areas of macular depigmentation, commonly on extensor aspects of extremities, on the face or neck, and in skin folds. Age of onset is often in young adulthood and the condition tends to progress gradually with lesions enlarging and extending until a quiescent state is reached. [NIH] 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] Voriconazole: A drug that treats infections caused by fungi. [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] 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'
Dictionary 197
and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [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] Zymogen: Inactive form of an enzyme which can then be converted to the active form, usually by excision of a polypeptide, e. g. trypsinogen is the zymogen of trypsin. [NIH]
199
INDEX A Abdominal, 139, 162, 179, 194 Abdominal Pain, 139, 162, 194 Abortion, 100, 103, 139 Acceptor, 139, 171, 178 Acetylcholine, 139, 150, 176, 177 Acetylcholinesterase, 101, 139 Acetylcysteine, 69, 139 Acquired Immunodeficiency Syndrome, 32, 54, 73, 139 Actin, 25, 34, 139, 173, 174, 175, 194 Actinin, 139, 157 Acute lymphoblastic leukemia, 50, 75, 139 Acute lymphocytic leukemia, 139 Acute renal, 40, 87, 139 Adaptability, 140, 149 Adenine, 14, 77, 140 Adenovirus, 6, 40, 41, 47, 140 Adjunctive Therapy, 21, 140 Adoptive Transfer, 4, 22, 140 Adrenal Cortex, 140, 141, 154, 183, 186 Adrenal Medulla, 140, 148, 160, 177 Adrenergic, 19, 100, 140, 143, 157, 160 Adverse Effect, 26, 140, 151, 181, 188 Aerobic, 140, 173 Aerospace Medicine, 43, 140 Affinity, 17, 27, 104, 140, 151, 189 Agar, 140, 181 Akathisia, 140, 143 Albumin, 140, 178 Aldosterone, 104, 141 Algorithms, 141, 146 Alkaline, 141, 147 Alkaloid, 141, 151, 194 Allergen, 141, 156, 188 Allo, 5, 141 Allogeneic, 141, 164 Allograft, 29, 61, 141 Alopecia, 141, 154 Alternative medicine, 110, 141 Alveolitis, 30, 141 Amino Acid Sequence, 24, 141, 142, 163 Amphetamines, 141, 151 Anaemia, 101, 141 Anaesthesia, 141, 168 Analogous, 142, 193 Anaphylatoxins, 142, 152 Androgens, 140, 142, 154
Anemia, 142, 150 Aneurysm, 78, 142 Angina, 10, 142 Angiotensinogen, 142, 186 Animal model, 4, 6, 7, 11, 23, 26, 32, 34, 142 Anions, 140, 142, 170, 191 Ankylosis, 102, 142 Annealing, 142, 182 Anorexia, 141, 142, 158, 162, 194 Antagonism, 142, 151 Antiallergic, 50, 142, 154 Antibacterial, 142, 189 Antibiotic, 142, 147, 148, 149, 189, 192 Antibodies, 5, 6, 11, 24, 51, 66, 103, 142, 143, 145, 160, 164, 165, 166, 167, 171, 174, 181 Anticoagulant, 143, 183 Anticonvulsant, 143, 180 Antiemetic, 143 Antigen-Antibody Complex, 143, 152 Antigen-presenting cell, 143, 156 Anti-infective, 143, 166 Anti-inflammatory, 86, 143, 144, 154, 163, 168 Anti-Inflammatory Agents, 143, 144, 154 Antineoplastic, 143, 154, 162 Antioxidant, 11, 30, 143, 178 Antipsychotic, 8, 36, 143, 151, 176, 187 Antiserum, 103, 143, 145 Antiviral, 13, 28, 29, 35, 98, 99, 139, 143, 162, 169 Antiviral Agents, 28, 143 Apoptosis, 4, 5, 11, 17, 19, 20, 25, 31, 41, 46, 144 Aqueous, 144, 155, 166 Arginine, 142, 144, 177 Arrhythmia, 90, 126, 144 Arterial, 27, 144, 163, 166, 184, 191 Arteries, 144, 147, 153, 173, 175, 184 Arterioles, 144, 147 Arteriolosclerosis, 144 Arteriosclerosis, 98, 144, 190 Artery, 27, 45, 58, 59, 98, 142, 144, 147, 153, 158, 179, 184, 186, 195 Articular, 102, 144, 171, 178 Aseptic, 14, 34, 144, 154, 178, 190 Aspirin, 76, 144
200
Myocarditis
Assay, 6, 12, 13, 17, 104, 144 Asymptomatic, 18, 58, 59, 144, 179 Ataxia, 144, 154 Atopic, 5, 144 Atrial, 42, 82, 104, 144, 145 Atrial Natriuretic Factor, 104, 145 Atrioventricular, 45, 50, 70, 75, 76, 145 Atrium, 144, 145, 195 Atrophy, 102, 145, 182 Attenuated, 145, 195 Attenuation, 145, 185 Atypical, 9, 145, 151, 168, 187 Autoantibodies, 18, 21, 24, 44, 86, 145 Autoantigens, 5, 19, 145 Autodigestion, 145, 179 Autoimmune disease, 16, 21, 22, 27, 29, 32, 52, 57, 145, 174, 175 Autoimmunity, 16, 22, 27, 29, 51, 52, 76, 145 Autologous, 77, 145 Autonomic, 139, 143, 145, 175, 177, 191 Autonomic Nervous System, 145, 191 Autopsy, 9, 11, 25, 41, 75, 86, 145 Avidity, 27, 145 Axonal, 35, 145 B Bacteria, 142, 143, 145, 146, 158, 160, 173, 181, 184, 185, 187, 188, 189, 190, 193, 195 Bacterial Infections, 6, 145, 152, 186 Bactericidal, 18, 145, 160 Bacteriophage, 145, 181, 193, 196 Bacterium, 18, 146 Basal Ganglia, 143, 144, 146, 150, 162 Basophils, 146, 171 Benign, 33, 144, 146, 162, 164, 176 Bile, 146, 165, 171, 190 Biliary, 146, 179 Biliary Tract, 146, 179 Biochemical, 11, 20, 24, 28, 34, 35, 42, 146, 163, 170, 178, 188, 192 Biochemical reactions, 146, 192 Bioengineering, 34, 120, 146 Biological Transport, 146, 156 Biopsy, 12, 41, 42, 46, 48, 50, 64, 66, 75, 81, 136, 137, 146, 180 Biopsy specimen, 75, 146 Bioreactors, 34, 146 Biotechnology, 36, 38, 110, 121, 146 Black Widow Spider, 39, 146 Bladder, 146, 150, 168, 174, 194 Blood Coagulation, 146, 147, 192 Blood Glucose, 146, 169
Blood Platelets, 147, 188, 192 Blood pressure, 147, 148, 149, 163, 166, 174, 184, 189 Blood vessel, 147, 148, 149, 159, 170, 171, 180, 189, 190, 192, 195 Blot, 34, 147 Body Burden, 147, 170 Bone Marrow, 73, 139, 147, 163, 167, 171, 172, 174 Bone Marrow Transplantation, 73, 147 Bowel, 147, 169, 194 Bradykinin, 147, 177 Breeding, 23, 100, 147 Broad-spectrum, 147, 148 Bronchitis, 147, 150 Buccal, 147, 171 C Calcification, 87, 144, 147 Calcium, 100, 147, 152, 173, 194 Capsid, 47, 147, 196 Carbohydrate, 148, 154, 163, 164, 182 Carcinogenic, 148, 168, 177, 183, 190 Carcinogens, 148, 178 Carcinoma, 148, 160 Cardiogenic, 24, 44, 61, 81, 148 Cardiomyopathy, Congestive, 10, 148 Cardiopulmonary, 30, 64, 70, 81, 148 Cardiotonic, 148, 156 Cardiovascular, 8, 9, 10, 20, 21, 31, 34, 36, 41, 43, 52, 55, 61, 64, 66, 67, 68, 73, 77, 82, 87, 100, 148, 188 Cardiovascular disease, 20, 34, 148 Cardiovascular System, 11, 21, 148 Case report, 39, 41, 43, 44, 45, 47, 50, 58, 59, 61, 64, 66, 68, 69, 71, 77, 80, 148, 151, 161 Case series, 148, 151 Catecholamine, 19, 53, 148, 157 Catheterization, 137, 148, 170 Causal, 19, 148, 188, 191 Cause of Death, 34, 148, 189 Cefaclor, 60, 148 Cell Adhesion, 7, 72, 149 Cell Cycle, 12, 20, 21, 149, 154 Cell Cycle Proteins, 20, 149 Cell Death, 5, 15, 95, 144, 149, 163, 176 Cell Division, 145, 149, 174, 181, 188 Cell membrane, 146, 149, 181 Cell proliferation, 20, 21, 144, 149, 169 Cell Respiration, 149, 173, 186
201
Central Nervous System, 35, 139, 141, 145, 149, 150, 151, 162, 163, 164, 174, 180, 182, 188 Cephalexin, 148, 149 Cerebrospinal, 104, 149 Cerebrospinal fluid, 104, 149 Cerebrovascular, 148, 149 Cervix, 139, 149 Chagas Disease, 4, 149 Chemokines, 7, 149 Chemoreceptor, 143, 149 Chemotactic Factors, 149, 152 Chemotherapy, 98, 150 Chicken Anemia Virus, 150 Cholera, 150, 188 Cholesterol, 62, 146, 150, 153, 171, 172, 190 Choline, 139, 150 Cholinergic, 143, 150 Cholinesterase Inhibitors, 101, 150 Chorea, 143, 150 Chromatin, 144, 149, 150 Chromosomal, 150, 163, 181, 186 Chromosome, 150, 162, 188 Chronic Disease, 11, 12, 150 Chronic Fatigue Syndrome, 12, 98, 103, 150 Chronic Obstructive Pulmonary Disease, 53, 150 Circovirus, 100, 150 CIS, 14, 17, 150 Clinical Medicine, 151, 183 Clinical study, 54, 151 Clinical trial, 3, 121, 151, 185 Clone, 4, 151 Cloning, 35, 36, 146, 151 Clozapine, 9, 36, 76, 151 Coca, 151 Cocaine, 10, 19, 151 Cofactor, 28, 151, 184, 192 Colitis, 101, 151 Collagen, 34, 101, 141, 151, 161, 181, 183 Collapse, 81, 151 Colon, 151, 170, 194 Common Variable Immunodeficiency, 56, 152 Complement, 24, 26, 29, 30, 101, 110, 142, 152, 163, 172, 188 Complementary and alternative medicine, 89, 93, 152 Complementary medicine, 89, 152 Complementation, 17, 152 Computational Biology, 121, 152
Conception, 139, 152, 161, 190 Concomitant, 17, 54, 152 Congestion, 143, 152 Congestive heart failure, 4, 23, 56, 91, 148, 152 Conjunctiva, 153, 168 Conjunctivitis, 14, 153, 154 Connective Tissue, 101, 147, 151, 153, 156, 161, 162, 163, 171, 186, 187, 191 Connective Tissue Cells, 153 Consciousness, 153, 155, 156, 157 Constipation, 143, 153 Constitutional, 153, 175 Constriction, 153, 170 Contamination, 153, 165, 187 Contractile Proteins, 4, 153 Contractility, 27, 99, 153 Contraindications, ii, 153 Contrast medium, 153 Coordination, 153, 174 Cornea, 153, 197 Coronary, 23, 27, 31, 45, 58, 59, 71, 98, 148, 153, 173, 175 Coronary Angiography, 71, 153 Coronary heart disease, 23, 148, 153 Coronary Thrombosis, 98, 153, 173, 175 Cortex, 144, 153 Corticosteroid, 53, 154, 183, 190 Cowpox, 26, 154, 195 Cowpox Virus, 26, 154, 195 Coxsackie virus, 7, 24, 63, 69, 73, 86, 154 Coxsackieviruses, 11, 12, 13, 154 Coxsackieviruses A, 13, 154 Crossing-over, 154, 185 Cultured cells, 21, 154, 181 Curative, 154, 192 Cutaneous, 154, 170, 171, 188, 195 Cyclic, 154, 164, 177, 181 Cyclin, 21, 149, 154 Cyclin-Dependent Kinases, 149, 154 Cyclophosphamide, 53, 63, 114, 154 Cysteine, 139, 149, 154 Cytochrome, 154, 155, 178, 186 Cytochrome b, 155, 186 Cytokine, 6, 12, 15, 23, 25, 26, 50, 59, 60, 155, 180 Cytomegalovirus, 37, 99, 155 Cytoplasm, 144, 146, 149, 153, 155, 159, 174, 175, 187 Cytoskeletal Proteins, 4, 149, 155, 157 Cytoskeleton, 32, 155, 173 Cytotoxic, 4, 9, 57, 155, 167
202
Myocarditis
Cytotoxicity, 70, 102, 155 D Degenerative, 155, 165, 178 Deletion, 27, 144, 155 Delirium, 143, 155 Dementia, 139, 143, 155 Denaturation, 156, 182 Dendrites, 156, 176 Dendritic, 31, 39, 44, 54, 156 Dendritic cell, 31, 39, 44, 54, 156 Density, 156, 171, 185 Depigmentation, 156, 196 Deprivation, 80, 156 Dermatitis, 5, 150, 156 Dermis, 156, 196 Desensitization, 156, 167 Detoxification, 14, 156 Deuterium, 156, 166 Device Removal, 67, 156 Diabetes Mellitus, 59, 103, 156, 163, 180 Diagnostic procedure, 97, 110, 156 Diarrhea, 156, 158 Diastole, 156 Diastolic, 12, 25, 156, 166 Diffusion, 25, 146, 156, 168 Digestion, 146, 147, 156, 169, 171, 190 Digitalis, 100, 156 Dilation, 4, 147, 156 Diploid, 152, 156, 181 Direct, iii, 5, 14, 17, 26, 27, 33, 95, 99, 102, 113, 151, 156, 157, 185, 191 Discrete, 156, 197 Disease Susceptibility, 16, 157 Disinfectant, 157, 160 Dissociation, 75, 140, 157 Dissociative Disorders, 157 Distal, 14, 145, 157, 183 Dominance, 15, 157 Dopamine, 143, 151, 157, 176, 180, 187 Drug Hypersensitivity, 55, 157 Drug Interactions, 115, 157 Drug Tolerance, 157, 192 Duct, 148, 157, 160, 172, 187 Dura mater, 157, 173, 179 Dyskinesia, 143, 157 Dyspnea, 57, 157 Dystrophin, 32, 49, 157, 175 Dystrophy, 157, 158 E Echocardiography, 11, 49, 75, 158 Echoviruses, 34, 158 Edema, 135, 136, 158, 194
Effector, 4, 18, 22, 23, 24, 31, 139, 152, 158, 176, 181 Effector cell, 4, 18, 22, 158, 176 Efficacy, 5, 25, 35, 50, 158 Ehrlichiosis, 18, 158 Elasticity, 144, 158 Elastin, 151, 158 Electrolyte, 23, 141, 154, 155, 158, 173, 182, 189, 194 Electrons, 143, 158, 170, 178, 185 Electrophysiological, 86, 89, 158, 195 Emaciation, 139, 158 Embolus, 158, 168 Embryo, 139, 158, 168 Embryology, 158, 161 Emphysema, 150, 158 Encephalitis, 5, 16, 17, 20, 35, 50, 83, 154, 158, 159 Encephalitis, Viral, 158, 159 Endemic, 4, 149, 150, 159 Endocarditis, 72, 101, 159 Endocardium, 159 Endogenous, 21, 99, 145, 157, 159, 178, 193 Endothelial cell, 17, 27, 53, 159, 192 Endothelium, 159, 177 Endothelium-derived, 159, 177 Endotoxins, 152, 159 Enterovirus, 13, 14, 37, 41, 47, 49, 51, 77, 109, 154, 159 Environmental Exposure, 103, 159 Environmental Health, 69, 120, 122, 159 Enzymatic, 141, 147, 152, 154, 159, 165, 173, 182 Enzyme Inhibitors, 41, 159 Eosinophil, 44, 76, 159 Eosinophilic, 40, 42, 44, 47, 50, 51, 61, 76, 79, 80, 159 Epidemics, 159, 182 Epidemiological, 103, 159, 161 Epigastric, 160, 179 Epinephrine, 140, 157, 160, 176, 177, 194 Epithelial, 6, 146, 160, 165 Epithelial Cells, 6, 160, 165 Epithelium, 159, 160, 197 Epitope, 6, 7, 46, 86, 100, 160 Epitope Mapping, 86, 160 Epstein-Barr virus, 74, 160, 168 Erythrocytes, 141, 142, 147, 160, 188 Ethanol, 14, 160 Eukaryotic Cells, 35, 155, 160, 177, 178 Exocrine, 160, 179 Exogenous, 159, 160, 162
203
Extensor, 160, 196 Extracellular, 7, 104, 153, 160, 161, 189 Extracellular Matrix, 153, 160, 161 Extracorporeal, 52, 81, 160 Extracorporeal Membrane Oxygenation, 81, 160 Extrapyramidal, 140, 143, 157, 160 Eye Infections, 140, 160 F Family Planning, 121, 161 Fat, 147, 153, 154, 158, 161, 163, 171, 174, 186, 189 Fatal Outcome, 49, 161 Fatigue, 98, 150, 161, 164 Fetal Heart, 18, 161 Fetus, 60, 139, 161, 167, 195 Fibrillation, 161 Fibroblasts, 21, 24, 153, 161, 169 Fibrosis, 74, 161, 187 Fixation, 142, 161, 188 Flaccid, 14, 161 Fluorescence, 12, 28, 161 Free Radicals, 143, 157, 161 Fungi, 160, 161, 173, 195, 196 G Galanthamine, 101, 162 Gamma-interferon, 89, 162, 169 Ganglia, 139, 162, 176, 191 Ganglion, 162, 197 Gangrenous, 162, 188 Gas, 156, 162, 166, 177, 185, 186 Gastrin, 162, 165 Gastroenteritis, 162, 187 Gastrointestinal, 34, 147, 150, 160, 162, 188 Gastrointestinal tract, 150, 160, 162, 188 Gene, 4, 7, 15, 23, 24, 26, 32, 35, 38, 40, 41, 47, 61, 102, 140, 146, 157, 162, 163, 165, 188 Gene Amplification, 47, 162 Gene Expression, 15, 23, 26, 162 Gene Targeting, 7, 162 Gene Therapy, 40, 140, 162 Genetic Code, 163, 177 Genetic Engineering, 146, 151, 163 Genetic Techniques, 16, 163 Genetic testing, 163, 182 Genetics, 35, 41, 157, 163 Genotype, 33, 163, 180 Gestation, 100, 163, 180 Giant Cells, 57, 163, 187 Gland, 140, 163, 171, 172, 179, 181, 188, 190, 192
Glomerular, 163, 186 Glucocorticoids, 140, 154, 163 Glucose, 9, 146, 156, 163, 164, 169, 187 Glucose Intolerance, 156, 163 Glutathione Peroxidase, 15, 163, 188 Glycerol, 164, 181 Glycerophospholipids, 164, 181 Glycine, 141, 164, 176 Glycolysis, 27, 164 Glycoprotein, 6, 8, 163, 164, 174, 192, 194 Gonadal, 164, 190 Governing Board, 164, 183 Graft, 5, 29, 164, 167 Graft Rejection, 5, 29, 164, 167 Grafting, 164, 167 Granule, 164, 187 Gravis, 39, 63, 103, 164 Guanine, 61, 164 Guanylate Cyclase, 164, 177 H Habitat, 164, 176 Haemorrhage, 139, 164 Haptens, 5, 140, 164 Headache, 158, 164, 168, 182 Heart attack, 137, 148, 164 Heart failure, 10, 11, 21, 29, 49, 64, 71, 99, 164 Heart Transplantation, 13, 29, 41, 51, 56, 57, 58, 61, 67, 77, 81, 126, 164 Heartbeat, 136, 165, 191, 195 Hemorrhage, 164, 165, 190, 191 Hepatitis, 16, 28, 35, 59, 65, 66, 71, 99, 165, 168 Hepatitis A, 28, 165 Hepatocytes, 35, 165 Hepatomegaly, 136, 165, 168 Hepatovirus, 165 Heredity, 101, 162, 163, 165 Heterogeneity, 140, 165 Heterozygotes, 157, 165 Histamine, 142, 143, 165, 166 Histology, 12, 23, 31, 68, 165 Homeostasis, 23, 165 Homologous, 103, 154, 162, 163, 165, 174, 188 Homotypic, 7, 165 Homozygotes, 157, 165 Hormonal, 37, 145, 154, 165 Hormone, 58, 141, 154, 160, 162, 165, 169, 183, 187, 192 Humoral, 19, 73, 164, 165 Humour, 165
204
Myocarditis
Hybrid, 20, 151, 165 Hybridomas, 165, 169 Hydrogen, 15, 139, 148, 156, 163, 165, 166, 171, 174, 178, 184, 191, 192 Hydrogen Peroxide, 15, 163, 166, 171, 191 Hydrolysis, 139, 166, 182, 184 Hydrophobic, 10, 164, 166, 171 Hydroxylysine, 151, 166 Hydroxyproline, 141, 151, 166 Hyperaemia, 153, 166 Hyperlipidemia, 9, 166 Hyperplasia, 17, 166 Hyperreflexia, 166, 192 Hypersensitivity, 4, 60, 61, 64, 76, 86, 90, 141, 156, 159, 166, 187, 188 Hypersensitivity, Immediate, 166 Hypertension, 23, 144, 148, 164, 166, 194 Hypertrophic cardiomyopathy, 14, 166 Hypertrophy, 4, 166 Hypogammaglobulinemia, 152, 166 Hypotension, 18, 143, 166 I Idiopathic, 13, 34, 39, 50, 52, 55, 60, 61, 66, 79, 90, 110, 166, 187 Immune Sera, 166, 167 Immune system, 24, 30, 143, 145, 158, 166, 167, 171, 172, 174, 180, 196 Immune Tolerance, 27, 166 Immunization, 6, 24, 140, 167, 188 Immunochemistry, 160, 167 Immunodeficiency, 17, 19, 30, 139, 152, 166, 167 Immunodeficiency syndrome, 152, 167 Immunofluorescence, 167, 181 Immunogen, 100, 167 Immunoglobulin, 40, 54, 59, 77, 78, 142, 167, 174 Immunohistochemistry, 34, 47, 70, 167 Immunologic, 62, 86, 140, 150, 167, 180 Immunology, 3, 5, 6, 39, 46, 47, 49, 52, 62, 71, 77, 79, 86, 91, 140, 167 Immunosuppression, 20, 59, 62, 150, 167, 172, 178 Immunosuppressive, 5, 29, 56, 62, 65, 154, 167 Immunosuppressive Agents, 167 Immunosuppressive therapy, 5, 56, 62, 65, 167 Immunotherapy, 32, 110, 140, 156, 167 Implantation, 45, 87, 152, 167 In vitro, 4, 5, 10, 16, 21, 22, 23, 25, 30, 34, 35, 71, 163, 167, 182, 192
In vivo, 5, 7, 10, 11, 16, 22, 23, 25, 29, 30, 32, 34, 35, 86, 163, 167, 172, 178 Incision, 167, 170 Incontinence, 168, 175 Incubation, 168, 181 Indomethacin, 86, 168 Induction, 8, 25, 26, 36, 37, 39, 52, 62, 89, 110, 142, 143, 168 Infancy, 60, 83, 168 Infantile, 168, 182 Infarction, 34, 168, 186 Infection, 6, 8, 9, 10, 11, 12, 13, 17, 18, 19, 20, 22, 24, 26, 27, 28, 29, 30, 31, 32, 33, 34, 37, 40, 46, 52, 55, 59, 60, 68, 69, 71, 72, 74, 78, 80, 83, 99, 100, 104, 110, 139, 144, 150, 154, 155, 158, 159, 160, 162, 166, 167, 168, 170, 171, 177, 187, 188, 189, 190, 194, 195, 196, 197 Infectious Mononucleosis, 42, 168 Infiltration, 11, 168, 197 Influenza, 26, 33, 77, 78, 99, 168 Infusion, 69, 168 Ingestion, 168, 182 Inhalation, 168, 182 Initiation, 4, 7, 17, 32, 35, 168, 193 Inotropic, 63, 100, 157, 168 Insight, 8, 18, 168 Insulator, 169, 174 Insulin, 12, 169, 179 Insulin-dependent diabetes mellitus, 12, 169 Intercellular Adhesion Molecule-1, 37, 169 Interferon, 8, 15, 21, 24, 37, 77, 90, 162, 169, 171 Interferon-alpha, 77, 169 Interleukin-1, 65, 102, 169 Interleukin-2, 169 Interleukin-6, 72, 169 Interleukins, 24, 167, 169 Intermediate Filaments, 25, 169 Interstitial, 31, 90, 169, 186 Intestinal, 159, 169 Intestine, 35, 147, 169, 170, 190 Intracellular, 17, 19, 24, 100, 163, 168, 169, 172, 177, 182, 187, 188, 196 Intravascular, 67, 169 Intravenous, 40, 59, 63, 64, 78, 114, 116, 168, 169 Intrinsic, 24, 140, 170 Intubation, 148, 170 Invasive, 39, 71, 170, 172 Involuntary, 150, 161, 170, 175
205
Ionizing, 159, 170 Ions, 157, 158, 166, 170 Ischemia, 9, 25, 27, 145, 170, 175, 186 K Kb, 120, 170 Kinetic, 28, 170 L Labile, 152, 170 Laceration, 170, 192 Lag, 103, 170 Large Intestine, 169, 170, 189 Latency, 82, 170 Latent, 12, 170 Lead Poisoning, 91, 170 Lectin, 70, 170 Left ventricular assist device, 41, 42, 54, 58, 170 Leishmaniasis, 170, 180 Lesion, 170, 171, 188, 191 Lethal, 64, 145, 170 Leucocyte, 159, 170, 171 Leukemia, 20, 163, 171 Leukocytes, 23, 75, 146, 147, 149, 150, 168, 169, 171, 174, 194 Leukopenia, 18, 171 Ligaments, 153, 171 Ligands, 32, 171 Lipid, 10, 11, 144, 150, 164, 169, 171, 174, 178 Lipid Peroxidation, 10, 11, 171, 178 Lipoprotein, 171, 196 Lithium, 114, 143, 171 Litter, 100, 171 Liver, 100, 139, 141, 146, 154, 155, 163, 165, 171, 186, 187 Localization, 20, 65, 95, 167, 171 Localized, 31, 78, 153, 157, 161, 168, 171, 175, 181, 187, 192 Lupus, 20, 63, 66, 70, 101, 126, 171, 191 Lymph, 102, 159, 165, 168, 171, 187 Lymph node, 171, 187 Lymphadenopathy, 102, 168, 171 Lymphatic, 159, 168, 171, 190, 192 Lymphatic system, 171, 190, 192 Lymphoblasts, 139, 171 Lymphocyte, 38, 56, 139, 143, 167, 171, 172 Lymphocyte Count, 139, 172 Lymphocyte Depletion, 167, 172 Lymphocytic, 21, 31, 36, 51, 54, 60, 62, 64, 172 Lymphoid, 142, 170, 172 Lymphoma, 160, 172
Lytic, 172, 196 M Macrophage, 31, 37, 169, 172 Maculopapular, 172, 188 Magnetic Resonance Imaging, 47, 172, 177 Major Histocompatibility Complex, 10, 36, 172 Malignant, 139, 143, 144, 172, 176, 187 Malnutrition, 141, 145, 172 Mammogram, 147, 172, 173 Manic, 143, 171, 172, 184 Manifest, 18, 22, 145, 172 Mastitis, 172, 188 Medial, 144, 172 Mediate, 7, 14, 27, 31, 40, 157, 172 Medical Records, 172, 186 MEDLINE, 121, 172 Melanin, 156, 172, 180, 194 Membrane Lipids, 172, 181 Memory, 4, 16, 22, 27, 142, 155, 173 Meninges, 149, 157, 173 Meningitis, 14, 16, 34, 154, 158, 173 Mental, iv, 3, 120, 122, 155, 157, 161, 173, 184, 187, 194 Mental Health, iv, 3, 120, 122, 173, 184 Mental Processes, 157, 173, 184 Mesolimbic, 143, 173 Methylprednisolone, 40, 173 MI, 62, 86, 98, 138, 173 Mice Minute Virus, 173, 179 Microbe, 173, 193 Microbiology, 3, 5, 6, 13, 34, 47, 49, 53, 68, 71, 79, 91, 145, 173 Microcalcifications, 147, 173 Microfilaments, 169, 173 Microorganism, 151, 173, 180, 196 Microtubules, 169, 173 Migration, 169, 173 Mineralocorticoids, 140, 154, 173 Mitochondria, 4, 25, 173, 178 Mitochondrial Swelling, 173, 176 Mitosis, 144, 174 Modification, 141, 163, 174 Modulator, 104, 174 Molecular, 4, 6, 11, 12, 14, 16, 20, 21, 22, 23, 24, 26, 28, 34, 41, 45, 54, 67, 68, 72, 81, 82, 86, 121, 123, 145, 146, 152, 174, 189, 191, 193, 194 Monitor, 51, 98, 174, 177 Monoclonal, 24, 36, 62, 104, 116, 165, 174 Monoclonal antibodies, 24, 36, 174 Monocytes, 169, 171, 174
206
Myocarditis
Mononuclear, 77, 168, 174, 194 Morphological, 34, 58, 158, 174 Morphology, 11, 174 Motility, 168, 174, 188 Mucolytic, 139, 174 Mucosa, 171, 174 Mucus, 174, 194 Multiple sclerosis, 16, 174 Multivalent, 145, 174 Muscle Contraction, 158, 174 Muscle Fibers, 175, 194 Muscle Proteins, 153, 175 Muscle relaxant, 175, 180 Muscle Spindles, 175, 180 Mutate, 33, 175 Myalgia, 50, 168, 175 Myasthenia, 39, 63, 103, 175 Mydriatic, 156, 175 Myelin, 174, 175, 188 Myelitis, 80, 175 Myocardial Contraction, 99, 175 Myocardial infarction, 10, 20, 28, 43, 44, 73, 110, 153, 173, 175, 195 Myocardium, 19, 21, 23, 27, 31, 34, 47, 52, 71, 102, 173, 175 Myofibrils, 158, 175 Myopathy, 12, 32, 175 Myosin, 5, 6, 11, 21, 24, 29, 46, 62, 65, 100, 174, 175, 194 Myositis, 39, 72, 175 N Nasal Mucosa, 168, 175 Nausea, 143, 162, 175, 194 NCI, 1, 119, 151, 175 Necrosis, 19, 21, 56, 71, 144, 168, 173, 175, 176, 186, 187 Neonatal, 34, 70, 71, 176 Neoplasm, 176, 187, 194 Nerve, 19, 140, 144, 145, 156, 162, 174, 176, 179, 186, 187, 190, 195, 197 Nerve Endings, 19, 176 Nervous System, 145, 149, 176, 183, 191 Neural, 72, 165, 176 Neuroeffector Junction, 176 Neuroleptic, 140, 143, 151, 176 Neuromuscular, 139, 176, 194 Neuromuscular Junction, 139, 176 Neuronal, 176 Neurons, 151, 156, 162, 175, 176, 191 Neuropeptides, 9, 176 Neurotransmitter, 139, 141, 147, 150, 157, 164, 165, 176, 177
Neutropenia, 18, 176 Neutrophil, 18, 169, 176 Niche, 5, 176 Nitrates, 25, 176 Nitric acid, 176 Nitric Oxide, 10, 23, 25, 27, 177 Nitrogen, 141, 142, 154, 161, 177, 194 Nitrosamines, 177 Nitrosation, 25, 177 Norepinephrine, 140, 157, 176, 177 Nuclear, 20, 46, 47, 48, 76, 146, 158, 160, 162, 176, 177 Nuclear magnetic resonance imaging, 46, 177 Nuclei, 158, 163, 172, 174, 177, 184 Nucleic acid, 28, 147, 163, 177, 196 Nucleolus, 177, 187 Nucleus, 144, 145, 146, 150, 154, 155, 156, 160, 169, 174, 177, 184, 190 Nutritional Status, 33, 177 O Occult, 44, 177 Odds Ratio, 177, 185 Opportunistic Infections, 18, 139, 177 Organ Culture, 178, 192 Organ Transplantation, 29, 178 Organelles, 155, 174, 178 Orthostatic, 143, 178 Osteoarthritis, 101, 178 Ovalbumin, 4, 31, 178 Ovum, 163, 178, 183 Oxidants, 25, 178 Oxidation, 139, 143, 155, 163, 171, 178 Oxidation-Reduction, 178 Oxidative Phosphorylation, 14, 27, 100, 178 Oxidative Stress, 9, 14, 30, 178 Oxygen Consumption, 100, 178, 186 Oxygenation, 52, 178 Oxygenator, 160, 178 P Pacemaker, 87, 179 Pachymeningitis, 173, 179 Palliative, 179, 192 Pancreas, 7, 18, 139, 169, 179 Pancreas Transplant, 18, 179 Pancreatic, 179 Pancreatitis, 6, 12, 58, 179 Papio, 36, 179 Paralysis, 14, 38, 79, 179, 182 Parasite, 20, 51, 179 Parasitic, 179, 187, 193
207
Parasitism, 37, 179 Parkinsonism, 143, 179 Parotid, 179, 187 Partial remission, 179, 185 Particle, 179, 193, 196 Parvovirus, 37, 40, 45, 53, 54, 55, 60, 64, 78, 79, 173, 179 Patch, 5, 34, 180 Pathogen, 4, 6, 33, 168, 180 Pathogenesis, 4, 5, 6, 7, 9, 11, 12, 19, 20, 22, 23, 31, 32, 34, 71, 95, 107, 180 Pathologic, 31, 32, 45, 51, 60, 100, 144, 146, 153, 166, 180 Pathologic Processes, 32, 144, 180 Pentamidine, 9, 180 Pentoxifylline, 24, 180 Peptide, 6, 10, 23, 24, 27, 29, 31, 35, 42, 77, 82, 104, 141, 145, 180, 182, 183, 184 Percutaneous, 70, 81, 180 Perfusion, 23, 146, 180 Pericarditis, 17, 61, 98, 180 Perinatal, 100, 180 Peripheral blood, 6, 77, 169, 180 Perivascular, 31, 180 Phagocyte, 178, 180 Pharmacologic, 180, 193 Pharynx, 168, 180 Phenotype, 10, 15, 17, 21, 23, 24, 152, 180 Phenylalanine, 180, 194 Phenytoin, 64, 180 Phosphodiesterase, 180, 181 Phospholipids, 62, 161, 171, 172, 181 Phosphorus, 147, 181 Phosphorylation, 20, 24, 154, 181 Physical Examination, 98, 181 Physiologic, 6, 23, 181, 185 Physiology, 27, 158, 181 Picornavirus, 11, 181 Pituitary Gland, 154, 181 Plants, 141, 147, 150, 151, 156, 163, 170, 174, 177, 181, 187, 193, 194 Plaque, 12, 181 Plaque Assay, 12, 181 Plasma, 12, 104, 140, 142, 149, 158, 163, 173, 181, 186, 196 Plasma cells, 142, 181 Plasmid, 65, 162, 181, 195 Platelet Aggregation, 142, 177, 180, 181 Platelets, 27, 177, 181, 182, 192 Pneumonia, 31, 153, 180, 182 Pneumonitis, 17, 54, 182 Poisoning, 90, 99, 155, 162, 175, 182
Poliomyelitis, 16, 34, 35, 182 Polymerase, 20, 28, 47, 144, 182 Polymerase Chain Reaction, 47, 182 Polymorphic, 44, 182 Polypeptide, 104, 141, 151, 182, 184, 197 Polysaccharide, 143, 182 Posterior, 144, 179, 182 Post-translational, 27, 182 Potassium, 141, 173, 182 Potentiates, 14, 169, 182 Potentiation, 150, 182 Practice Guidelines, 122, 182 Precordial, 74, 183 Precursor, 15, 142, 145, 150, 154, 157, 158, 159, 177, 180, 183, 194 Prednisolone, 173, 183 Presynaptic, 176, 183 Presynaptic Terminals, 176, 183 Prevalence, 66, 74, 78, 159, 177, 183 Probe, 25, 183 Progesterone, 183, 190 Progression, 4, 10, 13, 21, 54, 58, 142, 154, 183, 196 Progressive, 21, 56, 80, 101, 144, 156, 157, 176, 178, 183, 185, 194 Proline, 151, 166, 183 Promoter, 17, 21, 34, 183 Prophylaxis, 101, 143, 183, 195 Prostaglandins, 168, 183 Prostaglandins A, 168, 183 Protease, 32, 183 Protein C, 103, 140, 141, 145, 171, 175, 183, 184, 189, 194, 196 Protein Conformation, 141, 184 Protein S, 8, 17, 24, 32, 144, 146, 163, 184, 187, 192 Proteolytic, 152, 184 Protons, 166, 170, 184, 185 Protozoa, 170, 173, 184, 193, 194, 195 Protozoal, 184 Protozoan, 20, 184 Psychology, 157, 184 Psychosis, 143, 184 Public Health, 28, 122, 184 Public Policy, 121, 184 Publishing, 36, 184 Pulmonary, 17, 30, 31, 74, 109, 147, 159, 184, 189, 195 Pulmonary hypertension, 17, 30, 74, 109, 184 Pulse, 174, 184 Pupil, 153, 156, 175, 185
208
Myocarditis
Q Quiescent, 12, 185, 196 R Radiation, 159, 161, 167, 170, 185, 196 Radioactive, 147, 166, 167, 174, 177, 185 Radiological, 180, 185 Randomized, 158, 185 Rarefaction, 102, 185 Reactivation, 12, 20, 87, 91, 185 Reactive Oxygen Species, 14, 185 Receptor, 6, 7, 9, 10, 15, 23, 24, 34, 38, 39, 41, 52, 54, 65, 102, 110, 143, 149, 151, 157, 185, 188 Recombinant, 12, 146, 185, 195 Recombination, 17, 162, 163, 185 Reductase, 185, 192 Refer, 1, 147, 152, 161, 171, 176, 184, 185, 193 Refraction, 185, 189 Refractory, 11, 185 Regimen, 158, 185 Relative risk, 9, 185 Remission, 75, 185 Renal failure, 155, 185, 194 Renin, 23, 104, 142, 186 Renin-Angiotensin System, 23, 186 Reperfusion, 9, 25, 186 Reperfusion Injury, 186 Respiration, 149, 174, 186 Respiratory Burst, 18, 186 Respiratory failure, 160, 186 Retina, 186, 187 Retrospective, 70, 186 Retrospective study, 70, 186 Retrovirus, 11, 17, 186 Rhabdomyolysis, 87, 186 Rheology, 180, 186 Rheumatism, 57, 186, 187 Rheumatoid, 16, 27, 101, 178, 187 Rheumatoid arthritis, 16, 27, 101, 187 Rhinitis, 187, 188 Rhinovirus, 35, 187 Ribosome, 14, 187, 193 Rickettsiae, 187, 195 Risk factor, 9, 19, 185, 187 Risperidone, 9, 187 Rod, 34, 146, 187 Rotavirus, 54, 187 S Salivary, 155, 187 Salivary glands, 155, 187 Saponins, 187, 190
Sarcoidosis, 39, 57, 65, 78, 82, 187 Sarcoma, 17, 187 Sarcomere, 100, 187 Schizophrenia, 8, 187 Scleroderma, 40, 144, 187 Sclerosis, 101, 103, 144, 174, 187 Screening, 151, 187 Scrub Typhus, 67, 187 Secretion, 154, 163, 165, 169, 173, 174, 188 Sedentary, 98, 188 Segregation, 185, 188 Seizures, 155, 180, 188 Selenium, 33, 63, 86, 87, 188 Sensitization, 4, 29, 188 Sensory loss, 175, 188 Sepsis, 23, 25, 34, 188 Septic, 23, 25, 144, 188 Septicaemia, 188 Sequencing, 182, 188 Serotonin, 143, 151, 176, 187, 188, 194 Serotypes, 13, 154, 158, 188 Serum, 12, 31, 51, 62, 76, 77, 86, 92, 99, 140, 142, 143, 152, 166, 167, 172, 173, 188, 194 Shock, 18, 23, 44, 55, 61, 81, 92, 188, 193 Side effect, 113, 116, 140, 143, 154, 188, 193 Signs and Symptoms, 185, 189, 194 Skeletal, 10, 21, 32, 78, 142, 150, 175, 186, 189, 194 Skeleton, 139, 189 Skull, 189, 191 Small intestine, 165, 169, 189 Smallpox, 26, 51, 68, 69, 189, 195 Smoke Inhalation Injury, 160, 189 Smooth muscle, 24, 27, 31, 141, 142, 153, 165, 166, 186, 189 Sodium, 115, 141, 173, 189 Soft tissue, 147, 189 Solvent, 160, 164, 189 Somatic, 165, 174, 189 Specialist, 127, 156, 189 Specificity, 4, 6, 21, 27, 28, 140, 189 Spectrin, 157, 189 Spectrum, 14, 32, 100, 189 Spinal cord, 149, 150, 157, 162, 173, 175, 176, 179, 190, 191 Spinal Cord Vascular Diseases, 175, 190 Spleen, 25, 155, 171, 187, 190 Splenomegaly, 102, 168, 190 Stabilization, 180, 190 Steady state, 28, 190 Sterile, 144, 190 Sterility, 154, 190
209
Steroid, 50, 187, 190 Steroid therapy, 50, 190 Stimulus, 153, 158, 170, 190, 192 Stomach, 139, 145, 162, 165, 175, 180, 189, 190 Strand, 16, 28, 182, 190 Streptococcal, 6, 190 Streptococci, 36, 190 Streptococcus, 190 Stress, 9, 15, 73, 145, 148, 162, 175, 178, 187, 190 Stroke, 70, 120, 148, 190 Subacute, 11, 98, 168, 190 Subclinical, 168, 188, 190 Subcutaneous, 102, 158, 162, 190 Subspecies, 189, 191, 195 Substrate, 28, 159, 191 Sudden death, 21, 41, 78, 103, 191 Superoxide, 15, 18, 25, 186, 191 Superoxide Dismutase, 15, 25, 191 Suppression, 54, 154, 191 Sympathetic Nervous System, 104, 145, 191 Symptomatic, 179, 191 Synapse, 140, 176, 183, 191 Syncytium, 163, 191 Synergistic, 9, 19, 191 Synovial, 22, 191 Systemic disease, 95, 191 Systemic lupus erythematosus, 16, 52, 69, 191 Systolic, 12, 166, 191 T Tachycardia, 36, 44, 63, 66, 79, 80, 136, 191 Tamponade, 79, 191 Tardive, 143, 191 Temporal, 26, 191 Tetani, 191, 192 Tetanic, 191, 192 Tetanus, 40, 191 Tetracycline, 23, 192 Therapeutics, 115, 192 Thermal, 23, 157, 182, 192 Thioredoxin, 77, 81, 87, 192 Thorax, 183, 192 Threshold, 30, 166, 192 Thrombin, 181, 183, 192 Thrombocytes, 182, 192 Thrombocytopenia, 18, 192 Thrombomodulin, 183, 192 Thrombosis, 184, 190, 192 Thrombus, 153, 168, 181, 192
Thymoma, 39, 63, 192 Thymus, 93, 167, 171, 192 Thyroid, 71, 192, 194 Tissue Culture, 30, 192 Tolerance, 6, 22, 26, 29, 31, 52, 140, 163, 192 Tone, 104, 193 Tonus, 193 Topical, 114, 160, 166, 193 Torsion, 168, 193 Toxic, iv, 19, 39, 49, 148, 155, 156, 159, 176, 180, 188, 189, 193 Toxicity, 11, 15, 36, 157, 193 Toxicology, 76, 90, 122, 193 Toxin, 24, 191, 192, 193 Toxoplasma, 73, 75, 193 Trachea, 180, 192, 193 Transcriptase, 186, 193 Transcription Factors, 17, 21, 24, 149, 193 Transduction, 24, 193 Transfection, 21, 146, 163, 193 Transfer Factor, 167, 193 Translating, 14, 193 Translation, 13, 14, 16, 35, 141, 193 Translational, 5, 22, 193 Transplantation, 11, 29, 34, 41, 56, 57, 58, 61, 64, 67, 77, 81, 167, 172, 193 Trauma, 23, 155, 164, 176, 179, 193 Trigger zone, 143, 194 Tropism, 6, 7, 35, 194 Tropomyosin, 175, 194 Troponin, 31, 43, 49, 175, 194 Trypanosomiasis, 149, 180, 194 Tryptophan, 151, 188, 194 Tuberculosis, 171, 194 Tubocurarine, 162, 194 Tumor Necrosis Factor, 23, 52, 72, 194 Tumour, 56, 162, 194 Tyrosine, 24, 25, 157, 194 U Ulcerative colitis, 57, 194 Ultrasonography, 31, 194 Uraemia, 179, 194 Uremia, 185, 194 Urethra, 194 Urinary, 150, 168, 194 Urine, 22, 104, 136, 146, 168, 194 Uterine Contraction, 139, 195 Uterus, 139, 149, 183, 191, 195 V Vaccination, 26, 40, 51, 68, 195 Vaccines, 26, 35, 103, 150, 182, 195, 196
210
Myocarditis
Vaccinia, 26, 195 Vaccinia Virus, 26, 195 Vagina, 149, 191, 195 Varicella, 80, 82, 195 Variola, 195 Vascular, 11, 17, 23, 31, 101, 104, 153, 156, 159, 166, 168, 177, 190, 192, 195 Vasculitis, 102, 126, 179, 195 Vasodilators, 100, 177, 195 Vector, 100, 103, 193, 195 Vein, 142, 169, 177, 179, 195 Venom, 24, 62, 195 Venous, 184, 195 Ventricle, 145, 185, 191, 195 Ventricular Dysfunction, 31, 55, 64, 195 Ventricular fibrillation, 77, 195 Ventricular Function, 32, 195 Ventricular Remodeling, 21, 195 Vesicular, 189, 195 Veterinary Medicine, 121, 196 Viral Load, 100, 196 Viral Proteins, 7, 11, 17, 35, 196 Virion, 7, 196
Virulence, 33, 58, 145, 193, 196 Virulent, 33, 196 Virus Diseases, 143, 196 Virus Replication, 35, 37, 196 Visceral, 69, 145, 170, 196 Visceral Larva Migrans, 69, 196 Viscosity, 139, 186, 196 Vitiligo, 72, 196 Vitro, 5, 10, 16, 22, 34, 37, 196 Vivo, 5, 10, 30, 32, 37, 172, 196 Voriconazole, 77, 196 W White blood cell, 139, 142, 168, 171, 172, 174, 176, 181, 196 Windpipe, 180, 192, 196 X Xenograft, 142, 196 X-ray, 137, 153, 161, 172, 177, 196 Y Yeasts, 161, 180, 196 Z Zoster, 59, 197 Zymogen, 183, 197
211
212
Myocarditis
