METABOLIC ACIDOSIS 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., 1960Metabolic Acidosis: 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: 0-497-00718-5 1. Metabolic Acidosis-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 metabolic acidosis. 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 METABOLIC ACIDOSIS .............................................................................. 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Metabolic Acidosis ........................................................................ 4 E-Journals: PubMed Central ....................................................................................................... 21 The National Library of Medicine: PubMed ................................................................................ 24 CHAPTER 2. NUTRITION AND METABOLIC ACIDOSIS .................................................................... 67 Overview...................................................................................................................................... 67 Finding Nutrition Studies on Metabolic Acidosis ....................................................................... 67 Federal Resources on Nutrition ................................................................................................... 68 Additional Web Resources ........................................................................................................... 69 CHAPTER 3. ALTERNATIVE MEDICINE AND METABOLIC ACIDOSIS .............................................. 71 Overview...................................................................................................................................... 71 National Center for Complementary and Alternative Medicine.................................................. 71 Additional Web Resources ........................................................................................................... 74 General References ....................................................................................................................... 74 CHAPTER 4. PATENTS ON METABOLIC ACIDOSIS ........................................................................... 77 Overview...................................................................................................................................... 77 Patents on Metabolic Acidosis ..................................................................................................... 77 Patent Applications on Metabolic Acidosis ................................................................................. 80 Keeping Current .......................................................................................................................... 81 CHAPTER 5. BOOKS ON METABOLIC ACIDOSIS .............................................................................. 83 Overview...................................................................................................................................... 83 Book Summaries: Federal Agencies.............................................................................................. 83 Book Summaries: Online Booksellers........................................................................................... 86 Chapters on Metabolic Acidosis ................................................................................................... 86 CHAPTER 6. MULTIMEDIA ON METABOLIC ACIDOSIS .................................................................... 89 Overview...................................................................................................................................... 89 Video Recordings ......................................................................................................................... 89 CHAPTER 7. PERIODICALS AND NEWS ON METABOLIC ACIDOSIS ................................................. 91 Overview...................................................................................................................................... 91 News Services and Press Releases................................................................................................ 91 Newsletter Articles ...................................................................................................................... 93 Academic Periodicals covering Metabolic Acidosis ..................................................................... 93 APPENDIX A. PHYSICIAN RESOURCES ............................................................................................ 97 Overview...................................................................................................................................... 97 NIH Guidelines............................................................................................................................ 97 NIH Databases............................................................................................................................. 99 Other Commercial Databases..................................................................................................... 101 APPENDIX B. PATIENT RESOURCES ............................................................................................... 103 Overview.................................................................................................................................... 103 Patient Guideline Sources.......................................................................................................... 103 Finding Associations.................................................................................................................. 105 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 107 Overview.................................................................................................................................... 107 Preparation................................................................................................................................. 107 Finding a Local Medical Library................................................................................................ 107 Medical Libraries in the U.S. and Canada ................................................................................. 107 ONLINE GLOSSARIES................................................................................................................ 113
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Online Dictionary Directories ................................................................................................... 113 METABOLIC ACIDOSIS DICTIONARY................................................................................. 115 INDEX .............................................................................................................................................. 165
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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 metabolic acidosis 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 metabolic acidosis, 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 metabolic acidosis, 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 metabolic acidosis. 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 metabolic acidosis, 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 metabolic acidosis. 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 METABOLIC ACIDOSIS Overview In this chapter, we will show you how to locate peer-reviewed references and studies on metabolic acidosis.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and metabolic acidosis, you will need to use the advanced search options. First, go to http://chid.nih.gov/index.html. From there, select the “Detailed Search” option (or go directly to that page with the following hyperlink: http://chid.nih.gov/detail/detail.html). The trick in extracting studies is found in the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Journal Article.” At the top of the search form, select the number of records you would like to see (we recommend 100) and check the box to display “whole records.” We recommend that you type “metabolic acidosis” (or synonyms) into the “For these words:” box. Consider using the option “anywhere in record” to make your search as broad as possible. If you want to limit the search to only a particular field, such as the title of the journal, then select this option in the “Search in these fields” drop box. The following is what you can expect from this type of search: •
Metabolic Acidosis of Chronically Hemodialyzed Patients Source: American Journal of Nephrology. 23(3): 158-164. 2003. Summary: Metabolic acidosis is a condition that is commonly encountered in both chronic renal (kidney) failure (CRF) and in end stage renal disease (ESRD). Metabolic acidosis is associated with many adverse effects: negative nitrogen balance, increased protein decomposition, anorexia, fatigue, bone lesions, impaired function of the cardiovascular system, impaired function of the gastrointestinal system, hormonal disturbances, insulin resistance, hyperkalemia, altered gluconeogenesis and triglyceride metabolism, increased progression of chronic renal failure, and growth retardation in children. This article considers the problem of metabolic acidosis in chronically hemodialyzed patients. The authors caution that even 'minor' degrees of metabolic
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acidosis are harmful. Metabolic acidosis of ESRD patients could be successfully corrected with bicarbonate hemodialysis and with peroral bicarbonate-containing phosphate binders, i.e., calcium carbonate. 'High' dialysate bicarbonate is a safe, welltolerated and useful tool for better correction of the metabolic acidosis and must become a standard of hemodialysis treatment. Measured postdialysis blood bicarbonate concentration should be obtained at least every month and correction of metabolic acidosis should be a goal of the management of patients undergoing chronic hemodialysis. 90 references.
Federally Funded Research on Metabolic Acidosis The U.S. Government supports a variety of research studies relating to metabolic acidosis. 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 metabolic acidosis. 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 metabolic acidosis. The following is typical of the type of information found when searching the CRISP database for metabolic acidosis: •
Project Title: BICARBONATE TRANSPORT BY THE MATURING RENAL TUBULE Principal Investigator & Institution: Schwartz, George J.; Professor; Pediatrics; University of Rochester Orpa - Rc Box 270140 Rochester, Ny 14627 Timing: Fiscal Year 2002; Project Start 01-JUL-1990; Project End 30-JUN-2004 Summary: (Adapted from the Applicant's Abstract): Membrane-bound carbonic anhydrase (CA) is essential for HCO transport in the proximal tubule and collecting duct. Clinically, problems in neonatal renal acidification may be due to delayed membrane CA expression. Membrane CA includes CA isoform IV, which is anchored to the luminal membrane via a glycosylphosphatidylinositol (GPI) linkage. However, two anti-CA IV peptide antibodies show that CA IV is expressed on both apical and basolateral membranes of the proximal tubule, the latter not expected for a GPIanchored protein. Other membrane CA isoforms (CA XII, and XIV), could reside on the basolateral membrane and cross-react with these antibodies. The identity of the basolateral CA, the mechanisms for its targeting, and its regulation during acidosis and development will be examined in rabbit kidney. Aim 1 is to determine which CA isoform resides in the basolateral membrane of the proximal tubule. A PCR-based approach will be used to obtain cDNA probes for CAs XII, and XIV in rabbit. Peptides will be prepared from these sequences to test specificity of the CA IV antibodies and to generate CA XII- and XIV-specific antibodies. Another anti-CA IV peptide antibody
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Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
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(with no homology to CAs XII or XIV) will be made. The apical basolateral CAs will be compared and characterized. Aim 2 examines the targeting of membrane CAs. Membrane CA cDNAs will be FLAG-tagged and transiently transfected into immortalized mouse proximal tubule cells. The polarity of expressed membrane CAs will be examined and compared with the targeting of the C-terminus. This will establish whether GPI-linkage confers apical polarity and the C-terminal hydrophilic segment confers basolateral polarity to the membrane CA. The regulation of these CAs in response to metabolic acidosis and maturation will also be examined. Aim 3 investigates physiologic correlations. The presence of basolateral CA activity on HCO transport and cell pH will be examined in perfused proximal tubules. The regulation of basolateral CAs in response to acidosis and development will be studied. Finally, the mechanisms by which acidosis causes resistance to CA inhibition will be studied in outer medullary collecting ducts, which absorb HCO despite a luminal disequilibrium pH. The objective is to better understand the role of membrane carbonic anhydrases (CAs) in mediating renal acid-base transport. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CELL CYCLE PROTEINS IN RENAL GROWTH, INJURY, AND REPAIR Principal Investigator & Institution: Preisig, Patricia A.; Professor; Internal Medicine; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2002; Project Start 15-AUG-2000; Project End 31-JUL-2005 Summary: Renal epithelial cells are normally quiescent, but can increase their growth rate. In some situations, such as following an acute renal injury, the cell growth is essential to repairing the damaged epithelium, and appears tightly regulated. In contrast, unregulated, and ultimately destructive, growth occurs in renal cancer, polycystic kidney disease, and the progressive loss of renal function associated with loss of renal mass, diabetes mellitus, and most forms of glomerular injury. The growth changes that occur involve both hyperplasia (resulting in an increase in cell number) and hypertrophy (resulting in an increase in cell size). Using in vitro systems, two mechanisms of renal epithelial cell hypertrophy have been characterized; One involves regulation of the cell cycle process (referred to as being cell cycle-dependent) and is mediated by growth factors and cytokines, and the other is independent of cell cycle processes and mediated by agents that alkalinize intravesicular compartments, such as NH4C1. Using in vivo renal growth models, we have shown that: 1) Compensatory renal growth following uninephrectomy is a hypertrophic growth process that involves primarily activation of cyclin D kinase, without an increase in BrdU incorporation, and is not affected by inhibiting ammoniagenesis, suggesting that a cell cycle-dependent mechanism is involved; 2) Diabetes-induced renal growth involves an initial hyperplastic growth phase associated with activation of both G, kinase and an increase in BrdU incorporation, followed by a hypertrophic growth phase associated with continued activation of cyclin D kinase, inhibition of cyclin E kinase, and inhibition of BrdU incorporation; 3) The renal growth associated with chronic hypokalemia can be reversed when ammoniagenesis is inhibition by an alkaline diet, suggesting a cell cycleindependent mechanism of growth; and 4) In transgenic mice in which the endothelin B receptor has been knocked out, uninephrectomy does not lead to hypertrophy. Aim 1 will continue to characterize the role of cell cycle proteins in compensatory renal growth. Aim 2 will focus of diabetes-induced hypertrophy. Studies will examine the regulation of the cell cycle proteins in the switch between a hyperplastic and hypertrophic growth pattern. Studies will be done in 3 models of diabetes mellitus:
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streptozotocin-induced type I, in Nod mice (type I), and in db/db mice (type II). Studies will also be done to determine the role of the endothelin B receptor in diabetes-induced renal growth. Aim 3 will determine the mechanisms involved in the activation of cyclin D kinase and inhibition of cyclin E kinase in cell cycle-dependent hypertrophy. Aim 4 will determine if the endothelin B receptor plays a role in chronic metabolic acidosis and chronic potassium deficiency, models of renal hypertrophy thought to be mediated by the cell cycle-independent mechanism. Together these studies will afford us the opportunity to determine if direct regulation of cell cycle processes provides an avenue for therapeutic advances that will either improve upon the beneficial effects or reduce the detrimental sequelae of renal injury. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CHARACTERIZATION OF A NEW FAMILY OF PROTEIN KINASES Principal Investigator & Institution: Popov, Kirill M.; Assistant Professor; Molecular Biology and Biochem; University of Missouri Kansas City Kansas City, Mo 64110 Timing: Fiscal Year 2002; Project Start 01-JUL-1995; Project End 30-JUN-2004 Summary: (From the application abstract:) The mitochondrial pyruvate dehydrogenase complex (PDC) catalyzes the oxidative decarboxylation of pyruvate, the reaction that determines the metabolic fate of carbohydrates. The enzymatic activity of the mammalian PDC is regulated by reversible phosphorylation. The specific kinase (pyruvate dehydrogenase kinase or PDK) converts it to an inactive form that can be reactivated only by a specific phosphatase. The hyperphosphorylation of PDC observed in diabetes, ischemia, and metabolic acidosis directly contributes to the morbidity and mortality associated with these conditions. It is generally believed that the hyperphosphorylation is due, in part, to enhanced kinase activity. Recently this laboratory provided the first data indicating that, in humans and other mammals there are multiple isoenzymes of PDK. The physiological significance of multiple isoenzymes is currently unknown. The results available thus far strongly suggest that the isoenzymes are functionally different. The isoenzyme PDK2 is likely to be responsible for the * short-term regulation of PDC activity. The inducible isoenzyme PDK4, in contrast, may be mainly responsible for long-term control. Its over-expression in diabetes is likely a leading cause of the hyperphosphorylation of PDC that, in turn, contributes to hyperglycemia. This proposal is aimed to further elucidate the structure, function, regulation and physiological significance of the multiple isoenzymes of PDK. Its major goals are: 1) to determine the three dimensional structure of pyruvate dehydrogenase kinase; 2) to elucidate the molecular basis for catalysis and substrate recognition by pyruvate dehydrogenase kinase; 3) to further define the molecular mechanisms responsible for regulation of pyruvate dehydrogenase kinase activity; 4) to characterize the molecular interactions between isozymes, as well as between isozymes and pyruvate dehydrogenase complex under normal conditions, as well as under starvation and diabetes. These goals will be achieved though a combination of structure/functional analysis, biochemical characterization, as well as more physiologically oriented studies of isozymes under conditions such as starvation and diabetes. This will allow us to understand how this structurally unique protein kinase functions. It will also allow us to take the first step towards the design of isoenzymespecific drugs that may alleviate some of the symptoms and prevent complications associated with diabetes, ischemia and acidosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CONTROL OF RENAL GLUTAMINASE INDUCTION DURING ACIDOSIS Principal Investigator & Institution: Curthoys, Norman P.; Professor and Chairman; Biochem and Molecular Biology; Colorado State University-Fort Collins Fort Collins, Co 80523 Timing: Fiscal Year 2002; Project Start 01-OCT-1989; Project End 31-MAR-2006 Summary: During chronic metabolic acidosis, increased renal ammoniagenesis and gluconeogenesis from glutamine are sustained, in part, by a cell specific increase in expression of the mitochondrial glutaminase (GA) that results from the selective stabilization of the GA mRNA. Previous experiments identified an 8-base AU- sequence within the 3'- non-translated region of the GA mRNA that functions as a pH-response element (pHRE) when introduced into a chimeric reporter mRNA. This sequence was used as an affinity ligand to purify and identify zeta-crystallin/NADPH; quinone reductase as the pHRE-binding protein. The functional characterization of the pHRE was carried out in LLC-PK1-FBPase+ cells, a porcine proximal tubule-like cell line that expresses multiple forms of GA mRNAs. The corresponding porcine GA cDNAs were cloned and sequenced. Only the 4.5-kb GA mRNA contains pHREs that are identical to the sequence identified in the rat GA mRNA and only this form of GA mRNA is stabilized and increased by incubating the cells in acidic medium (Ph=6.9, 10 mM HCO3). Thus this cell lines provides a system to further characterized the molecular mechanism of GA mRNA stabilization and the associated signal transduction pathway. Finally, the 4.50kb GA mRNA is the ortholog of a newly identified isoform of the human kidney-type GA that is generated by alternative splicing of exons within the GA gene. This isoform contains a unique C-terminal domain of unknown function. The specific aims of the proposed research are: to express and characterize the isoforms of the kidney-type GA; to characterize the mechanism of GA mRNA turnover; to characterize the role of zeta-crystallin/NADPH; quinone reductase in the stabilization of the GA mRNA; and to identify the signal transduction pathway that leads to enhanced binding of zeta-crystallin/NADPH; quinone reductase to the pHRE. The results of the proposed experiments should significantly increase the understanding of the molecular mechanism that regulates this essential adaptive response and may provide insight to improve the clinical treatment of chronic acidosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: EFFECTS OF ACID ON BONE Principal Investigator & Institution: Bushinsky, David A.; Professor of Medicine and Physiology; Medicine; University of Rochester Orpa - Rc Box 270140 Rochester, Ny 14627 Timing: Fiscal Year 2002; Project Start 01-APR-2000; Project End 31-MAR-2005 Summary: Metabolic acidosis, present during many clinical disorders, has significant effects on bone. The proposed studies are designed to test hypotheses relating to the effects of increases in proton concentration ([H+]), acidosis, on the ionic composition of bone mineral and on bone cell function. We propose to study how acidosis affects mass spectroscopy and to study how acidosis alters signal transduction pathways and bone cell expression. With the microprobe we obtain sensitive, mass resolved images and spectra of the ionic composition of bone mineral. We propose three Specific Aims: 1) To test the hypothesis that there are specific changes in bone ion composition with respect to time and location after exposure to acidosis. To pursue this aim we will test the hypothesis that in vivo acidosis initially causes a preferential loss of mid-cortical
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bicarbonate, Na and K due to physicochemical dissolution, with subsequent additional loss of phosphate due to cell-mediated resorption. We will test the hypothesis that the magnitude of H+ buffering by bone increases with age as the carbonate content increase and the phosphate content decreases and that there are labile pools of Ca and K preferentially released during in vivo acidosis. We will test the hypothesis that mice deficient in osteopontin (OP), matrix gla protein (MGP) or c-src have altered basal bone ion composition and an altered osseous response (Jca and JH) to acidosis. 2) To test the hypothesis that the mechanism of acid-induced cell-mediated bone resorption involves activation of signal transduction pathways such as protein kinase A (PKA), protein kinase C (PKC) and/or mitogen-activated protein kinase (MAPK) by using specific inhibitors of PKA and PKC and measurements of PKA, PKC and MAPK during acidosis. 3) To test the hypothesis that metabolic acidosis selectively inhibits osteoblastic extracellular matrix gene expression via distinct transcriptional mechanisms, by testing acidosis effects on OP and MGP RNA transcription initiation. We will identify sequences in the mouse OP and MGP genes which are capable of conferring pH dependence to a reporter gene. These Specific Aims are interrelated as the effects of acidosis at the level of the gene lead to alterations in bone cell function which subsequently alter bone mineral. Our long term goal is to develop a model to describe how acidosis affects bone in order to devise therapy to preserve mineral while maintaining the H+ buffering properties of bone. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: FLUID RESUSCITATION IN PEDIATRIC FALCIPARUM MALARIA COMPLICATED BY ACIDOSIS Principal Investigator & Institution: Usen, Stanley; Michigan State University 301 Administration Bldg East Lansing, Mi 48824 Timing: Fiscal Year 2002 Summary: Fifty per cent of deaths in children hospitalized with severe pediatric malaria occur within 12 hours of admission to hospital. Rapidly acting interventions are required in order to address these early deaths. Metabolic acidosis has recently been recognized, by workers at the SMAC site in Kenya, as a complicating feature in patients with P. falciparum malaria. Acidosis may be the sole complication, in which case patients are fully alert, but present with deep breathing (an appropriate, involuntary, compensatory mechanism); the mortality rate in these patients is 24%. The mortality rate in patients with cerebral malaria and acidosis (32%) is significantly higher than in patients with cerebral malaria alone (19%). Clinical findings from this same site in Kenya suggest that many of the acidotic patients are hypovolemic, and that the acidosis improves quickly following, aggressive volume replacement (with intravenous fluids or blood). However, two of the SMAC sites (Kenya and Malawi) have data suggesting that brain swelling may be a cause of death. If this is tme, then the rapid administration of intravenous fluids might be harmful. Whether this particular intervention, the rapid administration of intravenous fluids, would be effective in terms of decreasing the mortality (early and late) in children with falciparum malaria complicated by acidosis, is the central question of this clinical trial. The clinical trial will be preceded by a pilot study, conducted in Kenya (the SMAC site most experienced in the required metabolic and hemodynamic monitoring). The purpose of the pilot study is to develop specific recommendations for fluid resuscitation which (a) are safe (b) can be evaluated in a multi-center study and (c) will be feasible in the district hospitals and health centers in which most of the African children with severe malaria are treated. Data regarding the safety and efficacy of various doses' of the intervention will be critical to our decision
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regarding the recommended regimen. In the intervention trial, parasitemic children with metabolic acidosis (plasma lactate concentration > 5.0 mmol\l or severe respiratory distress or pH and pCO2 measurements consisted with frank metabolic acidosis or compensated metabolic acidosis or base excess 5%). The execution of this study is the most difficult of the three studies contained in this proposal because the protocol must allow study clinicians to give fluid resuscitation to children who are obviously dehydrated. Data will be collected on other known predictors of outcome in severe malaria, in order to assess the comparability between treatment groups, but the sole measures of clinical efficacy will be clinical condition (dead or alive) at 12 hours, and overall outcome (survival or death). If rapid fluid administration is successful in decreasing mortality, especially the early mortality, then clinicians across Africa will have a new tool which can be deployed immediately in the treatment of severe pediatric malaria. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: H/HCO3 TRANSPORT IN THE COLLECTING DUCT Principal Investigator & Institution: Weiner, I. David.; Associate Professor; Medicine; University of Florida Gainesville, Fl 32611 Timing: Fiscal Year 2003; Project Start 01-AUG-1993; Project End 31-MAY-2007 Summary: (provided by applicant): Ammonia metabolism is critical for normal health. Inappropriate ammonia metabolism in the kidney leads to metabolic acidosis and in the liver leads to ammonia encephalopathy. In the central nervous system increased extracellular ammonia alters neuronal function and can lead to encephalopathy. Accordingly, understanding the cellular and molecular mechanisms of ammonia metabolism, which includes ammonia transport, is important. Recent studies have identified a novel family of ammonium ion (NH4+)-specific transporters. These proteins were first identified in yeast and in plants, and homologues are present throughout nature. In model systems, such as yeast, plants and bacteria, these are intrinsic membrane proteins that mediate high-affinity, ammonium-specific transport and whose expression is physiologically regulated. Two of these proteins, RhBG and RhCG are expressed in the connecting segment and the collecting duct of the kidney, and exhibit polarized expression. These observations lead us to postulate that RhBG and RhCG are integral membrane, physiologically-regulated ammonium-ion transporters that play critical roles in renal ammonia metabolism. The broad, long-term objectives of this project are to define the roles of RhBG and RhCG in mammalian renal physiology. To do so, the Specific Aims of the current proposal are to: (1) Define the regulation of mouse renal RhBG and RhCG expression and vesicular trafficking in response to specific clinical conditions associated with altered renal ammonia metabolism; (2) Determine the mechanism of extracellular ammonia-stimulated changes in RhBG- and RhCG-mediated ion transport; and, (3) identify the specific ion-transport characteristics of RhBG and RhCG. We will utilize in vivo animal models of altered renal ammonia metabolism, metabolic acidosis and alkalosis and hypokalemia, to define the regulation of RhBG and RhCG expression and cellular localization, a cultured collecting duct cell line, mIMCD-3, for in vitro studies examining the cellular mechanisms underlying regulation of RhBG and RhCG-mediated transport, and heterologous expression systems in which to define the specific ion transport characteristics of RhBG and RhCG. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: INTEGRATED ANALYSIS OF OVER AND UNDEREXPRESSION OF ENAC IN MICE Principal Investigator & Institution: Merrill, David; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2002 Summary: The epithelial sodium channel (ENaC) has been proposed to be a vital regulatory mechanism in renal sodium transport and arterial pressure control and has clear disease implications for humans. Liddle~s syndrome, a condition characterized by excessive sodium reabsorption, volume overload, and hypertension is caused by activating mutations in EnaC subunits (1-4). In contrast, loss-of- function ENaC mutations have been defined in families with pseudohypoaldostreronism type I (PHA1) associated with salt wasting, dehydration, and metabolic acidosis (5,6). Direct assessment of ENaC function in vivo has not therefore been possible. The overall goal of this proposal is to directly quantitate the relative importance of ENaC in renal sodium transport and arterial pressure control. To achieve this goal, we proposed the following Specific Aims. Aim # 1 to generate and characterize mice with an inactivated betasubunit of EnaC. Aim # 2 to generate and characterize transgenic mice with overexpression of a mutated GammahEnaC. Aim # 3 to characterize the role of ENaC in the acute and chronic regulation of renal sodium handling and arterial pressure in genetically manipulated mouse models. We will utilize the powerful methods of gene targeting and transgenic technology to generate murine models with under-and overexpression of ENaC activity. Generation of transgenic mice overexpressing a mutated Gamma hENaC has already been achieved, and correctly targeted embryonic stem (ES) cell clones with an inactivated Beta EnaC allele have been pro9duced. This set of constructs will uniquely enable us to dissect the relative importance of ENaC. In the proposed studies we will utilize a comprehensive approach which will entail molecular biological, electrophysiological, and conscious whole animal physiology experiments. Recent advances in our ability to culture murine inner medullary collecting duct (IMCD) cells will allow us to conduct direct electrophysiological studies of sodium transport in the distal nephron. Finally, we have developed the expertise and tools necessary to measure cardiovascular and renal function parameters in conscious, chronically instrumented mice, and thus have the ability to perform essential physiological experiments. Information gained from these studies will provide important new insights into the mechanisms involved in the physiology of sodium homeostasis and arterial pressure control. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISM OF RENAL ACID/BASE HOMEOSTASIS Principal Investigator & Institution: Dubose, Thomas D.; Chief, Division of Nephrology; Internal Medicine; University of Kansas Medical Center Msn 1039 Kansas City, Ks 66160 Timing: Fiscal Year 2002; Project Start 01-JUL-1981; Project End 31-AUG-2002 Summary: Abundant evidence has established a pivotal role for an H+, K+- ATPase in renal K+ homeostasis and acid-base balance. The regulatory response of the H+, K+ATPases to chronic hypokalemia and chronic acidosis has been localized to the outer medullary and inner medullary collecting ducts (OMCD and IMCD). Two, and perhaps more, alpha-subunit isoforms have been localized to the mammalian kidney, but uncertainties remain with respect to participation of specific alpha isoforms in segmental K+ and acid-base homeostasis. Transport studies have been forced to rely on the effect of "specific" inhibitors of the H+, K+-ATPase (such as Sch 28080) to identify
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that component of bicarbonate and/or K+ absorption attributable to this transporter. Since the H+, K+-ATPases exhibit differing sensitivities to ouabain and Sch 28080, it is not known with certainty if modulations in transport and the well established response to chronic metabolic acidosis and hypokalemia are the result of modulation in function of HKalpha1, HKalpha2, HKalpha4, or yet to be identified isoforms. This study is designed to elucidate the pathophysiologic factors which regulate at both molecular and functional levels, at H+, K+-ATPases in collecting duct segments, and in medullary collecting cells in culture. By transfecting mOMCD1, and mIMCD-3 cells with anti-sense HKalpah1, HKalpha2, and HKalpha4, we will define which isoform is responsible for the well-accepted adaptive response to chronic hypokalemia. We will then define the molecular equivalent of the H+, K+-ATPase enzymatic activity characterized as type III, which is upregulated by chronic K+ depletion. This approach will required the synthesis and screening of a subtraction cDNA library. Thirdly, we will determine if aldosterone or endothelin regulate H+, K+-ATPase function in mOMCD1 and mIMCD-3 cells in culture, and if so, we will delineate the alpha, H+, K+-ATPase iosoform responsible. Finally, we will define the contribution of the H+, K+-ATPases to net acid secretion in the OMCDis perfused in vitro during metabolic alkalosis without K+ depletion. Metabolic alkalosis with and without hypokalemia will then be simulated in mOMCD1, cells in culture to delineate whether hypokalemia or alkalemia per se upregulates the alpha H+, K+-ATPase, and if so, which alpha H+, K+-ATPase isoform responds specifically to each condition. These studies will help to elucidate the means by which K+ depletion can maintain metabolic alkalosis. The H+, K+- ATPase remains a candidate gene for abnormal structure and function in inherited and acquired forms of distal renal tubular acidosis. To understand this group of disorders more completely, fundamental studies which elucidate the molecular regulation of this family of transporters will be necessary to further our understanding of the pathophysiology of this disorder. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MECHANISM OF RENAL TUBULAR ANION TRANSPORT Principal Investigator & Institution: Aronson, Peter S.; Professor; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2002; Project Start 01-DEC-2001; Project End 30-NOV-2002 Summary: The principal focus of this project continues to be the mechanisms of anion transport in the proximal tubule. Studies during the past decade have supported a model by which transcellular CI-absorption in the proximal tubule involves uphill CIuptake across the luminal membrane by exchange with formate and oxalate. Recycling of formate occurs by H/+- couple formate transport in parallel with Na/+-H/+ exchange, whereas next project period we propose to investigate two aspects of proximal tubule anion transport. First, we plan to complete the cDNA cloning and carry out the physiological characterization of a novel transporter that is likely to play a role in mediating apical membrane anion transport. Specifically, we will isolate, clone and sequence cDNAs encoding the transporter, determine anion specificity and transport modes by functional expression in Xenopus oocytes; general specific antibodies, and determine cell and membrane sites of expression; determine whether different isoforms of the transporter exist; examine structure-function relationships by use of chimeric constructs; and estimate the contribution of the transporter to integrated tubule function in microperfusion studies in mice with targeted disruption of the transporter gene. Second, in collaboration with Gerhard Giebisch (project#1), we propose to continue studies of the mechanisms of regulation of transcellular NaHCO/3 and NaCI
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Metabolic Acidosis
reabsorption in the proximal tubule. Specifically, we will measure the activities of both anion exchanges (CI-formate and CI-oxalate) and recycling pathways (H+-coupled formate transport, Na/+- sulfate co-transport, oxalate-sulfate exchange) in renal brush border vesicles isolated from rats subjects to conditions that regulate proximal NaHCO/3 and NaCI reabsorption (eg. metabolic acidosis, hypokalemic alkalosis, furosemide-induced volume contraction). Activities of these pathways in membrane vesicles will be correlated with rates of transtubular HCO/3- and CI- reabsorption in the intact tubule under similar conditions. We will thereby test the hypothesis that activities of luminal membrane anion transporters are appropriate altered tot permit independent regulation of proximal tubule NaHCO/3 and NaCI reabsorption. The proposed project will provide new information on the molecular mechanisms and regulation of renal CItransport, and is therefore of relevance for understanding clinical disorders of NaCI balance. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MITOCHONDRIAL DYSFUNCTION IN PEDIATRIC HEAD INJURY Principal Investigator & Institution: Robertson, Courtney L.; Assistant Professor; Pediatrics; University of Maryland Balt Prof School Baltimore, Md 21201 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2007 Summary: (provided by applicant): Following traumatic brain injury (TBI), the immature rat brain experiences many secondary insults that lead to delayed cell death. Although considerable evidence indicates that mitochondria are primary mediators of ischemic and excitotoxic neural cell death and survival, relatively little is known regarding mitochondrial involvement in adult TBI, and nothing has been reported for models of pediatric TBI. Limited studies of the immature rat brain have demonstrated vulnerability to many known mediators of mitochondrial injury, including elevated intracellular calcium and oxidative stress. Mitochondrial alterations can also trigger the cascade of caspase activities that mediate apoptosis, a process of programmed cell death that appears particularly important in TBI. The working hypothesis for the proposed study is that the response of brain mitochondria to metabolic acidosis, elevated calcium, oxidative stress, and pro-apoptotic proteins plays an integral role in the neurochemical, histologic, and neurologic outcome following pediatric TBI. We will test the following mechanistic hypotheses using a clinically relevant model of pediatric TBI: 1) Mitochondrial injury early after TBI increases the sensitivity of mitochondria to cellular factors that promote apoptotic or necrotic cell death cascades. 2) Cerebral lactic acidosis after TBI promotes cytochrome c release, mediated by mitochondrial swelling due to activation of the membrane permeability transition. 3) Oxidative stress following TBI contributes to mitochondrial dysfunction, cell death and neurologic injury. This study will help define the molecular mechanisms by which mitochondria are injured after TBI in immature animals. This may identify novel targets for neuroprotection following TBI in infants and children. This proposal is intended to provide for the research experience and career development of the applicant, specifically involving the mechanisms of, and therapeutic strategies for, the treatment of acute brain injury. The Departments of Anesthesiology and Pediatrics, and the Brain Injury and Neuroprotection Research Group at the University of Maryland will provide a rich environment for the study of experimental brain injury, and have a strong commitment to fostering meaningful and contemporary research in this field. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MOLECULAR BASIS OF SKELETAL GROWTH IN RENAL FAILURE Principal Investigator & Institution: Kaskel, Frederick J.; Developmental Renal and Electrolyte Phys; Montefiore Medical Center (Bronx, Ny) Bronx, Ny 104672490 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 29-SEP-2004 Summary: (provided by applicant): Growth failure is highly prevalent in children with chronic kidney disease (CKD) both pre-and post-transplantation, and is a significant cause of morbidity and mortality. The causes of impaired linear growth may include protein energy malnutrition, chronic metabolic acidosis and anemia, recurrent infections, endocrinopathies, and steroid therapy. Despite aggressive supportive therapies, the condition persists and its impact on neurocognitive development is unknown. Identification of the molecular events controlling normal skeletal growth and development may: l ) allow better understanding of the pathophysiology of renal osteodystrophy and growth failure children with CKD; and, 2) direct new and improved therapies for these disorders resulting in the achievement of full growth potential and overall development. These goals serve as the basis for the International Pediatric Nephrology Association (IPNA)-sponsored Seventh Symposium on Growth and Development in Children with Chronic Renal Failure: The Molecular Basis of Skeletal Growth, to be held in Heidelberg, Germany, April 1-4, 2004. This conference builds on the success of the prior six such international scientific meetings and will continue to provide the opportunity for interaction between basic and clinical investigators studying skeletal growth and derangement secondary to CKD. Up to date scientific information regarding the molecular mechanisms for both normal and abnormal skeletal growth will be presented with the goal of developing new directions for research and treatment of the pathophysiology of growth failure in CKD. Participation of young investigators and trainees in nephrology and endocrinology with special consideration given to individuals who are underrepresented in science, will be a primary goal of this symposium and will be achieved by travel grants. Two poster sessions selected by the Scientific Organizing Committee will provide a forum for these participants to present their work for critical review prior to publication in a supplemental issue of the International Journal of Pediatric Nephrology. Meeting announcements via mail, journals, websites, and emails will reach the North and South American, European, Asian, and other International Societies of Pediatric Nephrology. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NOVEL ASSAY FOR ETHYLENE GLYCOL TOXICITY Principal Investigator & Institution: Kloepfer, Hans G.; Micronix, Inc. 14950 Greyhound Ct, Ste 307 Carmel, in 46032 Timing: Fiscal Year 2002; Project Start 01-AUG-1999; Project End 31-MAY-2003 Summary: (Applicant's abstract) Poisoning from ethylene glycol is a potentially lethal medical emergency but can be treated effectively when recognized early. Conversely, when diagnosis is late, the outcome is usually poor. The major pathogenic factor is metabolic acidosis from glycolic acid (glycolate). Because laboratory testing for ethylene glycol and glycolate is severely restricted, timely diagnosis depends on comparatively nonspecific physical signs and laboratory tests. Lack of access to specific testing and need for differentiation from conditions featuring similar symptoms constitute a unique medical dilemma. Recognizing these deficiencies we propose to develop novel, specific enzymic assays for ethylene glycol and glycolate. Two product configurations are perceived: 1) aqueous reagents for existing clinical analyzers (serum, quantitative); 2) a dry-chemistry, dual-analyte point-of-care testrip method (whole blood, semi-
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Metabolic Acidosis
quantitative).The POC method is a dual-analyte test tab device for the simultaneous estimation of ethylene glycol and glycolate from approximately two (2) microliters of whole blood without centrifugation or any other form of sample or reagent handling. To make such a level of miniaturization and simplicity feasible, we have developed a capillary fill sampling technique permitting specimen dosing, plasma separation, and red cell removal in one wholly integrated step. Because of rapid metabolism of (flontoxic) ethylene glycol and the longer half life of (toxic) glycolate, the latter provides better prognostic information and improved clinical sensitivity, especially late postingestion. Thus, rapid and simultaneous availability of test results for both analytes expands the window of diagnostic/therapeutic opportunity. Socioeconomic benefits are: 1) reducing expensive gas chromatographic screening, confirmatory and other testing; 2) averting late or unnecessary treatment; 3) cutting intensive care and hospital stay; 4) abating long term morbidity (renal dialysis). PROPOSED COMMERCIAL APPLICATION: Most current gas chromatographic screening and confirmatory methods for ethylene glycol require derivatization, sample pretreatment and special columns. Direct methods are fraught with analytical problems such as peak overlap and trailing. Cases have been reported where other compounds were identified as ethylene glycol with serious consequences. All methods require specialized equipment unavailable in most laboratories, are technically demanding, time consuming, and relatively insensitive. For these reasons access to timely and reliable testing for ethylene glycol is extremely limited. Testing for the clinically more sensitive and relevant toxic metabolite glycolic acid is essentially non-existant. Not a single routine clinical analyzer currently exists offering either an ethylene glycol or glycolate method. The proposed products would solve these problems. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PATHOGENESIS OF RETINOPATHY OF PREMATURITY Principal Investigator & Institution: Holmes, Jonathan M.; Professor and Chairman; Mayo Clinic Coll of Medicine, Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2002; Project Start 01-FEB-2000; Project End 31-JAN-2004 Summary: (Adapted from the applicant's abstract): Retinopathy of prematurity (ROP) is a blinding disease of premature infants resulting from development of abnormal blood vessels in the immature retina. It has been well established that excess oxygen is an important causative factor in the pathogenesis of ROP. Nevertheless, despite the more careful use of oxygen, the incidence of ROP is increasing in the United States. In addition, current treatments for severe ROP fail to prevent blindness in a large proportion of infants. Therefore, further research into the pathogenesis of ROP is critical to increase our understanding of the disease and to develop new methods of prevention and treatment. Infants who never experience hyperoxia (e.g., those with congenital heart disease) may also develop ROP. For these infants in particular, and for premature neonates in general, systemic acidosis has been implicated as a risk factor in the development of ROP. A new neonatal animal model has been developed that allows study of metabolic acidosis and retinal neovascularization. The investigator has confirmed that metabolic acidosis alone leads to preretinal neovascularization in the retina of immature animals, and has termed this model "metabolic acidosis-induced retinopathy" (MAIR). Using this model, the investigator proposes to characterize the effect of acidosis on the immature retina and investigate biochemical and molecular mechanisms. These studies may lead to new avenues of prevention and treatment of ROP. The primary hypothesis for this series of experiments is that: "acidosis is a risk factor for ROP in human neonates." This leads to the following secondary hypotheses
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that will be tested in the MAIR model, which is that: (1) a dose-response relationship exists between the extent of metabolic acidosis and the severity of retinopathy in the neonatal rat model; (2) neovascularization in the acidotic model is mediated by downregulation followed by up-regulation of one or more growth factors including vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and insulin-like growth factor 1 (IGF-1); and (3) the retinopathy can be prevented by reversal of acidosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PH REGULATION IN VENTRICULAR CELLS Principal Investigator & Institution: Spitzer, Kenneth W.; Cardiovascular Research and Training Institute; University of Utah Salt Lake City, Ut 84102 Timing: Fiscal Year 2002; Project Start 01-JUL-1989; Project End 30-JUN-2003 Summary: The long-term goal of this research is to better understand the mechanisms that regulate intracellular pH (pHi) in adult mammalian heart muscle. In this project we focus on three main areas: 1) peptide modulation of sarcolemmal ion transporters involved in cardiac pHi control, 2) H+ diffusion within cardiac cells and 3) H+ diffusion between cardiac cells, through gap junctions. These topics are closely related since the pHi changes induced by the ion transporters, which are initially confined to the subsarcolemmal space, must eventually reach the cell interior and neighboring cells to exert their full physiologic effect. The peptide studies focus on angiotensin II (AngII), endothelin 1 (ET1) and atrial natriuretic peptide (ANP). These agents exert a wide range of potent effects on cardiac function under both normal and pathological conditions. We will examine peptide effects on HCO3-CI exchange and CI-OH exchange. These acid loading systems are critically important in mediating pHi recovery from intracellular alkalosis and the fall in pHi during metabolic acidosis. The ANP studies focus on identifying its effects on Na-H exchange, Na-HCO3 cotransport, HCO3-CI exchange and CI-OH exchange. The peptide experiments will be performed on ventricular and atrial myocytes, enzymatically isolated from adult rabbits. pHi will be measured in single cells using epifluoresence techniques and the H+ sensitive indicator, SNARF-1. The H+ diffusion studies are designed to characterize H+ diffusion within and between single cardiac cells under a variety of conditions which are likely to create regional pHj gradients. The experiments will be performed on both single myocytes and myocyte pairs (ventricular and Purkinje, rabbit) using confocal microscopy and SNARF-1 to measure pHi. The results of this project will yield new information concerning hormonal modulation of cardiac pHi control systems and the action of intracellular and intercellular H+ diffusion to dissipate regional pHi gradients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PHYSIOLOGY OF ELECTROGENIC NA/HCO3 COTRANSPORTERS Principal Investigator & Institution: Boron, Walter F.; Cellular/Molecular Physiology; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2002; Project Start 01-JAN-1982; Project End 30-NOV-2006 Summary: A major task of the kidney tubule is to reabsorb filtered HCO-3 and generate "new" HCO-3, thereby preventing a fatal metabolic acidosis. About 80 percent of HCO3 reabsorption and generation occurs in the proximal tubule (PT), which secretes H+ into the tubule lumen, titrating HCO-3 to CO2 + H2O. After entering the PT cell, the CO2 + H2O regenerate HCO-3, which exits across the basolateral membrane via the electrogenic Na/HCO3 cotransporter (NBCe1-A). Since the Pl's laboratory reported the expression cloning of this cotransporter nearly 5 yrs ago, both "pancreatic" (NBCe1-B)
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and "brain" (NBCe1-C) splice variants have been identified. These cotransporters play key roles in HCO-3 transport by other epithelia, and in pHi regulation by many cell types. NBCe1 is part of the Bicarbonate Transporter (BT) superfamily, along with the C1-HCO3 exchangers (AEs), two other Na+ -coupled HCO-3 transporters (the electroneutral NBC and the Na+ -driven C1-HCO3 exchanger), related proteins not yet fully characterized, and at least one new gene (known from human genome sequence). The major goal of this project is to elucidate the molecular physiology of electrogenic NBCs, particularly in the kidney. An ancillary goal is to elucidate the expression of other Na+ -coupled HCO-3 transporters in key renal cell types. The proposed work has three aims: (i) Develop molecular tools. We will obtain the cDNA for a new NBCe-related sequence identified in the genome, extend our panel of type-specific antibodies, and determine the localization of Na+ -coupled HCO-3 transporters in the kidney. (ii) Determine properties of wild- type electrogenic NBCs. Using heterologous expression in oocytes, we will determine the function of two cDNA clones likely to encode electrogenic NBCs. We will also determine the stoichiometry of the electro-genic NBCs; assess their dependence on Na+, HCO-3 and pH; ask whether they transport CO=3; characterize the interaction between NBCe1 and carbonic anhydrase II; and examine the action of PKA on NBCe1 in oocytes. (iii) Analyze structure-function relationships. We will determine the structural requirements for extra- and intracellular DIDS sensitivity, ask whether conserved putative DIDS-reaction motifs are involved in electrostatic trapping of HCO-3, assess naturally occurring human NBCe1 mutations, explore the topology of NBCe1, and-in collaboration with another laboratory-study the biochemistry of the isolated cytoplasmic N termini of NBCe1-A and -B. The proposed work should elucidate the role that the electrogenic Na/HCO3 cotransporter plays in renal function, both in health and disease. The results could have important implications for understanding the normal control of acid-base balance and renal-tubule acidosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PILOT STUDY--REGIONAL BLOOD FLOW IN FRESH WATER TURTLES Principal Investigator & Institution: Crocker, Carlos E.; San Francisco State University 1600 Holloway Ave San Francisco, Ca 941321722 Timing: Fiscal Year 2003; Project Start 01-JAN-2003; Project End 31-DEC-2006 Summary: The primary goal of this study is to increase understanding of the physiology of diving in North American freshwater turtles. This research will quantify how environmental hypoxia (severe < 50% oxygen saturation), and/or moderate hypoxia (75 - 50% saturation), which leads to hypoxic hypoxia, affects the cardiovascular system. Ischemic hypoxia can cause irreversible damage to tissues; the protection of brain and heart function during long-term submergence is critical to survival. Hypoxic hypoxia produces cardiac insufficiency and alters peripheral vascular resistance, and it is currently hypothesized that it results in significant changes in the regional distribution of cardiac output to the vital organs (e.g. brain, heart, liver), at the expense of non-vital tissues/organs (e.g. skeletal muscle, gastrointestinal tract). To test this hypothesis, experimental animals will be fitted with indwelling catheters and one or more surgically implanted ultrasonic flow probes, for the measurement of blood flow to specific organs/tissues during prolonged aquatic submergence. Periodic sampling from the indwelling arterial cannula will provide blood samples for analysis of physiologically important acid-base relevant ions, plasma stress hormone concentrations (primarily epinephrine and cortisol), blood gases (O2 and CO2) and pH. Overall, this research will show that systemic hypoxia, cold-induced metabolic depression, and the progressive
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metabolic acidosis associated with prolonged aquatic submergence results in preferential blood distribution that favors the vital organs over the 'less critical' tissue masses. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PILOT--REGULATION OF RENAL PYRUVATE DEHYDROGENASE DURING ACIDOSIS Principal Investigator & Institution: Harris, Robert A.; Professor of Pharmacology; Indiana Univ-Purdue Univ at Indianapolis 620 Union Drive, Room 618 Indianapolis, in 462025167 Timing: Fiscal Year 2002; Project Start 01-JUN-2002; Project End 31-MAY-2007 Summary: The objective of this work is to establish the importance of regulation of the pyruvate dehydrogenase (PDH) complex in the kidney in maintenance of acid-base balance. Activity of the pyruvate dehydrogenase complex is regulated by covalent modification. Phosphorylation and inactivation of the complex is catalyzed by four pyruvate dehydrogenase kinase (PDK) isoenzymes; dephosphorylation by two pyruvate dehydrogenase phosphatase (PDP) isoenzymes. Unique regulatory properties of these isoenzymes and differences in their levels of expression in different cell types provide tissue specific control of the activity of the pyruvate dehydrogenase complex. The basis for this proposed work is our preliminary data indicating that two of the PDK isoenzymes, PDK2 and PDK4, are increased in the kidney by metabolic acidosis. We propose therefore that increased expression of these PDKs results in inactivation of pyruvate dehydrogenase complex, which promotes generation of new bicarbonate by the kidney. Our working hypothesis is that alterations in the expression of the PDK2 and PDK4 isoenzymes cause hyperphosphorylation and therefore inactivation of pyruvate dehydrogenase complex in kidney during metabolic acidosis. The hypothesis will be tested by: (a) determining the effects of acute and chronic metabolic acidosis and alkalosis on activity state of the PDH complex and the expression levels of its kinases and phosphatases in rat kidney; (b) determining whether the compensatory mechanism for metabolic acidosis is abnormal in the kidney of the PDK4 null mouse; and (c) establish factors and mechanisms that regulate expression of PDK2, PDK4, and PDP2 in the kidney. The findings are expected to provide new insight with respect to an important compensatory mechanism for life threatening metabolic acidosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PROTEIN METABOLISM IN CHRONIC RENAL FAILURE PATIENTS Principal Investigator & Institution: Lim, Victoria S.; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2002 Summary: To study protein metabolism in patients with end-stage renal disease, we measured leucine kinetics in 8 patients. Study was performed twice before and once after (period III)( initiation of maintenance dialysis treatment. Before dialysis, one measurement was done when the patients are acidotic (period I), and the other during sodium bicarbonate supplementation when acidosis was corrected (period II). Sequence of Periods I and II were randomized. Subjects were on identical constant diet during all three periods. Leucine kinetics was measured during primed-constant infusion of [113C]leucine, [1-13C]KIC or ( keto-isocaproate and expired breath CO2 enrichment were directly determined. These values were used to calculate leucine appearance rates into the plasma leucine pool and into the total body leucine pool and leucine oxidation rate.
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The former represents protein degradation rat; protein synthesis rate was indirectly estimated by mass balance equation. The h igher leuc ine oxidation rate without bicarbonate supplementation was not due to higher VCO2 as total CO2 production rate was not different during the three periods. Alternatively, higher proportion of endogenously produced CO2 may be excreted than in the non-acidotic state. Finally, these findings may represent a real enhancement of amino acid oxidation in the presence of metabolic acidosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PROTEIN NUTRITION IN EXPERIMENTAL UREMIA Principal Investigator & Institution: Mitch, William E.; Professor and Chairman; Internal Medicine; University of Texas Medical Br Galveston 301 University Blvd Galveston, Tx 77555 Timing: Fiscal Year 2002; Project Start 01-SEP-1987; Project End 30-NOV-2005 Summary: Uremia is often associated with weight loss, reduced muscle mass and a low serum albumin. Our long-term goal is to identify cellular mechanisms causing protein malnutrition in uremia to improve treatment. In rats with chronic renal failure (CRF), we identified metabolic acidosis as a stimulus for accelerated muscle protein degradation. This proteolytic response was confirmed in patients and is now vigorously treated to improve their nutritional status but the mechanism(s) underlying muscle catabolism is unknown. Factors that we identified as activators of the ubiquitinproteasome (Ub-P'some) Proteolytic pathway in muscle are a low extracellular pH, glucocorticoids and a low insulin level. Important problems to be solved are: first, myofibrillar proteins are not degraded and adding actin blocks myosin degradation by the Ub-P'some system. Our Preliminary Results indicate that the protease, caspase 3, is induced by acidification and plays a role in the early stages of muscle cell proteolysis by degrading myofibrillar proteins and actin to a stage where degradation proceeds via the Ub-P'some pathway. A second problem is how to integrate multiple signals that can activate the Ub-P'some system. We propose that depressed phoshatidylinositol 3-kinase (PI 3-kinase) is a key step as: we find CRF reduces muscle PI 3-kinase activity and insulin (or IGF- 1) blocks caspase 3 activation in muscle cells. A third problem is to understand how signals that initiate muscle proteolysis invariably stimulate transcription of genes encoding components of the Ub-P'some pathway. Since clinical evidence suggests an important role for TNFalpha in causing muscle wasting in CRF, we will examine the opposing actions between glucocorticoids and a TNFalphainducible transcription factor, NF-kB, on transcription of the C3 proteasome subunit to understand the requirement for glucocorticoids in stimulating transcription in many catabolic conditions. Finally, we will examine how TNFalpha influences protein degradation in muscle of CRF rats and in cultured muscle cells. Our results will uncover cellular mechanisms regulating protein turnover in uremia and other catabolic conditions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RENAL BASIS OF HYPOCITRATURIA Principal Investigator & Institution: Alpern, Robert J.; Dean; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2002 Summary: (Taken directly from the application) Hypocitraturia is an important cause of kidney stones. Citrate is freely filtered in the glomerulus, and urinary citrate excretion is
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regulated principally by the rate of citrate reabsorption and metabolism in the proximal tubule. Reabsorption is mediated by an apical membrane 3Na+/citrate cotransporter encoded by the NaDC-1 gene, and metabolism is mediate by one of two pathways: a mitochondrial pathway that mediates citrate metabolism in the tricarboxylic acid cycle; and a cytoplasmic pathway in which ATP citrate lyase metabolizes citrate to acetyl CoA and oxaloacetate. The proposed studies will examine the molecular mechanisms responsible for regulation of citrate reabsorption and metabolism, focusing on NaDC-1. Studies in Aim 1 will address the molecular mechanisms of NaDC-1 regulation in rats with chronic metabolic acidosis, K+ deficiency, alkali feeding, and starvation. Studies in Aim 2 will further address the molecular mechanisms of NaDC-1 regulation in cultured proximal tubule cells exposed to acidic extracellular fluid. These studies will utilize cells expressing native NaDC-1, as well as cells expressing stably transfected tagged NaDC-1, and transiently transfected reporter constructs. Aim 1 and 2 together will address the regulation of NaDC-1. Studies in Aim 3 will address the role of signaling pathways known to be activated by acidosis in the regulation of NaDC-1. These pathways include: 1) tyrosine kinase and MAP kinase pathways; 2) glucocorticoids; and 3) endothelin. Studies in Aim 4 will quantitate citrate metabolism in mitochondrial and cytoplasmic pathways of the renal proximal tubule using 13C NMR spectroscopy. Lastly, studies in Aim 5 will address whether hyperkalemia causes hypercitraturia and thus is responsible for the lack of predisposition to nephrolithiasis in hyperkalemic renal distal tubular acidosis. These studies will allow us to continue to pursue an understanding of the mechanisms of regulation of renal citrate handling in the proximal tubule. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: RENAL CONTRANSPORTER
NET
ACID
SECRETION
AND
THE
NA/K/2C1
Principal Investigator & Institution: Wall, Susan M.; Professor; Internal Medicine; University of Texas Hlth Sci Ctr Houston Box 20036 Houston, Tx 77225 Timing: Fiscal Year 2002; Project Start 01-APR-1993; Project End 31-JAN-2004 Summary: Two distinct genes (BSC-1 and BSC-2) encode the NA/+-K/+-2CI- cotransporter. BSC-1, or the "absorptive isoform", is kidney-specific and localizes to the apical membrane of the thick ascending limb. BSC-2, the "secretory" isoform, is widely distributed BSC-1 is responsible for the "single effect" of the countercurrent multiplier, and thereby generates an axial gradient in the medullary interstitium for ammonium and other solutes, facilitating net acid secretion and urinary concentration. In the thick ascending limb, NH/4 uptake by the Na/+-K/+-2CI-co-transporter (BSC-1) is highly regulated. Since BSC-2 localizes to the basolateral membrane of the rat alpha intercalated cell and since it is both an NH/4 amd a CO/transporter, it likely mediates net acid secretion. However, regulation of BSC-2 in the kidney and its role in net acid secretion are untested. Regulation of net CI- and H/+ secretion by the collecting duct requires transport of these ions to be regulated in parallel across the apical and the basolateral membrane of the collecting duct cell. With perturbations in acid-base balance such as chronic metabolic acidosis an increase in apical proton secretion is observed which results from up- regulation of the apical H/+-ATPase in parallel with the basolateral CI- HCO/3-exchanger. However, in the rat contribution of CI-/HCO/3exchange to transepithelial net acid and CI-secretion has not been established. Thus, another mechanism for net H/+ and/or CI-uptake across the basolateral membrane may be important in mediating or modulating transepithelial net acid secretion. We will determine the contribution of BSC-2 to transepithelial net acid and net CI-secretion. Moreover, we will determine if activity of the co-transporter is modulated in a fashion
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Metabolic Acidosis
appropriate for correction of perturbations in acid-base balance. With the recent cloning of both isoforms of the co-transporter, the published structure has been exploited to raise antibodies against co-transporter peptides. These antibodies can be used to study the long term regulation of the co-transporter. Changes in protein immunoreactivity and mRNA can be correlated with changes in transport activity to determine the role of the co-transporter in acid-base homeostasis. Specific Aims are to determine the following in the rat OMCD: 1. If BSC-2 modulates net acid secretion through direct NH/4+ uptake. 2. If BSC-2 is a major contributor to transepithelial net CI- secretion. 4. To determine the mechanism of BSC-2 transport regulation. To answer these questions, isolated renal tubules perfused in vitro will be studied. Transport will be studied with microfluorimetry as well as pH sensitive fluorescent probes. Transporter immunoreactivity and message abundance will be studied using immunoblots, immunocytochemistry and RT PCR. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE EXCHANGERS
AND
REGULATION
OF
INTESTINAL
SODIUM/H+
Principal Investigator & Institution: Chang, Eugene B,.; Martin Boyer Professor of Medicine; Medicine; University of Chicago 5801 S Ellis Ave Chicago, Il 60637 Timing: Fiscal Year 2002; Project Start 01-JUL-1986; Project End 31-MAR-2003 Summary: Intestinal epithelial cell Na-H exchanger (NHE) isoforms have very specialized functions, regulatory systems, cellular distribution, and regional patterns of expression which are inherently important in adapting to acute and chronic metabolic demands and changes in liminal Na load. Until now, the regulation of NHE isoforms has largely been studied in mutant, NHE-deficient, non-epithelial cells where some findings, particularly with the epithelial-specific NHE-2 and NHE-3 isoforms, substantially differ from NHE function and regulation in intact enterocytes. These isoforms are believed to be the major route for non-nutrient dependent Na absorption by the gut. Therefore, the goal of this proposal is to test the hypothesis that the role and regulation of intestinal epithelial NHE isoforms are unique and best studied in intestinal epithelial cells in vivo and in vitro. The first Specific Aim is to characterize the role of intestinal epithelial NHEs in mediating the adaptation of intestinal Na absorption following massive small bowel resection and chronic metabolic acidosis in the rat. Preliminary studies show striking isoform-, region-, and cell-specific changes in NHE function and expression in response to these conditions. Additional studies will be performed to define the cellular and molecular bases for these adaptive responses. Potential determinants of the adaptive changes in the NHE expression, i.e. alterations in Na luminal load or metabolic/hormonal perturbations, will be experimentally assessed. In Specific Aim #2, Caco-2/C2BBE (C2) intestinal epithelial cell monolayers will be used to examine specific mechanisms of NHE function, regulation, and expression in response to extracellular metabolic perturbations and stimuli. C2 cells spontaneously differentiate in culture, have endogenous NHE-1, but little apical NHE expression, and, when transfected with NHE-2 or NHE-3, demonstrate correct sorting and functional and regulatory characteristics of these proteins that correlate with observations made in native enterocytes. NHE isoform activities expressed in C2 cells can also be separately measured. The roles of protein phosphorylation, membrane recycling, post-translational modifications, and potential regulatory roles of NHE binding proteins in mediating NHE responses to hormonal stimuli, luminal Na load, metabolic acidosis, and states of cellular differentiation will be examined. These studies will provide important insights into the gut-specific cellular and molecular mechanisms for regulation of intestinal
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epithelial NHEs and into physiologically-relevant mechanisms mediating the Na absorptive response of the gut to acute and chronic metabolic perturbations. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SUBUNIT STRUCTURE AND FUNCTION IN VACUOLAR H+ATPASE Principal Investigator & Institution: Kane, Patricia M.; Professor; Biochem and Molecular Biology; Upstate Medical University Research Administration Syracuse, Ny 13210 Timing: Fiscal Year 2003; Project Start 01-MAR-1994; Project End 31-MAY-2007 Summary: (provided by applicant): Vacuolar proton-translocating ATPases (V-ATPases) couple hydrolysis of cytosolic ATP to proton transport into organelles of all eukaryotic cells and across the plasma membrane of some cell types. Organelle acidification, the major constitutive function of V-ATPases, is essntial for many physiological processes, but is also linked to a number of disease states. For example, acidification of phagosomes is essential for killing invading bacteria, but many viruses and toxins exploit the acidic environment generated by V-ATPases to facilitate their escape from organelles into the cytoplasm where they become biologically active. Plasma membrane V-ATPases are involved in renal acid secretion and osteoclast bone dissolution; mutations in tissue-specific V-ATPase subunit isoforms necessary for these processes result in genetic diseases characterized by metabolic acidosis and osteoporosis. The long-term goal of the lab is to understand the structure, function, assembly and regulation of V-ATPases by studying the yeast V-ATPase, which has proven to be an excellent model for all eukaryotic V-ATPases. All V-ATPases are composed of two multisubunit domains, a peripheral membrane complex involved in ATP hydrolysis and an integral membrane complex required for proton transport. In this proposal, we focus on the "stalk" subunits that structurally and functionally bridge these two domains. These subunits are responsible for transmission of conformational changes resulting from ATP hydrolysis to the proton pore, and are also key players in regulated disassembly of V-ATPases, an important regulatory mechanism. The aims of this proposal are: 1) to position the stalk subunits in the yeast V-ATPase, by a combination of electron microscopy, hydrodynamic studies of subcomplexes, mutagenesis, and crosslinking experiments, 2) to elucidate the roles of the C and H subunits, particularly in the functionally important conformational change accompanying release of the peripheral sector from the membrane sector, 3) to examine protein-protein interactions with two isoforms of the "a" subunit and test their importance in regulated disassembly, and 4) to follow V-ATPase assembly and disassembly in vivo using GFP-tagged VATPase subunits. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National
3
Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.
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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 “metabolic acidosis” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for metabolic acidosis in the PubMed Central database: •
Acute metabolic acidosis enhances circulating parathyroid hormone, which contributes to the renal response against acidosis in the rat. by Bichara M, Mercier O, Borensztein P, Paillard M.; 1990 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=296745
•
Changes in Bone Sodium and Carbonate in Metabolic Acidosis and Alkalosis in the Dog. by Burnell JM.; 1971 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291928
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Chronic metabolic acidosis causes an adaptation in the apical membrane Na/H antiporter and basolateral membrane Na(HCO3)3 symporter in the rat proximal convoluted tubule. by Preisig PA, Alpern RJ.; 1988 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=442703
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Chronic metabolic acidosis decreases albumin synthesis and induces negative nitrogen balance in humans. by Ballmer PE, McNurlan MA, Hulter HN, Anderson SE, Garlick PJ, Krapf R.; 1995 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=295365
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Chronic metabolic acidosis increases the serum concentration of 1,25dihydroxyvitamin D in humans by stimulating its production rate. Critical role of acidosis-induced renal hypophosphatemia. by Krapf R, Vetsch R, Vetsch W, Hulter HN.; 1992 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=443402
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Contribution of individual superficial nephron segments to ammonium handling in chronic metabolic acidosis in the rat. Evidence for ammonia disequilibrium in the renal cortex. by Simon E, Martin D, Buerkert J.; 1985 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=423918
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EFFECT OF ACUTE METABOLIC ACIDOSIS AND ALKALOSIS ON ACETATE AND CITRATE METABOLISM IN THE RAT. by Gordon EE.; 1963 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=289262
4
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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•
Effect of in vitro metabolic acidosis on luminal Na+/H+ exchange and basolateral Na+:HCO3- cotransport in rabbit kidney proximal tubules. by Soleimani M, Bizal GL, McKinney TD, Hattabaugh YJ.; 1992 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=443083
•
Glucose Utilization and Production by the Dog Kidney In Vivo in Metabolic Acidosis and Alkalosis. by Costello J, Scott JM, Wilson P, Bourke E.; 1973 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=302299
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Metabolism of Glutamine by the Intact Functioning Kidney of the Dog STUDIES IN METABOLIC ACIDOSIS AND ALKALOSIS. by Pitts RF, Pilkington LA, MacLeod MB, Leal-Pinto E.; 1972 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=302161
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Parallel adaptation of the rabbit renal cortical sodium/proton antiporter and sodium/bicarbonate cotransporter in metabolic acidosis and alkalosis. by Akiba T, Rocco VK, Warnock DG.; 1987 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=442239
•
Renal ammoniagenesis in an early stage of metabolic acidosis in man. by Tizianello A, Deferrari G, Garibotto G, Robaudo C, Acquarone N, Ghiggeri GM.; 1982 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=371188
•
Renal Metabolic Response to Acid-Base Changes. II. THE EARLY EFFECTS OF METABOLIC ACIDOSIS ON RENAL METABOLISM IN THE RAT. by Alleyne GA.; 1970 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=322557
•
Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs. by Adrogue HJ, Chap Z, Ishida T, Field JB.; 1985 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=423607
•
Studies of the Mechanism by Which Chronic Metabolic Acidosis Augments Urinary Calcium Excretion in Man. by Lemann J Jr, Litzow JR, Lennon EJ.; 1967 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=297133
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The influence of salt intake on the metabolic acidosis of chronic renal failure. by Espinel GH.; 1975 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=436586
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Metabolic Acidosis
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 metabolic acidosis, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “metabolic acidosis” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for metabolic acidosis (hyperlinks lead to article summaries): •
A 27-year-old homeless man with mental obtundation and a metabolic acidosis. Author(s): Szerlip HM. Source: Chest. 1999 May; 115(5): 1447-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10334168
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A 52-year-old acyanotic man with severe hypoxia and profound metabolic acidosis following an industry chemical exposure. Author(s): Zavotsky KE, Mentler P, Gronczewski C, Torres P. Source: Journal of Emergency Nursing: Jen : Official Publication of the Emergency Department Nurses Association. 2004 April; 30(2): 113-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15039666
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A chronic glue sniffer with hyperchloraemia metabolic acidosis, rhabdomyolysis, irreversible quadriplegia, central pontine myelinolysis, and hypothyroidism. Author(s): Hong JJ, Lin JL, Wu MS, Huang CC, Verberckmoes R. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1996 September; 11(9): 1848-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8918637
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A conceptual approach to the patient with metabolic acidosis. Application to a patient with diabetic ketoacidosis. Author(s): Shafiee MA, Kamel KS, Halperin ML. Source: Nephron. 2002; 92 Suppl 1: 46-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12401937
6
PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.
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•
A guide for predicting arterial CO2 tension in metabolic acidosis. Author(s): Fulop M. Source: American Journal of Nephrology. 1997; 17(5): 421-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9382159
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A newborn girl with watery diarrhea, weight loss, and severe metabolic acidosis. Author(s): Nizet V, Priebe CJ. Source: Current Opinion in Pediatrics. 1994 April; 6(2): 163-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8032396
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A non-insulin dependent diabetic man with metabolic acidosis. Author(s): Watterson MK, Patrick ST, Coleman MD, Morgan HJ. Source: Tenn Med. 1998 December; 91(12): 469-70. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9846083
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A stepwise approach to acid-base disorders. Practical patient evaluation for metabolic acidosis and other conditions. Author(s): Fall PJ. Source: Postgraduate Medicine. 2000 March; 107(3): 249-50, 253-4, 257-8 Passim. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10728149
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Absence of high anion gap metabolic acidosis in severe ethylene glycol poisoning: a potential effect of simultaneous lithium carbonate ingestion. Author(s): Leon M, Graeber C. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1994 February; 23(2): 313-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8311092
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Absence of metabolic acidosis in toxic methanol ingestion: a case report and review. Author(s): Sullivan M, Chen CL, Madden JF. Source: Del Med J. 1999 October; 71(10): 421-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10565083
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Accidental metabolic acidosis during hemodialysis. Author(s): Hartmann A, Reisaeter A, Holdaas H, Rolfsen B, Fauchald P. Source: Artificial Organs. 1994 March; 18(3): 214-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8185487
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•
Accidental substitution of acidic concentrate for acetate in dialysis fluid concentrate: a cause of severe metabolic acidosis. Author(s): Gainza FJ, Zarraga S, Minguela I, Lampreabe I. Source: Nephron. 1995; 69(4): 480-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7777118
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ACE-inhibitors-induced metabolic acidosis in a child with nephrotic syndrome. Author(s): Bruno I, Pennesi M, Marchetti F. Source: Pediatric Nephrology (Berlin, Germany). 2003 December; 18(12): 1293-4. Epub 2003 October 24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14579142
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Acetazolamide, alternate carbonic anhydrase inhibitors and hypoglycaemic agents: comparing enzymatic with diuresis induced metabolic acidosis following intraocular surgery in diabetes. Author(s): Zaidi FH, Kinnear PE. Source: The British Journal of Ophthalmology. 2004 May; 88(5): 714-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15090429
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Acid-base and endocrine effects of aldosterone and angiotensin II inhibition in metabolic acidosis in human patients. Author(s): Henger A, Tutt P, Riesen WF, Hulter HN, Krapf R. Source: The Journal of Laboratory and Clinical Medicine. 2000 November; 136(5): 379-89. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11079465
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Acute abdomen and unexplained metabolic acidosis in a chronic alcoholic. Author(s): McClelland A, Kannan S, Milligan KR. Source: Anaesthesia. 2000 September; 55(9): 926-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10947777
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Acute correction of metabolic acidosis increases serum procollagen type I carboxyterminal propeptide in patients with chronic renal failure. Author(s): Chu P, Lu KC, Lin YF. Source: J Formos Med Assoc. 2001 November; 100(11): 748-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11802533
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Acute mental status changes and hyperchloremic metabolic acidosis with long-term topiramate therapy. Author(s): Stowe CD, Bollinger T, James LP, Haley TM, Griebel ML, Farrar HC 3rd. Source: Pharmacotherapy. 2000 January; 20(1): 105-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10641984
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Acute metabolic acidosis decreases muscle protein synthesis but not albumin synthesis in humans. Author(s): Kleger GR, Turgay M, Imoberdorf R, McNurlan MA, Garlick PJ, Ballmer PE. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2001 December; 38(6): 1199-207. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11728951
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Acute metabolic acidosis in chronic alcoholism: ketoacidosis as differential diagnosis. Author(s): Fumeaux T, de Werra P. Source: Intensive Care Medicine. 1996 December; 22(12): 1462-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8986506
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Acute respiratory and metabolic acidosis induced by excessive muscle contraction during spinal evoked stimulation. Author(s): Tohdoh Y, Sumita S, Kawamata T, Omote K, Kawana S, Namiki A. Source: British Journal of Anaesthesia. 2001 April; 86(4): 589-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11573641
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Alcoholic ketoacidosis as the cause of repeated episodes of severe metabolic acidosis. Author(s): Newton P, Standing SJ, Kay JD, Hart G. Source: Annals of Clinical Biochemistry. 1999 November; 36 ( Pt 6): 783-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10586321
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Alkali therapy in the treatment of acute metabolic acidosis. Author(s): Offenstadt G. Source: Minerva Anestesiol. 1999 May; 65(5): 202-4. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10389392
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Alkali therapy versus sodium chloride supplement in low birthweight infants with incipient late metabolic acidosis. Author(s): Kalhoff H, Diekmann L, Kunz C, Stock GJ, Manz F. Source: Acta Paediatrica (Oslo, Norway : 1992). 1997 January; 86(1): 96-101. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9116434
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Alkaline buffers for correction of metabolic acidosis during cardiopulmonary resuscitation with focus on Tribonat--a review. Author(s): Bjerneroth G. Source: Resuscitation. 1998 June; 37(3): 161-71. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9715776
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Alterations of protein metabolism by metabolic acidosis in children with chronic renal failure. Author(s): Boirie Y, Broyer M, Gagnadoux MF, Niaudet P, Bresson JL. Source: Kidney International. 2000 July; 58(1): 236-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10886568
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Ammonium chloride poisoning: a misunderstood cause of metabolic acidosis with normal anion gap. Author(s): Megarbane B, Bruneel F, Bedos JP, Regnier B. Source: Intensive Care Medicine. 2000 December; 26(12): 1869. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11271099
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An uncommon cause of metabolic acidosis in a haemodialysis patient. Author(s): Woywodt A, Kielstein JT, Haller H. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 2002 May; 17(5): 92930. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11981087
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Arterial CO2 tension in metabolic acidosis. Author(s): Fulop M. Source: American Journal of Nephrology. 1998; 18(4): 351-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9653843
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Assessing metabolic acidosis in the intensive care unit: does the method make a difference? Author(s): Carreira F, Anderson RJ. Source: Critical Care Medicine. 2004 May; 32(5): 1227-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15190979
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Benylin dependence, metabolic acidosis and hyperglycaemia. Author(s): MacRury S, Neilson R, Goodwin K. Source: Postgraduate Medical Journal. 1987 July; 63(741): 587-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3658871
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Better correction of metabolic acidosis, blood pressure control, and phagocytosis with bicarbonate compared to lactate solution in acute peritoneal dialysis. Author(s): Thongboonkerd V, Lumlertgul D, Supajatura V. Source: Artificial Organs. 2001 February; 25(2): 99-108. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11251475
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Bialaphos poisoning with apnea and metabolic acidosis. Author(s): Matsukawa Y, Hachisuka H, Sawada S, Horie T, Kitammi Y, Nishijima S. Source: Journal of Toxicology. Clinical Toxicology. 1991; 29(1): 141-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2005662
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Bicarbonate therapy of metabolic acidosis. Author(s): Kaehny WD, Anderson RJ. Source: Critical Care Medicine. 1994 October; 22(10): 1525-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7924360
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Blood flow to the human uterus during maternal metabolic acidosis. Author(s): Blechner JN, Stenger VG, Prystowsky H. Source: American Journal of Obstetrics and Gynecology. 1975 March 15; 121(6): 789-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1119488
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Butoxyethanol ingestion with prolonged hyperchloremic metabolic acidosis treated with ethanol therapy. Author(s): McKinney PE, Palmer RB, Blackwell W, Benson BE. Source: Journal of Toxicology. Clinical Toxicology. 2000; 38(7): 787-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11192467
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Catabolism in uremia: metabolic acidosis and activation of specific pathways. Author(s): Greiber S, Mitch WE. Source: Contrib Nephrol. 1992; 98: 20-7. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1337319
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Catabolism in uremia: the impact of metabolic acidosis. Author(s): Franch HA, Mitch WE. Source: Journal of the American Society of Nephrology : Jasn. 1998 December; 9(12 Suppl): S78-81. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11443773
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Cause of metabolic acidosis in prolonged surgery. Author(s): Waters JH, Miller LR, Clack S, Kim JV. Source: Critical Care Medicine. 1999 October; 27(10): 2142-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10548196
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Cellular mechanisms of catabolism activated by metabolic acidosis. Author(s): Mitch WE. Source: Blood Purification. 1995 November-December; 13(6): 368-74. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8821202
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Cerebral pathology in the very low birthweight infant: predictive value of peripartum metabolic acidosis. Author(s): Mires GJ, Agustsson P, Forsyth JS, Patel NB. Source: European Journal of Obstetrics, Gynecology, and Reproductive Biology. 1991 December 13; 42(3): 181-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1773871
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Cerebrovascular response to acute metabolic acidosis in humans. Author(s): van de Ven M, Colier WN, Kersten BT, Oeseburg B, Folgering H. Source: Advances in Experimental Medicine and Biology. 2003; 530: 707-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14562769
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Changes in serum leptin levels in chronic renal failure patients with metabolic acidosis. Author(s): Zheng F, Qiu X, Yin S, Li Y. Source: Journal of Renal Nutrition : the Official Journal of the Council on Renal Nutrition of the National Kidney Foundation. 2001 October; 11(4): 207-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11680001
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Cholestyramine-induced hyperchloremic metabolic acidosis. Author(s): Scheel PJ Jr, Whelton A, Rossiter K, Watson A. Source: Journal of Clinical Pharmacology. 1992 June; 32(6): 536-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1634640
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Chronic metabolic acidosis decreases albumin synthesis and induces negative nitrogen balance in humans. Author(s): Ballmer PE, McNurlan MA, Hulter HN, Anderson SE, Garlick PJ, Krapf R. Source: The Journal of Clinical Investigation. 1995 January; 95(1): 39-45. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7814640
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Chronic metabolic acidosis increases the serum concentration of 1,25dihydroxyvitamin D in humans by stimulating its production rate. Critical role of acidosis-induced renal hypophosphatemia. Author(s): Krapf R, Vetsch R, Vetsch W, Hulter HN. Source: The Journal of Clinical Investigation. 1992 December; 90(6): 2456-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1469097
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Citric acid ingestion: a life-threatening cause of metabolic acidosis. Author(s): DeMars CS, Hollister K, Tomassoni A, Himmelfarb J, Halperin ML. Source: Annals of Emergency Medicine. 2001 November; 38(5): 588-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11679874
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Clinical and biochemical aspects of thiamine treatment for metabolic acidosis during total parenteral nutrition. Author(s): Nakasaki H, Ohta M, Soeda J, Makuuchi H, Tsuda M, Tajima T, Mitomi T, Fujii K. Source: Nutrition (Burbank, Los Angeles County, Calif.). 1997 February; 13(2): 110-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9106788
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Clinical significance of the fractional excretion of anions in metabolic acidosis. Author(s): Kim HY, Han JS, Jeon US, Joo KW, Earm JH, Ahn C, Kim S, Lee JS, Kim GH. Source: Clinical Nephrology. 2001 June; 55(6): 448-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11434355
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Coma and metabolic acidosis related to the use of muscle liniment. Author(s): van Wijngaarden M, Mock T, Dinwoodie A, LeGatt D, Yatscoff R. Source: Critical Care Medicine. 1995 June; 23(6): 1143-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7774229
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Comparison of albumin versus bicarbonate treatment for neonatal metabolic acidosis. Author(s): Dixon H, Hawkins K, Stephenson T. Source: European Journal of Pediatrics. 1999 May; 158(5): 414-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10333127
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Comparison of urine anion gap, urine osmolal gap and modified urine osmolal gap in assessing the urine ammonium in metabolic acidosis. Author(s): Tapaneya-Olarn C, Tapaneya-Olarn W, Phuaksungnern R, Petchthong T. Source: J Med Assoc Thai. 1999 November; 82 Suppl 1: S98-103. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10730527
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Control of metabolic acidosis after pancreas transplantation using acetazolamide. Author(s): Elkhammas EA, Henry ML, Tesi RJ, Sommer BG, Ferguson RM. Source: Transplantation Proceedings. 1991 February; 23(1 Pt 2): 1623-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1989310
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Conventional or physicochemical approach in intensive care unit patients with metabolic acidosis. Author(s): Moviat M, van Haren F, van der Hoeven H. Source: Critical Care (London, England). 2003 June; 7(3): R41-5. Epub 2003 May 01. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12793889
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Correction of chronic metabolic acidosis in haemodialysed patients by acetate-free biofiltration does not influence parathyroid function. Author(s): de Precigout V, Combe C, Blanchetier V, Larroumet N, Pommereau A, Potaux L, Aparicio M. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1995; 10(6): 821-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7566610
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Correction of metabolic acidosis and changes in plasma acetate levels in acetate and bicarbonate dialyses and acetate-free biofiltration. Author(s): Suzuki M, Hirasawa Y. Source: Contrib Nephrol. 1994; 108: 114-20. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8039392
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Correction of metabolic acidosis and its effect on albumin in chronic hemodialysis patients. Author(s): Brady JP, Hasbargen JA. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1998 January; 31(1): 35-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9428449
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Correction of metabolic acidosis and the protein catabolic rate in PD patients. Author(s): Stein A, Baker F, Larratt C, Bennett S, Harris K, Feehally J, Walls J. Source: Perit Dial Int. 1994; 14(2): 187-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8043680
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Correction of metabolic acidosis increases serum albumin concentrations and decreases kinetically evaluated protein intake in haemodialysis patients: a prospective study. Author(s): Movilli E, Zani R, Carli O, Sangalli L, Pola A, Camerini C, Cancarini GC, Scolari F, Feller P, Maiorca R. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1998 July; 13(7): 1719-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9681718
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Correlation of metabolic acidosis with outcome following injury and its value as a scoring tool. Author(s): Falcone RE, Santanello SA, Schulz MA, Monk J, Satiani B, Carey LC. Source: World Journal of Surgery. 1993 September-October; 17(5): 575-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8273377
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Deep breathing in children with severe malaria: indicator of metabolic acidosis and poor outcome. Author(s): English M, Waruiru C, Amukoye E, Murphy S, Crawley J, Mwangi I, Peshu N, Marsh K. Source: The American Journal of Tropical Medicine and Hygiene. 1996 November; 55(5): 521-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8940984
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Defense of hydrogen ion concentration in chronic metabolic acidosis. A new evaluation of an old approach. Author(s): Lennon EJ, Lemann J Jr. Source: Annals of Internal Medicine. 1966 August; 65(2): 265-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5912890
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Detection and differentiation of metabolic acidosis in parturients. Author(s): Marx GF, Desai PK, Habib NS. Source: Anesthesia and Analgesia. 1980 December; 59(12): 929-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7192513
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D-Glyceric acidemia in a patient with chronic metabolic acidosis. Author(s): Wadman SK, Duran M, Ketting D, Bruinvis L, De Bree PK, Kamerling JP, Gerwig GJ, Vliegenthart JF, Przyrembel H, Becker K, Bremer HJ. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 1976 September 20; 71(3): 477-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=971536
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Diagnosing the cause of a hyperosmolar anion-gap metabolic acidosis. Author(s): Markowitz DH. Source: Journal of Intensive Care Medicine. 2003 May-June; 18(3): 160-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14984636
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Diagnosis and treatment of an unusual cause of metabolic acidosis: ethylene glycol poisoning. Author(s): Piagnerelli M, Lejeune P, Vanhaeverbeek M. Source: Acta Clin Belg. 1999 December; 54(6): 351-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10686708
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Diagnosis of anion gap metabolic acidosis. Author(s): Reyman L, Price D, Goldfrank L. Source: Journal of Toxicology. Clinical Toxicology. 1985-86; 23(7-8): 615-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3831382
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Dichloroacetate treatment for severe refractory metabolic acidosis during neonatal sepsis. Author(s): Arnon S, Litmanovits I, Regev R, Elpeleg O, Dolfin T. Source: The Pediatric Infectious Disease Journal. 2001 February; 20(2): 218-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11224847
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Dietary protein, metabolic acidosis, and calcium balance. Author(s): Brosnan JT, Brosnan ME. Source: Adv Nutr Res. 1982; 4: 77-105. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7039265
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Diet-induced metabolic acidosis and the performance of high intensity exercise in man. Author(s): Greenhaff PL, Gleeson M, Maughan RJ. Source: European Journal of Applied Physiology and Occupational Physiology. 1988; 57(5): 583-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3396576
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Double gaps metabolic acidosis and bilateral basal ganglion lesions in methanol intoxication. Author(s): Yu FC, Lin SH, Lin YF, Lu KC, Shyu WC, Tsao WL. Source: The American Journal of Emergency Medicine. 1995 May; 13(3): 369-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7755836
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Drug and chemical-induced metabolic acidosis. Author(s): Kreisberg RA, Wood BC. Source: Clin Endocrinol Metab. 1983 July; 12(2): 391-411. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6347452
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Early metabolic acidosis and coma after acetaminophen ingestion. Author(s): Roth B, Woo O, Blanc P. Source: Annals of Emergency Medicine. 1999 April; 33(4): 452-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10092726
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Effect of chronic metabolic acidosis on the growth hormone/IGF-1 endocrine axis: new cause of growth hormone insensitivity in humans. Author(s): Brungger M, Hulter HN, Krapf R. Source: Kidney International. 1997 January; 51(1): 216-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8995736
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Effect of chronic metabolic acidosis on thyroid hormone homeostasis in humans. Author(s): Brungger M, Hulter HN, Krapf R. Source: The American Journal of Physiology. 1997 May; 272(5 Pt 2): F648-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9176376
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Effect of extreme metabolic acidosis on oxygen delivery capacity of the blood--an in vitro investigation of changes in the oxyhemoglobin dissociation curve in blood with pH values of approximately 6.30. Author(s): Refsum HE, Opdahl H, Leraand S. Source: Critical Care Medicine. 1997 September; 25(9): 1497-501. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9295823
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Effect of induced metabolic acidosis on human skeletal muscle metabolism during exercise. Author(s): Hollidge-Horvat MG, Parolin ML, Wong D, Jones NL, Heigenhauser GJ. Source: The American Journal of Physiology. 1999 October; 277(4 Pt 1): E647-58. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10516124
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Effect of metabolic acidosis on branched-chain amino acids in uremia. Author(s): Mak RH. Source: Pediatric Nephrology (Berlin, Germany). 1999 May; 13(4): 319-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10454782
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Effect of metabolic acidosis on hyperlipidemia in uremia. Author(s): Mak RH. Source: Pediatric Nephrology (Berlin, Germany). 1999 November; 13(9): 891-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10603143
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Effect of metabolic acidosis on insulin action and secretion in uremia. Author(s): Mak RH. Source: Kidney International. 1998 August; 54(2): 603-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9690228
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Effect of the correction of metabolic acidosis on nutritional status in elderly patients with chronic renal failure. Author(s): Verove C, Maisonneuve N, El Azouzi A, Boldron A, Azar R. Source: Journal of Renal Nutrition : the Official Journal of the Council on Renal Nutrition of the National Kidney Foundation. 2002 October; 12(4): 224-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12382214
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Effects of acid-base abnormalities on blood capacity of transporting CO(2): adverse effect of metabolic acidosis. Author(s): Cavaliere F, Antonelli M, Arcangeli A, Conti G, Pennisi MA, Proietti R. Source: Intensive Care Medicine. 2002 May; 28(5): 609-15. Epub 2002 April 12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12029410
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Effects of methamphetamine on trauma patients: a cause of severe metabolic acidosis? Author(s): Burchell SA, Ho HC, Yu M, Margulies DR. Source: Critical Care Medicine. 2000 June; 28(6): 2112-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10890674
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Enhanced Na(+)-H+ exchanger activity and NHE-1 mRNA levels in human lymphocytes during metabolic acidosis. Author(s): Quednau B, Rosskopf D, Reusch HP, Luft FC, Siffert W. Source: The American Journal of Physiology. 1994 February; 266(2 Pt 1): C480-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7511337
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Enterovesical fistula presenting as life-threatening normal anion gap metabolic acidosis. Author(s): Saxena R, Rutecki GW, Whittier FC. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1997 July; 30(1): 131-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9214413
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Errors in the selection of dialysate concentrates cause severe metabolic acidosis during bicarbonate hemodialysis. Author(s): Navarro JF, Mora-Fernandez C, Garcia J. Source: Artificial Organs. 1997 September; 21(9): 966-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9288865
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Ethylene glycol intoxication presenting as a metabolic acidosis associated with a motor vehicle crash: case report. Author(s): Buell JF, Sterling R, Mandava S, Berger AC, Paulilio LM, Bar-Lavie Y, Trimbach CA, Gens DR. Source: The Journal of Trauma. 1998 October; 45(4): 811-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9783626
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Ethylene glycol, glycolic acid, and metabolic acidosis of unknown origin. Author(s): Fraser AD. Source: Clinical Chemistry. 1993 August; 39(8): 1753-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8353976
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Evaluating a critically ill patient with metabolic acidosis: the ifosfamide paradigm. Author(s): Lehrich RW, Moll S, Luft FC. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1999 January; 14(1): 226-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10052517
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Evaluation of urine acidification by urine anion gap and urine osmolal gap in chronic metabolic acidosis. Author(s): Kim GH, Han JS, Kim YS, Joo KW, Kim S, Lee JS. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1996 January; 27(1): 42-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8546137
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Evidence for an independent role of metabolic acidosis on nutritional status in haemodialysis patients. Author(s): Movilli E, Bossini N, Viola BF, Camerini C, Cancarini GC, Feller P, Strada A, Maiorca R. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1998 March; 13(3): 674-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9550646
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Expression of carbonic anhydrase IV mRNA in rabbit kidney: stimulation by metabolic acidosis. Author(s): Winkler CA, Kittelberger AM, Schwartz GJ. Source: The American Journal of Physiology. 1997 April; 272(4 Pt 2): F551-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9140058
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Face-mask CPAP and sodium bicarbonate infusion in acute, severe asthma and metabolic acidosis. Author(s): Mansel JK, Stogner SW, Norman JR. Source: Chest. 1989 October; 96(4): 943-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2551599
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Factors which influence alterations of phosphates and pH in exercising human skeletal muscle: measurement error, reproducibility, and effects of fasting, carbohydrate loading, and metabolic acidosis. Author(s): Miller RG, Carson PJ, Moussavi RS, Green A, Baker A, Boska MD, Weiner MW. Source: Muscle & Nerve. 1995 January; 18(1): 60-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7799999
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Fasting hypoglycaemia and metabolic acidosis associated with deficiency of hepatic fructose-1,6-diphosphatase activity. Author(s): Baker L, Winegrad AI. Source: Lancet. 1970 July 4; 2(7662): 13-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4193749
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Fatal hypocalcemic, hyperphosphatemic, metabolic acidosis following sequential sodium phosphate-based enema administration. Author(s): Pitcher DE, Ford RS, Nelson MT, Dickinson WE. Source: Gastrointestinal Endoscopy. 1997 September; 46(3): 266-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9378217
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Fatal ingestion of sodium hypochlorite bleach with associated hypernatremia and hyperchloremic metabolic acidosis. Author(s): Ross MP, Spiller HA. Source: Vet Hum Toxicol. 1999 April; 41(2): 82-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10192136
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Fatal metabolic acidosis caused by thiamine deficiency. Author(s): Klein M, Weksler N, Gurman GM. Source: The Journal of Emergency Medicine. 2004 April; 26(3): 301-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15028327
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Fatal metabolic acidosis in a pediatric patient receiving an infusion of propofol in the intensive care unit: is there a relationship? Author(s): Strickland RA, Murray MJ. Source: Critical Care Medicine. 1995 February; 23(2): 405-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7867366
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Fatal metabolic acidosis, hyperglycemia, and coma after steroid therapy for KearnsSayre syndrome. Author(s): Curless RG, Flynn J, Bachynski B, Gregorios JB, Benke P, Cullen R. Source: Neurology. 1986 June; 36(6): 872-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3703301
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Free circulating magnesium and renal magnesium handling during acute metabolic acidosis in humans. Author(s): Blumberg D, Bonetti A, Jacomella V, Capillo S, Truttmann AC, Luthy CM, Colombo JP, Bianchetti MG. Source: American Journal of Nephrology. 1998; 18(3): 233-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9627040
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General aspects of physiology and pathophysiology of metabolic acidosis in the critically ill. Author(s): Van Biesen W, Lameire N. Source: Acta Clin Belg. 2000 May-June; 55(3): 133-40. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10981320
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Glucose intolerance following chronic metabolic acidosis in man. Author(s): DeFronzo RA, Beckles AD. Source: The American Journal of Physiology. 1979 April; 236(4): E328-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=434194
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Graft failure of autologous peripheral blood stem cell transplantation due to acute metabolic acidosis associated with total parenteral nutrition in a patient with relapsed breast cancer. Author(s): Sawada M, Tsurumi H, Hara T, Goto H, Yamada T, Oyama M, Moriwaki H. Source: Acta Haematologica. 2000; 102(3): 157-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10692681
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Grocery store baking soda. A source of sodium bicarbonate in the management of chronic metabolic acidosis. Author(s): Booth BE, Gates J, Morris RC Jr. Source: Clinical Pediatrics. 1984 February; 23(2): 94-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6319065
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Growth and mineral metabolism in very low birth weight infants. I. Comparison of the effects of two modes of NaHCO3 treatment of late metabolic acidosis. Author(s): Radde IC, Chance GW, Bailey K, O'Brien J, Day GM, Sheepers J. Source: Pediatric Research. 1975 July; 9(7): 564-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1161344
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Growth failure in children with metabolic alkalosis and with metabolic acidosis. Author(s): Tsuru N, Chan JC. Source: Nephron. 1987; 45(3): 182-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3574565
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Growth hormone stimulation tests in chronic renal failure with metabolic acidosis. Author(s): Bircan Z, Kervancioglu M, Soran M, Yildirim I. Source: Acta Paediatr Jpn. 1998 February; 40(1): 70-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9583205
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Growth retardation with chronic hyperkalemic metabolic acidosis: a consequence of selective colonic mucosa resistance to mineralocorticoid. Author(s): Preeyasombat C, Varavithya W, Sriboonruang S, Sriphrapradang A. Source: J Med Assoc Thai. 1986 August; 69(8): 438-51. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3783071
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Haematopoietic indicators of fetal metabolic acidosis. Author(s): Spencer MK, Khong TY, Matthews BL, MacLennan AH. Source: The Australian & New Zealand Journal of Obstetrics & Gynaecology. 2000 August; 40(3): 286-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11065035
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High anion gap metabolic acidosis associated with aminocaproic acid. Author(s): Budris WA, Roxe DM, Duvel JM. Source: The Annals of Pharmacotherapy. 1999 March; 33(3): 308-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10200855
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High anion gap metabolic acidosis in suicide: don't forget metformin intoxication-two patients' experiences. Author(s): Chang CT, Chen YC, Fang JT, Huang CC. Source: Renal Failure. 2002 September; 24(5): 671-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12380915
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Hippurate participates in the correction of metabolic acidosis. Author(s): Dzurik R, Spustova V, Krivosikova Z, Gazdikova K. Source: Kidney International. Supplement. 2001 February; 78: S278-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11169026
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How to assess fetal metabolic acidosis from cord samples. Author(s): Rosen KG, Murphy KW. Source: Journal of Perinatal Medicine. 1991; 19(3): 221-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1748945
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Hyperchloraemia causes metabolic acidosis by reducing strong ion difference. Author(s): Dorje P, Bree SE, Adhikary G, Mclaren DI. Source: Anaesthesia. 2000 January; 55(1): 94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10594451
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Hyperchloremic metabolic acidosis is a predictable consequence of intraoperative infusion of 0.9% saline. Author(s): Prough DS, Bidani A. Source: Anesthesiology. 1999 May; 90(5): 1247-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10319767
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Hyperglycemia, ketosis and mild metabolic acidosis in two patients subsequently found not to require insulin. Author(s): O'Dell ML. Source: Kans Med. 1990 February; 91(2): 40-3. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2108273
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Hyperkalemic hyperchloremic metabolic acidosis in a patient with sickle cell betathalassemia. Author(s): Elisaf M, Katopodis K, Bouradas K, Siamopoulos KC. Source: American Journal of Hematology. 1995 October; 50(2): 151-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7573002
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Hyperkalemic hyperchloremic metabolic acidosis: pathophysiologic insights. Author(s): DuBose TD Jr. Source: Kidney International. 1997 February; 51(2): 591-602. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9027745
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Hyperkalemic metabolic acidosis. Author(s): DuBose TD Jr. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1999 May; 33(5): Xlv-Xlviii. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10213664
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Hyperlactataemia and metabolic acidosis during haemofiltration using lactatebuffered fluids. Author(s): Davenport A, Will EJ, Davison AM. Source: Nephron. 1991; 59(3): 461-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1758538
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Hyperlactatemia and increasing metabolic acidosis in hepatorenal failure treated by hemofiltration. Author(s): Davenport A, Aulton K, Payne RB, Will EJ. Source: Renal Failure. 1990; 12(2): 99-101. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2236733
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Hyperleukocytosis presenting as myocardial ischemia, altered sensorium, and metabolic acidosis. Author(s): Jacob S, Jain H, Mathew M, Gay R, Goldberg JB, Dollard DJ. Source: The American Journal of Emergency Medicine. 2004 March; 22(2): 127-9. Erratum In: Am J Emerg Med. 2004 May; 22(3): 248. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15011235
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Hyperosmolar metabolic acidosis and intravenous Lorazepam. Author(s): Mullins ME, Barnes BJ. Source: The New England Journal of Medicine. 2002 September 12; 347(11): 857-8; Author Reply 857-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12226165
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Hyperplasia of pulmonary arterial media in infantile familial pulmonary hypertension associated with severe metabolic acidosis. Author(s): Cullinane C, Clarke JT, Rabinovitch M, Bohn D, Silver MM. Source: Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc. 1993 November; 6(6): 699-706. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8302812
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Hypokalaemic, hyperchloraemic metabolic acidosis requiring ventilation. Author(s): Dunn SR, Farnsworth TA, Karunaratne WU. Source: Anaesthesia. 1999 June; 54(6): 566-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10403871
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Hypokalemic metabolic acidosis attributed to cough mixture abuse. Author(s): Wong KM, Chak WL, Cheung CY, Chan YH, Choi KS, Chau KF, Li CS. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2001 August; 38(2): 390-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11479167
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Hypomagnesemia following correction of metabolic acidosis: a case of hungry bones. Author(s): Frisch LS, Mimouni F. Source: Journal of the American College of Nutrition. 1993 December; 12(6): 710-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8294727
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Hypoxia enhances induction of endothelial ICAM-1: role for metabolic acidosis and proteasomes. Author(s): Zund G, Uezono S, Stahl GL, Dzus AL, McGowan FX, Hickey PR, Colgan SP. Source: The American Journal of Physiology. 1997 November; 273(5 Pt 1): C1571-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9374642
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Ibuprofen overdose complicated by renal failure, adult respiratory distress syndrome, and metabolic acidosis. Author(s): Le HT, Bosse GM, Tsai Y. Source: Journal of Toxicology. Clinical Toxicology. 1994; 32(3): 315-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8007040
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Impact of metabolic acidosis on serum albumin and other nutritional parameters in long-term CAPD patients. Author(s): Kang SW, Lee SW, Lee IH, Kim BS, Choi KH, Lee HY, Han DS. Source: Adv Perit Dial. 1997; 13: 249-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9360692
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Impairment of ventilatory response to metabolic acidosis in insulin-dependent diabetic patients with advanced nephropathy. Author(s): Ikegaya N, Yonemura K, Suzuki T, Kato-Ohishi H, Taminato T, Hishida A. Source: Renal Failure. 1999 September; 21(5): 495-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10516994
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Incidence and severity of neovascularization in oxygen- and metabolic acidosisinduced retinopathy depend on rat source. Author(s): Kitzmann A, Leske D, Chen Y, Kendall A, Lanier W, Holmes J. Source: Current Eye Research. 2002 October; 25(4): 215-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12658554
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Indications for use of bicarbonate in patients with metabolic acidosis. Author(s): Arieff AI. Source: British Journal of Anaesthesia. 1991 August; 67(2): 165-77. Review. Erratum In: Br J Anaesth 1992 March; 68(3): 326. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1653584
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Influence of metabolic acidosis on nutrition. Author(s): Mitch WE. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1997 May; 29(5): Xlvi-Xlviii. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9159296
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Influence of metabolic acidosis on serum 1,25(OH)2D3 levels in chronic renal failure. Author(s): Lu KC, Lin SH, Yu FC, Chyr SH, Shieh SD. Source: Mineral and Electrolyte Metabolism. 1995; 21(6): 398-402. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8592483
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Influence of rapid correction of metabolic acidosis on serum osteocalcin level in chronic renal failure. Author(s): Lin YF, Shieh SD, Diang LK, Lin SH, Chyr SH, Li BL, Lu KC. Source: Asaio Journal (American Society for Artificial Internal Organs : 1992). 1994 JulySeptember; 40(3): M440-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8555554
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Initial severity of metabolic acidosis predicts the development of acute lung injury in severely traumatized patients. Author(s): Eberhard LW, Morabito DJ, Matthay MA, Mackersie RC, Campbell AR, Marks JD, Alonso JA, Pittet JF. Source: Critical Care Medicine. 2000 January; 28(1): 125-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10667511
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Interorgan glutamine flow in metabolic acidosis. Author(s): Welbourne TC. Source: The American Journal of Physiology. 1987 December; 253(6 Pt 2): F1069-76. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3322041
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Interrelationship between plasma leptin concentration and severity of metabolic acidosis in haemodialysed patients with chronical renal failure. Author(s): Kokot F, Chudek J, Adamczak M, Wiecek A. Source: Experimental and Clinical Endocrinology & Diabetes : Official Journal, German Society of Endocrinology [and] German Diabetes Association. 2001; 109(7): 370-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11573148
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Intracisternal papaverine administration associated with acute onset of hyperthermia and metabolic acidosis in a craniotomy. Author(s): McLoughlin AL. Source: Journal of Neurosurgical Anesthesiology. 1997 January; 9(1): 21-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9016436
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Intraocular pressure changes during hemodialysis: prevention of excessive dialytic rise and development of severe metabolic acidosis following acetazolamide therapy. Author(s): De Marchi S, Cecchin E, Tesio F. Source: Renal Failure. 1989; 11(2-3): 117-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2623197
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Intrapartum computerized fetal heart rate parameters and metabolic acidosis at birth. Author(s): Boog G. Source: Obstetrics and Gynecology. 2004 May; 103(5 Pt 1): 1002-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15121588
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Intrapartum computerized fetal heart rate parameters and metabolic acidosis at birth. Author(s): Agrawal SK, Doucette F, Gratton R, Richardson B, Gagnon R. Source: Obstetrics and Gynecology. 2003 October; 102(4): 731-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14551003
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Irrelevance of bone buffering to acid-base homeostasis in chronic metabolic acidosis. Author(s): Oh MS. Source: Nephron. 1991; 59(1): 7-10. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1944749
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Is chloride or dilution of bicarbonate the cause of metabolic acidosis from fluid administration? Author(s): Mathes DD. Source: Anesthesiology. 2001 September; 95(3): 809; Author Reply 810-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11575564
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Is it necessary to treat metabolic acidosis in chronic renal insufficiency? Author(s): Horl WH. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1995; 10(9): 1542-3. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8559464
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Isoniazid toxicity presenting as seizures and metabolic acidosis. Author(s): Watkins RC, Hambrick EL, Benjamin G, Chavda SN. Source: Journal of the National Medical Association. 1990 January; 82(1): 57, 62, 64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2304098
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Kussmaul respiration and abdominal pain secondary to metabolic acidosis in AIDS patients with disseminated Mycobacterium avium complex infection receiving clofazimine. Author(s): Soriano V, Moreno V, Alba A, Laguna F, Gonzalez-Lahoz J. Source: Aids (London, England). 1993 June; 7(6): 894-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8363767
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Late metabolic acidosis and poor weight gain in moderately pre-term babies fed with a casein-predominant formula: a continuing need for caution. Author(s): Fok TF, So LY, Lee NN, Leung RK, Wong W, Cheung KL, Davies DP. Source: Annals of Tropical Paediatrics. 1989 December; 9(4): 243-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2482007
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Late metabolic acidosis in low-birth-weight babies: report of four cases. Author(s): Teng RJ, Wen HH, Cheung TC, Ho MM. Source: Zhonghua Min Guo Xiao Er Ke Yi Xue Hui Za Zhi. 1991 July-August; 32(4): 2338. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1663687
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Late metabolic acidosis in premature infants. Prevalence and significance. Author(s): Ranlov P, Siggaard-Andersen O. Source: Acta Paediatr Scand. 1965 November; 54(6): 531-40. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5832145
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Late metabolic acidosis in preterm infants: clinical profile and response to oral sodium bicarbonate therapy. Author(s): Singhi S, Marwah RK, Singh M. Source: The Indian Journal of Medical Research. 1979 March; 69: 440-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=447382
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Late metabolic acidosis of prematurity. Author(s): Singhi S, Singhi P, Singh M. Source: Indian J Pediatr. 1980 March-April; 47(385): 129-32. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7450831
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Late metabolic acidosis. Author(s): Essin D. Source: The Journal of Pediatrics. 1980 September; 97(3): 509-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6774076
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Late metabolic acidosis: a reassessment of the definition. Author(s): Schwartz GJ, Haycock GB, Edelmann CM Jr, Spitzer A. Source: The Journal of Pediatrics. 1979 July; 95(1): 102-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=479989
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L-cysteine in metabolic acidosis of low-birth-weight infants. Author(s): Manz F. Source: The American Journal of Clinical Nutrition. 1993 March; 57(3): 455-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8438783
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Leiner's disease associated with metabolic acidosis. Author(s): Goodyear HM, Harper JI. Source: Clinical and Experimental Dermatology. 1989 September; 14(5): 364-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2532987
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Letter: Cholestyramine and metabolic acidosis. Author(s): Kleinman PK. Source: The New England Journal of Medicine. 1974 April 11; 290(15): 861. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4817847
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Letter: Hyperchloremia, metabolic acidosis, and cholestyramine. Author(s): Hartline JV. Source: The Journal of Pediatrics. 1976 July; 89(1): 155. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=932886
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Letter: Metabolic acidosis in the acute abdomen. Author(s): Mendelow D, Mieny CJ. Source: South African Medical Journal. Suid-Afrikaanse Tydskrif Vir Geneeskunde. 1975 April 26; 49(18): 727. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1138380
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Letter: Metabolic acidosis in the acute abdomen. Author(s): Buchanan N. Source: South African Medical Journal. Suid-Afrikaanse Tydskrif Vir Geneeskunde. 1975 March 1; 49(9): 300. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1114419
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Letter: Recovery from severe metabolic acidosis. Author(s): Goldstein MR. Source: Jama : the Journal of the American Medical Association. 1975 December 15; 234(11): 1119. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1242424
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Letter: Severe metabolic acidosis associated with nalidixic acid overdose. Author(s): Dash H, Mills J. Source: Annals of Internal Medicine. 1976 May; 84(5): 570-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1275361
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Letter: Use of bicarbonate and K in metabolic acidosis. Author(s): Bennett CM. Source: The New England Journal of Medicine. 1975 February 27; 292(9): 479-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=803641
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Leucocyte intracellular pH in patients with the metabolic acidosis of renal failure. Author(s): Levin GE, Baron DN. Source: Clin Sci Mol Med. 1977 March; 52(3): 325-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14806
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Life-threatening metabolic acidosis from cholestyramine in an infant with renal insufficiency. Author(s): Pattison M, Lee SM. Source: Am J Dis Child. 1987 May; 141(5): 479-80. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3578154
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Lithium and metabolic acidosis. Author(s): Jefferson JW. Source: Annals of Internal Medicine. 1978 March; 88(3): 434. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=629520
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Mechanism of increased renal gene expression during metabolic acidosis. Author(s): Curthoys NP, Gstraunthaler G. Source: American Journal of Physiology. Renal Physiology. 2001 September; 281(3): F381-90. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11502586
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Metabolic acidosis and coma in a child with acetaminophen toxicity. Author(s): Steelman R, Goodman A, Biswas S, Zimmerman A. Source: Clinical Pediatrics. 2004 March; 43(2): 201-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15024447
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Metabolic acidosis and hepatic steatosis in two HIV-infected patients on stavudine (d4T) treatment. Author(s): Cornejo-Juarez P, Sierra-Madero J, Volkow-Fernandez P. Source: Archives of Medical Research. 2003 January-February; 34(1): 64-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12604378
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Metabolic acidosis and hyperventilation induced by acetazolamide in patients with central nervous system pathology. Author(s): Venkatesha SL, Umamaheswara Rao GS. Source: Anesthesiology. 2000 December; 93(6): 1546-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11149457
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Metabolic acidosis associated with a new formulation of propofol. Author(s): Badr AE, Mychaskiw G 2nd, Eichhorn JH. Source: Anesthesiology. 2001 March; 94(3): 536-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11374620
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Metabolic acidosis associated with propofol in the absence of other causative factors. Author(s): Burow BK, Johnson ME, Packer DL. Source: Anesthesiology. 2004 July; 101(1): 239-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15220796
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Metabolic acidosis in HIV-infected patients. Author(s): Bonnet F, Bonarek M, Abrij A, Beylot J, Morlat P. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 2002 May 1; 34(9): 1289-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11941568
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Metabolic acidosis in maintenance dialysis patients: clinical considerations. Author(s): Mehrotra R, Kopple JD, Wolfson M. Source: Kidney International. Supplement. 2003 December; (88): S13-25. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14870874
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Metabolic acidosis in the intensive care unit. Author(s): Gauthier PM, Szerlip HM. Source: Critical Care Clinics. 2002 April; 18(2): 289-308, Vi. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12053835
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Metabolic acidosis of chronically hemodialyzed patients. Author(s): Kovacic V, Roguljic L, Kovacic V. Source: American Journal of Nephrology. 2003 May-June; 23(3): 158-64. Epub 2003 March 21. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12649614
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Metabolic acidosis stimulates intestinal glutamine absorption. Author(s): Epler MJ, Souba WW, Meng Q, Lin C, Karinch AM, Vary TC, Pan M. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2003 December; 7(8): 1045-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14675714
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Metabolic acidosis, core-peripheral temperature difference and blood pressure response to albumin infusion in hypotensive, very premature infants. Author(s): Dimitriou G, Greenough A, Mantagos J, Skinner S. Source: Journal of Perinatal Medicine. 2001; 29(5): 442-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11723846
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Metabolic acidosis, rhabdomyolysis, and cardiovascular collapse after prolonged propofol infusion. Author(s): Cannon ML, Glazier SS, Bauman LA. Source: Journal of Neurosurgery. 2001 December; 95(6): 1053-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11765823
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Metabolic acidosis. Author(s): Swenson ER. Source: Respiratory Care. 2001 April; 46(4): 342-53. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11262554
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Metabolic acidosis: separation methods and biological relevance of organic acids and lactic acid enantiomers. Author(s): Ewaschuk JB, Zello GA, Naylor JM, Brocks DR. Source: Journal of Chromatography. B, Analytical Technologies in the Biomedical and Life Sciences. 2002 December 5; 781(1-2): 39-56. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12450652
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Metabolic and endocrine effects of metabolic acidosis in humans. Author(s): Wiederkehr M, Krapf R. Source: Swiss Medical Weekly : Official Journal of the Swiss Society of Infectious Diseases, the Swiss Society of Internal Medicine, the Swiss Society of Pneumology. 2001 March 10; 131(9-10): 127-32. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11416968
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Mitochondrial DNA depletion, near-fatal metabolic acidosis, and liver failure in an HIV-infected child treated with combination antiretroviral therapy. Author(s): Church JA, Mitchell WG, Gonzalez-Gomez I, Christensen J, Vu TH, Dimauro S, Boles RG. Source: The Journal of Pediatrics. 2001 May; 138(5): 748-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11343055
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Moderate metabolic acidosis and its effects on serum parameters in hemodialysis patients. Author(s): Gao H, Lew SQ, Bosch JP. Source: Nephron. 2000 October; 86(2): 135-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11014982
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Mortality and the nature of metabolic acidosis in children with shock. Author(s): Hatherill M, Waggie Z, Purves L, Reynolds L, Argent A. Source: Intensive Care Medicine. 2003 February; 29(2): 286-91. Epub 2003 January 08. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12594588
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Must metabolic acidosis be associated with malnutrition in haemodialysed patients? Author(s): Lin SH, Lin YF, Chin HM, Wu CC. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 2002 November; 17(11): 2006-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12401862
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Na+/H+ exchange in human lymphocytes and platelets in chronic and subacute metabolic acidosis. Author(s): Reusch HP, Reusch R, Rosskopf D, Siffert W, Mann JF, Luft FC. Source: The Journal of Clinical Investigation. 1993 August; 92(2): 858-65. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8394388
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Neonatal cerebral arterial flow velocity waveforms in term infants with and without metabolic acidosis at delivery. Author(s): Morrison FK, Patel NB, Howie PW, Mires GJ, Herd RM. Source: Early Human Development. 1995 August 18; 42(3): 155-68. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7493584
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Neonatal metabolic acidosis. Author(s): Koo W. Source: Jpen. Journal of Parenteral and Enteral Nutrition. 1988 September-October; 12(5): 534. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3141652
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Neonatal metabolic acidosis: effect of chloride from normal saline flushes. Author(s): Groh-Wargo S, Ciaccia A, Moore J. Source: Jpen. Journal of Parenteral and Enteral Nutrition. 1988 March-April; 12(2): 15961. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3129591
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New autosomal-recessive syndrome of Leber congenital amaurosis, short stature, growth hormone insufficiency, mental retardation, hepatic dysfunction, and metabolic acidosis. Author(s): Ehara H, Nakano C, Ohno K, Goto YI, Takeshita K. Source: American Journal of Medical Genetics. 1997 August 22; 71(3): 258-66. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9268092
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Newborn complications after intrapartum asphyxia with metabolic acidosis in the preterm fetus. Author(s): Low JA, Panagiotopoulos C, Derrick EJ. Source: American Journal of Obstetrics and Gynecology. 1995 March; 172(3): 805-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7892868
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Newborn complications after intrapartum asphyxia with metabolic acidosis in the term fetus. Author(s): Low JA, Panagiotopoulos C, Derrick EJ. Source: American Journal of Obstetrics and Gynecology. 1994 April; 170(4): 1081-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8166190
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Nitroprusside-induced metabolic acidosis. Author(s): MacRae WR. Source: Anesthesiology. 1976 November; 45(5): 578-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=823836
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Nonanion gap metabolic acidosis in a newborn. Author(s): Jorquera P, Wu J, Bockenhauer D. Source: Current Opinion in Pediatrics. 1999 April; 11(2): 169-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10202628
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Onset of metabolic acidosis (anaerobic threshold) as a criterion measure of submaximum fitness. Author(s): Weltman A, Katch V, Sady S, Freedson P. Source: Res Q. 1978 May; 49(2): 218-27. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=725288
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Osmolar gap metabolic acidosis in a 60-year-old man treated for hypoxemic respiratory failure. Author(s): Arbour R, Esparis B. Source: Chest. 2000 August; 118(2): 545-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10936154
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Osmotic kaliuresis in metabolic acidosis and alkalosis. Author(s): Jasinski K, Szereszewska H, Wachowiak A. Source: Pol Med J. 1967; 6(3): 547-55. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6038076
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Oxygenation of the human fetus and newborn infant during maternal metabolic acidosis. Author(s): Blechner JN, Stenger VG, Eitzman DV, Prystowsky H. Source: American Journal of Obstetrics and Gynecology. 1970 September 1; 108(1): 47-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5454583
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Paracetamol-associated coma, metabolic acidosis, renal and hepatic failure. Author(s): Kritharides L, Fassett R, Singh B. Source: Intensive Care Medicine. 1988; 14(4): 439-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3403780
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Pathogenesis of cardiac dysfunction during metabolic acidosis: therapeutic implications. Author(s): Shapiro JI. Source: Kidney International. Supplement. 1997 October; 61: S47-51. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9328965
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Patterns of metabolic acidosis in patients with chronic renal failure: impact of hemodialysis. Author(s): Cohen E, Liu K, Batlle DC. Source: Int J Artif Organs. 1988 November; 11(6): 440-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3203972
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Perinatal brain damage: predictive value of metabolic acidosis and the Apgar score. Author(s): Ruth VJ, Raivio KO. Source: Bmj (Clinical Research Ed.). 1988 July 2; 297(6640): 24-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2457406
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Persistent non-gastrointestinal metabolic acidosis in pediatric HIV-1 infection. Author(s): Chakraborty R, Uy CS, Oleske JM, Coen PG, McSherry GD. Source: Aids (London, England). 2003 March 28; 17(5): 673-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12646789
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Pharmacokinetics of TRIS (hydroxymethyl-)aminomethane in healthy subjects and in patients with metabolic acidosis. Author(s): Brasch H, Thies E, Iven H. Source: European Journal of Clinical Pharmacology. 1982; 22(3): 257-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7106159
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Phenformin-associated metabolic acidosis. Author(s): Fulop M, Hoberman HD. Source: Diabetes. 1976 April; 25(4): 292-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=817951
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Picolax; an unusual cause of metabolic acidosis. Author(s): Burden RJ, Way CF, Spargo PM. Source: Paediatric Anaesthesia. 1998; 8(4): 365. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9672941
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Plasticity of intercalated cell polarity: effect of metabolic acidosis. Author(s): Schwartz GJ. Source: Nephron. 2001 April; 87(4): 304-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11287773
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Potential effect of metabolic acidosis on beta 2-microglobulin generation: in vivo and in vitro studies. Author(s): Sonikian M, Gogusev J, Zingraff J, Loric S, Quednau B, Bessou G, Siffert W, Drueke TB, Reusch HP, Luft FC. Source: Journal of the American Society of Nephrology : Jasn. 1996 February; 7(2): 350-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8785408
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Predictive value of electronic fetal monitoring for intrapartum fetal asphyxia with metabolic acidosis. Author(s): Low JA, Victory R, Derrick EJ. Source: Obstetrics and Gynecology. 1999 February; 93(2): 285-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9932571
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Predisposition to metabolic acidosis induced by topiramate. Author(s): Montenegro MA, Guerreiro MM, Scotoni AE, Guerreiro CA. Source: Arquivos De Neuro-Psiquiatria. 2000 December; 58(4): 1021-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11105067
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Profound hyperglycemia and metabolic acidosis after verapamil overdose. Author(s): Enyeart JJ, Price WA, Hoffman DA, Woods L. Source: Journal of the American College of Cardiology. 1983 December; 2(6): 1228-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6355245
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Propofol anaesthesia and metabolic acidosis in children. Author(s): Ozlu O, Ozkara HA, Eris S, Ocal T. Source: Paediatric Anaesthesia. 2003 January; 13(1): 53-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12535040
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Protein and amino acid metabolism in splanchnic organs in metabolic acidosis. Author(s): Deferrari G, Garibotto G, Robaudo C, Saffioti S, Russo R, Sofia A. Source: Mineral and Electrolyte Metabolism. 1997; 23(3-6): 229-33. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9387123
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Protein and amino acid metabolism in uremia: influence of metabolic acidosis. Author(s): Mitch WE, May RC, Maroni BJ, Druml W. Source: Kidney International. Supplement. 1989 November; 27: S205-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2636659
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Protein catabolic rate (PCR), dietary protein intake (DPI) and metabolic acidosis. Author(s): Grzegorzewska A. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1999 September; 14(9): 2266-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10489257
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Pyroglutamic acidemia: a cause of high anion gap metabolic acidosis. Author(s): Dempsey GA, Lyall HJ, Corke CF, Scheinkestel CD. Source: Critical Care Medicine. 2000 June; 28(6): 1803-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10890623
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Quantitative displacement of acid-base equilibrium in metabolic acidosis. Author(s): Albert MS, Dell RB, Winters RW. Source: Annals of Internal Medicine. 1967 February; 66(2): 312-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6016545
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Quiz of the month. Question 2. Mixed metabolic acidosis and alkalosis. Author(s): Kurtzman NA. Source: American Journal of Nephrology. 1981; 1(3-4): 198, 223. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7349053
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Quiz page. Severe metabolic acidosis, caused by an enteric augmentation of urinary tract and renal impairment. Decompensation was caused by lack of selfcatheterization. Author(s): Jones G, Wheeler D, Davenport A; American Journal of Kidney Diseases. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2004 February; 43(2): Ra42, E1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14750125
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Rapid correction of metabolic acidosis in chronic renal failure: effect on parathyroid hormone activity. Author(s): Lu KC, Shieh SD, Li BL, Chu P, Jan SY, Lin YF. Source: Nephron. 1994; 67(4): 419-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7969674
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Rate of production of carbon dioxide in patients with a severe degree of metabolic acidosis. Author(s): Kamel KS, Richardson RM, Goguen JM, Fine A, Levin A, Halperin ML. Source: Nephron. 1993; 64(4): 514-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8366976
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Recovery from prolonged metabolic acidosis due to accidental ethylene glycol poisoning. Author(s): Wisse B, Thakur S, Baran D. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1999 February; 33(2): E4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10074604
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Recovery of metabolic acidosis in term infants with postasphyxial hypoxic-ischemic encephalopathy. Author(s): Shah PS, Raju NV, Beyene J, Perlman M. Source: Acta Paediatrica (Oslo, Norway : 1992). 2003 August; 92(8): 941-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12948070
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Recurrent severe anion gap metabolic acidosis secondary to episodic ethylene glycol intoxication. Author(s): Moossavi S, Wadhwa NK, Nord EP. Source: Clinical Nephrology. 2003 September; 60(3): 205-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14524585
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Regulation of renal ammoniagenesis in metabolic acidosis. Author(s): Schoolwerth AC. Source: Kidney International. 1991 November; 40(5): 961-73. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1762300
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Relationship between metabolic acidosis and calcium phosphate urinary stone formation in women. Author(s): Kohri K, Kodama M, Ishikawa Y, Katayama Y, Takada M, Katoh Y, Kataoka K, Iguchi M, Kurita T. Source: International Urology and Nephrology. 1991; 23(4): 307-16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1938225
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Relationship between severity of hyperglycemia and metabolic acidosis in diabetic ketoacidosis. Author(s): Brandt KR, Miles JM. Source: Mayo Clinic Proceedings. 1988 November; 63(11): 1071-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3143031
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Relationship of CSF pH, O2, and CO2 responses in metabolic acidosis and alkalosis in humans. Author(s): Irsigler GB, Stafford MJ, Severinghaus JW. Source: Journal of Applied Physiology (Bethesda, Md. : 1985). 1980 February; 48(2): 35561. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6767670
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Renal ammoniagenesis and interorgan flow of glutamine in chronic metabolic acidosis. Author(s): Deferrari G, Garibotto G, Robaudo C, Saffioti S, Russo R, Sala MR, Bruzzone M, Tizianello A. Source: Contrib Nephrol. 1994; 110: 144-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7956248
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Renal ammoniagenesis during the adaptation to metabolic acidosis in man. Author(s): Tizianello A, Deferrari G, Garibotto G, Robaudo C, Bruzzone M, Passerone GC. Source: Contrib Nephrol. 1982; 31: 40-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7105750
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Renal ammoniagenesis in an early stage of metabolic acidosis in man. Author(s): Tizianello A, Deferrari G, Garibotto G, Robaudo C, Acquarone N, Ghiggeri GM. Source: The Journal of Clinical Investigation. 1982 January; 69(1): 240-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7054241
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Renal bicarbonate handling in low birth weight infants during metabolic acidosis. Author(s): Zilleruelo G, Sultan S, Bancalari E, Steele B, Strauss J. Source: Biology of the Neonate. 1986; 49(3): 132-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3006803
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Renal excretion of calcium and phosphorus in premature infants with incipient late metabolic acidosis. Author(s): Kalhoff H, Diekmann L, Rudloff S, Manz F. Source: Journal of Pediatric Gastroenterology and Nutrition. 2001 November; 33(5): 5659. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11740230
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Renal hypercalciuria and metabolic acidosis associated with medullary sponge kidney: effect of alkali therapy. Author(s): Higashihara E, Nutahara K, Niijima T. Source: Urological Research. 1988; 16(2): 95-100. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2835848
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Renal salt wasting and metabolic acidosis with trimethoprim-sulfamethoxazole therapy. Author(s): Kaufman AM, Hellman G, Abramson RG. Source: The Mount Sinai Journal of Medicine, New York. 1983 May-June; 50(3): 238-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6604867
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Respiratory compensation for the metabolic acidosis of severe exercise as a modulator of muscular capillary O2-unloading. Author(s): Fukuba Y, Whipp BJ. Source: Advances in Experimental Medicine and Biology. 1995; 393: 153-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8629473
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Respiratory response to acute metabolic acidosis in man. Author(s): Verdon F. Source: Intensive Care Medicine. 1979 November; 5(4): 204. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=533788
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Respiratory response to acute metabolic acidosis. Author(s): Verdon F, van Melle G, Perret C. Source: Bull Eur Physiopathol Respir. 1981; 17(2): 223-35. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6793113
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Role of the carotid bodies in the respiratory compensation for the metabolic acidosis of exercise in humans. Author(s): Rausch SM, Whipp BJ, Wasserman K, Huszczuk A. Source: The Journal of Physiology. 1991 December; 444: 567-78. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1822563
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Safety and efficacy of intravenous Carbicarb in patients undergoing surgery: comparison with sodium bicarbonate in the treatment of mild metabolic acidosis. SPI Research Group. Study of Perioperative Ischemia. Author(s): Leung JM, Landow L, Franks M, Soja-Strzepa D, Heard SO, Arieff AI, Mangano DT. Source: Critical Care Medicine. 1994 October; 22(10): 1540-9. Erratum In: Crit Care Med 1995 February; 23(2): 420. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7924363
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Saline-induced hyperchloremic metabolic acidosis. Author(s): Kellum JA. Source: Critical Care Medicine. 2002 January; 30(1): 259-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11902280
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Serum anion gap in the differential diagnosis of metabolic acidosis in critically ill newborns. Author(s): Lorenz JM, Kleinman LI, Markarian K, Oliver M, Fernandez J. Source: The Journal of Pediatrics. 1999 December; 135(6): 751-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10586180
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Severe acute metabolic acidosis and Wernicke's encephalopathy following chemotherapy with 5-fluorouracil and cisplatin: case report and review of the literature. Author(s): Kondo K, Fujiwara M, Murase M, Kodera Y, Akiyama S, Ito K, Takagi H. Source: Japanese Journal of Clinical Oncology. 1996 August; 26(4): 234-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8765181
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Severe hyperosmolar metabolic acidosis due to a large dose of intravenous lorazepam. Author(s): Tayar J, Jabbour G, Saggi SJ. Source: The New England Journal of Medicine. 2002 April 18; 346(16): 1253-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11961161
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Severe metabolic acidosis and heart failure due to thiamine deficiency. Author(s): Blanc P, Henriette K, Boussuges A. Source: Nutrition (Burbank, Los Angeles County, Calif.). 2002 January; 18(1): 118. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11827785
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Severe metabolic acidosis and heart failure due to thiamine deficiency. Author(s): Ozawa H, Homma Y, Arisawa H, Fukuuchi F, Handa S. Source: Nutrition (Burbank, Los Angeles County, Calif.). 2001 April; 17(4): 351-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11369178
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Severe metabolic acidosis and renal failure in an HIV-1 patient receiving tenofovir. Author(s): Hansen AB, Mathiesen S, Gerstoft J. Source: Scandinavian Journal of Infectious Diseases. 2004; 36(5): 389-92. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15287389
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Severe metabolic acidosis complicating massive ibuprofen overdose. Author(s): Downie A, Ali A, Bell D. Source: Postgraduate Medical Journal. 1993 July; 69(813): 575-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8415347
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Severe metabolic acidosis during haemodialysis: a rare but life threatening complication. Author(s): Fourtounas C, Kopelias I, Dimitriadis G, Paraskevopoulos A, Agroyannis B. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 2001 December; 16(12): 2416-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11733636
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Severe metabolic acidosis in nalidixic acid overdosage. Author(s): Suganthi AR, Ramanan AS, Pandit N, Yeshwanth M. Source: Indian Pediatrics. 1993 August; 30(8): 1025-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8125574
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Severe metabolic acidosis in the alcoholic: differential diagnosis and management. Author(s): Hojer J. Source: Human & Experimental Toxicology. 1996 June; 15(6): 482-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8793530
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Severe metabolic acidosis resulting from a dislocated gastric band. Author(s): Bruegger D, Rehm M, Da Silva L, Christ F, Finsterer U. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2004 April; 14(4): 555-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15130238
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Shock, metabolic acidosis, and coma following ibuprofen overdose in a child. Author(s): Zuckerman GB, Uy CC. Source: The Annals of Pharmacotherapy. 1995 September; 29(9): 869-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8547735
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Sodium lactate as an alternative to sodium bicarbonate in the management of metabolic acidosis after pancreas transplantation. Author(s): Peltenburg HG, Mutsaerts KJ, Hardy EL, van Hooff JP. Source: Transplantation. 1992 January; 53(1): 225-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1310172
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Somnolence, hypotension, and metabolic acidosis following high-dose teniposide treatment in children with leukemia. Author(s): McLeod HL, Baker DK Jr, Pui CH, Rodman JH. Source: Cancer Chemotherapy and Pharmacology. 1991; 29(2): 150-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1760858
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Spurious metabolic acidosis in hemodialysis patients. Author(s): Kirschbaum B. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2000 June; 35(6): 1068-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10845818
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Strong ion difference: metabolic acidosis or alkalosis? Author(s): Roncoroni AJ. Source: Respiratory Care. 2002 January; 47(1): 94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11811151
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Succinylcholine-induced hyperkalemic arrest in a patient with severe metabolic acidosis and exsanguinating hemorrhage. Author(s): Schwartz DE, Kelly B, Caldwell JE, Carlisle AS, Cohen NH. Source: Anesthesia and Analgesia. 1992 August; 75(2): 291-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1632545
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Sulthiame-associated mild compensated metabolic acidosis. Author(s): Troger U, Fritzsch C, Darius J, Gedschold J, Meyer FP. Source: Int J Clin Pharmacol Ther. 1996 December; 34(12): 542-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8996849
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The aetiology and pathogenesis of cardiopulmonary bypass-associated metabolic acidosis using polygeline pump prime. Author(s): Hayhoe M, Bellomo R, Liu G, McNicol L, Buxton B. Source: Intensive Care Medicine. 1999 July; 25(7): 680-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10470571
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The clinical spectrum of chronic metabolic acidosis: homeostatic mechanisms produce significant morbidity. Author(s): Alpern RJ, Sakhaee K. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1997 February; 29(2): 291-302. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9016905
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The effect of metabolic acidosis on serum apolipoprotein A I and apolipoprotein B levels in children with chronic renal failure. Author(s): Bircan Z, Kaplan A, Soran M, Soker M, Kervancioglu M, Sahin A, Kilinc M. Source: International Urology and Nephrology. 1997; 29(5): 603-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9413770
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The effects of diaspirin cross-linked hemoglobin on hemodynamics, metabolic acidosis, and survival in burned rats. Author(s): Soltero RG, Hansbrough JF. Source: The Journal of Trauma. 1999 February; 46(2): 286-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10029035
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The implications of metabolic acidosis in intensive care unit patients. Author(s): Bailey JL, Mitch WE. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1998 April; 13(4): 837-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9568833
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The search for the uremic toxin: the case for metabolic acidosis. Author(s): Bailey JL, Mitch WE. Source: Wiener Klinische Wochenschrift. 1997 January 17; 109(1): 7-12. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9037742
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The value of the chloride: sodium ratio in differentiating the aetiology of metabolic acidosis. Author(s): Durward A, Skellett S, Mayer A, Taylor D, Tibby SM, Murdoch IA. Source: Intensive Care Medicine. 2001 May; 27(5): 828-35. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11430538
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Threshold of metabolic acidosis associated with newborn complications. Author(s): Low JA, Lindsay BG, Derrick EJ. Source: American Journal of Obstetrics and Gynecology. 1997 December; 177(6): 1391-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9423740
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Topical dorzolamide and metabolic acidosis in a neonate. Author(s): Morris S, Geh V, Nischal KK, Sahi S, Ahmed MA. Source: The British Journal of Ophthalmology. 2003 August; 87(8): 1052-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12881361
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Topiramate and metabolic acidosis in infants and toddlers. Author(s): Philippi H, Boor R, Reitter B. Source: Epilepsia. 2002 July; 43(7): 744-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12102678
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Topiramate and metabolic acidosis in pediatric epilepsy. Author(s): Takeoka M, Holmes GL, Thiele E, Bourgeois BF, Helmers SL, Duffy FH, Riviello JJ. Source: Epilepsia. 2001 March; 42(3): 387-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11442157
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Topiramate-induced metabolic acidosis: report of two cases. Author(s): Ko CH, Kong CK. Source: Developmental Medicine and Child Neurology. 2001 October; 43(10): 701-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11665828
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Transient 5-oxoprolinuria and high anion gap metabolic acidosis: clinical and biochemical findings in eleven subjects. Author(s): Pitt JJ, Hauser S. Source: Clinical Chemistry. 1998 July; 44(7): 1497-503. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9665429
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Treatment of metabolic acidosis. Author(s): Levraut J, Grimaud D. Source: Current Opinion in Critical Care. 2003 August; 9(4): 260-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12883279
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Trimethoprim/sulfamethoxazole and metabolic acidosis in HIV-infected patients. Author(s): Porras MC, Lecumberri JN, Castrillon JL. Source: The Annals of Pharmacotherapy. 1998 February; 32(2): 185-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9496402
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Twice-told tales of metabolic acidosis, glucocorticoids, and protein wasting: what do results from rats tell us about patients with kidney disease? Author(s): Bailey JL, Mitch WE. Source: Seminars in Dialysis. 2000 July-August; 13(4): 227-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10923349
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Two reports of propofol anesthesia associated with metabolic acidosis in adults. Author(s): Funston JS, Prough DS. Source: Anesthesiology. 2004 July; 101(1): 6-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15220765
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Unaccounted for anion in metabolic acidosis during severe sepsis in humans. Author(s): Mecher C, Rackow EC, Astiz ME, Weil MH. Source: Critical Care Medicine. 1991 May; 19(5): 705-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2026034
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Unexpected metabolic acidosis during rectal surgery. Author(s): Hurdley J. Source: Anaesthesia. 1978 May; 33(5): 478-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=665965
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Unexpected metabolic acidosis in severe lye poisoning. Author(s): Okonek S, Bierbach H, Atzpodien W. Source: Clin Toxicol. 1981 February; 18(2): 225-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7226735
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Unexplained metabolic acidosis in critically ill patients: the role of pyroglutamic acid. Author(s): Mizock BA, Belyaev S, Mecher C. Source: Intensive Care Medicine. 2004 March; 30(3): 502-5. Epub 2003 December 19. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14685659
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Unusual case of metabolic acidosis. Author(s): McGrath RP. Source: Critical Care Medicine. 1989 January; 17(1): 108. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2909311
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Urinary ammonia content as a determinant or urinary pH during chronic metabolic acidosis. Author(s): Schloeder FX, Stinebaugh BJ. Source: Metabolism: Clinical and Experimental. 1977 December; 26(12): 1321-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=22017
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Urinary excretion of N-acetyl-beta-D-glucosaminidase in children with NH4Cl metabolic acidosis. Author(s): Guignard JP, Sulyok E, Gyorke Z. Source: Acta Paediatr Scand. 1990 November; 79(11): 1116-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2267932
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Urinary net charge in hyperchloremic metabolic acidosis. Author(s): Kumar S, Vaswani M, Srivastava RN, Bagga A. Source: Indian Pediatrics. 1998 January; 35(1): 13-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9707899
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Urinary sodium in the evaluation of hyperchloremic metabolic acidosis. Author(s): Batlle DC, von Riotte A, Schlueter W. Source: The New England Journal of Medicine. 1987 January 15; 316(3): 140-4. Erratum In: N Engl J Med 1987 June 11; 316(24): 1556. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3796685
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Ventilatory management casebook. Error in blood gas sampling resulting in a spurious interpretation of compensated metabolic acidosis. Author(s): Goldsmith JP. Source: Journal of Perinatology : Official Journal of the California Perinatal Association. 1993 March-April; 13(2): 165-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8515314
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Ventilatory response in metabolic acidosis and cerebral blood volume in humans. Author(s): Van de Ven MJ, Colier WN, van der Sluijs MC, Oeseburg B, Folgering H. Source: Respiration Physiology. 2001 January; 124(2): 105-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11164202
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Ventilatory responses to the metabolic acidosis of treadmill and cycle ergometry. Author(s): Koyal SN, Whipp BJ, Huntsman D, Bray GA, Wasserman K. Source: Journal of Applied Physiology (Bethesda, Md. : 1985). 1976 June; 40(6): 864-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=931922
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What is the relationship between metabolic acidosis and nutritional status in dialysis patients? Author(s): Goodship TH. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1998 May; 31(5): 884-6; Discussion 886-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9590204
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CHAPTER 2. NUTRITION AND METABOLIC ACIDOSIS Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and metabolic acidosis.
Finding Nutrition Studies on Metabolic Acidosis 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 “metabolic acidosis” (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 “metabolic acidosis” (or a synonym): •
Comparison of the measurement of total carbon dioxide and strong ion difference for the evaluation of metabolic acidosis in diarrhoeic calves. Author(s): Department of Veterinary Clinical Studies, University of Liverpool, Neston, Wirral. Source: Grove White, D H Michell, A R Vet-Rec. 2001 March 24; 148(12): 365-70 00424900
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Diagnosis and treatment of metabolic acidosis in calves: a field study. Author(s): Department of Farm Animal Medicine, Royal Veterinary College, University of London, Hatfield, Hertfordshire. Source: Grove White, D H White, D G Vet-Rec. 1993 November 13; 133(20): 499-501 0042-4900
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Hyperlactataemia and metabolic acidosis following paracetamol overdose. Author(s): West Midlands Poisons Unit, Dudley Road Hospital, Birmingham. Source: Gray, T A Buckley, B M Vale, J A Q-J-Med. 1987 October; 65(246): 811-21 00335622
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Severe metabolic acidosis and “muti” (traditional herbal medicine) ingestion in young children. Author(s): Department of Paediatrics, Faculty of Medicine, University of Zimbabwe. Source: Nkrumah, F K Nathoo, K J Gomo, Z A Pirie, D J Cent-Afr-J-Med. 1990 January; 36(1): 16-9 0008-9176
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The acute reversal of a diet-induced metabolic acidosis does not restore endurance capacity during high-intensity exercise in man. Author(s): Department of Enviromental and Occupational Medicine, University Medical School, Foresterhill, Aberdeen, UK. Source: Ball, D Greenhaff, P L Maughan, R J Eur-J-Appl-Physiol-Occup-Physiol. 1996; 73(1-2): 105-12 0301-5548
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
The following is a specific Web list relating to metabolic acidosis; 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: •
Minerals Sodium Bicarbonate Source: Healthnotes, Inc.; www.healthnotes.com
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CHAPTER 3. ALTERNATIVE MEDICINE AND METABOLIC ACIDOSIS Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to metabolic acidosis. 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 metabolic acidosis 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 “metabolic acidosis” (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 metabolic acidosis: •
A lamb-meat-based formula for infants allergic to casein hydrolysate formulas. Author(s): Weisselberg B, Dayal Y, Thompson JF, Doyle MS, Senior B, Grand RJ. Source: Clinical Pediatrics. 1996 October; 35(10): 491-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8902326
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Carbon monoxide poisoning treated with hyperbaric oxygen: metabolic acidosis as a predictor of treatment requirements. Author(s): Turner M, Esaw M, Clark RJ. Source: Journal of Accident & Emergency Medicine. 1999 March; 16(2): 96-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10191440
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Chronic metabolic acidosis increases mRNA levels for components of the ubiquitinmediated proteolytic pathway in skeletal muscle of dairy cows. Author(s): Mutsvangwa T, Gilmore J, Squires JE, Lindinger MI, McBride BW. Source: The Journal of Nutrition. 2004 March; 134(3): 558-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14988446
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Comparison of lactate or BE during out-of-hospital cardiac arrest to determine metabolic acidosis. Author(s): Prause G, Ratzenhofer-Comenda B, Smolle-Juttner F, Heydar-Fadai J, Wildner G, Spernbauer P, Smolle J, Hetz H. Source: Resuscitation. 2001 December; 51(3): 297-300. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11738782
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Intravenous pyridoxine-induced metabolic acidosis. Author(s): Lovecchio F, Curry SC, Graeme KA, Wallace KL, Suchard J. Source: Annals of Emergency Medicine. 2001 July; 38(1): 62-4. Erratum In: Ann Emerg Med 2001 September; 38(3): 341. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11423814
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Late metabolic acidosis of the premature infant. Author(s): Brackemyre P, Schreiner RL. Source: Journal of the American Dietetic Association. 1978 March; 72(3): 298-301. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=564920
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Management of cardiac arrest, with special reference to metabolic acidosis. Author(s): STEWART JS. Source: British Medical Journal. 1964 February 22; 5381: 476-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14084675
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Metabolic acidosis following external cardiac massage. Author(s): RAISON JC. Source: Lancet. 1962 December 29; 2: 1379-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=13990530
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Pathogenesis and treatment of metabolic acidosis in open heart surgery under surface induced deep hypothermia. Author(s): Shida H. Source: Jpn J Surg. 1974 December; 4(4): 198-203. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4465470
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Postnatal growth of infants of less than 1.3 kg birth weight: effects of metabolic acidosis, of caloric intake, and of calcium, sodium, and phosphate supplementation. Author(s): Chance GW, Radde IC, Willis DM, Roy RN, Park E, Ackerman I.
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Source: The Journal of Pediatrics. 1977 November; 91(5): 787-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=909021 •
Proceedings: Metabolic acidosis following regional circulatory arrest: treatment by THAM, hyperventilation and hyperbaric oxygen. Author(s): Benichoux R. Source: The Journal of Cardiovascular Surgery. 1973 November-December; 14(6): 573-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4764807
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Severe metabolic acidosis and “muti” (traditional herbal medicine) ingestion in young children. Author(s): Nkrumah FK, Nathoo KJ, Gomo ZA, Pirie DJ. Source: Cent Afr J Med. 1990 January; 36(1): 16-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2397494
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Sublimed (inorganic) sulfur ingestion. A cause of life-threatening metabolic acidosis with a high anion gap. Author(s): Schwartz SM, Carroll HM, Scharschmidt LA. Source: Archives of Internal Medicine. 1986 July; 146(7): 1437-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3718141
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The acute reversal of a diet-induced metabolic acidosis does not restore endurance capacity during high-intensity exercise in man. Author(s): Ball D, Greenhaff PL, Maughan RJ. Source: European Journal of Applied Physiology and Occupational Physiology. 1996; 73(1-2): 105-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8861677
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The influence of bicarbonate supplementation on plasma levels of branched-chain amino acids in haemodialysis patients with metabolic acidosis. Author(s): Kooman JP, Deutz NE, Zijlmans P, van den Wall Bake A, Gerlag PG, van Hooff JP, Leunissen KM. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 1997 November; 12(11): 2397-401. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9394330
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Thiamine deficiency as a cause of metabolic acidosis. Author(s): Logan G, Goli SA, McGonagle M, Byrd RP Jr, Roy TM. Source: Tenn Med. 2003 December; 96(12): 553-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15077560
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Topiramate and metabolic acidosis. Author(s): Wilner A, Raymond K, Pollard R. Source: Epilepsia. 1999 June; 40(6): 792-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10368081
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 metabolic acidosis; 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: •
Herbs and Supplements Garcinia Cambogia Alternative names: Citrin, Gambooge Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html.
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This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 4. PATENTS ON METABOLIC ACIDOSIS 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 “metabolic acidosis” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on metabolic acidosis, we have not necessarily excluded non-medical patents in this bibliography.
Patents on Metabolic Acidosis By performing a patent search focusing on metabolic acidosis, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We will tell you how to obtain this information later in the chapter. 8Adapted
from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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The following is an example of the type of information that you can expect to obtain from a patent search on metabolic acidosis: •
Method of preventing development of severe metabolic derangement in inborn errors of metabolism Inventor(s): Kang; Chunghee Kimberly (16 Forest Gate Cir., Oak Brook, IL 60523), Kang; David S. (16 Forest Gate Cir., Oak Brook, IL 60523) Assignee(s): none reported Patent Number: 6,503,530 Date filed: November 1, 2001 Excerpt(s): The present invention provides a method of avoiding rapid development of extreme hyperammonemia and metabolic acidosis in undiagnosed metabolically abnormal infants having an inherited metabolic disorder. Inborn errors of metabolism occur when there is a block in a pathway in a metabolic sequence. The block results in a rapid accumulation of normal intermediary products in abnormally large amounts and also of products of usually little used metabolic pathways. This biochemical abnormality is when characterized by hyperammonemia and/or ketoacidosis in neonatal-onset metabolic disorder. Restricting the intake of the essential substance from which the toxic metabolite is derived can treat the accumulated toxic effects of these intermediary metabolites. This minimizes the accumulation of intermediates that damage organs, particularly the nervous system, and affects the extent of mental retardation. Conventional management of infants diagnosed with certain inborn errors of amino acid or nitrogen metabolism requires the restriction of the specific amino acid(s) to the minimum amount required for normal growth and development. The amount of the restricted amino acid provided by the diet must be sufficient to meet the metabolic requirements dependent on it, but it must not permit an excess accumulation in the body fluids of the amino acid or its derivatives, or of nitrogen. Web site: http://www.delphion.com/details?pn=US06503530__
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Methods for treating renal failure Inventor(s): Hsu; Chen Hsing (3720 Tremont Dt., Ann Harbor, MI 48105) Assignee(s): none reported Patent Number: 5,753,706 Date filed: February 3, 1997 Abstract: Methods of controlling phosphate metabolism and metabolic acidosis in patients suffering from renal failure and associated hyperphosphatemia or patients predisposed to development of a hyperphosphatemic condition are provided. The method in accordance with this invention comprises administering to a patient a ferriccontaining compound selected from the group consisting of ferric citrate, ferric acetate, and combinations thereof. Therapeutic benefit can be realized in accordance with such method by administering the compound orally to a patient to contact and bind with ingested phosphate in the patient's digestive tract, and thereby prevent its intestinal absorption. Excerpt(s): The present invention relates generally to the control of phosphate retention and particularly, to methods for treating patients suffering from renal failure and
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associated hyperphosphatemia. Phosphate is primarily excreted through the kidney. Phosphate retention therefore inevitably occurs in renal failure. Phosphate restriction plays an important role in slowing down deterioration of renal function as well as soft tissue calcification in renal failure. A high intake of dietary phosphorus in experimental renal failure worsens renal function (Haut, L. L., Kidney Int 17:722-731 (1980); Karlinsky, D. et al., Kidney Int 17:293-302 (1980)) and a low phosphate intake arrests progression of chronic renal failure. Lumlertgul, D. et al., Kidney Int 29:658-666 (1986). Recent studies have demonstrated that phosphate restriction either increases plasma calcitriol (the most potent vitamin D metabolite) and suppresses secondary hyperparathyroidism (Portale, A. A. et al., J. Clin. Invest 73:1580-1589 (1989); Kilav, R. et al., J Clin. Invest 96:327-333 (1995); Lopez, H. et al., Am. J Physiol 259:F432-437 (1990)), or directly inhibits parathyroid cell proliferation. Naveh-Many, T. et al., Am. Soc. Nephrol 6:968 (1995). Taken together, maintaining a normal plasma concentration and tissue content of phosphate is an important means to prevent secondary hyperparathyroidism, renal osteodystrophy and soft tissue calcification in renal failure. Dietary restriction of phosphate is difficult to achieve and thrice weekly dialysis alone can not remove daily absorbed phosphate. Therefore, phosphate binding agents have generally been employed to control phosphate metabolism in renal failure. For the last 30 years nephrologist have been using aluminum carbonate or aluminum hydroxide as phosphate binding agents. Concerns about aluminum toxicity in renal failure have prompted increased use of calcium carbonate and calcium acetate and a cessation in the use of aluminum compounds. However, calcium carbonate or other calcium preparations are not only inadequate to remove all the ingested dietary phosphate, but also provide too much calcium to end stage renal disease (ESRD) patients. Web site: http://www.delphion.com/details?pn=US05753706__ •
Synthetic buffer composition for clinical use Inventor(s): Swan; Henry (Lakewood, CO) Assignee(s): Henry Swan II Trust (Lakewood, CO) Patent Number: 5,256,660 Date filed: March 17, 1992 Abstract: Methods of administering aqueous synthetic buffer compositions of an Nsubstituted aminosulfonic acid and a sodium salt of a different substituted aminosulfonic acid suitable to treat oligemic, respiratory and metabolic acidosis are disclosed. Methods of administering aqueous synthetic buffer compositions of a different N-substituted aminosulfonic acid, a sodium salt of an N-substituted aminosulfonic acid and tris(hydroxymethyl)aminomethane which may be similarly employed are also disclosed. Excerpt(s): This invention relates to synthetic buffer compositions, methods of making same and methods of using same. More specifically, this invention relates to synthetic buffer compositions finding particular but not exclusive utility in the treatment of disturbed metabolism in vertebrates. Even more specifically, this invention relates to aqueous buffering solutions finding particular but not exclusive utility in the treatment of disturbed metabolism in humans associated with disease, trauma or manipulative procedures. Stabilization and preservation of hydrogen ion concentration in both intracellular and extra-cellular body fluids is critical to the health of vertebrates. Considerable attention and scientific study have been devoted to this crucial aspect of maintaining internal homeostasis in humans. 3) the PHO.sub.3 /PO.sub.4 phosphate
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buffer system. Of these three chemical systems, the phosphate buffer system is the least effective, primarily because of the phosphate buffer system's inefficiency as a buffer above pH 7.2, and also because excessive phosphate causes undesirable side effects. For these reasons and others, phosphate buffers have had very limited clinical utility. Web site: http://www.delphion.com/details?pn=US05256660__
Patent Applications on Metabolic Acidosis 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 metabolic acidosis: •
Biochemically balanced peritoneal dialysis solutions Inventor(s): Henderson, Lee W.; (Lake Forest, IL), Martis, Leo; (Long Grove, IL) Correspondence: Charles R. Mattenson, ESQ.; Renal Division; Baxter International INC.; One Baxter Parkway; Deerfield; IL; 60015-4633; US Patent Application Number: 20020037329 Date filed: September 17, 2001 Abstract: A peritoneal dialysis solution that is biochemically balanced to correct metabolic acidosis associated with chronic renal failure in a more physiological manner. The peritoneal dialysis solution has a physiological pH, e.g., pH of 7.0 to 7.4, and contains bicarbonate at a concentration that is found in blood involved in Additionally, the solution contains carbon dioxide at a partial pressure that is similar to partial pressure of carbon dioxide found in the blood capillaries. The peritoneal dialysis solution also contains a weak acid with a pKa of less than 5.0. Excerpt(s): The present invention relates generally to peritoneal dialysis. More specifically, the present invention relates to peritoneal dialysis solutions. It is known to use dialysis to support a patient whose renal function has decreased to the point where the kidneys no longer sufficiently function. Two principal dialysis methods are utilized: hemodialysis; and peritoneal dialysis. In hemodialysis, the patient's blood is passed through an artificial kidney dialysis machine. A membrane in the machine acts as an artificial kidney for cleansing the blood. Because it is an extracorporeal treatment that requires special machinery, there are certain inherent disadvantages with hemodialysis. 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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•
Calcium glutarate supplement and phosphorus binder Inventor(s): Alexandrides, George; (San Antonio, TX), Walsdorf, Neill B. SR.; (San Antonio, TX) Correspondence: Thomas D. Paul; Fulbright & Jaworski, L.L.P.; 1301 Mckinney, Suite 5100; Houston; TX; 77010-3095; US Patent Application Number: 20030077331 Date filed: July 31, 2001 Abstract: Methods of controlling calcium intake and phosphate metabolism and metabolic acidosis in patients suffering from renal failure and associated hyperphosphatemia or patients predisposed to development of a hyperphosphatemic condition are provided. The method in accordance with this invention comprises administering to a patient a calcium glutarate compound. Therapeutic benefit can be realized in accordance with such method by administering the compound orally to a patient to increase available calcium and contact and bind with ingested phosphate in the patient's digestive tract, and thereby prevent its intestinal absorption. Excerpt(s): The present invention relates generally to calcium supplementation and controlling phosphate retention and particularly, to methods for treating patients on dialysis and suffering from renal failure and associated hyperphosphatemia. Phosphorus is the sixth most abundant element in the human body. It is critical for bone mineralization, cellular structure, genetic coding, and energy metabolism. Many organic and inorganic forms exist. Approximately 1,000 g of phosphorus is present in an adult, of which 80-90% is in bone. An additional 10-14% is intracellular and the remaining 1%, is extracellular. The phosphorus in plasma is 12-17% protein bound. Free serum compounds represent much less than 1% of the total body phosphorus content. This fraction also varies with shifts between the intracellular and extracellular compartments. Thus, serum phosphorus levels may not accurately reflect the total body phosphorus content. Levels are expressed in terms of serum phosphorus mass (mg/dL). One mg/dL of phosphorus is equal to 0.32 mmol of phosphate. The normal adult range is 2.5 to 4.5 mg/dL (0.81 to 1.45 mmol/L). Levels are 50% higher in infants and 30% higher in children due to growth hormone effects. Hyperphosphatemia is an abnormally elevated serum phosphate level. Normal serum phosphate levels are in the range of 2.5 to 4.5 mg/dl. 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 metabolic acidosis, 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 “metabolic acidosis” (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 metabolic acidosis.
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You can also use this procedure to view pending patent applications concerning metabolic acidosis. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.
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CHAPTER 5. BOOKS ON METABOLIC ACIDOSIS Overview This chapter provides bibliographic book references relating to metabolic acidosis. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on metabolic acidosis include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.
Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “metabolic acidosis” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on metabolic acidosis: •
Renal Failure: Blackwell's Basics of Medicine Source: Oxford, England: Blackwell Science Ltd. 1995. 295 p. Contact: Available from Blackwell Science, Inc. 238 Main Street, Cambridge, MA 02142. (800) 215-1000 or (617) 876-7000. Fax (617) 492-5263. PRICE: $24.95. ISBN: 0865424306. Summary: This book for health professionals on renal failure is from a series that examines relevant topics in medicine using concepts that pertain to the basic sciences. In this series, readers learn to interpret clinical data based on pathophysiological concepts. Four sections in this book cover the following issues: essentials, pathophysiology, clinical picture, and management of renal failure. Each section offers questions, with answers of one or two paragraphs on relevant topics. The 555 questions are numbered for ease of access through the subject index. Specific topics covered include: the anatomy of the kidneys, the kidney function tests used for diagnosis and monitoring, electrolyte
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function, urine concentration and dilution, oral water load, the roles of aldosterone, the role of the kidney in acid base balance, potassium, dietary therapy, chronic renal failure, polyuria, water and salt homeostasis, metabolic acidosis, renal tubular acidosis, hyperkalemia, acute tubular necrosis, uremia, renal impairment associated with diabetes mellitus, etiology of renal failure, hepatorenal syndrome, obstructive uropathy, anemia and erythropoietin, osteodystrophy, dialysis, prognosis, cost factors, and kidney transplantation. •
Pathogenetic and Therapeutic Aspects of Chronic Renal Failure Source: New York, NY: Marcel Dekker, Inc. 1997. 242 p. Contact: Available from Marcel Dekker, Inc. 270 Madison Avenue, New York, NY 10016. (212) 696-9000. Fax (212) 685-4540. PRICE: $115.00. ISBN: 0824798945. Summary: This book is based on an international workshop, Chronic Renal Failure: Pathogenetic and Therapeutic Aspects, held in Berlin in May 1996. The first part of the book deals with arterial hypertension, hyperlipidemia, and metabolic acidosis as factors that accelerate the progression of chronic renal failure (CRF) and with the effect of dietary protein restriction as a measure to slow the advance of renal insufficiency. The second part addresses the etiology and pathophysiology of myocardial hypertrophy in general, and especially in uremia, and the influence of the dialysis regimen on the development of myocardial hypertrophy. The final section discusses the correction of renal anemia via treatment with recombinant human erythropoietin (rhEPO), with special emphasis on its effects on cardiac function and hypertrophy and on the function of parts of the endocrine system. Also included are an analysis of the use of rhEPO in renal transplant patients and an overview of the problems of iron supplementation in rhEPO treatment. The 17 chapters, each written by experts in the field, include reference lists; a subject index concludes the book.
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Acid-Base, Fluids, and Electrolytes Made Ridiculously Simple Source: Miami, FL: Medmaster, Inc. 1997. 160 p. Contact: Available from Medmaster, Inc. P.O. Box 640028, Miami, FL 33164. (954) 9628414. Fax (954) 962-4508. E-mail:
[email protected]. Website: www.medmaster.net. PRICE: $17.95 plus shipping and handling. ISBN: 0940780313. Summary: This book on acid base, fluids, and electrolytes is from a series of publications that select material that is most clinically relevant to the medical student and other health professionals. The text then offers a clear conceptual understanding of the subject as a whole, along with those clinically relevant facts that are important to learn (leaving out those facts that can be looked up in a reference text). The book is designed for medical students, interns and residents, nurses, nephrologists, primary care physicians, surgeons, and other clinicians responsible for intravenous fluid therapy. Ten chapters cover the basics, intravenous (IV) solutions and IV orders, hyponatremia (low blood levels of sodium), hypernatremia, hypokalemia (low blood levels of potassium), hyperkalemia, metabolic acidosis, metabolic alkalosis, and mixed acid base disorders. Each chapter concludes with questions and clinical situations for readers to use to review the specific material presented in that chapter. A final chapter offers seven case examples for readers to summarize and combine the concepts presented. Extensive figures and tables also summarize the material in each chapter. The book concludes with a subject index.
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Primer on Kidney Diseases. 2nd ed Source: San Diego, CA: Academic Press. 1998. 542 p. Contact: Available from Academic Press. Order Fulfillment Department, 6277 Sea Harbor Drive, Orlando, FL 32887. (800) 321-5068 or (407) 345-3800. Fax (800) 874-6418 or (407) 345-4060. E-mail:
[email protected]. Website: www.apnet.com. PRICE: $57.95 plus shipping and handling. ISBN: 0122990900. Summary: This comprehensive textbook on kidney diseases is designed for medical students, house staff, and practitioners. The text offers a summary of the management of renal disease and fluid and electrolyte disorders. The 79 chapters are categorized in 11 sections, covering renal function and its assessment, electrolyte disorders, glomerular disease, the kidney in systemic disease, acute renal failure, drugs and the kidney, hereditary renal diseases, tubulointerstitial diseases, the kidney in special circumstances, chronic renal disease, and hypertension. Specific chapter topics include the characteristics of kidney function in the very young and in the very old, tubulointerstitial diseases, analgesic abuse nephropathy and the effects of NSAIDs on the kidneys, hematuria (blood in the urine), proteinuria, renal imaging techniques, metabolic acidosis and alkalosis, edema and the clinical use of diuretics, immunopathogenesis, minimal change nephropathy, IgA nephropathy, Goodpasture's syndrome, renal function in congestive heart failure, renal function in liver disease, renal manifestations of systemic lupus erythematosus, diabetic nephropathy, dysproteinemias and amyloidosis, renal and urologic complications of cancer and its treatment, hemolytic uremic syndrome, the renal manifestations of HIV, interstitial nephritis, sickle cell nephropathy, Alport's syndrome, medullary cystic disease, tubulointerstitial disease, lead nephrotoxicity, lithium induced renal disease, medullary sponge kidney, obstructive uropathy, nephrolithiasis (kidney stones), urinary tract infections, the kidney in pregnancy, the uremic syndrome, hemodialysis and hemofiltration, peritoneal dialysis, nutrition and renal disease, renal osteodystrophy, renal transplantation, and the pathogenesis of hypertension. Each chapter is written by an established expert in the field. The book is illustrated with full color and black and white photographs, figures, and tables. Each chapter concludes with suggested readings. An extensive subject index concludes the text.
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Renal and Electrolyte Disorders, Fourth Edition Source: Boston, MA: Little, Brown and Company. 1992. 857 p. Contact: Available from Little, Brown and Company. Order Department, 200 West Street, Waltham, MA 02154. (800) 343-9204. PRICE: $57.95. ISBN: 0316774944. Summary: This medical textbook presents a pathophysiologic approach to understanding renal and electrolyte disorders. Topics in the fifteen chapters include: disorders of water metabolism; renal sodium excretion, edematous disorders, and diuretic use; the pathogenesis and management of metabolic acidosis; the pathogenesis and management of respiratory and mixed acid-base disorders; disorders of potassium metabolism; disorders of calcium, phosphorus, vitamin D, and parathyroid hormone activity; normal and abnormal magnesium metabolism; disorders of the reninangiotensin-aldosterone system; the kidney in hypertension; the pathogenesis, diagnosis and management of acute renal failure; the manifestations and pathogenesis of chronic renal failure; obstructive nephropathy; renal function in pregnancy; proteinuria and the nephrotic syndrome; and the glomerulopathies. A subject index is appended. 3862 references.
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Renal and Electrolyte Disorders, Sixth Edition Source: Philadelphia, PA: Lippincott Williams and Wilkins. 2003. 703 p. Contact: Available from Lippincott Williams and Wilkins. P.O. Box 1600, Hagerstown, MD 21741. (800) 638-3030 or (301) 223-2300. Fax (301) 223-2365. PRICE: $75.00 plus shipping and handling. ISBN: 0781737494. Summary: This textbook on renal (kidney) pathophysiology is designed for physicians in training who wish to maintain a current knowledge base and update their clinical skills. The text features clinically focused coverage of kidney pathophysiology. Fifteen chapters cover disorders of water metabolism; renal sodium excretion, edematous disorders, and diuretic use; the pathogenesis and management of metabolic acidosis and alkalosis; the pathogenesis and management of respiratory and mixed acid-base disorders; disorders of potassium metabolism; disorders of calcium, phosphorus, vitamin D, and parathyroid hormone (PTH) activity; normal and abnormal magnesium metabolism; disorders of the renin-angiotensin-aldosterone system; the kidney in hypertension (high blood pressure); the pathogenesis, diagnosis, and management of acute renal failure (ARF); the manifestations and pathogenesis of chronic renal failure (CFR); obstructive nephropathy; renal function in pregnancy; proteinuria and the nephrotic syndrome; and the glomerulopathies. Each chapter concludes with a lengthy reference list and the text concludes with a detailed subject index.
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 “metabolic acidosis” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “metabolic acidosis” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “metabolic acidosis” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •
No.87 Metabolic Acidosis (CIBA Foundation Symposium); ISBN: 0272796514; http://www.amazon.com/exec/obidos/ASIN/0272796514/icongroupinterna
Chapters on Metabolic Acidosis In order to find chapters that specifically relate to metabolic acidosis, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and metabolic acidosis using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Book Chapter.” Type “metabolic acidosis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on metabolic acidosis:
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Metabolic Acidosis Source: in Suki, W.N.; Massry, S.G., eds. Therapy of Renal Diseases and Related Disorders, 2nd ed. Hingham, MA: Kluwer Academic Publishers. 1991. p. 177-191. Contact: Available from Kluwer Academic Publishers. P.O. Box 358, Accord Station, Hingham, MA 02018. (617) 871-6600. PRICE: $315. ISBN: 0792306767. Summary: This chapter, from a medical text on the therapy of renal disease and related disorders, discusses metabolic acidosis. The authors briefly review the pathogenesis of and diagnostic approach to metabolic acidosis, provide some general principles of treatment, and then discuss individual disorders separately. Specific topics include the calculation of the quantity of bicarbonate to administer in treating acidosis; therapeutic options; and treatment of ketoacidosis, lactic acidosis, salicylate intoxication, methanol intoxication, ethylene glycol intoxication, organic acid load from the gastrointestinal tract, and renal acidoses. 3 appendixes. 8 figures. 7 tables. 27 references.
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CHAPTER 6. MULTIMEDIA ON METABOLIC ACIDOSIS Overview In this chapter, we show you how to keep current on multimedia sources of information on metabolic acidosis. We start with sources that have been summarized by federal agencies, and then show you how to find bibliographic information catalogued by the National Library of Medicine.
Video Recordings An excellent source of multimedia information on metabolic acidosis is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “metabolic acidosis” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find video productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Videorecording (videotape, videocassette, etc.).” Type “metabolic acidosis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on metabolic acidosis: •
Nephrology Update Source: Cleveland, OH: Cleveland Clinic Foundation. 1992. (videocassettes, proceedings/minutes). Contact: Available from CME Video. 2000 Crawford Place, Suite 100, Mount Laurel, NJ 08054. (800) 284-8433. PRICE: $495; plus $18.25 shipping and handling; Group Practice Package $150 plus $5.25 shipping and handling. Program Number 076. Summary: This Video Education Program presents 23 hours of presentations and problem-solving workshops. Topics include the clinical applications of basic renal physiology; the biology of mesangial cell structure and function; the diagnosis and management of hypercalcemia; mechanisms of dialysis-induced hypotension; HIV nephropathy; renal artery stenosis; the pathogenesis of renal stones; glomerulonephritis; dietary treatment in chronic renal disease; drug-induced acute and chronic interstitial nephritis; issues in metabolic acidosis; prostatic disease; hypertension; systemic lupus
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erythematosus nephritis; and the thrombotic angiopathies. Workshops cover topics including: management issues in dialysis patients, access, adequacy and nutrition; complex acid-base disorders; and intensive care unit (ICU) nephrology. All tapes are indexed with Quik-Scan for fast reference to presentations of special interest to the viewer. The program is accompanied by the original course syllabus, including supplemental reference information.
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CHAPTER 7. PERIODICALS AND NEWS ON METABOLIC ACIDOSIS Overview In this chapter, we suggest a number of news sources and present various periodicals that cover metabolic acidosis.
News Services and Press Releases One of the simplest ways of tracking press releases on metabolic acidosis 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 “metabolic acidosis” (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 metabolic acidosis. 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 “metabolic acidosis” (or synonyms).
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The NIH Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine. Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name. Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “metabolic acidosis” (or synonyms) into the search box, and click on “Search News.” As this service is technology oriented, you may wish to use it when searching for press releases covering diagnostic procedures or tests. Search Engines Medical news is also available in the news sections of commercial Internet search engines. See the health news page at Yahoo (http://dir.yahoo.com/Health/News_and_Media/), or you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “metabolic acidosis” (or synonyms). If you know the name of a company that is relevant to metabolic acidosis, 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 “metabolic acidosis” (or synonyms).
Periodicals and News
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Newsletter Articles Use the Combined Health Information Database, and limit your search criteria to “newsletter articles.” Again, you will need to use the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter Article.” Type “metabolic acidosis” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months. The following is a typical result when searching for newsletter articles on metabolic acidosis: •
Management of Laxative Abuse in Eating Disorders Source: SCAN'S PULSE. 18(3): 7-8. Fall 1999. Contact: Available from American Dietetic Association. SCAN Office, 90 S. Cascade Avenue, Suite 1230, Colorado Springs, CO 80903. (719) 475-7751. Fax (719) 475-8748. Summary: Health professionals who treat eating disorders eventually encounter clients with anorexia nervosa or bulimia who use laxatives as a method of weight control. This article reviews the management of laxative abuse in patients with eating disorders. Women who abuse laxatives believe that taking laxatives after food consumption prevents the absorption of calories in the intestine. However, studies show that laxative use only decreases caloric absorption by 12 percent, because laxatives primarily exert their effect in the large intestine. In addition to being ineffective in weight control, chronic laxative use is also medically dangerous. Serious problems that may occur include electrolyte and fluid imbalance leading to metabolic acidosis or alkalosis, permanent structural and functional damage to the colon, interstitial renal (kidney) disease, and rectal prolapse. The successful management of chronic laxative abuse requires a team of professionals that includes a physician, nutrition therapist, and psychotherapist. The author reviews the treatment protocol for these patients, which includes adequate dietary fiber and fluids intake, limited consumption of high sodium and gas forming foods, regular exercise, and patient education. During weekly appointments, the nutrition therapist should evaluate the client's compliance with the prescribed treatment plan. The author cautions that discontinuing long term laxative abuse is extremely difficult, and some clients may require inpatient treatment to be successful. Body image issues become predominant as the client experiences severe fluid retention, often in the range of 10 to 20 pounds, until natural diuresis occurs after about 4 to 6 weeks of laxative abstinence. 9 references.
Academic Periodicals covering Metabolic Acidosis Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to metabolic acidosis. In addition to these sources, you can search for articles covering metabolic acidosis 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
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name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”
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APPENDICES
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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute10: •
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
•
National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
•
National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
•
National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
•
National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
•
National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
•
National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
•
National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
10
These publications are typically written by one or more of the various NIH Institutes.
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•
National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
•
National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
•
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
•
National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
•
National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
•
National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
•
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
•
National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
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National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
•
National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
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National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
•
National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
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National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
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Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
•
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 “metabolic acidosis” (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 9618 47 598 26 1520 11809
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 “metabolic acidosis” (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 metabolic acidosis can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internetbased 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 metabolic acidosis. 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 metabolic acidosis. 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 “metabolic acidosis”:
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Gaucher's Disease http://www.nlm.nih.gov/medlineplus/gauchersdisease.html Genetic Brain Disorders http://www.nlm.nih.gov/medlineplus/geneticbraindisorders.html Laboratory Tests http://www.nlm.nih.gov/medlineplus/laboratorytests.html Leukodystrophies http://www.nlm.nih.gov/medlineplus/leukodystrophies.html Metabolic Disorders http://www.nlm.nih.gov/medlineplus/metabolicdisorders.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 metabolic acidosis. 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. PEDBASE Similar to NORD, PEDBASE covers relatively rare disorders, limited mainly to pediatric conditions. PEDBASE was designed by Dr. Alan Gandy. To access the database, which is more oriented to researchers than patients, you can view the current list of health topics covered at the following Web site: http://www.icondata.com/health/pedbase/pedlynx.htm. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
•
Family Village: http://www.familyvillage.wisc.edu/specific.htm
Patient Resources
•
Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
•
Med Help International: http://www.medhelp.org/HealthTopics/A.html
•
Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
•
Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
•
WebMDHealth: http://my.webmd.com/health_topics
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Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to metabolic acidosis. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with metabolic acidosis. 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 metabolic acidosis. 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 “metabolic acidosis” (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 “metabolic acidosis”. Type the following hyperlink into
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your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “metabolic acidosis” (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 “metabolic acidosis” (or a synonym) into the search box, and click “Submit Query.”
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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.
Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.21
Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.
Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of
21
Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.
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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)22: •
Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/
•
Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)
•
Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
•
California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
•
California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
•
California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html
•
California: Gateway Health Library (Sutter Gould Medical Foundation)
•
California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
•
California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
•
California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
•
California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
•
California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
•
California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
•
California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
•
California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
•
Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
•
Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
•
Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
22
Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
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•
Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
•
Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm
•
Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
•
Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm
•
Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp
•
Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/
•
Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm
•
Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html
•
Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/
•
Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
•
Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
•
Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
•
Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
•
Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm
•
Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html
•
Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm
•
Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
•
Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
•
Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
•
Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
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•
Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html
•
Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp
•
Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp
•
Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/
•
Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
•
Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
•
Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
•
Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
•
Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
•
Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
•
Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
•
Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
•
Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html
•
Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm
•
Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
•
Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
•
National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
•
National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/
•
National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
Finding Medical Libraries
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Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
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New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
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New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
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New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
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New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
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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 metabolic acidosis: •
Basic Guidelines for Metabolic Acidosis Metabolic acidosis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000335.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
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MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html
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Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/
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Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
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METABOLIC ACIDOSIS DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. Abdomen: That portion of the body that lies between the thorax and the pelvis. [NIH] Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Abdominal Pain: Sensation of discomfort, distress, or agony in the abdominal region. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] ACE: Angiotensin-coverting enzyme. A drug used to decrease pressure inside blood vessels. [NIH]
Acetaminophen: Analgesic antipyretic derivative of acetanilide. It has weak antiinflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage. [NIH] Acid-Base Equilibrium: The balance between acids and bases in the blood plasma. Normally it results in a slightly alkaline state with an excess of hydroxyl ions in comparison to hydrogen. The balance is achieved by the offset of the ingestion and production of acidic and basic material by the amount of acidic and basic material metabolized and excreted by the body. [NIH] Acidemia: Increased acidity of blood. [NIH] Acidity: The quality of being acid or sour; containing acid (hydrogen ions). [EU] Acidosis: A pathologic condition resulting from accumulation of acid or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, and characterized by an increase in hydrogen ion concentration. [EU] Actin: Essential component of the cell skeleton. [NIH] Acute renal: A condition in which the kidneys suddenly stop working. In most cases, kidneys can recover from almost complete loss of function. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adaptation: 1. The adjustment of an organism to its environment, or the process by which it enhances such fitness. 2. The normal ability of the eye to adjust itself to variations in the intensity of light; the adjustment to such variations. 3. The decline in the frequency of firing of a neuron, particularly of a receptor, under conditions of constant stimulation. 4. In dentistry, (a) the proper fitting of a denture, (b) the degree of proximity and interlocking of restorative material to a tooth preparation, (c) the exact adjustment of bands to teeth. 5. In microbiology, the adjustment of bacterial physiology to a new environment. [EU] Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adipocytes: Fat-storing cells found mostly in the abdominal cavity and subcutaneous tissue. Fat is usually stored in the form of tryglycerides. [NIH]
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Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH] Adjuvant: A substance which aids another, such as an auxiliary remedy; in immunology, nonspecific stimulator (e.g., BCG vaccine) of the immune response. [EU] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Adrenal Glands: Paired glands situated in the retroperitoneal tissues at the superior pole of each kidney. [NIH] Adrenal 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] Aetiology: Study of the causes of disease. [EU] Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Aldosterone: (11 beta)-11,21-Dihydroxy-3,20-dioxopregn-4-en-18-al. A hormone secreted by the adrenal cortex that functions in the regulation of electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium. [NIH] Alertness: A state of readiness to detect and respond to certain specified small changes occurring at random intervals in the environment. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU]
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Alkalemia: Decreased acidity of blood. [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] Alkalosis: A pathological condition that removes acid or adds base to the body fluids. [NIH] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Alternative Splicing: A process whereby multiple protein isoforms are generated from a single gene. Alternative splicing involves the splicing together of nonconsecutive exons during the processing of some, but not all, transcripts of the gene. Thus a particular exon may be connected to any one of several alternative exons to form messenger RNA. The alternative forms produce proteins in which one part is common while the other part is different. [NIH] Aluminum: A metallic element that has the atomic number 13, atomic symbol Al, and atomic weight 26.98. [NIH] Aluminum Compounds: Inorganic compounds that contain aluminum as an integral part of the molecule. [NIH] Aluminum Hydroxide: Hydrated aluminum. A compound with many biomedical applications: as a gastric antacid, an antiperspirant, in dentifrices, as an emulsifier, as an adjuvant in bacterins and vaccines, in water purification, etc. [NIH] Alveolar Process: The thickest and spongiest part of the maxilla and mandible hollowed out into deep cavities for the teeth. [NIH] Alveoli: Tiny air sacs at the end of the bronchioles in the lungs. [NIH] Amaurosis: Partial or total blindness from any cause. [NIH] Amenorrhea: Absence of menstruation. [NIH] 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] Amino-terminal: The end of a protein or polypeptide chain that contains a free amino group (-NH2). [NIH] Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH] Amyloidosis: A group of diseases in which protein is deposited in specific organs (localized amyloidosis) or throughout the body (systemic amyloidosis). Amyloidosis may be either primary (with no known cause) or secondary (caused by another disease, including some
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types of cancer). Generally, primary amyloidosis affects the nerves, skin, tongue, joints, heart, and liver; secondary amyloidosis often affects the spleen, kidneys, liver, and adrenal glands. [NIH] Anaerobic: 1. Lacking molecular oxygen. 2. Growing, living, or occurring in the absence of molecular oxygen; pertaining to an anaerobe. [EU] Anaerobic Threshold: The oxygen consumption level above which aerobic energy production is supplemented by anaerobic mechanisms during exercise, resulting in a sustained increase in lactate concentration and metabolic acidosis. The anaerobic threshold is affected by factors that modify oxygen delivery to the tissues; it is low in patients with heart disease. Methods of measurement include direct measure of lactate concentration, direct measurement of bicarbonate concentration, and gas exchange measurements. [NIH] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Anal: Having to do with the anus, which is the posterior opening of the large bowel. [NIH] Analgesic: An agent that alleviates pain without causing loss of consciousness. [EU] Analog: In chemistry, a substance that is similar, but not identical, to another. [NIH] Analytes: A component of a test sample the presence of which has to be demonstrated. The term "analyte" includes where appropriate formed from the analyte during the analyses. [NIH]
Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anesthesia: A state characterized by loss of feeling or sensation. This depression of nerve function is usually the result of pharmacologic action and is induced to allow performance of surgery or other painful procedures. [NIH] Anesthetics: Agents that are capable of inducing a total or partial loss of sensation, especially tactile sensation and pain. They may act to induce general anesthesia, in which an unconscious state is achieved, or may act locally to induce numbness or lack of sensation at a targeted site. [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] Anionic: Pertaining to or containing an anion. [EU] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Anode: Electrode held at a positive potential with respect to a cathode. [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] Anorexia Nervosa: The chief symptoms are inability to eat, weight loss, and amenorrhea. [NIH]
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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] 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] 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] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Antimetabolite: A chemical that is very similar to one required in a normal biochemical reaction in cells. Antimetabolites can stop or slow down the reaction. [NIH] Antimicrobial: Killing microorganisms, or suppressing their multiplication or growth. [EU] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] 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] Antipruritic: Relieving or preventing itching. [EU] Antipyretic: An agent that relieves or reduces fever. Called also antifebrile, antithermic and febrifuge. [EU] Anus: The opening of the rectum to the outside of the body. [NIH] Anxiety: Persistent feeling of dread, apprehension, and impending disaster. [NIH] Aorta: The main trunk of the systemic arteries. [NIH] Apnea: A transient absence of spontaneous respiration. [NIH] Aponeurosis: Tendinous expansion consisting of a fibrous or membranous sheath which serves as a fascia to enclose or bind a group of muscles. [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
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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] 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] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Asphyxia: A pathological condition caused by lack of oxygen, manifested in impending or actual cessation of life. [NIH] Asymptomatic: Having no signs or symptoms of disease. [NIH] Atmospheric Pressure: The pressure at any point in an atmosphere due solely to the weight of the atmospheric gases above the point concerned. [NIH] Atrial: Pertaining to an atrium. [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] Attenuated: Strain with weakened or reduced virulence. [NIH] Autologous: Taken from an individual's own tissues, cells, or DNA. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacterial Physiology: Physiological processes and activities of bacteria. [NIH] Bactericidal: Substance lethal to bacteria; substance capable of killing bacteria. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its subdivisions is the basal (basement) lamina. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]
Beta 2-Microglobulin: An 11 kDa protein associated with the outer membrane of many cells including lymphocytes. It is the small subunit of the MHC class I molecule. Association with beta 2-microglobulin is generally required for the transport of class I heavy chains from the endoplasmic reticulum to the cell surface. Beta 2-microglobulin is present in small amounts in serum, csf, and urine of normal people, and to a much greater degree in the urine and plasma of patients with tubular proteinemia, renal failure, or kidney transplants. [NIH]
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Beta-Thalassemia: A disorder characterized by reduced synthesis of the beta chains of hemoglobin. There is retardation of hemoglobin A synthesis in the heterozygous form (thalassemia minor), which is asymptomatic, while in the homozygous form (thalassemia major, Cooley's anemia, Mediterranean anemia, erythroblastic anemia), which can result in severe complications and even death, hemoglobin A synthesis is absent. [NIH] Bilateral: Affecting both the right and left side of body. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [NIH] Bilirubin: A bile pigment that is a degradation product of heme. [NIH] Binding agent: A substance that makes a loose mixture stick together. For example, binding agents can be used to make solid pills from loose powders. [NIH] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biogenic Monoamines: Biogenic amines having only one amine moiety. Included in this group are all natural monoamines formed by the enzymatic decarboxylation of natural amino acids. [NIH] Biological therapy: Treatment to stimulate or restore the ability of the immune system to fight infection and disease. Also used to lessen side effects that may be caused by some cancer treatments. Also known as immunotherapy, biotherapy, or biological response modifier (BRM) therapy. [NIH] Biological Transport: The movement of materials (including biochemical substances and drugs) across cell membranes and epithelial layers, usually by passive diffusion. [NIH] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Bladder: The organ that stores urine. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blood Volume: Volume of circulating blood. It is the sum of the plasma volume and erythrocyte volume. [NIH] Body Fluids: Liquid components of living organisms. [NIH] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and
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is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bone Resorption: Bone loss due to osteoclastic activity. [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] Brain Diseases: Pathologic conditions affecting the brain, which is composed of the intracranial components of the central nervous system. This includes (but is not limited to) the cerebral cortex; intracranial white matter; basal ganglia; thalamus; hypothalamus; brain stem; and cerebellum. [NIH] Brain Stem: The part of the brain that connects the cerebral hemispheres with the spinal cord. It consists of the mesencephalon, pons, and medulla oblongata. [NIH] Bronchi: The larger air passages of the lungs arising from the terminal bifurcation of the trachea. [NIH] Buffers: A chemical system that functions to control the levels of specific ions in solution. When the level of hydrogen ion in solution is controlled the system is called a pH buffer. [NIH]
Bulbar: Pertaining to a bulb; pertaining to or involving the medulla oblongata, as bulbar paralysis. [EU] Bulimia: Episodic binge eating. The episodes may be associated with the fear of not being able to stop eating, depressed mood, or self-deprecating thoughts (binge-eating disorder) and may frequently be terminated by self-induced vomiting (bulimia nervosa). [NIH] Calcifediol: The major circulating metabolite of vitamin D3 produced in the liver and the best indicator of the body's vitamin D stores. It is effective in the treatment of rickets and osteomalacia, both in azotemic and non-azotemic patients. Calcifediol also has mineralizing properties. [NIH] Calcification: Deposits of calcium in the tissues of the breast. Calcification in the breast can be seen on a mammogram, but cannot be detected by touch. There are two types of breast calcification, macrocalcification and microcalcification. Macrocalcifications are large deposits and are usually not related to cancer. Microcalcifications are specks of calcium that may be found in an area of rapidly dividing cells. Many microcalcifications clustered together may be a sign of cancer. [NIH] Calcitriol: The physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (calcifediol). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calcium Carbonate: Carbonic acid calcium salt (CaCO3). An odorless, tasteless powder or crystal that occurs in nature. It is used therapeutically as a phosphate buffer in hemodialysis patients and as a calcium supplement. [NIH] Calcium channel blocker: A drug used to relax the blood vessel and heart muscle, causing
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pressure inside blood vessels to drop. It also can regulate heart rhythm. [NIH] Calcium Channels: Voltage-dependent cell membrane glycoproteins selectively permeable to calcium ions. They are categorized as L-, T-, N-, P-, Q-, and R-types based on the activation and inactivation kinetics, ion specificity, and sensitivity to drugs and toxins. The L- and T-types are present throughout the cardiovascular and central nervous systems and the N-, P-, Q-, & R-types are located in neuronal tissue. [NIH] Calcium Oxalate: The calcium salt of oxalic acid, occurring in the urine as crystals and in certain calculi. [NIH] Caloric intake: Refers to the number of calories (energy content) consumed. [NIH] Cannula: A tube for insertion into a duct or cavity; during insertion its lumen is usually occupied by a trocar. [EU] Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carbonate Dehydratase: A zinc-containing enzyme of erythrocytes with molecular weight of 30 kD. It is among the most active of known enzymes and catalyzes the reversible hydration of carbon dioxide, which is significant in the transport of CO2 from the tissues to the lungs. The enzyme is inhibited by acetazolamide. EC 4.2.1.1. [NIH] Carbonic Anhydrase Inhibitors: A class of compounds that reduces the secretion of H+ ions by the proximal kidney tubule through inhibition of carbonic anhydrase (carbonate dehydratase). [NIH] Carcinogenic: Producing carcinoma. [EU] Cardiac: Having to do with the heart. [NIH] Cardiac arrest: A sudden stop of heart function. [NIH] Cardiac Output: The volume of blood passing through the heart per unit of time. It is usually expressed as liters (volume) per minute so as not to be confused with stroke volume (volume per beat). [NIH] Cardiopulmonary: Having to do with the heart and lungs. [NIH] Cardiopulmonary Bypass: Diversion of the flow of blood from the entrance of the right atrium directly to the aorta (or femoral artery) via an oxygenator thus bypassing both the heart and lungs. [NIH] Cardiopulmonary Resuscitation: The artificial substitution of heart and lung action as indicated for heart arrest resulting from electric shock, drowning, respiratory arrest, or other causes. The two major components of cardiopulmonary resuscitation are artificial ventilation and closed-chest cardiac massage. [NIH] Cardiopulmonary Resuscitation: The artificial substitution of heart and lung action as indicated for heart arrest resulting from electric shock, drowning, respiratory arrest, or other causes. The two major components of cardiopulmonary resuscitation are artificial
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ventilation and closed-chest cardiac massage. [NIH] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular System: The heart and the blood vessels by which blood is pumped and circulated through the body. [NIH] Carotene: The general name for a group of pigments found in green, yellow, and leafy vegetables, and yellow fruits. The pigments are fat-soluble, unsaturated aliphatic hydrocarbons functioning as provitamins and are converted to vitamin A through enzymatic processes in the intestinal wall. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Caspase: Enzyme released by the cell at a crucial stage in apoptosis in order to shred all cellular proteins. [NIH] Catabolism: Any destructive metabolic process by which organisms convert substances into excreted compounds. [EU] 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] Catheters: A small, flexible tube that may be inserted into various parts of the body to inject or remove liquids. [NIH] Cations: Postively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis. [NIH] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Cecum: The beginning of the large intestine. The cecum is connected to the lower part of the small intestine, called the ileum. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell 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 Polarity: Orientation of intracellular structures especially with respect to the apical and basolateral domains of the plasma membrane. Polarized cells must direct proteins from the
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Golgi apparatus to the appropriate domain since tight junctions prevent proteins from diffusing between the two domains. [NIH] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Cell Size: The physical dimensions of a cell. It refers mainly to changes in dimensions correlated with physiological or pathological changes in cells. [NIH] Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. [NIH] Cell Transplantation: Transference of cells within an individual, between individuals of the same species, or between individuals of different species. [NIH] Cellulose: A polysaccharide with glucose units linked as in cellobiose. It is the chief constituent of plant fibers, cotton being the purest natural form of the substance. As a raw material, it forms the basis for many derivatives used in chromatography, ion exchange materials, explosives manufacturing, and pharmaceutical preparations. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Centrifugation: A method of separating organelles or large molecules that relies upon differential sedimentation through a preformed density gradient under the influence of a gravitational field generated in a centrifuge. [NIH] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] Chemotherapy: Treatment with anticancer drugs. [NIH] Chin: The anatomical frontal portion of the mandible, also known as the mentum, that contains the line of fusion of the two separate halves of the mandible (symphysis menti). This line of fusion divides inferiorly to enclose a triangular area called the mental protuberance. On each side, inferior to the second premolar tooth, is the mental foramen for the passage of blood vessels and a nerve. [NIH] 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] Cholestyramine: Strongly basic anion exchange resin whose main constituent is polystyrene trimethylbenzylammonium as Cl(-) anion. It exchanges chloride ions with bile salts, thus decreasing their concentration and that of cholesterol. It is used as a hypocholesteremic in diarrhea and biliary obstruction and as an antipruritic. [NIH] Chondrocytes: Polymorphic cells that form cartilage. [NIH] Choroid: The thin, highly vascular membrane covering most of the posterior of the eye between the retina and sclera. [NIH] Chromaffin System: The cells of the body which stain with chromium salts. They occur along the sympathetic nerves, in the adrenal gland, and in various other organs. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all
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human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic renal: Slow and progressive loss of kidney function over several years, often resulting in end-stage renal disease. People with end-stage renal disease need dialysis or transplantation to replace the work of the kidneys. [NIH] Circulatory system: The system that contains the heart and the blood vessels and moves blood throughout the body. This system helps tissues get enough oxygen and nutrients, and it helps them get rid of waste products. The lymph system, which connects with the blood system, is often considered part of the circulatory system. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Cisplatin: An inorganic and water-soluble platinum complex. After undergoing hydrolysis, it reacts with DNA to produce both intra and interstrand crosslinks. These crosslinks appear to impair replication and transcription of DNA. The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle. [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] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [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] Colloidal: Of the nature of a colloid. [EU] Colon: The long, coiled, tubelike organ that removes water from digested food. The remaining material, solid waste called stool, moves through the colon to the rectum and leaves the body through the anus. [NIH] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the
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classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] 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] Compliance: Distensibility measure of a chamber such as the lungs (lung compliance) or bladder. Compliance is expressed as a change in volume per unit change in pressure. [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] Cones: One type of specialized light-sensitive cells (photoreceptors) in the retina that provide sharp central vision and color vision. [NIH] Confusion: A mental state characterized by bewilderment, emotional disturbance, lack of clear thinking, and perceptual disorientation. [NIH] Congestive heart failure: Weakness of the heart muscle that leads to a buildup of fluid in body tissues. [NIH] Conjugated: Acting or operating as if joined; simultaneous. [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] Connexins: A group of homologous proteins which form the intermembrane channels of
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gap junctions. The connexins are the products of an identified gene family which has both highly conserved and highly divergent regions. The variety contributes to the wide range of functional properties of gap junctions. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Constriction: The act of constricting. [NIH] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Convulsions: A general term referring to sudden and often violent motor activity of cerebral or brainstem origin. Convulsions may also occur in the absence of an electrical cerebral discharge (e.g., in response to hypotension). [NIH] Cor: The muscular organ that maintains the circulation of the blood. c. adiposum a heart that has undergone fatty degeneration or that has an accumulation of fat around it; called also fat or fatty, heart. c. arteriosum the left side of the heart, so called because it contains oxygenated (arterial) blood. c. biloculare a congenital anomaly characterized by failure of formation of the atrial and ventricular septums, the heart having only two chambers, a single atrium and a single ventricle, and a common atrioventricular valve. c. bovinum (L. 'ox heart') a greatly enlarged heart due to a hypertrophied left ventricle; called also c. taurinum and bucardia. c. dextrum (L. 'right heart') the right atrium and ventricle. c. hirsutum, c. villosum. c. mobile (obs.) an abnormally movable heart. c. pendulum a heart so movable that it seems to be hanging by the great blood vessels. c. pseudotriloculare biatriatum a congenital cardiac anomaly in which the heart functions as a three-chambered heart because of tricuspid atresia, the right ventricle being extremely small or rudimentary and the right atrium greatly dilated. Blood passes from the right to the left atrium and thence disease due to pulmonary hypertension secondary to disease of the lung, or its blood vessels, with hypertrophy of the right ventricle. [EU] 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 Arteriosclerosis: Thickening and loss of elasticity of the coronary arteries. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Corticosteroid: Any of the steroids elaborated by the adrenal cortex (excluding the sex hormones of adrenal origin) in response to the release of corticotrophin (adrenocorticotropic hormone) by the pituitary gland, to any of the synthetic equivalents of these steroids, or to angiotensin II. They are divided, according to their predominant biological activity, into three major groups: glucocorticoids, chiefly influencing carbohydrate, fat, and protein metabolism; mineralocorticoids, affecting the regulation of electrolyte and water balance; and C19 androgens. Some corticosteroids exhibit both types of activity in varying degrees, and others exert only one type of effect. The corticosteroids are used clinically for hormonal replacement therapy, for suppression of ACTH secretion by the anterior pituitary, as antineoplastic, antiallergic, and anti-inflammatory agents, and to suppress the immune response. Called also adrenocortical hormone and corticoid. [EU] Cortisol: A steroid hormone secreted by the adrenal cortex as part of the body's response to stress. [NIH]
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Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Criterion: A standard by which something may be judged. [EU] CSF: Cerebrospinal fluid. The fluid flowing around the brain and spinal cord. CSF is produced in the ventricles of the brain. [NIH] Curative: Tending to overcome disease and promote recovery. [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] Cystine: A covalently linked dimeric nonessential amino acid formed by the oxidation of cysteine. Two molecules of cysteine are joined together by a disulfide bridge to form cystine. [NIH]
Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, . New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytokines: Non-antibody proteins secreted by inflammatory leukocytes and some nonleukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner. [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] Cytoplasmic Vesicles: Membrane-limited structures derived from the plasma membrane or various intracellular membranes which function in storage, transport or metabolism. [NIH] 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]
Cytotoxicity: Quality of being capable of producing a specific toxic action upon cells of special organs. [NIH] Decarboxylation: The removal of a carboxyl group, usually in the form of carbon dioxide,
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from a chemical compound. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Dehydration: The condition that results from excessive loss of body water. [NIH] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Dentifrices: Any preparations used for cleansing teeth; they usually contain an abrasive, detergent, binder and flavoring agent and may exist in the form of liquid, paste or powder; may also contain medicaments and caries preventives. [NIH] Depressive Disorder: An affective disorder manifested by either a dysphoric mood or loss of interest or pleasure in usual activities. The mood disturbance is prominent and relatively persistent. [NIH] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Dextroamphetamine: The d-form of amphetamine. It is a central nervous system stimulant and a sympathomimetic. It has also been used in the treatment of narcolepsy and of attention deficit disorders and hyperactivity in children. Dextroamphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulating release of monamines, and inhibiting monoamine oxidase. It is also a drug of abuse and a psychotomimetic. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diabetic Ketoacidosis: Complication of diabetes resulting from severe insulin deficiency coupled with an absolute or relative increase in glucagon concentration. The metabolic acidosis is caused by the breakdown of adipose stores and resulting increased levels of free fatty acids. Glucagon accelerates the oxidation of the free fatty acids producing excess ketone bodies (ketosis). [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Dialysate: A cleansing liquid used in the two major forms of dialysis--hemodialysis and peritoneal dialysis. [NIH] Dialysis Solutions: Solutions prepared for exchange across a semipermeable membrane of solutes below a molecular size determined by the cutoff threshold of the membrane material. [NIH] Dialyzer: A part of the hemodialysis machine. (See hemodialysis under dialysis.) The dialyzer has two sections separated by a membrane. One section holds dialysate. The other holds the patient's blood. [NIH] Diarrhea: Passage of excessively liquid or excessively frequent stools. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Dietary Fiber: The remnants of plant cell walls that are resistant to digestion by the alimentary enzymes of man. It comprises various polysaccharides and lignins. [NIH] 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]
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Digestive tract: The organs through which food passes when food is eaten. These organs are the mouth, esophagus, stomach, small and large intestines, and rectum. [NIH] 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] Dihydrotestosterone: Anabolic agent. [NIH] Dihydroxy: AMPA/Kainate antagonist. [NIH] Dilution: A diluted or attenuated medicine; in homeopathy, the diffusion of a given quantity of a medicinal agent in ten or one hundred times the same quantity of water. [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] 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] Diuresis: Increased excretion of urine. [EU] Diuretic: A drug that increases the production of urine. [NIH] Dorsum: A plate of bone which forms the posterior boundary of the sella turcica. [NIH] Drive: A state of internal activity of an organism that is a necessary condition before a given stimulus will elicit a class of responses; e.g., a certain level of hunger (drive) must be present before food will elicit an eating response. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Duct: A tube through which body fluids pass. [NIH] Eating Disorders: A group of disorders characterized by physiological and psychological disturbances in appetite or food intake. [NIH] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [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] Electric shock: A dangerous patho-physiological effect resulting from an electric current passing through the body of a human or animal. [NIH] Electrolysis: Destruction by passage of a galvanic electric current, as in disintegration of a
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chemical compound in solution. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electrons: Stable elementary particles having the smallest known negative charge, present in all elements; also called negatrons. Positively charged electrons are called positrons. The numbers, energies and arrangement of electrons around atomic nuclei determine the chemical identities of elements. Beams of electrons are called cathode rays or beta rays, the latter being a high-energy biproduct of nuclear decay. [NIH] 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] 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] Encephalopathy: A disorder of the brain that can be caused by disease, injury, drugs, or chemicals. [NIH] Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] Endocrine Glands: Ductless glands that secrete substances which are released directly into the circulation and which influence metabolism and other body functions. [NIH] Endocrine System: The system of glands that release their secretions (hormones) directly into the circulatory system. In addition to the endocrine glands, included are the chromaffin system and the neurosecretory systems. [NIH] Endocrinology: A subspecialty of internal medicine concerned with the metabolism, physiology, and disorders of the endocrine system. [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] Endotoxins: Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells. [NIH] End-stage renal: Total chronic kidney failure. When the kidneys fail, the body retains fluid and harmful wastes build up. A person with ESRD needs treatment to replace the work of the failed kidneys. [NIH] Enema: The injection of a liquid through the anus into the large bowel. [NIH] Energy balance: Energy is the capacity of a body or a physical system for doing work. Energy balance is the state in which the total energy intake equals total energy needs. [NIH] Enterocytes: Terminally differentiated cells comprising the majority of the external surface of the intestinal epithelium (see intestinal mucosa). Unlike goblet cells, they do not produce or secrete mucins, nor do they secrete cryptdins as do the paneth cells. [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]
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Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] 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] Ergometer: An instrument for measuring the force of muscular contraction. [NIH] Ergometry: Any method of measuring the amount of work done by an organism, usually during exertion. Ergometry also includes measures of power. Some instruments used in these determinations include the hand crank and the bicycle ergometer. [NIH] Erythrocyte Volume: Volume of circulating erythrocytes. It is usually measured by radioisotope dilution technique. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Erythropoietin: Glycoprotein hormone, secreted chiefly by the kidney in the adult and the liver in the fetus, that acts on erythroid stem cells of the bone marrow to stimulate proliferation and differentiation. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [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] Ethylene Glycol: A colorless, odorless, viscous dihydroxy alcohol. It has a sweet taste, but is poisonous if ingested. Ethylene glycol is the most important glycol commercially available and is manufactured on a large scale in the United States. It is used as an antifreeze and coolant, in hydraulic fluids, and in the manufacture of low-freezing dynamites and resins. [NIH]
Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Evacuation: An emptying, as of the bowels. [EU] Evoke: The electric response recorded from the cerebral cortex after stimulation of a peripheral sense organ. [NIH] Excrete: To get rid of waste from the body. [NIH] Exhaustion: The feeling of weariness of mind and body. [NIH] Exocrine: Secreting outwardly, via a duct. [EU] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Exon: The part of the DNA that encodes the information for the actual amino acid sequence of the protein. In many eucaryotic genes, the coding sequences consist of a series of exons alternating with intron sequences. [NIH]
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Expiration: The act of breathing out, or expelling air from the lungs. [EU] Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extracorporeal: Situated or occurring outside the body. [EU] Eye Movements: Voluntary or reflex-controlled movements of the eye. [NIH] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]
Femoral: Pertaining to the femur, or to the thigh. [EU] Femoral Artery: The main artery of the thigh, a continuation of the external iliac artery. [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] Fetal Monitoring: Physiologic or biochemical monitoring of the fetus. It is usually done during labor and may be performed in conjunction with the monitoring of uterine activity. It may also be performed prenatally as when the mother is undergoing surgery. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibroblast Growth Factor: Peptide isolated from the pituitary gland and from the brain. It is a potent mitogen which stimulates growth of a variety of mesodermal cells including chondrocytes, granulosa, and endothelial cells. The peptide may be active in wound healing and animal limb regeneration. [NIH] Fistula: Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body. [NIH] Flatus: Gas passed through the rectum. [NIH] Fluid Therapy: Therapy whose basic objective is to restore the volume and composition of the body fluids to normal with respect to water-electrolyte balance. Fluids may be administered intravenously, orally, by intermittent gavage, or by hypodermoclysis. [NIH] Fluorouracil: A pyrimidine analog that acts as an antineoplastic antimetabolite and also has immunosuppressant. It interferes with DNA synthesis by blocking the thymidylate synthetase conversion of deoxyuridylic acid to thymidylic acid. [NIH] Forearm: The part between the elbow and the wrist. [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] Furosemide: A sulfamyl saluretic and diuretic. It has a fast onset and short duration of
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action and is used in edema and chronic renal insufficiency. [NIH] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Ganglion: 1. A knot, or knotlike mass. 2. A general term for a group of nerve cell bodies located outside the central nervous system; occasionally applied to certain nuclear groups within the brain or spinal cord, e.g. basal ganglia. 3. A benign cystic tumour occurring on a aponeurosis or tendon, as in the wrist or dorsum of the foot; it consists of a thin fibrous capsule enclosing a clear mucinous fluid. [EU] Gap Junctions: Connections between cells which allow passage of small molecules and electric current. Gap junctions were first described anatomically as regions of close apposition between cells with a narrow (1-2 nm) gap between cell membranes. The variety in the properties of gap junctions is reflected in the number of connexins, the family of proteins which form the junctions. [NIH] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gas exchange: Primary function of the lungs; transfer of oxygen from inhaled air into the blood and of carbon dioxide from the blood into the lungs. [NIH] Gastric: Having to do with the stomach. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]
Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gavage: Feeding by a tube passed into the stomach; called also tube feeding. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]
Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Targeting: The integration of exogenous DNA into the genome of an organism at sites where its expression can be suitably controlled. This integration occurs as a result of homologous recombination. [NIH] 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] Germ Cells: The reproductive cells in multicellular organisms. [NIH] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]
Glomeruli: Plural of glomerulus. [NIH] Glomerulonephritis: Glomerular disease characterized by an inflammatory reaction, with leukocyte infiltration and cellular proliferation of the glomeruli, or that appears to be the result of immune glomerular injury. [NIH]
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Glomerulus: A tiny set of looping blood vessels in the nephron where blood is filtered in the kidney. [NIH] Glucocorticoids: A group of corticosteroids that affect carbohydrate metabolism (gluconeogenesis, liver glycogen deposition, elevation of blood sugar), inhibit corticotropin secretion, and possess pronounced anti-inflammatory activity. They also play a role in fat and protein metabolism, maintenance of arterial blood pressure, alteration of the connective tissue response to injury, reduction in the number of circulating lymphocytes, and functioning of the central nervous system. [NIH] Gluconeogenesis: The process by which glucose is formed from a non-carbohydrate source. [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] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH]
Glutamine: A non-essential amino acid present abundantly throught the body and is involved in many metabolic processes. It is synthesized from glutamic acid and ammonia. It is the principal carrier of nitrogen in the body and is an important energy source for many cells. [NIH] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycogen: A sugar stored in the liver and muscles. It releases glucose into the blood when cells need it for energy. Glycogen is the chief source of stored fuel in the body. [NIH] Glycoside: Any compound that contains a carbohydrate molecule (sugar), particularly any such natural product in plants, convertible, by hydrolytic cleavage, into sugar and a nonsugar component (aglycone), and named specifically for the sugar contained, as glucoside (glucose), pentoside (pentose), fructoside (fructose) etc. [EU] Goblet Cells: Cells of the epithelial lining that produce and secrete mucins. [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] Gram-negative: Losing the stain or decolorized by alcohol in Gram's method of staining, a primary characteristic of bacteria having a cell wall composed of a thin layer of peptidoglycan covered by an outer membrane of lipoprotein and lipopolysaccharide. [EU] Gram-Negative Bacteria: Bacteria which lose crystal violet stain but are stained pink when treated by Gram's method. [NIH] Gram-positive: Retaining the stain or resisting decolorization by alcohol in Gram's method of staining, a primary characteristic of bacteria whose cell wall is composed of a thick layer of peptidologlycan with attached teichoic acids. [EU] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH]
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Haemodialysis: The removal of certain elements from the blood by virtue of the difference in the rates of their diffusion through a semipermeable membrane, e.g., by means of a haemodialyzer. [EU] Haploid: An organism with one basic chromosome set, symbolized by n; the normal condition of gametes in diploids. [NIH] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or 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 Arrest: Sudden and usually momentary cessation of the heart beat. This sudden cessation may, but not usually, lead to death, sudden, cardiac. [NIH] Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Hematuria: Presence of blood in the urine. [NIH] Heme: The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins. [NIH] Hemodialysis: The use of a machine to clean wastes from the blood after the kidneys have failed. The blood travels through tubes to a dialyzer, which removes wastes and extra fluid. The cleaned blood then flows through another set of tubes back into the body. [NIH] Hemodynamics: The movements of the blood and the forces involved in systemic or regional blood circulation. [NIH] Hemofiltration: Extracorporeal ultrafiltration technique without hemodialysis for treatment of fluid overload and electrolyte disturbances affecting renal, cardiac, or pulmonary function. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemolytic: A disease that affects the blood and blood vessels. It destroys red blood cells, cells that cause the blood to clot, and the lining of blood vessels. HUS is often caused by the Escherichia coli bacterium in contaminated food. People with HUS may develop acute renal failure. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hepatic: Refers to the liver. [NIH] Hepatorenal Syndrome: Renal failure in those with liver disease, usually liver cirrhosis or obstructive jaundice. Historically called Heyd disease, urohepatic syndrome, or bile nephrosis. [NIH]
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Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one generation to another. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]
Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydroxylation: Hydroxylate, to introduce hydroxyl into (a compound or radical) usually by replacement of hydrogen. [EU] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hyperammonemia: Metabolic disorder characterized by elevated level of ammonia in blood. [NIH] Hyperbaric: Characterized by greater than normal pressure or weight; applied to gases under greater than atmospheric pressure, as hyperbaric oxygen, or to a solution of greater specific gravity than another taken as a standard of reference. [EU] Hyperbaric oxygen: Oxygen that is at an atmospheric pressure higher than the pressure at sea level. Breathing hyperbaric oxygen to enhance the effectiveness of radiation therapy is being studied. [NIH] Hypercalcemia: Abnormally high level of calcium in the blood. [NIH] Hypercalciuria: Abnormally large amounts of calcium in the urine. [NIH] Hyperglycemia: Abnormally high blood sugar. [NIH] Hyperlipidemia: An excess of lipids in the blood. [NIH] Hyperoxia: An abnormal increase in the amount of oxygen in the tissues and organs. [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] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels
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are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hyperthermia: A type of treatment in which body tissue is exposed to high temperatures to damage and kill cancer cells or to make cancer cells more sensitive to the effects of radiation and certain anticancer drugs. [NIH] 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] Hyperventilation: A pulmonary ventilation rate faster than is metabolically necessary for the exchange of gases. It is the result of an increased frequency of breathing, an increased tidal volume, or a combination of both. It causes an excess intake of oxygen and the blowing off of carbon dioxide. [NIH] Hypnotic: A drug that acts to induce sleep. [EU] Hypoglycaemia: An abnormally diminished concentration of glucose in the blood, which may lead to tremulousness, cold sweat, piloerection, hypothermia, and headache, accompanied by irritability, confusion, hallucinations, bizarre behaviour, and ultimately, convulsions and coma. [EU] Hypotension: Abnormally low blood pressure. [NIH] Hypotensive: Characterized by or causing diminished tension or pressure, as abnormally low blood pressure. [EU] Hypothermia: Lower than normal body temperature, especially in warm-blooded animals; in man usually accidental or unintentional. [NIH] Hypothyroidism: Deficiency of thyroid activity. In adults, it is most common in women and is characterized by decrease in basal metabolic rate, tiredness and lethargy, sensitivity to cold, and menstrual disturbances. If untreated, it progresses to full-blown myxoedema. In infants, severe hypothyroidism leads to cretinism. In juveniles, the manifestations are intermediate, with less severe mental and developmental retardation and only mild symptoms of the adult form. When due to pituitary deficiency of thyrotropin secretion it is called secondary hypothyroidism. [EU] Hypotonic Solutions: Solutions that have a lesser osmotic pressure than a reference solution such as blood, plasma, or interstitial fluid. [NIH] Hypoxia: Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood. [EU] Hypoxic: Having too little oxygen. [NIH] Ibuprofen: A nonsteroidal anti-inflammatory agent with analgesic properties used in the therapy of rheumatism and arthritis. [NIH] Ifosfamide: Positional isomer of cyclophosphamide which is active as an alkylating agent and an immunosuppressive agent. [NIH] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunology: The study of the body's immune system. [NIH] Immunosuppressant: An agent capable of suppressing immune responses. [EU] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Impotence: The inability to perform sexual intercourse. [NIH] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH]
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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]
Infiltration: The diffusion or accumulation in a tissue or cells of substances not normal to it or in amounts of the normal. Also, the material so accumulated. [EU] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH] 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] Inorganic: Pertaining to substances not of organic origin. [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] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Insulin-like: Muscular growth factor. [NIH] Intensive Care: Advanced and highly specialized care provided to medical or surgical patients whose conditions are life-threatening and require comprehensive care and constant monitoring. It is usually administered in specially equipped units of a health care facility. [NIH]
Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU]
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Intestinal: Having to do with the intestines. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH] Intracellular Membranes: Membranes of subcellular structures. [NIH] Intramuscular: IM. Within or into muscle. [NIH] Intraocular: Within the eye. [EU] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Intubation: Introduction of a tube into a hollow organ to restore or maintain patency if obstructed. It is differentiated from catheterization in that the insertion of a catheter is usually performed for the introducing or withdrawing of fluids from the body. [NIH] Intussusception: A rare disorder. A part of the intestines folds into another part of the intestines, causing blockage. Most common in infants. Can be treated with an operation. [NIH]
Involuntary: Reaction occurring without intention or volition. [NIH] Ion Transport: The movement of ions across energy-transducing cell membranes. Transport can be active or passive. Passive ion transport (facilitated diffusion) derives its energy from the concentration gradient of the ion itself and allows the transport of a single solute in one direction (uniport). Active ion transport is usually coupled to an energy-yielding chemical or photochemical reaction such as ATP hydrolysis. This form of primary active transport is called an ion pump. Secondary active transport utilizes the voltage and ion gradients produced by the primary transport to drive the cotransport of other ions or molecules. These may be transported in the same (symport) or opposite (antiport) direction. [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] Isoenzyme: Different forms of an enzyme, usually occurring in different tissues. The isoenzymes of a particular enzyme catalyze the same reaction but they differ in some of their properties. [NIH] Isozymes: The multiple forms of a single enzyme. [NIH] Jaundice: A clinical manifestation of hyperbilirubinemia, consisting of deposition of bile pigments in the skin, resulting in a yellowish staining of the skin and mucous membranes. [NIH]
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] Keto: It consists of 8 carbon atoms and within the endotoxins, it connects poysaccharide and lipid A. [NIH] Ketoacidosis: Acidosis accompanied by the accumulation of ketone bodies (ketosis) in the body tissues and fluids, as in diabetic acidosis. [EU] Ketone Bodies: Chemicals that the body makes when there is not enough insulin in the blood and it must break down fat for its energy. Ketone bodies can poison and even kill
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body cells. When the body does not have the help of insulin, the ketones build up in the blood and then "spill" over into the urine so that the body can get rid of them. The body can also rid itself of one type of ketone, called acetone, through the lungs. This gives the breath a fruity odor. Ketones that build up in the body for a long time lead to serious illness and coma. [NIH] Ketosis: A condition of having ketone bodies build up in body tissues and fluids. The signs of ketosis are nausea, vomiting, and stomach pain. Ketosis can lead to ketoacidosis. [NIH] Kidney Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Kidney Failure: The inability of a kidney to excrete metabolites at normal plasma levels under conditions of normal loading, or the inability to retain electrolytes under conditions of normal intake. In the acute form (kidney failure, acute), it is marked by uremia and usually by oliguria or anuria, with hyperkalemia and pulmonary edema. The chronic form (kidney failure, chronic) is irreversible and requires hemodialysis. [NIH] Kidney stone: A stone that develops from crystals that form in urine and build up on the inner surfaces of the kidney, in the renal pelvis, or in the ureters. [NIH] Kidney Transplantation: The transference of a kidney from one human or animal to another. [NIH] Kinetics: The study of rate dynamics in chemical or physical systems. [NIH] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Laxative: An agent that acts to promote evacuation of the bowel; a cathartic or purgative. [EU]
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] Leptin: A 16-kD peptide hormone secreted from white adipocytes and implicated in the regulation of food intake and energy balance. Leptin provides the key afferent signal from fat cells in the feedback system that controls body fat stores. [NIH] Lesion: An area of abnormal tissue change. [NIH] Lethal: Deadly, fatal. [EU] Lethargy: Abnormal drowsiness or stupor; a condition of indifference. [EU] Leucine: An essential branched-chain amino acid important for hemoglobin formation. [NIH] Leukemia: Cancer of blood-forming tissue. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Liminal: The main auxiliary method for diagnosing impairment of hearing and determining its localization. Routine tests are carried out within the register of frequencies 125 to 8000 Hz. [NIH]
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Linkage: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Lipid: Fat. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lithium: An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight 6.94. Salts of lithium are used in treating manic-depressive disorders. [NIH]
Lithium Carbonate: A lithium salt, classified as a mood-stabilizing agent. Lithium ion alters the metabolism of biogenic monoamines in the central nervous system, and affects multiple neurotransmission systems. [NIH] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Liver Cirrhosis: Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Lorazepam: An anti-anxiety agent with few side effects. It also has hypnotic, anticonvulsant, and considerable sedative properties and has been proposed as a preanesthetic agent. [NIH] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [NIH] Lye: Generally speaking, it is the alkaline substance obtained from wood ashes by percolation. Preparations of lye can either be solutions of potassium or sodium hydroxide. The term lye, is also used to refer to the household product which is a mixture of sodium hydroxide and sodium carbonate. [NIH] 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] Lymphocytes: White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each); those with characteristics of neither major class are called null cells. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lysine: An essential amino acid. It is often added to animal feed. [NIH] Lysosome: A sac-like compartment inside a cell that has enzymes that can break down cellular components that need to be destroyed. [NIH] Malaria: A protozoan disease caused in humans by four species of the genus Plasmodium (P. falciparum (malaria, falciparum), P. vivax (malaria, vivax), P. ovale, and P. malariae) and transmitted by the bite of an infected female mosquito of the genus Anopheles. Malaria is
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endemic in parts of Asia, Africa, Central and South America, Oceania, and certain Caribbean islands. It is characterized by extreme exhaustion associated with paroxysms of high fever, sweating, shaking chills, and anemia. Malaria in animals is caused by other species of plasmodia. [NIH] Malaria, Falciparum: Malaria caused by Plasmodium falciparum. This is the severest form of malaria and is associated with the highest levels of parasites in the blood. This disease is characterized by irregularly recurring febrile paroxysms that in extreme cases occur with acute cerebral, renal, or gastrointestinal manifestations. [NIH] Malaria, Vivax: Malaria caused by Plasmodium vivax. This form of malaria is less severe than malaria, falciparum, but there is a higher probability for relapses to occur. Febrile paroxysms often occur every other day. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]
Mammogram: An x-ray of the breast. [NIH] Mandible: The largest and strongest bone of the face constituting the lower jaw. It supports the lower teeth. [NIH] Manic: Affected with mania. [EU] Meat: The edible portions of any animal used for food including domestic mammals (the major ones being cattle, swine, and sheep) along with poultry, fish, shellfish, and game. [NIH]
Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Medullary: Pertaining to the marrow or to any medulla; resembling marrow. [EU] Melanin: The substance that gives the skin its color. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Membrane Proteins: Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Processes: Conceptual functions or thinking in all its forms. [NIH] Mental Retardation: Refers to sub-average general intellectual functioning which originated during the developmental period and is associated with impairment in adaptive behavior. [NIH]
Metabolic disorder: A condition in which normal metabolic processes are disrupted, usually because of a missing enzyme. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Methamphetamine: A central nervous system stimulant and sympathomimetic with actions and uses similar to dextroamphetamine. The smokable form is a drug of abuse and is referred to as crank, crystal, crystal meth, ice, and speed. [NIH]
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Methanol: A colorless, flammable liquid used in the manufacture of formaldehyde and acetic acid, in chemical synthesis, antifreeze, and as a solvent. Ingestion of methanol is toxic and may cause blindness. [NIH] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microcalcifications: Tiny deposits of calcium in the breast that cannot be felt but can be detected on a mammogram. A cluster of these very small specks of calcium may indicate that cancer is present. [NIH] Mineralization: The action of mineralizing; the state of being mineralized. [EU] 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 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] Mitotic: Cell resulting from mitosis. [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] Motor Activity: The physical activity of an organism as a behavioral phenomenon. [NIH] Mucinous: Containing or resembling mucin, the main compound in mucus. [NIH] Mucins: A secretion containing mucopolysaccharides and protein that is the chief constituent of mucus. [NIH] Mucosa: A mucous membrane, or tunica mucosa. [EU] 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] 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]
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Muscular Diseases: Acquired, familial, and congenital disorders of skeletal muscle and smooth muscle. [NIH] Mutagenesis: Process of generating genetic mutations. It may occur spontaneously or be induced by mutagens. [NIH] Mutagens: Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes. [NIH] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Myocardial Ischemia: A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (coronary arteriosclerosis), to obstruction by a thrombus (coronary thrombosis), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (myocardial infarction). [NIH] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myosin: Chief protein in muscle and the main constituent of the thick filaments of muscle fibers. In conjunction with actin, it is responsible for the contraction and relaxation of muscles. [NIH] Nalidixic Acid: Synthetic antimicrobial agent used in urinary tract infections. It is active against gram-negative bacteria but has little activity against gram-positive organisms or Pseudomonas. [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] Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Nephritis: Inflammation of the kidney; a focal or diffuse proliferative or destructive process which may involve the glomerulus, tubule, or interstitial renal tissue. [EU] Nephrolithiasis: Kidney stones. [NIH] Nephrologist: A doctor who treats patients with kidney problems or hypertension. [NIH] Nephrology: A subspecialty of internal medicine concerned with the anatomy, physiology, and pathology of the kidney. [NIH] Nephropathy: Disease of the kidneys. [EU] Nephrosis: Descriptive histopathologic term for renal disease without an inflammatory component. [NIH] Nephrotic: Pertaining to, resembling, or caused by nephrosis. [EU] Nephrotic Syndrome: Clinical association of heavy proteinuria, hypoalbuminemia, and generalized edema. [NIH] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH]
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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] Neurologic: Having to do with nerves or the nervous system. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU] Neuromuscular Diseases: A general term encompassing lower motor neuron disease; peripheral nervous system diseases; and certain muscular diseases. Manifestations include muscle weakness; fasciculation; muscle atrophy; spasm; myokymia; muscle hypertonia, myalgias, and musclehypotonia. [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] Neurosecretory Systems: A system of neurons that has the specialized function to produce and secrete hormones, and that constitutes, in whole or in part, an endocrine organ or system. [NIH] Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins, endorphins, and serotonin. [EU] Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nutritional Status: State of the body in relation to the consumption and utilization of nutrients. [NIH] Obtundation: A dulled or reduced level of alertness or consciousness. [NIH] Oocytes: Female germ cells in stages between the prophase of the first maturation division and the completion of the second maturation division. [NIH] Opium: The air-dried exudate from the unripe seed capsule of the opium poppy, Papaver somniferum, or its variant, P. album. It contains a number of alkaloids, but only a few morphine, codeine, and papaverine - have clinical significance. Opium has been used as an analgesic, antitussive, antidiarrheal, and antispasmodic. [NIH]
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Opsin: A protein formed, together with retinene, by the chemical breakdown of metarhodopsin. [NIH] Optic Nerve: The 2nd cranial nerve. The optic nerve conveys visual information from the retina to the brain. The nerve carries the axons of the retinal ganglion cells which sort at the optic chiasm and continue via the optic tracts to the brain. The largest projection is to the lateral geniculate nuclei; other important targets include the superior colliculi and the suprachiasmatic nuclei. Though known as the second cranial nerve, it is considered part of the central nervous system. [NIH] 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] Osmotic: Pertaining to or of the nature of osmosis (= the passage of pure solvent from a solution of lesser to one of greater solute concentration when the two solutions are separated by a membrane which selectively prevents the passage of solute molecules, but is permeable to the solvent). [EU] Osteoblasts: Bone-forming cells which secrete an extracellular matrix. Hydroxyapatite crystals are then deposited into the matrix to form bone. [NIH] Osteocalcin: Vitamin K-dependent calcium-binding protein synthesized by osteoblasts and found primarily in bone. Serum osteocalcin measurements provide a noninvasive specific marker of bone metabolism. The protein contains three residues of the amino acid gammacarboxyglutamic acid (GLA), which, in the presence of calcium, promotes binding to hydroxyapatite and subsequent accumulation in bone matrix. [NIH] Osteodystrophy: Defective bone formation. [EU] Osteoporosis: Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis and age-related (or senile) osteoporosis. [NIH] Ouabain: A cardioactive glycoside consisting of rhamnose and ouabagenin, obtained from the seeds of Strophanthus gratus and other plants of the Apocynaceae; used like digitalis. It is commonly used in cell biological studies as an inhibitor of the NA(+)-K(+)-exchanging atpase. [NIH] Overdosage: 1. The administration of an excessive dose. 2. The condition resulting from an excessive dose. [EU] Overdose: An accidental or deliberate dose of a medication or street drug that is in excess of what is normally used. [NIH] Oxalate: A chemical that combines with calcium in urine to form the most common type of kidney stone (calcium oxalate stone). [NIH] Oxaloacetate: An anionic form of oxaloacetic acid. [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]
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]
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Oxygen Consumption: The oxygen consumption is determined by calculating the difference between the amount of oxygen inhaled and exhaled. [NIH] Oxygenator: An apparatus by which oxygen is introduced into the blood during circulation outside the body, as during open heart surgery. [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] Pancreas Transplantation: The transference of a pancreas from one human or animal to another. [NIH] Pancreatic: Having to do with the pancreas. [NIH] Papaverine: An alkaloid found in opium but not closely related to the other opium alkaloids in its structure or pharmacological actions. It is a direct-acting smooth muscle relaxant used in the treatment of impotence and as a vasodilator, especially for cerebral vasodilation. The mechanism of its pharmacological actions is not clear, but it apparently can inhibit phosphodiesterases and it may have direct actions on calcium channels. [NIH] Paralysis: Loss of ability to move all or part of the body. [NIH] Parathyroid: 1. Situated beside the thyroid gland. 2. One of the parathyroid glands. 3. A sterile preparation of the water-soluble principle(s) of the parathyroid glands, ad-ministered parenterally as an antihypocalcaemic, especially in the treatment of acute hypoparathyroidism with tetany. [EU] Parathyroid Glands: Two small paired endocrine glands in the region of the thyroid gland. They secrete parathyroid hormone and are concerned with the metabolism of calcium and phosphorus. [NIH] Parathyroid hormone: A substance made by the parathyroid gland that helps the body store and use calcium. Also called parathormone, parathyrin, or PTH. [NIH] Parenteral: Not through the alimentary canal but rather by injection through some other route, as subcutaneous, intramuscular, intraorbital, intracapsular, intraspinal, intrasternal, intravenous, etc. [EU] Parenteral Nutrition: The administering of nutrients for assimilation and utilization by a patient who cannot maintain adequate nutrition by enteral feeding alone. Nutrients are administered by a route other than the alimentary canal (e.g., intravenously, subcutaneously). [NIH] Particle: A tiny mass of material. [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]
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Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]
Pelvis: The lower part of the abdomen, located between the hip bones. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Perfusion: Bathing an organ or tissue with a fluid. In regional perfusion, a specific area of the body (usually an arm or a leg) receives high doses of anticancer drugs through a blood vessel. Such a procedure is performed to treat cancer that has not spread. [NIH] Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Peripheral Nervous System Diseases: Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves. [NIH] Peritoneal: Having to do with the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Peritoneal Cavity: The space enclosed by the peritoneum. It is divided into two portions, the greater sac and the lesser sac or omental bursa, which lies behind the stomach. The two sacs are connected by the foramen of Winslow, or epiploic foramen. [NIH] Peritoneal Dialysis: Dialysis fluid being introduced into and removed from the peritoneal cavity as either a continuous or an intermittent procedure. [NIH] Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] Peroral: Performed through or administered through the mouth. [EU] Phagocytosis: The engulfing of microorganisms, other cells, and foreign particles by phagocytic cells. [NIH] Phagosomes: Membrane-bound cytoplasmic vesicles formed by invagination of phagocytized material. They fuse with lysosomes to form phagolysosomes in which the hydrolytic enzymes of the lysosome digest the phagocytized material. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phosphates: Inorganic salts of phosphoric acid. [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] Physicochemical: Pertaining to physics and chemistry. [EU]
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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] Pigments: Any normal or abnormal coloring matter in plants, animals, or micro-organisms. [NIH]
Piloerection: Involuntary erection or bristling of hairs. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasma protein: One of the hundreds of different proteins present in blood plasma, including carrier proteins ( such albumin, transferrin, and haptoglobin), fibrinogen and other coagulation factors, complement components, immunoglobulins, enzyme inhibitors, precursors of substances such as angiotension and bradykinin, and many other types of proteins. [EU] Plasma Volume: Volume of plasma in the circulation. It is usually measured by indicator dilution techniques. [NIH] Plastids: Self-replicating cytoplasmic organelles of plant and algal cells that contain pigments and may synthesize and accumulate various substances. Plastids are used in phylogenetic studies. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Platinum: Platinum. A heavy, soft, whitish metal, resembling tin, atomic number 78, atomic weight 195.09, symbol Pt. (From Dorland, 28th ed) It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as "alutiae". [NIH]
Pneumonia: Inflammation of the lungs. [NIH] Podophyllotoxin: The main active constituent of the resin from the roots of may apple or mandrake (Podophyllum peltatum and P. emodi). It is a potent spindle poison, toxic if taken internally, and has been used as a cathartic. It is very irritating to skin and mucous membranes, has keratolytic actions, has been used to treat warts and keratoses, and may have antineoplastic properties, as do some of its congeners and derivatives. [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Polycystic: An inherited disorder characterized by many grape-like clusters of fluid-filled cysts that make both kidneys larger over time. These cysts take over and destroy working kidney tissue. PKD may cause chronic renal failure and end-stage renal disease. [NIH]
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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] Polyuria: Urination of a large volume of urine with an increase in urinary frequency, commonly seen in diabetes. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postmenopausal: Refers to the time after menopause. Menopause is the time in a woman's life when menstrual periods stop permanently; also called "change of life." [NIH] 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] Potassium Compounds: Inorganic compounds that contain potassium as an integral part of the molecule. [NIH] Potassium, Dietary: Potassium or potassium compounds used in foods or as foods. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Predisposition: A latent susceptibility to disease which may be activated under certain conditions, as by stress. [EU] Procollagen: A biosynthetic precursor of collagen containing additional amino acid sequences at the amino-terminal ends of the three polypeptide chains. Protocollagen, a precursor of procollagen consists of procollagen peptide chains in which proline and lysine have not yet been hydroxylated. [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] Prophase: The first phase of cell division, in which the chromosomes become visible, the nucleus starts to lose its identity, the spindle appears, and the centrioles migrate toward opposite poles. [NIH] Propofol: A widely used anesthetic. [NIH] Prospective study: An epidemiologic study in which a group of individuals (a cohort), all
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free of a particular disease and varying in their exposure to a possible risk factor, is followed over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] 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] Protein Isoforms: Different forms of a protein that may be produced from different genes, or from the same gene by alternative splicing. [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Protozoan: 1. Any individual of the protozoa; protozoon. 2. Of or pertaining to the protozoa; protozoal. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychology: The science dealing with the study of mental processes and behavior in man and animals. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]
Pulmonary: Relating to the lungs. [NIH] Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs. [NIH] Pulmonary hypertension: Abnormally high blood pressure in the arteries of the lungs. [NIH] Pulmonary Ventilation: The total volume of gas per minute inspired or expired measured in liters per minute. [NIH]
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Purgative: 1. Cathartic (def. 1); causing evacuation of the bowels. 2. A cathartic, particularly one that stimulates peristaltic action. [EU] Pyruvate Dehydrogenase Complex: An organized assembly of three kinds of enzymes; catalyzes the oxidative decarboxylation of pyruvate. [NIH] Quadriplegia: Severe or complete loss of motor function in all four limbs which may result from brain diseases; spinal cord diseases; peripheral nervous system diseases; neuromuscular diseases; or rarely muscular diseases. The locked-in syndrome is characterized by quadriplegia in combination with cranial muscle paralysis. Consciousness is spared and the only retained voluntary motor activity may be limited eye movements. This condition is usually caused by a lesion in the upper brain stem which injures the descending cortico-spinal and cortico-bulbar tracts. [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] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radioactive: Giving off radiation. [NIH] 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] Reabsorption: 1. The act or process of absorbing again, as the selective absorption by the kidneys of substances (glucose, proteins, sodium, etc.) already secreted into the renal tubules, and their return to the circulating blood. 2. Resorption. [EU] Reagent: A substance employed to produce a chemical reaction so as to detect, measure, produce, etc., other substances. [EU] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] Rectal: By or having to do with the rectum. The rectum is the last 8 to 10 inches of the large intestine and ends at the anus. [NIH] Rectal Prolapse: Protrusion of the rectal mucous membrane through the anus. There are various degrees: incomplete with no displacement of the anal sphincter muscle; complete with displacement of the anal sphincter muscle; complete with no displacement of the anal sphincter muscle but with herniation of the bowel; and internal complete with rectosigmoid or upper rectum intussusception into the lower rectum. [NIH] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called
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erythrocytes. [NIH] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Refractory: Not readily yielding to treatment. [EU] Regeneration: The natural renewal of a structure, as of a lost tissue or part. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Relaxant: 1. Lessening or reducing tension. 2. An agent that lessens tension. [EU] Renal Artery: A branch of the abdominal aorta which supplies the kidneys, adrenal glands and ureters. [NIH] Renal Dialysis: Removal of certain elements from the blood based on the difference in their rates of diffusion through a semipermeable membrane. [NIH] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [NIH] Renal pelvis: The area at the center of the kidney. Urine collects here and is funneled into the ureter, the tube that connects the kidney to the bladder. [NIH] Renal tubular: A defect in the kidneys that hinders their normal excretion of acids. Failure to excrete acids can lead to weak bones, kidney stones, and poor growth in children. [NIH] Renal tubular acidosis: A rare disorder in which structures in the kidney that filter the blood are impaired, producing using that is more acid than normal. [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] Resection: Removal of tissue or part or all of an organ by surgery. [NIH] Resorption: The loss of substance through physiologic or pathologic means, such as loss of dentin and cementum of a tooth, or of the alveolar process of the mandible or maxilla. [EU] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Respiratory distress syndrome: A lung disease that occurs primarily in premature infants; the newborn must struggle for each breath and blueing of its skin reflects the baby's inability to get enough oxygen. [NIH] Respiratory failure: Inability of the lungs to conduct gas exchange. [NIH] Respiratory Physiology: Functions and activities of the respiratory tract as a whole or of any of its parts. [NIH] Resuscitation: The restoration to life or consciousness of one apparently dead; it includes such measures as artificial respiration and cardiac massage. [EU] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH]
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Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retinal Neovascularization: Formation of new blood vessels originating from the retinal veins and extending along the inner (vitreal) surface of the retina. [NIH] Retinal Vein: Central retinal vein and its tributaries. It runs a short course within the optic nerve and then leaves and empties into the superior ophthalmic vein or cavernous sinus. [NIH]
Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous membranes. Retinol is being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Retinopathy: 1. Retinitis (= inflammation of the retina). 2. Retinosis (= degenerative, noninflammatory condition of the retina). [EU] Rhabdomyolysis: Necrosis or disintegration of skeletal muscle often followed by myoglobinuria. [NIH] Rhamnose: A methylpentose whose L- isomer is found naturally in many plant glycosides and some gram-negative bacterial lipopolysaccharides. [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] Rhodopsin: A photoreceptor protein found in retinal rods. It is a complex formed by the binding of retinal, the oxidized form of retinol, to the protein opsin and undergoes a series of complex reactions in response to visible light resulting in the transmission of nerve impulses to the brain. [NIH] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Rods: One type of specialized light-sensitive cells (photoreceptors) in the retina that provide side vision and the ability to see objects in dim light (night vision). [NIH] Salicylate: Non-steroidal anti-inflammatory drugs. [NIH] Saline: A solution of salt and water. [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] Screening: Checking for disease when there are no symptoms. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Secretory: Secreting; relating to or influencing secretion or the secretions. [NIH] Sedative: 1. Allaying activity and excitement. 2. An agent that allays excitement. [EU]
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Sedimentation: The act of causing the deposit of sediment, especially by the use of a centrifugal machine. [EU] Segmental: Describing or pertaining to a structure which is repeated in similar form in successive segments of an organism, or which is undergoing segmentation. [NIH] Segmentation: The process by which muscles in the intestines move food and wastes through the body. [NIH] 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] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Sensibility: The ability to receive, feel and appreciate sensations and impressions; the quality of being sensitive; the extend to which a method gives results that are free from false negatives. [NIH] Sepsis: The presence of bacteria in the bloodstream. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Serum Albumin: A major plasma protein that serves in maintaining the plasma colloidal osmotic pressure and transporting large organic anions. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock. [NIH]
Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] 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] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]
Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Sodium Bicarbonate: A white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH]
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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] 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] 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] Sphincter: A ringlike band of muscle fibres that constricts a passage or closes a natural orifice; called also musculus sphincter. [EU] 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 Diseases: Pathologic conditions which feature spinal cord damage or dysfunction, including disorders involving the meninges and perimeningeal spaces surrounding the spinal cord. Traumatic injuries, vascular diseases, infections, and inflammatory/autoimmune processes may affect the spinal cord. [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] Stabilization: The creation of a stable state. [EU] Stavudine: A dideoxynucleoside analog that inhibits reverse transcriptase and has in vitro activity against HIV. [NIH] Steatosis: Fatty degeneration. [EU] Stem cell transplantation: A method of replacing immature blood-forming cells that were destroyed by cancer treatment. The stem cells are given to the person after treatment to help the bone marrow recover and continue producing healthy blood cells. [NIH] Stem Cells: Relatively undifferentiated cells of the same lineage (family type) that retain the ability to divide and cycle throughout postnatal life to provide cells that can become specialized and take the place of those that die or are lost. [NIH] Stenosis: Narrowing or stricture of a duct or canal. [EU] Sterile: Unable to produce children. [NIH] 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] Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on
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muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU]
Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stricture: The abnormal narrowing of a body opening. Also called stenosis. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU] 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] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]
Substrate: A substance upon which an enzyme acts. [EU] Sulfur: An element that is a member of the chalcogen family. It has an atomic symbol S, atomic number 16, and atomic weight 32.066. It is found in the amino acids cysteine and methionine. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Sweat: The fluid excreted by the sweat glands. It consists of water containing sodium chloride, phosphate, urea, ammonia, and other waste products. [NIH] Sympathomimetic: 1. Mimicking the effects of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. 2. An agent that produces effects similar to those of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. Called also adrenergic. [EU] 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] Tendon: A discrete band of connective tissue mainly composed of parallel bundles of collagenous fibers by which muscles are attached, or two muscles bellies joined. [NIH] Teniposide: A semisynthetic derivative of podophyllotoxin that exhibits antitumor activity. Teniposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA.
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This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent cells from entering into the mitotic phase of the cell cycle, and lead to cell death. Teniposide acts primarily in the G2 and S phases of the cycle. [NIH] Testosterone: A hormone that promotes the development and maintenance of male sex characteristics. [NIH] Tetany: 1. Hyperexcitability of nerves and muscles due to decrease in concentration of extracellular ionized calcium, which may be associated with such conditions as parathyroid hypofunction, vitamin D deficiency, and alkalosis or result from ingestion of alkaline salts; it is characterized by carpopedal spasm, muscular twitching and cramps, laryngospasm with inspiratory stridor, hyperreflexia and choreiform movements. 2. Tetanus. [EU] Thalassemia: A group of hereditary hemolytic anemias in which there is decreased synthesis of one or more hemoglobin polypeptide chains. There are several genetic types with clinical pictures ranging from barely detectable hematologic abnormality to severe and fatal anemia. [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] Thiamine: 3-((4-Amino-2-methyl-5-pyrimidinyl)methyl)-5-(2methylthiazolium chloride. [NIH]
hydroxyethyl)-4-
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] 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] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Thyroid Gland: A highly vascular endocrine gland consisting of two lobes, one on either side of the trachea, joined by a narrow isthmus; it produces the thyroid hormones which are concerned in regulating the metabolic rate of the body. [NIH] Thyrotropin: A peptide hormone secreted by the anterior pituitary. It promotes the growth of the thyroid gland and stimulates the synthesis of thyroid hormones and the release of thyroxine by the thyroid gland. [NIH] Thyroxine: An amino acid of the thyroid gland which exerts a stimulating effect on thyroid metabolism. [NIH]
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Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Topical: On the surface of the body. [NIH] 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] 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] Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Translocating: The attachment of a fragment of one chromosome to a non-homologous chromosome. [NIH] 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] Triglyceride: A lipid carried through the blood stream to tissues. Most of the body's fat tissue is in the form of triglycerides, stored for use as energy. Triglycerides are obtained primarily from fat in foods. [NIH] Trimethoprim-sulfamethoxazole: An antibiotic drug used to treat infection and prevent pneumocystis carinii pneumonia. [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;
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called also neoplasm. [EU] Tunica: A rather vague term to denote the lining coat of hollow organs, tubes, or cavities. [NIH]
Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Ubiquitin: A highly conserved 76 amino acid-protein found in all eukaryotic cells. [NIH] Ultrafiltration: The separation of particles from a suspension by passage through a filter with very fine pores. In ultrafiltration the separation is accomplished by convective transport; in dialysis separation relies instead upon differential diffusion. Ultrafiltration occurs naturally and is a laboratory procedure. Artificial ultrafiltration of the blood is referred to as hemofiltration or hemodiafiltration (if combined with hemodialysis). [NIH] Urea: A compound (CO(NH2)2), formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids. [NIH] Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [NIH] Ureters: Tubes that carry urine from the kidneys to the bladder. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]
Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary tract: The organs of the body that produce and discharge urine. These include the kidneys, ureters, bladder, and urethra. [NIH] Urinary tract infection: An illness caused by harmful bacteria growing in the urinary tract. [NIH]
Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH] Vaccines: Suspensions of killed or attenuated microorganisms (bacteria, viruses, fungi, protozoa, or rickettsiae), antigenic proteins derived from them, or synthetic constructs, administered for the prevention, amelioration, or treatment of infectious and other diseases. [NIH]
Vacuoles: Any spaces or cavities within a cell. They may function in digestion, storage, secretion, or excretion. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vascular endothelial growth factor: VEGF. A substance made by cells that stimulates new blood vessel formation. [NIH] Vascular Resistance: An expression of the resistance offered by the systemic arterioles, and to a lesser extent by the capillaries, to the flow of blood. [NIH] Vasoconstriction: Narrowing of the blood vessels without anatomic change, for which constriction, pathologic is used. [NIH] Vasodilation: Physiological dilation of the blood vessels without anatomic change. For dilation with anatomic change, dilatation, pathologic or aneurysm (or specific aneurysm) is used. [NIH]
Dictionary 163
Vasodilator: An agent that widens blood vessels. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venous: Of or pertaining to the veins. [EU] Ventilation: 1. In respiratory physiology, the process of exchange of air between the lungs and the ambient air. Pulmonary ventilation (usually measured in litres per minute) refers to the total exchange, whereas alveolar ventilation refers to the effective ventilation of the alveoli, in which gas exchange with the blood takes place. 2. In psychiatry, verbalization of one's emotional problems. [EU] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Verapamil: A calcium channel blocker that is a class IV anti-arrhythmia agent. [NIH] Vesicular: 1. Composed of or relating to small, saclike bodies. 2. Pertaining to or made up of vesicles on the skin. [EU] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Vitreous: Glasslike or hyaline; often used alone to designate the vitreous body of the eye (corpus vitreum). [EU] Vitreous Body: The transparent, semigelatinous substance that fills the cavity behind the crystalline lens of the eye and in front of the retina. It is contained in a thin hyoid membrane and forms about four fifths of the optic globe. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] Volition: Voluntary activity without external compulsion. [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] Womb: A hollow, thick-walled, muscular organ in which the impregnated ovum is
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developed into a child. [NIH] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xenograft: The cells of one species transplanted to another species. [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]
165
INDEX A Abdomen, 26, 47, 115, 122, 133, 141, 143, 150, 158, 159, 160 Abdominal, 45, 115, 149, 150, 155 Abdominal Pain, 45, 115 Acceptor, 115, 143, 148 ACE, 26, 115 Acetaminophen, 34, 48, 115 Acid-Base Equilibrium, 55, 115 Acidemia, 33, 55, 115 Acidity, 115, 117 Acidosis, 3, 4, 6, 7, 8, 9, 10, 12, 14, 16, 17, 19, 20, 22, 23, 30, 86, 87, 115, 141 Actin, 18, 115, 145, 146 Acute renal, 5, 85, 86, 115, 137 Adaptability, 115, 124, 125 Adaptation, 20, 22, 23, 57, 115 Adenosine, 115, 150 Adipocytes, 115, 142 Adjustment, 115, 116 Adjuvant, 116, 117 Adrenal Cortex, 116, 128, 152 Adrenal Glands, 116, 118, 155 Adrenal Medulla, 116, 133 Adrenergic, 116, 133, 159 Adverse Effect, 3, 36, 116, 157 Aerobic, 116, 118, 145 Aetiology, 61, 62, 116 Afferent, 116, 142 Affinity, 7, 9, 116, 157 Albumin, 22, 27, 30, 31, 32, 49, 116, 151 Aldosterone, 11, 26, 84, 85, 86, 116 Alertness, 116, 147 Algorithms, 116, 121 Alimentary, 49, 116, 130, 149 Alkalemia, 11, 117 Alkaline, 5, 27, 115, 117, 122, 143, 160 Alkaloid, 117, 149 Alkalosis, 9, 11, 12, 15, 17, 22, 23, 39, 52, 55, 57, 61, 84, 85, 86, 93, 117, 160 Alternative medicine, 92, 117 Alternative Splicing, 7, 117, 153 Aluminum, 79, 117 Aluminum Compounds, 79, 117 Aluminum Hydroxide, 79, 117 Alveolar Process, 117, 155 Alveoli, 117, 163 Amaurosis, 51, 117
Amenorrhea, 117, 118 Amino acid, 18, 35, 54, 55, 73, 78, 117, 118, 119, 121, 129, 133, 136, 142, 143, 145, 148, 150, 152, 153, 159, 160, 161, 162 Amino Acid Sequence, 117, 119, 133, 152 Amino-terminal, 117, 152 Ammonia, 9, 22, 64, 117, 136, 138, 159, 162 Amyloidosis, 85, 117 Anaerobic, 52, 118 Anaerobic Threshold, 52, 118 Anaesthesia, 26, 27, 40, 42, 43, 53, 54, 64, 118, 140 Anal, 118, 154 Analgesic, 85, 115, 118, 139, 147 Analog, 118, 134, 158 Analytes, 14, 118 Anatomical, 118, 120, 125, 139 Anemia, 13, 84, 118, 121, 144, 160 Anesthesia, 33, 61, 63, 118 Anesthetics, 118, 133 Angiotensinogen, 118, 155 Animal model, 9, 14, 118 Anionic, 118, 148 Anions, 31, 116, 118, 141, 157 Anode, 118 Anorexia, 3, 93, 118 Anorexia Nervosa, 93, 118 Antibacterial, 119, 158 Antibiotic, 119, 158, 161 Antibodies, 4, 11, 16, 20, 119, 137, 151 Antibody, 4, 116, 119, 126, 129, 137, 138, 139, 140, 154, 158 Anticoagulant, 119, 153 Anticonvulsant, 119, 143 Antigen, 116, 119, 127, 138, 140 Anti-inflammatory, 115, 119, 128, 136, 139, 156 Antimetabolite, 119, 134 Antimicrobial, 119, 146 Antineoplastic, 119, 128, 129, 134, 151 Antioxidant, 119, 148 Antipruritic, 119, 125 Antipyretic, 115, 119 Anus, 118, 119, 126, 132, 154 Anxiety, 119, 143 Aorta, 119, 123, 155, 163 Apnea, 29, 119 Aponeurosis, 119, 135
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Apoptosis, 12, 119, 124 Aqueous, 13, 79, 120, 129 Arrhythmia, 120, 163 Arterial, 10, 16, 25, 28, 42, 51, 84, 120, 128, 136, 138, 153, 159 Arteries, 119, 120, 121, 128, 145, 146, 153 Arterioles, 120, 121, 123, 146, 162 Artery, 120, 128, 134 Asphyxia, 51, 52, 54, 120 Asymptomatic, 120, 121 Atmospheric Pressure, 120, 138 Atrial, 15, 120, 128 Atrium, 120, 123, 128, 163 Attenuated, 120, 131, 162 Autologous, 39, 120 B Bacteria, 9, 21, 119, 120, 136, 145, 157, 158, 161, 162 Bacterial Physiology, 115, 120 Bactericidal, 120, 133 Bacteriophage, 120, 161 Bacterium, 120, 137 Basal Ganglia, 120, 122, 135 Basement Membrane, 120, 134 Benign, 120, 135, 137 Beta 2-Microglobulin, 54, 120 Beta-Thalassemia, 41, 121 Bilateral, 34, 121 Bile, 121, 125, 135, 137, 141, 143, 158 Biliary, 121, 125 Bilirubin, 116, 121 Binding agent, 79, 121 Biochemical, 6, 14, 31, 63, 78, 119, 121, 134, 142 Biogenic Monoamines, 121, 143 Biological therapy, 121, 136 Biological Transport, 121, 130 Biotechnology, 21, 24, 92, 99, 121 Bladder, 121, 127, 155, 162 Blood Coagulation, 121, 122, 160 Blood Glucose, 121, 137, 140 Blood pressure, 28, 49, 86, 121, 136, 138, 139, 153, 157 Blood Volume, 65, 121 Body Fluids, 78, 79, 117, 121, 131, 134, 157 Bone Marrow, 121, 133, 143, 158 Bone Resorption, 8, 122 Bowel, 20, 118, 122, 132, 141, 142, 150, 154, 159 Brain Diseases, 122, 154 Brain Stem, 122, 154 Bronchi, 122, 133, 161
Buffers, 27, 80, 122 Bulbar, 122, 154 Bulimia, 93, 122 C Calcifediol, 122 Calcification, 79, 122 Calcitriol, 79, 122 Calcium, 4, 12, 23, 34, 56, 57, 72, 79, 81, 85, 86, 122, 123, 127, 138, 145, 148, 149, 160, 163 Calcium Carbonate, 4, 79, 122 Calcium channel blocker, 122, 163 Calcium Channels, 123, 149 Calcium Oxalate, 123, 148 Caloric intake, 72, 123 Cannula, 16, 123 Capillary, 14, 58, 123, 163 Carbohydrate, 37, 123, 128, 136 Carbon Dioxide, 56, 68, 80, 123, 129, 135, 139, 155 Carbonate Dehydratase, 123 Carbonic Anhydrase Inhibitors, 26, 123 Carcinogenic, 123, 140, 158 Cardiac, 15, 16, 53, 72, 84, 123, 124, 128, 133, 137, 146, 155, 158 Cardiac arrest, 72, 123 Cardiac Output, 16, 123 Cardiopulmonary, 27, 61, 123 Cardiopulmonary Bypass, 61, 123 Cardiopulmonary Resuscitation, 27, 123 Cardiovascular, 3, 10, 15, 16, 50, 73, 123, 124 Cardiovascular System, 3, 16, 124 Carotene, 124, 156 Case report, 25, 36, 59, 124 Caspase, 12, 18, 124 Catabolism, 18, 29, 124 Catheterization, 55, 124, 141 Catheters, 16, 124 Cations, 124, 141 Cause of Death, 8, 124 Cecum, 124, 142 Cell, 5, 7, 9, 10, 11, 12, 14, 15, 17, 18, 19, 20, 21, 41, 54, 79, 85, 89, 115, 119, 120, 121, 123, 124, 125, 126, 127, 129, 130, 132, 134, 135, 136, 140, 141, 142, 143, 145, 146, 147, 148, 151, 152, 154, 155, 160, 161, 162, 163 Cell Cycle, 5, 124, 126, 129, 160 Cell Cycle Proteins, 5, 124 Cell Death, 12, 119, 124, 146, 160
167
Cell Division, 120, 124, 125, 136, 145, 151, 152 Cell membrane, 121, 123, 124, 135, 141 Cell Polarity, 54, 124 Cell proliferation, 79, 125 Cell Respiration, 125, 145, 155 Cell Size, 5, 125 Cell Survival, 125, 136 Cell Transplantation, 125 Cellulose, 125, 151 Central Nervous System, 9, 48, 122, 123, 125, 130, 135, 136, 137, 143, 144, 148 Centrifugation, 14, 125 Cerebral, 8, 12, 30, 51, 65, 120, 122, 125, 128, 133, 144, 149 Cerebrum, 125 Chemotherapy, 59, 60, 125 Chin, 51, 125, 144 Cholesterol, 121, 125, 158 Cholestyramine, 30, 47, 48, 125 Chondrocytes, 125, 134 Choroid, 125, 155 Chromaffin System, 125, 132 Chromatin, 119, 124, 125, 143 Chromosome, 125, 137, 143, 161 Chronic renal, 3, 18, 23, 26, 28, 30, 35, 39, 43, 44, 45, 53, 55, 61, 79, 80, 84, 85, 86, 89, 126, 135, 151 Circulatory system, 126, 132 CIS, 126, 156 Cisplatin, 59, 126 Clinical trial, 4, 8, 99, 126, 153, 154 Clone, 11, 126 Cloning, 11, 15, 20, 121, 126 Cofactor, 126, 153, 160 Collagen, 117, 120, 126, 152 Collapse, 50, 126 Colloidal, 116, 126, 157 Colon, 93, 126, 142 Complement, 126, 127, 135, 151 Complementary and alternative medicine, 71, 74, 127 Complementary medicine, 71, 127 Compliance, 93, 127 Computational Biology, 99, 127 Conception, 127, 134 Cones, 127, 156 Confusion, 127, 139, 162 Congestive heart failure, 85, 127 Conjugated, 127, 129 Connective Tissue, 122, 126, 127, 135, 136, 156, 159
Connexins, 127, 135 Consciousness, 118, 128, 131, 147, 154, 155 Constriction, 128, 141, 162 Contraindications, ii, 128 Convulsions, 119, 128, 139 Cor, 128, 136 Coronary, 128, 145, 146 Coronary Arteriosclerosis, 128, 146 Coronary Thrombosis, 128, 145, 146 Cortex, 22, 122, 128, 133 Cortical, 7, 23, 128, 157 Corticosteroid, 128, 158 Cortisol, 16, 116, 128 Cranial, 129, 137, 148, 150, 154 Criterion, 52, 129 CSF, 57, 120, 129 Curative, 129, 160 Cyclin, 5, 124, 129 Cyclin-Dependent Kinases, 124, 129 Cyclophosphamide, 129, 139 Cysteine, 46, 129, 159 Cystine, 129 Cytochrome, 12, 129 Cytokines, 5, 129 Cytoplasm, 21, 119, 124, 129, 132, 143 Cytoplasmic Vesicles, 129, 150 Cytoskeletal Proteins, 124, 129 Cytotoxicity, 126, 129 D Decarboxylation, 6, 121, 129, 154 Degenerative, 130, 156 Dehydration, 10, 130 Deletion, 119, 130 Density, 125, 130 Dentifrices, 117, 130 Depressive Disorder, 130, 143 Deuterium, 130, 138 Dextroamphetamine, 130, 144 Diabetes Mellitus, 5, 84, 130, 136, 137 Diabetic Ketoacidosis, 24, 56, 130 Diagnostic procedure, 77, 92, 130 Dialysate, 4, 36, 130 Dialysis Solutions, 80, 130 Dialyzer, 130, 137 Diarrhea, 25, 125, 130 Diastolic, 130, 139 Dietary Fiber, 93, 130 Diffusion, 15, 121, 130, 131, 137, 140, 141, 155, 162 Digestion, 116, 121, 122, 130, 141, 143, 159, 162 Digestive tract, 78, 81, 131, 157
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Digitalis, 131, 148 Dihydrotestosterone, 131, 155 Dihydroxy, 116, 131, 133 Dilution, 45, 84, 131, 133, 151 Diploid, 131, 151 Direct, iii, 6, 10, 13, 14, 20, 118, 124, 131, 149, 155 Disinfectant, 131, 133 Dissociation, 35, 116, 131 Dissociative Disorders, 131 Distal, 10, 11, 19, 131 Diuresis, 26, 93, 131 Diuretic, 85, 86, 131, 134 Dorsum, 131, 135 Drive, ii, vi, 17, 67, 85, 131, 141 Drug Interactions, 131 Duct, 4, 9, 10, 11, 19, 123, 124, 131, 133, 158 E Eating Disorders, 93, 131 Edema, 85, 131, 135, 142, 146 Efficacy, 8, 58, 131 Electric shock, 123, 131 Electrolysis, 118, 124, 131 Electrolyte, 13, 43, 54, 83, 85, 86, 93, 116, 128, 132, 134, 137, 152, 157 Electrons, 119, 132, 141, 148, 154 Electrophysiological, 10, 132 Embryo, 132, 140 Embryology, 132, 134 Encephalopathy, 9, 56, 59, 132 Endemic, 132, 144 Endocrine Glands, 132, 149 Endocrine System, 84, 132 Endocrinology, 13, 44, 132 Endogenous, 20, 132, 161 Endothelial cell, 132, 134, 160 Endotoxins, 127, 132, 141 End-stage renal, 17, 126, 132, 151 Enema, 38, 132 Energy balance, 132, 142 Enterocytes, 20, 132 Environmental Health, 98, 100, 132 Enzymatic, 6, 11, 26, 117, 121, 122, 124, 127, 129, 132, 156 Enzyme, 115, 123, 124, 132, 133, 141, 144, 151, 153, 155, 159, 160, 161, 163, 164 Epigastric, 133, 149 Epinephrine, 16, 116, 133, 147, 162 Epithelial, 5, 10, 20, 121, 133, 136 Epithelial Cells, 5, 20, 133 Epithelium, 5, 120, 132, 133 Ergometer, 133
Ergometry, 65, 133 Erythrocyte Volume, 121, 133 Erythrocytes, 118, 122, 123, 133, 155 Erythropoietin, 84, 133 Esophagus, 131, 133, 159 Ethanol, 29, 133 Ethylene Glycol, 13, 25, 33, 56, 87, 133 Eukaryotic Cells, 21, 129, 133, 148, 162 Evacuation, 133, 142, 154 Evoke, 133, 159 Excrete, 133, 142, 155 Exhaustion, 133, 144 Exocrine, 133, 149 Exogenous, 132, 133, 135 Exon, 117, 133 Expiration, 134, 155 Extracellular, 8, 9, 18, 19, 20, 81, 127, 134, 148, 157, 160 Extracellular Matrix, 8, 127, 134, 148 Extracellular Space, 134 Extracorporeal, 80, 134, 137 Eye Movements, 134, 154 F Family Planning, 99, 134 Fat, 115, 121, 124, 128, 134, 136, 141, 142, 143, 156, 157, 161 Fatigue, 3, 134, 137 Femoral, 123, 134 Femoral Artery, 123, 134 Fetal Heart, 44, 45, 134 Fetal Monitoring, 54, 134 Fetus, 51, 52, 133, 134, 162 Fibroblast Growth Factor, 15, 134 Fistula, 36, 134 Flatus, 134, 135 Fluid Therapy, 84, 134 Fluorouracil, 59, 134 Forearm, 121, 134 Free Radicals, 119, 131, 134 Furosemide, 12, 134 G Gallbladder, 115, 121, 135 Ganglia, 135, 147, 150 Ganglion, 34, 135, 148 Gap Junctions, 15, 128, 135 Gas, 14, 65, 93, 117, 118, 123, 130, 134, 135, 138, 147, 153, 155, 163 Gas exchange, 118, 135, 155, 163 Gastric, 60, 117, 135 Gastrin, 135, 138 Gastrointestinal, 3, 16, 38, 49, 53, 87, 133, 135, 144, 159
169
Gastrointestinal tract, 16, 87, 133, 135 Gavage, 134, 135 Gene, 7, 8, 10, 11, 16, 19, 48, 117, 121, 128, 135, 153 Gene Expression, 8, 48, 135 Gene Targeting, 10, 135 Genetic Engineering, 121, 126, 135 Germ Cells, 135, 147 Gland, 116, 125, 135, 149, 151, 156, 159, 160 Glomerular, 5, 85, 135, 155 Glomeruli, 135 Glomerulonephritis, 89, 135 Glomerulus, 18, 135, 136, 146 Glucocorticoids, 18, 19, 63, 116, 128, 136 Gluconeogenesis, 3, 7, 136 Glucose, 23, 39, 121, 125, 130, 136, 137, 139, 140, 154, 156 Glucose Intolerance, 130, 136 Glutamic Acid, 136, 147, 152 Glutamine, 7, 23, 44, 49, 57, 136 Glycine, 117, 136, 147 Glycogen, 136 Glycoside, 136, 148, 156 Goblet Cells, 132, 136 Gonadal, 136, 158 Governing Board, 136, 152 Gram-negative, 136, 146, 156 Gram-Negative Bacteria, 136, 146, 156 Gram-positive, 136, 146 Growth factors, 5, 15, 136 H Haemodialysis, 28, 32, 37, 60, 73, 137 Haploid, 137, 151 Haptens, 116, 137 Headache, 137, 139 Heart Arrest, 123, 137 Heart failure, 59, 137 Hematuria, 85, 137 Heme, 121, 129, 137 Hemodialysis, 4, 25, 32, 36, 44, 50, 53, 61, 80, 85, 122, 130, 137, 142, 162 Hemodynamics, 62, 137 Hemofiltration, 41, 85, 137, 162 Hemoglobin, 62, 118, 121, 133, 137, 142, 160 Hemolytic, 85, 137, 160 Hemorrhage, 61, 137, 159 Hepatic, 38, 48, 51, 53, 116, 137, 143 Hepatorenal Syndrome, 84, 137 Hereditary, 85, 138, 160 Heredity, 135, 138
Heterogeneity, 116, 138 Homeostasis, 10, 20, 35, 45, 79, 84, 138 Homologous, 127, 135, 138, 161 Hormonal, 3, 15, 20, 128, 138 Hormone, 16, 34, 35, 39, 51, 81, 116, 122, 128, 133, 135, 138, 140, 142, 144, 152, 160 Hybrid, 126, 138 Hydrogen, 33, 79, 115, 122, 123, 130, 138, 143, 145, 148, 153 Hydrolysis, 21, 126, 138, 141, 152, 153 Hydroxylation, 122, 138 Hydroxyproline, 117, 126, 138 Hyperammonemia, 78, 138 Hyperbaric, 71, 73, 138 Hyperbaric oxygen, 71, 73, 138 Hypercalcemia, 89, 138 Hypercalciuria, 57, 138 Hyperglycemia, 6, 38, 41, 54, 56, 138 Hyperlipidemia, 35, 84, 138 Hyperoxia, 14, 138 Hyperplasia, 5, 42, 138 Hypertension, 10, 84, 85, 86, 89, 137, 138, 146 Hyperthermia, 44, 139 Hypertrophy, 5, 84, 128, 138, 139 Hyperventilation, 48, 73, 139 Hypnotic, 139, 143 Hypoglycaemia, 38, 139 Hypotension, 60, 89, 128, 139 Hypotensive, 49, 139 Hypothermia, 72, 139 Hypothyroidism, 24, 139 Hypotonic Solutions, 139, 145 Hypoxia, 16, 24, 42, 139 Hypoxic, 16, 56, 139 I Ibuprofen, 43, 59, 60, 139 Ifosfamide, 37, 139 Immunoglobulin, 119, 139 Immunology, 116, 139 Immunosuppressant, 134, 139 Immunosuppressive, 129, 139 Impairment, 43, 55, 84, 139, 142, 144 Impotence, 139, 149 In vitro, 5, 9, 11, 20, 23, 35, 54, 139, 158 In vivo, 5, 7, 9, 10, 20, 21, 54, 139 Induction, 42, 140 Infancy, 140 Infantile, 42, 140 Infarction, 140 Infection, 45, 53, 121, 140, 143, 159, 161, 163
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Infiltration, 135, 140 Inflammation, 116, 119, 140, 146, 151, 156, 158, 159 Infusion, 17, 37, 38, 41, 49, 50, 140 Ingestion, 14, 25, 29, 30, 34, 38, 68, 73, 115, 140, 145, 151, 160 Inhalation, 140, 151 Initiation, 8, 17, 140, 161 Inorganic, 73, 81, 117, 126, 140, 150, 152 Insight, 7, 17, 140 Insulin, 3, 15, 18, 25, 35, 41, 43, 130, 140, 141, 149 Insulin-dependent diabetes mellitus, 140 Insulin-like, 15, 140 Intensive Care, 14, 27, 28, 31, 33, 36, 38, 49, 50, 53, 58, 61, 62, 64, 90, 140 Intermittent, 134, 140, 150 Interstitial, 85, 89, 93, 134, 139, 140, 146, 155 Intestinal, 20, 49, 78, 81, 122, 124, 132, 141 Intestine, 93, 122, 141, 142 Intoxication, 34, 36, 40, 56, 87, 141 Intracellular, 12, 15, 16, 47, 81, 124, 129, 140, 141, 144, 152 Intracellular Membranes, 129, 141, 144 Intramuscular, 141, 149 Intraocular, 26, 44, 141 Intravenous, 8, 42, 58, 59, 72, 84, 140, 141, 149 Intrinsic, 9, 116, 120, 141 Intubation, 124, 141 Intussusception, 141, 154 Involuntary, 8, 141, 146, 151 Ion Transport, 9, 15, 141 Ions, 16, 19, 115, 122, 123, 125, 131, 132, 138, 141 Ischemia, 6, 58, 141 Isoenzyme, 6, 141 Isozymes, 6, 141 J Jaundice, 137, 141 K Kb, 7, 98, 141 Keto, 17, 141 Ketoacidosis, 27, 78, 87, 141, 142 Ketone Bodies, 130, 141, 142 Ketosis, 41, 130, 141, 142 Kidney Disease, 5, 13, 25, 27, 32, 36, 37, 41, 42, 43, 55, 56, 61, 63, 65, 85, 98, 142 Kidney Failure, 132, 142 Kidney stone, 18, 85, 142, 146, 148, 155 Kidney Transplantation, 84, 142
Kinetics, 17, 123, 142 L Labile, 8, 126, 142 Large Intestine, 93, 124, 131, 141, 142, 154, 157 Latent, 142, 152 Laxative, 93, 142 Lectin, 142, 144 Leptin, 30, 44, 142 Lesion, 142, 143, 154 Lethal, 13, 120, 142 Lethargy, 139, 142 Leucine, 17, 142 Leukemia, 60, 142 Leukocytes, 122, 129, 142 Liminal, 20, 142 Linkage, 4, 143 Lipid, 140, 141, 143, 148, 161 Lipid Peroxidation, 143, 148 Lithium, 25, 48, 85, 143 Lithium Carbonate, 25, 143 Liver, 9, 16, 50, 85, 115, 116, 118, 121, 122, 129, 133, 135, 136, 137, 143, 162 Liver Cirrhosis, 137, 143 Localization, 9, 16, 142, 143 Localized, 10, 117, 140, 143, 151 Locomotion, 143, 151 Lorazepam, 42, 59, 143 Lupus, 143, 159 Lye, 64, 143 Lymphatic, 140, 143, 158 Lymphocytes, 36, 51, 119, 120, 136, 142, 143, 158, 163 Lymphoid, 119, 143 Lysine, 143, 152 Lysosome, 143, 150 M Malaria, 8, 33, 143, 144 Malaria, Falciparum, 143, 144 Malaria, Vivax, 143, 144 Malnutrition, 13, 18, 51, 116, 144 Mammogram, 122, 144, 145 Mandible, 117, 125, 144, 155 Manic, 143, 144 Meat, 71, 144 Mediate, 9, 12, 19, 144 MEDLINE, 99, 144 Medullary, 5, 10, 19, 57, 85, 144 Melanin, 144, 150, 162 Membrane Proteins, 9, 144 Memory, 118, 144 Meninges, 125, 144, 158
171
Mental, iv, 4, 24, 26, 51, 78, 98, 100, 125, 127, 131, 134, 139, 144, 153, 162 Mental Processes, 131, 144, 153 Mental Retardation, 51, 78, 144 Metabolic disorder, 78, 138, 144 Metabolite, 14, 78, 79, 122, 144 Methamphetamine, 36, 144 Methanol, 25, 34, 87, 145 Methionine, 145, 159 MI, 72, 78, 113, 145 Microbe, 145, 161 Microbiology, 115, 145 Microcalcifications, 122, 145 Mineralization, 81, 145 Mitochondria, 12, 145, 148 Mitochondrial Swelling, 12, 145, 146 Mitosis, 120, 145 Mitotic, 145, 160 Modification, 17, 117, 135, 145 Modulator, 58, 145 Molecular, 6, 7, 9, 10, 11, 12, 13, 14, 15, 16, 19, 20, 21, 99, 101, 118, 121, 123, 127, 130, 145, 161 Molecule, 117, 119, 120, 127, 129, 131, 136, 138, 142, 145, 148, 152, 154, 161, 163 Motor Activity, 128, 145, 154 Mucinous, 135, 145 Mucins, 132, 136, 145 Mucosa, 40, 132, 143, 145 Muscle Contraction, 27, 145 Muscle Fibers, 145, 146 Muscular Diseases, 146, 147, 154 Mutagenesis, 21, 146 Mutagens, 146 Myocardial infarction, 128, 145, 146 Myocardial Ischemia, 42, 146 Myocardium, 145, 146 Myosin, 18, 145, 146 N Nalidixic Acid, 47, 60, 146 Nausea, 142, 146, 162 Necrosis, 84, 119, 140, 145, 146, 156 Neonatal, 4, 14, 31, 34, 51, 78, 146 Nephritis, 85, 89, 146 Nephrolithiasis, 19, 85, 146 Nephrologist, 79, 146 Nephropathy, 43, 85, 86, 89, 142, 146 Nephrosis, 137, 146 Nephrotic, 26, 85, 86, 146 Nephrotic Syndrome, 26, 85, 86, 146 Nerve, 37, 116, 118, 125, 135, 146, 147, 148, 150, 156, 159
Nervous System, 78, 116, 125, 146, 147, 150, 159 Neural, 12, 116, 147 Neurologic, 12, 147 Neuromuscular, 147, 154 Neuromuscular Diseases, 147, 154 Neuronal, 9, 123, 147 Neurons, 135, 147 Neurosecretory Systems, 132, 147 Neurotransmitter, 115, 117, 136, 147, 159 Nitrogen, 3, 22, 30, 78, 117, 129, 136, 147 Nuclear, 120, 132, 133, 135, 146, 147 Nuclei, 132, 135, 145, 147, 148, 153 Nucleic acid, 146, 147 Nucleus, 119, 125, 129, 130, 133, 143, 147, 152, 153 Nutritional Status, 18, 35, 37, 65, 147 O Obtundation, 24, 147 Oocytes, 11, 16, 147 Opium, 147, 149 Opsin, 148, 156 Optic Nerve, 148, 155, 156 Organelles, 21, 125, 129, 148, 151 Osmotic, 52, 116, 139, 145, 148, 157 Osteoblasts, 148 Osteocalcin, 44, 148 Osteodystrophy, 13, 79, 84, 85, 148 Osteoporosis, 21, 148 Ouabain, 11, 148 Overdosage, 60, 148 Overdose, 43, 47, 54, 59, 60, 68, 148 Oxalate, 11, 148 Oxaloacetate, 19, 148 Oxidation, 17, 115, 119, 129, 130, 143, 148 Oxidative Stress, 12, 148 Oxygen Consumption, 118, 149, 155 Oxygenator, 123, 149 P Palliative, 149, 160 Pancreas, 23, 31, 60, 115, 140, 149 Pancreas Transplant, 31, 60, 149 Pancreas Transplantation, 31, 60, 149 Pancreatic, 15, 149 Papaverine, 44, 147, 149 Paralysis, 122, 149, 154 Parathyroid, 22, 32, 55, 79, 85, 86, 122, 149, 160 Parathyroid Glands, 149 Parathyroid hormone, 22, 55, 85, 86, 122, 149 Parenteral, 31, 39, 51, 149
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Metabolic Acidosis
Parenteral Nutrition, 31, 39, 149 Particle, 149, 161 Pathogenesis, 14, 53, 61, 72, 85, 86, 87, 89, 149 Pathologic, 115, 120, 122, 128, 149, 155, 158, 162 Pathologic Processes, 120, 149 Pathophysiology, 11, 13, 39, 83, 84, 86, 150 Patient Education, 93, 108, 110, 113, 150 Pelvis, 115, 150, 162 Peptide, 4, 15, 117, 134, 142, 150, 152, 153, 160 Perfusion, 139, 150 Peripheral blood, 39, 150 Peripheral Nervous System, 147, 150, 154, 159 Peripheral Nervous System Diseases, 147, 150, 154 Peritoneal, 28, 80, 85, 130, 150 Peritoneal Cavity, 150 Peritoneal Dialysis, 28, 80, 85, 130, 150 Peritoneum, 150 Peroral, 4, 150 Phagocytosis, 28, 150 Phagosomes, 21, 150 Pharmacologic, 118, 150, 161 Phenylalanine, 150, 162 Phosphates, 37, 150 Phosphorus, 57, 79, 81, 85, 86, 122, 149, 150 Phosphorylation, 6, 17, 20, 129, 150 Physicochemical, 8, 31, 150 Physiologic, 5, 15, 134, 151, 154, 155 Physiology, 7, 9, 10, 15, 16, 34, 35, 36, 37, 39, 42, 44, 48, 57, 58, 65, 73, 89, 132, 146, 151 Pigments, 124, 141, 151, 156 Piloerection, 139, 151 Pilot study, 8, 151 Pituitary Gland, 128, 134, 151 Plants, 9, 117, 123, 131, 136, 142, 148, 151, 156, 161 Plasma cells, 119, 151 Plasma protein, 116, 151, 157 Plasma Volume, 121, 151 Plastids, 148, 151 Platelets, 51, 151, 160 Platinum, 126, 151 Pneumonia, 128, 151, 161 Podophyllotoxin, 151, 159 Poisoning, 13, 25, 28, 29, 33, 56, 64, 71, 141, 146, 151
Polycystic, 5, 151 Polypeptide, 117, 126, 152, 160, 164 Polyuria, 84, 152 Posterior, 118, 125, 131, 149, 152 Postmenopausal, 148, 152 Post-translational, 20, 152 Potassium, 6, 84, 85, 86, 116, 143, 152 Potassium Compounds, 152 Potassium, Dietary, 84, 152 Practice Guidelines, 100, 152 Precursor, 118, 129, 132, 150, 152, 162 Predisposition, 19, 54, 152 Procollagen, 26, 152 Progesterone, 152, 158 Progression, 3, 79, 84, 118, 129, 152 Progressive, 5, 16, 126, 146, 152, 155, 161 Proline, 126, 138, 152 Prophase, 147, 152 Propofol, 38, 48, 49, 50, 54, 63, 152 Prospective study, 32, 152 Protease, 18, 153 Protein C, 32, 116, 117, 120, 148, 153, 162 Protein Isoforms, 117, 153 Protein S, 18, 27, 121, 148, 153 Proteinuria, 85, 86, 146, 153 Proteolytic, 18, 72, 127, 153 Protocol, 9, 93, 153 Protons, 138, 153, 154 Protozoan, 143, 153 Psychiatry, 153, 163 Psychic, 144, 153, 157 Psychology, 131, 153 Public Policy, 99, 153 Publishing, 22, 153 Pulmonary, 42, 121, 128, 137, 139, 142, 153, 163 Pulmonary Artery, 121, 153, 163 Pulmonary hypertension, 42, 128, 153 Pulmonary Ventilation, 139, 153 Purgative, 142, 154 Pyruvate Dehydrogenase Complex, 6, 17, 154 Q Quadriplegia, 24, 154 Quiescent, 5, 154 R Radiation, 134, 138, 139, 154 Radiation therapy, 138, 154 Radioactive, 138, 147, 154 Randomized, 17, 131, 154 Reabsorption, 10, 12, 15, 19, 154 Reagent, 14, 154
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Receptor, 5, 115, 119, 154 Recombinant, 84, 154, 163 Recombination, 135, 154 Rectal, 64, 93, 154 Rectal Prolapse, 93, 154 Rectum, 119, 126, 131, 134, 135, 142, 154 Red blood cells, 133, 137, 154, 156 Reductase, 7, 155 Refer, 1, 126, 143, 155, 161 Refraction, 155, 158 Refractory, 34, 155 Regeneration, 134, 155 Regimen, 9, 84, 131, 155 Relaxant, 149, 155 Renal Artery, 89, 155 Renal Dialysis, 14, 155 Renal pelvis, 142, 155 Renal tubular, 11, 84, 155 Renal tubular acidosis, 11, 84, 155 Renin, 85, 86, 118, 155 Resection, 20, 155 Resorption, 8, 154, 155 Respiration, 45, 65, 119, 123, 155 Respiratory distress syndrome, 43, 155 Respiratory failure, 52, 155 Respiratory Physiology, 155, 163 Resuscitation, 8, 27, 72, 123, 155 Retina, 14, 125, 127, 148, 155, 156, 163 Retinal, 14, 148, 156 Retinal Neovascularization, 14, 156 Retinal Vein, 156 Retinol, 156 Retinopathy, 14, 43, 156 Rhabdomyolysis, 24, 50, 156 Rhamnose, 148, 156 Rheumatism, 139, 156 Rhodopsin, 148, 156 Risk factor, 14, 153, 156 Rods, 156 S Salicylate, 87, 156 Saline, 41, 51, 58, 156 Saponins, 156, 158 Screening, 11, 14, 126, 156 Secretion, 11, 19, 21, 35, 123, 128, 136, 139, 140, 145, 156, 162 Secretory, 19, 156 Sedative, 143, 156 Sedimentation, 125, 157 Segmental, 10, 157 Segmentation, 157 Seizures, 45, 157
Semisynthetic, 157, 159 Senile, 148, 157 Sensibility, 118, 157 Sepsis, 34, 63, 157 Serum, 13, 18, 22, 26, 30, 32, 43, 44, 50, 59, 61, 81, 116, 120, 126, 148, 157 Serum Albumin, 18, 32, 43, 157 Shock, 50, 60, 157, 161 Side effect, 80, 116, 121, 129, 143, 157, 161 Skeletal, 13, 16, 35, 37, 72, 146, 156, 157 Skeleton, 115, 157 Small intestine, 124, 138, 141, 157 Smooth muscle, 146, 149, 157, 159 Sodium Bicarbonate, 17, 37, 39, 46, 58, 60, 69, 157 Soft tissue, 79, 121, 157 Solvent, 133, 145, 148, 158 Specialist, 105, 158 Species, 125, 133, 138, 143, 145, 158, 161, 163, 164 Specificity, 4, 11, 116, 123, 158 Spectrum, 61, 158 Sphincter, 154, 158 Spinal cord, 122, 125, 129, 135, 144, 147, 150, 154, 158 Spinal Cord Diseases, 154, 158 Spleen, 118, 143, 158 Stabilization, 7, 79, 158 Stavudine, 48, 158 Steatosis, 48, 158 Stem cell transplantation, 39, 158 Stem Cells, 133, 158 Stenosis, 89, 158, 159 Sterile, 149, 158 Steroid, 13, 38, 128, 156, 158 Steroid therapy, 13, 38, 158 Stimulant, 130, 144, 158 Stimulus, 18, 131, 159, 160 Stomach, 115, 131, 133, 135, 138, 142, 146, 150, 157, 158, 159 Stool, 126, 142, 159 Stress, 12, 16, 128, 146, 148, 152, 159 Stricture, 158, 159 Stroke, 98, 123, 159 Subacute, 51, 140, 159 Subclinical, 140, 157, 159 Subcutaneous, 115, 131, 149, 159 Substance P, 144, 156, 159 Substrate, 6, 159 Sulfur, 73, 145, 159 Supplementation, 17, 72, 73, 81, 84, 159 Sweat, 139, 159
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Metabolic Acidosis
Sympathomimetic, 130, 133, 144, 159 Systemic, 14, 16, 85, 89, 117, 119, 121, 133, 137, 140, 154, 157, 159, 162 Systemic disease, 85, 159 Systemic lupus erythematosus, 85, 90, 159 Systolic, 139, 159 T Tendon, 135, 159 Teniposide, 60, 159 Testosterone, 155, 160 Tetany, 149, 160 Thalassemia, 121, 160 Therapeutics, 160 Thermal, 131, 160 Thiamine, 31, 38, 59, 73, 160 Thorax, 115, 160 Threshold, 62, 118, 130, 138, 160 Thrombin, 153, 160 Thrombocytes, 151, 160 Thrombomodulin, 153, 160 Thrombosis, 153, 159, 160 Thrombus, 128, 140, 146, 160 Thyroid, 35, 139, 149, 160, 162 Thyroid Gland, 149, 160 Thyrotropin, 139, 160 Thyroxine, 116, 150, 160 Tissue, 17, 21, 79, 115, 119, 120, 121, 123, 127, 129, 131, 134, 138, 139, 140, 142, 143, 144, 145, 146, 147, 150, 151, 155, 157, 159, 161, 164 Tooth Preparation, 115, 161 Topical, 62, 133, 157, 161 Toxic, iv, 14, 25, 78, 129, 131, 145, 151, 161 Toxicity, 45, 48, 79, 131, 161 Toxicology, 29, 33, 43, 60, 100, 161 Toxin, 62, 161 Trachea, 122, 160, 161 Transcriptase, 158, 161 Transcription Factors, 124, 161 Transduction, 7, 161 Transfection, 121, 161 Translation, 117, 161 Translational, 161 Translocating, 21, 161 Transplantation, 13, 24, 28, 31, 32, 37, 45, 51, 55, 60, 62, 73, 85, 126, 161 Trauma, 36, 62, 79, 137, 146, 161 Triglyceride, 3, 161 Trimethoprim-sulfamethoxazole, 58, 161 Tumour, 135, 161 Tunica, 145, 162 Tyrosine, 19, 162
U Ubiquitin, 18, 72, 162 Ultrafiltration, 137, 162 Urea, 159, 162 Uremia, 18, 29, 35, 55, 84, 142, 155, 162 Ureters, 142, 155, 162 Urethra, 162 Urinary, 18, 19, 23, 55, 56, 64, 65, 85, 146, 152, 162 Urinary tract, 55, 85, 146, 162 Urinary tract infection, 85, 146, 162 Urine, 31, 37, 84, 85, 120, 121, 123, 131, 137, 138, 142, 148, 152, 153, 155, 162 Uterus, 29, 152, 162 V Vaccines, 117, 162, 163 Vacuoles, 148, 162 Vascular, 15, 16, 125, 140, 143, 158, 160, 162 Vascular endothelial growth factor, 15, 162 Vascular Resistance, 16, 162 Vasoconstriction, 133, 162 Vasodilation, 149, 162 Vasodilator, 149, 163 Vector, 161, 163 Vein, 141, 147, 156, 163 Venous, 153, 163 Ventilation, 42, 123, 124, 163 Ventricle, 128, 153, 159, 163 Ventricular, 15, 128, 163 Venules, 121, 123, 163 Verapamil, 54, 163 Vesicular, 9, 163 Veterinary Medicine, 99, 163 Viral, 161, 163 Virulence, 120, 161, 163 Virus, 120, 135, 161, 163 Vitreous, 155, 163 Vitreous Body, 155, 163 Vitro, 163 Vivo, 8, 23, 163 Volition, 141, 163 W White blood cell, 119, 142, 143, 151, 163 Windpipe, 160, 163 Womb, 162, 163 Wound Healing, 134, 164 X Xenograft, 118, 164 Z Zymogen, 153, 164
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Metabolic Acidosis
