RIC CID 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., 1960Uric Acid: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-84669-3 1. Uric Acid-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 uric acid. 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 URIC ACID ................................................................................................ 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Uric Acid....................................................................................... 4 E-Journals: PubMed Central ....................................................................................................... 21 The National Library of Medicine: PubMed ................................................................................ 24 CHAPTER 2. NUTRITION AND URIC ACID ...................................................................................... 69 Overview...................................................................................................................................... 69 Finding Nutrition Studies on Uric Acid ..................................................................................... 69 Federal Resources on Nutrition ................................................................................................... 71 Additional Web Resources ........................................................................................................... 71 CHAPTER 3. ALTERNATIVE MEDICINE AND URIC ACID ................................................................ 73 Overview...................................................................................................................................... 73 National Center for Complementary and Alternative Medicine.................................................. 73 Additional Web Resources ........................................................................................................... 77 General References ....................................................................................................................... 80 CHAPTER 4. DISSERTATIONS ON URIC ACID .................................................................................. 81 Overview...................................................................................................................................... 81 Dissertations on Uric Acid .......................................................................................................... 81 Keeping Current .......................................................................................................................... 82 CHAPTER 5. PATENTS ON URIC ACID ............................................................................................. 83 Overview...................................................................................................................................... 83 Patents on Uric Acid.................................................................................................................... 83 Patent Applications on Uric Acid.............................................................................................. 109 Keeping Current ........................................................................................................................ 119 CHAPTER 6. BOOKS ON URIC ACID............................................................................................... 121 Overview.................................................................................................................................... 121 Book Summaries: Federal Agencies............................................................................................ 121 Book Summaries: Online Booksellers......................................................................................... 122 Chapters on Uric Acid ............................................................................................................... 122 CHAPTER 7. PERIODICALS AND NEWS ON URIC ACID ................................................................. 133 Overview.................................................................................................................................... 133 News Services and Press Releases.............................................................................................. 133 Newsletter Articles .................................................................................................................... 135 Academic Periodicals covering Uric Acid.................................................................................. 137 CHAPTER 8. RESEARCHING MEDICATIONS .................................................................................. 139 Overview.................................................................................................................................... 139 U.S. Pharmacopeia..................................................................................................................... 139 Commercial Databases ............................................................................................................... 140 Researching Orphan Drugs ....................................................................................................... 141 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 145 Overview.................................................................................................................................... 145 NIH Guidelines.......................................................................................................................... 145 NIH Databases........................................................................................................................... 147 Other Commercial Databases..................................................................................................... 149 The Genome Project and Uric Acid ........................................................................................... 149 APPENDIX B. PATIENT RESOURCES ............................................................................................... 153 Overview.................................................................................................................................... 153 Patient Guideline Sources.......................................................................................................... 153 Finding Associations.................................................................................................................. 159
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APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 161 Overview.................................................................................................................................... 161 Preparation................................................................................................................................. 161 Finding a Local Medical Library................................................................................................ 161 Medical Libraries in the U.S. and Canada ................................................................................. 161 ONLINE GLOSSARIES................................................................................................................ 167 Online Dictionary Directories ................................................................................................... 169 URIC ACID DICTIONARY ......................................................................................................... 171 INDEX .............................................................................................................................................. 253
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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 uric acid 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 uric acid, 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 uric acid, 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 uric acid. 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 uric acid, 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 uric acid. 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 URIC ACID Overview In this chapter, we will show you how to locate peer-reviewed references and studies on uric acid.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and uric acid, 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 “uric acid” (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: •
Holmium: YAG Lithotripsy: Photothermal Mechanism Converts Uric Acid Calculi to Cyanide Source: Journal of Urology. 160(2): 320-324. August 1998. Contact: Available from Lippincott Williams and Wilkins. 12107 Insurance Way, Hagerstown, MD 21740. (800) 638-3030 or (301) 714-2334. Fax: (301) 824-7290. Website: www.lippincott.com. Summary: Holmium YAG lithotripsy fragments stones through a photothermal mechanism. Uric acid when heated is known to be converted to cyanide. This article reports on a study that tested the hypothesis that holmium YAG lithotripsy of uric acid calculi (stones) produces cyanide. Human calculi of known uric acid composition were irradiated with holmium YAG energy in water. The water in which lithotripsy was
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performed was then analyzed for cyanide concentration. The results showed the holmium YAG lithotripsy of uric acid calculi in vitro (in the laboratory) produced cyanide consistently. Cyanide production correlated with total holmium YAG energy. The authors conclude that their results raise significant safety issues. 2 appendices. 1 figure. 3 tables. 24 references. •
Drugs to Lower Uric Acid Levels: How to Avoid Misuse in Gouty Arthritis Source: Postgraduate Medicine. 89(2): 111-113, 116. February 1, 1991. Summary: This article discusses ways to avoid misuse of drugs to lower uric acid levels in patients with gouty arthritis. Topics include the characteristics of gout, drug therapy for gouty arthritis, and when to use drugs to lower uric acid levels. The author stresses that the latter agents are not useful in the management of acute gout and must be initiated at low doses with gradual increments. Due in part to the fact that these uricosuric agents tend to interact with a number of drugs, careful and frequent monitoring is needed during the first several months of therapy with these drugs. 2 tables. 6 references. (AA-M).
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Uric Acid Nephrolithiasis: Current Concepts and Controversies Source: Journal of Urology. 168(4 Part 1): 1307-1314. October 2002. Contact: Available from Lippincott Williams and Wilkins. 12107 Insurance Way, Hagerstown, MD 21740. (800) 638-3030 or (301) 714-2334. Fax (301) 824-7290. Summary: Uric acid calculi (stones) with or without a calcium component comprise a significant proportion of urinary stones. Knowledge of the pathophysiology of stone formation is important to direct medical treatment. This review article provides an update on the epidemiology, pathophysiology, and management of uric acid renal (kidney) stones. The incidence of uric acid stones varies between countries and accounts for 5 percent to 40 percent of all urinary calculi. Hyperuricuria (high levels of uric acid in the urine), low urinary output, and acidic urine are well known contributing factors. However, the most important factor for uric acid stone formation is persistently acidic urine. Gout and myeloproliferative disorders are associated with uric acid stones. The pathophysiological basis for persistent urine acidity remains unclear, although various mechanisms have been proposed. Urinary alkalization with potassium citrate or sodium bicarbonate is a highly effective treatment, resulting in dissolution of existing stones and prevention of recurrence. 2 figures. 81 references.
Federally Funded Research on Uric Acid The U.S. Government supports a variety of research studies relating to uric acid. 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.
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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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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 uric acid. 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 uric acid. The following is typical of the type of information found when searching the CRISP database for uric acid: •
Project Title: BIOCHEMICAL DETERMINANTS OF LOCAL DOSE GOVERN O3 TOXICITY Principal Investigator & Institution: Postlethwait, Edward M.; Professor and Vice Chair; University of Alabama Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: Exposure to ozone (O3) continues as a significant public health concern especially with regards to sensitive populations. However, responses to a given exposure demonstrate marked heterogeneity with respect to age, anatomic site, species, and exposure history. The respiratory tract surfaces are covered by an aqueous layer (epithelial lining fluid; ELF) that inhaled gases first encounter and is a complex mixture that contains significant concentrations of small molecular weight antioxidants, principally ascorbic acid (AH2), glutathione (GSH), and uric acid (UA). The standard paradigm proposes that ELF antioxidants provide a protective screen against the injurious effect of inhaled O3. Nonetheless, compelling evidence suggests that reactions between O3 and ELF constituents are critical to the induction of exposure-related cell injury. Due to the unique absorption properties of O3, the endogenous pools and regulation of ELF constituents will dictate the profile of bioactive/cytotoxic species generated during exposure. We hypothesize that the spatial distribution, magnitude, and temporal pattern of biological responses to O3 exposure are dependent on the extracellular chemistry occurring between O3 and constituents of the ELF. As part of the overall Program Project, Project 1 will characterize how surface interactions function to dictate the local dose. Both the surface chemistry and the ELF pharmacodynamics, in combination with O3 flux rates, function to dictate the local dose. Our hypothesis will be addressed by four specific aims that will characterize, in nasal and pulmonary compartments, the surface chemistry and product formation; pharmacokinetics of AH2, GSH, and UA in the ELF; the spatial distribution of the local dose; and the contribution of the local dose to the expression of pathology across animal age (30 --> 189 days), exposure pattern (acute vs. episodic), and airway sensitization in the rhesus monkey model. These characterizations will provide key new insights regarding the mechanisms of differential susceptibility, how surface phenomena govern the impact of exposure in the developing lung, and the utility of the nose to serve as a sentinel for the lung. It is anticipated that these studies can be extended into the human population. The project will facilitate the program as a whole and directly interact with all the other projects and cores. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CER ON CAM ANTIOXIDANT THERAPIES (CERCAT) Principal Investigator & Institution: Frei, Balz B.; Professor and Endowed Chair; None; Oregon State University Corvallis, or 973391086 Timing: Fiscal Year 2003; Project Start 26-SEP-2003; Project End 31-MAY-2008
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Summary: This Program Project is based in the Linus Pauling Institute, an emerging international leader in research and education on micronutrients and antioxidants, and one of a few centers in the US to focus entirely on health promotion and disease prevention by dietary and CAM approaches. The Center of Excellence for Research on Complementary and Alternative Medicine (CAM) Antioxidant Therapies (CERCAT) will investigate two specific categories of CAM antioxidants: (i) Antioxidants that modulate the cellular redox environment and, thus, cell signaling and transcriptional activation, e.g. by affecting critical thiols with a low pKa or upregulating endogenous antioxidant systems. The CAM antioxidants to be investigated from this category are dithiol compounds (e.g. alpha-Iipoic acid) and metal chelators (e.g. EDTA and desferrioxamine). (ii) Highly conjugated or aromatic compounds that inhibit tyrosine nitration by peroxynitrite and other reactive nitrogen species. The principal antioxidant to be examined in this category is uric acid. Using cell culture studies and relevant animal models, CERCAT will determine the molecular and cellular mechanisms of action of these CAM antioxidants, and their safety and efficacy in treating amyotrophic lateral sclerosis (ALS) and cardiovascular diseases (CVD) and reversing the loss of cellular resistance to stress that occurs with aging. These goals of CERCAT are buttressed by NCCAM's "increased emphasis on studies of the mechanism underlying CAM approaches" and its "FY 2003 Research Priorities" of "studies of the biology of EDTA chelation therapy in animal models of CVD" and "neurodegenerative disorders using in vitro studies and animal models." CERCAT's research goals will be accomplished through three highly interactiveprojects: 1) "Metal chelators and thiols in endothelial function, and CVD" (Balz Frei); 2) "Lower vulnerability to toxins in aging by treatment with lipoic acid" (Tory Hagen); and 3) "CAM antioxidants and ALS" (Joseph Beckman). Center Investigators will be aided by an Administrative Core, which handles budgetary, reporting, and external advisory needs. In summary, CERCAT will investigate the efficacy of CAM antioxidants in ALS, CVD and aging, and provide the essential knowledge about the underlying mechanisms, dose-response effects, and relevant biological targets to advance these CAM therapies to human trials; equally important, the studies will test for untoward effects that might discourage CAM antioxidant therapies from proceeding to human studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CRYSTAL INTERACTIONS IN RENAL STONE DISEASE Principal Investigator & Institution: Mandel, Neil S.; Professor; Medicine; Medical College of Wisconsin Po Box26509 Milwaukee, Wi 532260509 Timing: Fiscal Year 2002; Project Start 01-JUL-1982; Project End 30-NOV-2005 Summary: Kidney stone disease is a substantial health problem associated with significant pain, suffering, and economic costs. 5% to 15% of the population will have a symptomatic episode of a stone within the urinary tract by the age of 70 and at least 50% of these individuals will have recurrent stone disease. This grant focuses on the attachment of urinary crystals to injured kidney papillary tip epithelium. Our investigations are driven by the working hypothesis that crystal attachment to papillary epithelium requires cell/tissue injury that includes loss of cell plasma lipid asymmetry and/or loss of cell polarity. Two specific inner medullary collecting duct (IMCD) cell injury models will be employed. (i) the loss of plasma membrane lipid asymmetry resulting in the presentation of phosphatidylserine from the inner to the outer leaflet of the cell plasma membrane, and (ii) the loss of cell polarity as a result of intracellular tight junction breakdown resulting in the mixing of plasma membrane basolateral and apical membrane components to an altered luminal cell surface. In both models, injury
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leads to altered apical membrane composition/structure, and more importantly converts a non-crystal attaching cell into one that does attach crystals. The proposed studies are divided into three Specific Aims that test three specific hypotheses. They will utilize established cell culture and isolated perfused tubule systems and a hyperoxaluric animal model of stone disease. Investigations will be limited to the four most common crystalline components of human urinary tract stones, namely calcium oxalate monohydrate (COM) and calcium oxalate dihydrate (COD), basic calcium phosphate (apatite, AP), and uric acid (UA) crystals. The Specific Aims are: Specific Aim I: To determine in injured papillary collecting duct cells the influence of urinary environment on the molecular nature of crystal attachment in molecules on the altered plasma membrane surface. Specific Aim II: To determine the relative susceptibility of two specific nephron segments to defined injury and subsequent attachment of crystals. Specific Aim III: To determine in an animal model if mild chronic hyperoxaluria produces the localized nephron cell injury that precedes crystal attachment during supersaturation conditions and episodes of crystalluria. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EFFECTS OF ANTIOXIDANTS AND INFLAMMATION IN OLDER PEOPLE Principal Investigator & Institution: Hu, Peifeng; Medicine; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2004; Project Start 01-FEB-2004; Project End 31-JAN-2008 Summary: (provided by applicant): The candidate, Peifeng Hu, M.D., Ph.D., seeks support for further training in clinical epidemiology research. Specifically, he will focus on exploring the interactions of serum antioxidant levels and inflammation in predicting adverse health outcomes in older persons. His long-term goals are to develop an independent research program studying antioxidants and their relations to inflammation markers and cardiovascular risk. Dr. Hu's previous research experience includes: examining the predictive value of natural killer cells in the progression of HIV disease; exploring the association between serum uric acid and mortality; investigating whether the low cholesterol-high mortality association in older persons is attributable to inflammation and malnutrition; and analyzing the effects of managed care on the duration of ambulatory visits by older patients. Dr. Hu's sponsors are Drs. David Reuben, Teresa Seeman, and Alan Fogelman. The sponsors have extensive experience in clinical and basic research into the effects of inflammation and antioxidants on atherosclerosis and mortality risk. As part of his training activities, Dr. Hu will participate in a series of courses, seminars and tutorials to develop additional content expertise regarding antioxidants and atherosclerosis and enhance his ability to analyze complex physiologic data. He will receive training in primary data collection and bioassay techniques. He will also conduct new studies using stored serum specimens from the cohort to examine the basic mechanism of the effects of antioxidants and inflammation. The primary objective of his proposed research is to elaborate the relations between antioxidants and inflammation in elderly persons and explore how an understanding of these relations will enhance our ability to predict overall, cardiovascular, and cancer mortality; incident cardiovascular and cancer events; and decline of cognitive and physical functioning. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: FORMULATION OF RATIONAL THERAPY OF NEPHROLITHIASIS Principal Investigator & Institution: Pak, Charles Yc.; Professor of Internal Medicine; Internal Medicine; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2004; Project Start 01-SEP-1977; Project End 30-NOV-2008 Summary: Kidney stones (nephrolithiasis) is a common disorder in the United States. Kidney stones can be of different compostion and each type can result from a wide variety of causes. A great number of these underlying causes are either not yet identified or we do not know how the underlying condition leads to nephrolitiasis. The long-term objective of this work is to understand the pathophysiology of nephroliathisis and to provide a database to improve diagnosis and treatment of kidney stones. The aim of the current proposal is to address five specific areas of the pathophysiology of nephrolithiasis using a combination of human, animal and basic science approaches. (1) A common cause of calcium stones is a hereditary condition called absorptive hypercalciuria. This Program has defined a gene associated with this condition. In the proposal, the molecular mechanism of how this disease gene leads to kidney stones will be defined. (2). In a subset of patients, uric acid stones may be linked to defects in insulin action in the kidney. This proposal seeks to prove that insulin resistance can cause kidney stones. (3) One complication of popular weight reduction diets with high protein contents is calcium nephrololithiasis. The calcium stone is caused by high calcium and low citrate levels in the urine (citrate normally protects against calcium stones). This proposal will work out how these high protein diets lead to the urine abnormalities and put the subjects at risk for calcium stones. (4) While women have a lower incidence of kidney stones than men throughout life, kidney stones suddenly become quite frequent at the time of menopause. There are several reasons for this change including the calcium from bone loss passively being excreted in the urine. An additional mechanism is direct calcium leaking into the urine from the kidney due to estrogen lack. This proposal will define the mechanism of this primary renal calcium leak. (5) There has been a lot of publicity and controversy regarding whether dietary calcium restriction, a previously accepted therapy, is actually protective or may even be harmful for patients with calcium nephrolithiasis. Some of the disparate results and hence controversy stem from varying degrees of calcium interacting with another substance oxalate in the intestine and urine. This proposal will address the nature of calcium-oxalate interaction and how it impacts on the risk of developing kidney stones. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GENETIC EPIDEMIOLOGY OF AGING IN UTAH PEDIGREES Principal Investigator & Institution: Hunt, Steven C.; Professor; Internal Medicine; University of Utah Salt Lake City, Ut 84102 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-AUG-2003 Summary: (Abstract from application) This application is a response to an RFA on longitudinal genetic epidemiologic studies on aging. The goal of this application is to provide the foundation to identify specific gene mutations involved in changes with aging of cardiovascular phenotypes and how these gene mutations interact with the environment to determine the rate of aging and absence or presence of disease. The study population consists of 98 large, multigenerational Utah pedigrees of 2500 individuals. These individuals already have been examined up to three times over 10 years (starting in 1980) with a wide variety of phenotypes measured, including environmental risk factors for cardiovascular disease. There were four themes in the biochemical variables collected: The renin-angiotensin-aldosterone system, the
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kallikrein-prostaglandin system, the cellular ion transport systems, and the multiple metabolic syndrome including abnormal lipids, insulin and obesity. Additional collected variables associated with aging include blood pressure, heart rates, body temperature, albumin, bilirubin, uric acid, glucose. C-reactive protein and apoA-IV will be measured. Other strengths are 400 anonymous genetic markers being genotyped at the Mammalian Genotyping Service on almost 2000 of these persons. The combination of a large array of phenotypes and genotypes in large pedigrees from a low-risk Utah population provides a unique setting to study the genetic epidemiology-of aging. The goals of this pilot study are to analyze the newly obtained genetic marker data to identify chromosomal regions linked to each of the measured phenotypes and 10-year longitudinal changes in phenotypes. Environmental factors related to the phenotypes will be analyzed and those that are significant will be tested for interactions with these genetic regions within segregation/linkage models. Candidate genes will be prioritized from these regions. In addition, we will collect 20-year follow-up medical history data on each subject to obtain the number of death and incident cardiovascular events (CHD, stroke, diabetes, hypertension). These data will be used for survival analyses. We will assess the feasibility of performing a 25-year follow-up fourth exam during a full-scale study, in which all measured phenotypes at the first and second visits will be remeasured. Twenty-five year changes in these variables will provide an extremely powerful setting to identify specific genes related to aging changes in cardiovascular risk factors. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENOTYPE AND PHENOTYPE OF FAMILIAL NEPHROPATHY WITH GOUT Principal Investigator & Institution: Hart, Thomas C.; Associate Professor; Oral Medicine and Pathology; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2002; Project Start 15-JUL-2002; Project End 31-MAY-2006 Summary: (provided by applicant): Familial Nephropathy with Gout (FGN) is a rare kidney disorder characterized by reduced fractional excretion of uric acid, precocious and tophaceous gout, and development of chronic renal failure leading to end-stage renal disease. FGN is transmitted as an autosomal dominant trait, clinical fmdings are variable, response to treatment not predictable and the disease pathophysiology is poorly understood. The goals of this proposal are to identify the gene(s) responsible for FGN and to characterize the clinical manifestations of this condition. We have identified two large families with FGN providing unique opportunities to characterize clinical manifestations and progression of FGN and to identify the gene responsible. Our preliminary studies sublocalize an FGN gene to a 2.0 cM region of chromosome l6p in one family. Linkage data from a second, smaller family is consistent with a broader candidate interval. Additional studies will determine if the same gene is responsible for FGN in both families. The genetic interval we have mapped FGN to is not well characterized. Genetic and physical maps of the region are incomplete and there are no obvious candidate genes for FGN. We propose an integrated clinical and laboratory approach to identify the gene(s) responsible for FGN. We will longitudinally follow affected family members to better characterize clinical manifestations of FGN (Specific Aim#1). To identify the FGN gene (Specific Aim #2) we propose a hierarchical strategy to 1). Clarify and integrate genetic and physical maps of the candidate interval(s), 2). Continue linkage studies to narrow the candidate interval(s), and 3). Systematically evaluate genes within the interval to identify the gene mutation(s) responsible for FGN
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in these families. Identification of the specific gene mutation will provide an important discovery that will (a) elucidate important aspects of uric acid tubular transport, (b) provide an understanding of interstitial kidney disease and chronic renal failure, and (c) help to better define relationships between hyperuricemia, uric acid excretion, and the development of renal failure. Completion of these studies will permit pre-symptomatic diagnosis for individuals with FGN and enhance our ability to evaluate current treatment strategies as well as to develop new, more effective intervention strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GOUTY DIATHESIS--PATHOPHYSIOLOGY AND MOLECULAR GENETIC BASIS Principal Investigator & Institution: Sakhaee, Khashayar; Professor; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2002; Project Start 01-DEC-2001; Project End 30-NOV-2002 Summary: (Taken directly from the application) A disturbance in urate metabolism has been shown to lead to the development of both uric acid and calcium stones. In addition, primary gout is frequently observed with uric acid lithiasis, where undue urinary pH from defective ammonium production is believed to promote uric acid crystallization. We have used the term gouty diathesis to describe stone formation associate with primary gout, and that it is comprised of acquired and primary (genetic) variants. This hypothesis will be tested by (1) assessing whether defective ammonium production in gouty diathesis is evident by controlling acid intake and imposing phosphate restriction and that, in the acquired form of the disease, insulin resistance is responsible for undue acidity and other biochemical features of this disease, and (2) identifying the molecular defect in the "primary" genetic form of the disease. These studies will help elucidate the pathophysiology of gouty diathesis and may lead to improvements in the diagnosis and treatment of this form of urolithiasis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: INOSINE IN THE OVER-THE-COUNTER TREATMENT OF MS Principal Investigator & Institution: Hooper, Douglas C.; Microbiology and Immunology; Thomas Jefferson University Office of Research Administration Philadelphia, Pa 191075587 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 31-MAR-2005 Summary: (provided by applicant): For a number of years, inosine, a purine nucleoside, has been marketed by health and dietary supplement distributors as an energy or performance enhancer although there is little scientific evidence that inosine has these properties. Recently, interest has been raised in the possibility that inosine may have therapeutic effects in neurodegenerative disorders, such as multiple sclerosis (MS), through its metabolic product uric acid (UA), a natural inhibitor of peroxynitrite. The highly reactive oxidant peroxynitrite contributes to the pathogenesis of MS and animal models of central nervous system (CNS) inflammation through damaging tissue as well as inducing functional changes in the blood-brain barrier (BBB) that facilitate inflammatory cell invasion into CNS tissues. UA is an intermediate of purine metabolism in lower mammals but the excreted end product in humans. Consequently, serum levels of UA are normally relatively high in humans, offering natural protection against ONOO- -mediated pathological processes. With respect to this concept, it is notable that MS patients most often have lower serum UA levels than age- and sexmatched healthy controls and gout (hyperuricemia) patients rarely, if ever, develop MS.
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These observations have led us to examine the possibility that raising serum UA levels in MS patients using inosine may have therapeutic value. An FDA-approved clinical trial concerning the use of inosine to treat MS is now underway. In addition, publication of the results of these ongoing studies has evidently resulted in a number of individuals with MS independently taking inosine purchased over-the-counter. Nevertheless, little effort has been made to determine whether or not oral ingestion of inosine has therapeutic effects that are consistent with those of UA in animal models of CNS inflammation. The objective of this proposal is therefore to test the validity of two plausible hypotheses concerning the therapeutic effects of inosine ingestion on neuroinflammatory diseases believed to involve peroxynitrite: 1/inosine is therapeutic by raising serum UA levels and inactivating peroxynitrite; 2/inosine is therapeutic by suppressing the immune functions responsible for disease pathogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MASS SPECTROMETRIC IDENTIFICATION OF NEW LIPID MEDIATORS Principal Investigator & Institution: Balazy, Michael; Pharmacology; New York Medical College Valhalla, Ny 10595 Timing: Fiscal Year 2002; Project Start 01-MAR-2001; Project End 28-FEB-2006 Summary: (Applicant's abstract): The overall aim of this application is to characterize new mechanisms of biological membrane injury resulting form infection with bacterial endotoxin (LPS). The role of free radicals in LPS-induced endotoxemia is becoming well established, however, little is known about the processes involved in the damage to biomembrane lipids by nitrogen dioxide (NO2) radical (a product of nitric oxide oxidation). We have developed a new methodology based on electrospray tandem mass spectrometry, which allows identification and quantification of specific lipid products formed by the reaction of NO2 with arachidonic acid. Preliminary studies have revealed that this reaction generates a complex mixture of lipids containing characteristic products: trans isomers of arachidonic acid and lipids containing nitrogen-carbon bond (nitroeicosanoids). In addition, plasmalogen phospholipids reacted with NO2, which resulted in complete removal of this group of lipids and generation of 1 -lysophospholipids. We hypothesize that increased production of NO generates NO2. which is a key radical that targets arachidonic acid and phospholipids. thereby causing membrane injury. Specific aims are to: 1) study relationships between the magnitude of trans-arachidonic acid generation and other markers of free radical damage (isoprostaglandin, nitrite/nitrate, nitrotyrosine); 2) examine the nitration of arachidonic acid and the effects of nitroeicosanoids on NO and cGMP levels in tissues; 3) characterize modifications of plasmalogen phospholipids in endotoxemia. In order to address the role of NO, L-NMA, a NO synthase inhibitor will be used to prevent generation of NO. Uric acid was shown to scavenge NO2, and thus serve as a good probe to study effects of NO2 in LPS-induced injury. Thus these probes will be used to determine the role of NO and NO2 in arachidonic acid isomerization, nitration and plasmalogen degradation. We anticipate that in the long term the proposed studies will provide a foundation for a rational design of new strategies for development of new drugs (inhibitors of lipid isomexization and nitration), and therapies to treat symptoms of sepsis related to the N02-induced cytotoxicity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISMS OF NEURONAL APOPTOSIS IN VIVO Principal Investigator & Institution: Martin, Lee J.; Associate Professor; Pathology; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 01-MAR-2000; Project End 28-FEB-2004 Summary: (Adapted from the applicant's abstract): The mechanisms for neuronal degeneration in adult-onset central nervous system (CNS) diseases, including Alzheimer's disease (AD) and amyotrophic lateral sclerosis (ALS), are not understood. Recent studies suggest that neurodegeneration in AD and ALS is apoptosis, occurring by programmed cell death (PCD). The investigator has developed an animal model to study neuronal apoptosis. Occipital cortex ablation in adult rat and mice, a model of axotomy and target deprivation, causes progressive retrograde neuronal degeneration in thalamus that is structurally apoptosis. This apoptosis is associated with accumulation of active mitochondria within the neuronal cell body and oxidative damage to DNA. The investigator proposes to evaluate the mechanisms for neuronal apoptosis in vivo. The investigator will test the hypothesis that apoptosis in neurons is signaled by subcellular translocation of Bcl-2 and Bax and release of cytochrome C from mitochondria, which correspond temporally with activation of caspases and DNA fragmentation factors. The participation Bcl-2 and Bax to the mechanisms for neuronal apoptosis will be determined by evaluating whether neuronal loss is reduced in lesioned transgenic mice overexpressing Bcl-2 and in mice deficient in Bax. The participation of mitochondrial permeability transition and cytochrome C release will be determined by post-injury treatment with the permeability transition blocker cyclosporin A. In addition, the investigator proposes that a signal for PCD in these neurons is oxidative stress. The investigator will test the hypothesis that retrograde neuronal death after axotomy is nuclear DNA damage-induced, p53-dependent apoptosis. The investigator will evaluate whether dying neurons sustain oxidative damage to DNA and proteins during the transition between chromatolysis and early apoptosis. The participation of oxidative stress as a mechanism for the induction of neuronal apoptosis in vivo after axotomy/target deprivation will be further examined by determining whether oxidative injury and apoptosis are attenuated in transgenic mice that are deficient in neuronal or inducible nitric oxide synthase and in mice that overexpress human wild-type superoxide dismutase 1. The dependence of this neuronal apoptosis on p53 will be evaluated in lesioned p53-deficient mice. The investigator will then use antioxidant therapies (Trolox and uric acid) to prevent or delay neuronal apoptosis. These studies will identify possible molecular mechanisms of neuronal apoptosis in vivo and could lead to the design of new therapeutic neuroprotection experiments critical for the future treatment of AD and ALS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: METABOLIC DEFECTS IN RECURRENT NEPHROLITHIASIS Principal Investigator & Institution: Rothstein, Marcos; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2002 Summary: This protocol evaluates patients with recurrent nephrolithiasis to investigate the pathogenic role of distal renal tubular acidosis. Studies include the excretion of sodium, calcium, magnesium phosphorus, uric acid, oxalate, citrate and creatinine in the baseline state and in response to oral calcium ammonium chloride and bicarbonate loading and to neutral phosphate infusion. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NONLINEAR MODELING OF MYOCARDIAL TRANSPORT & ENERGY METABOLISM Principal Investigator & Institution: Kroll, Keith; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2002 Summary: The capillary endothelial enzyme, xanthine oxidase/dehydrogenase, which mediates oxidation of hypoxathine to xanthine, and xanthine to uric acid, was investigated in the perfused beating heart. Intracoronary bolus injections were made of [14C]-hypoxanthine (together with reference tracers [131I]-albumin and [3H]-L-glucose), while measuring venous concentrations of the injected tracers and [14C]-xanthine and [14C]-uric acid, formed in endothelial cells. Sufficient unlabeled carrier hypoxanthine was co-injected that peak concentrations swept through the likely concentration range of the enzyme Km. The dilution curves showed strikingly low levels of coronary efflux of [14C]-xanthine, suggesting very low endothelial membrane permeability. However, the possibility of low permeability had to be discarded as a result of additional experiments in which [14C]-xanthine was injected in the tracer bolus instead of hypoxanthine, and it was observed that the peak extraction of xanthine was nearly as high as that of hypoxanthine (0.5). Fitting the dilution curves using a multiple species nonlinear model of capillary-tissue transport, binding and reaction indicated that prolonged retention of xanthine following hypoxanthine injection was likely due to slow dissociation of the enzyme-xanthine product complex. This appears to favor subsequent reaction to uric acid over release of free xanthine. Consistent with this interpretation was the finding that when [14C]-xanthine was injected in the bolus, there was less formation of end product [14C]-uric acid, than when [14C]-hypoxanthine was injected. Therefore, it seems that the high affinity binding of the enzyme to xanthine serves to insure that most of the hypoxanthine oxidized in the first step of the reaction is not released from the enzyme until it is further oxidized to uric acid in the second step. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NOVEL INHIBITOR OF CRYSTAL ADHESION TO RENAL CELLS Principal Investigator & Institution: Lieske, John C.; Associate Professor; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2002; Project Start 01-MAY-1999; Project End 30-APR-2004 Summary: Nephrolithiasis, the formation of kidney stones, is a common condition seen in up to 12 percent of adults during their lifetime. As the mechanisms by which stones form are poorly understood, new knowledge is required to identify susceptible patients for early treatment and to formulate new therapeutic strategies to prevent the appearance of single and/or recurrent stones. How nascent crystals that nucleate in tubular fluid are retained in the nephron and form calculi is not known. My studies during the past 8 years demonstrate that calcium oxalate monohydrate (COM) crystals bind within seconds to anionic, sialic acid- containing glycoproteins on the apical surface of cultured monkey kidney epithelial cells (BSC-1), employed to model the tubule, suggesting one mechanism whereby crystals could be retained in the kidney in vivo. Preliminary studies have identified constitutive release of a protein by BSC-1 cells that blocks adhesion of COM crystals to the apical cell surface; it has been named the Crystal Adhesion Inhibitor, or CAI. A novel method employing COM crystal affinity chromatography was used to purify CAI. Evidence provided in this revised application demonstrates that CAI is a constituent of normal human urine. Biochemical characterization identifies it as a sialic acid-containing glycoprotein. Microsequencing of
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the amino terminus and 9 fragments generated by lys-C and asp-N protease cleavage reveal that CAI is novel. Two monospecific antibodies against synthetic peptides prepared using amino acid sequence information each recognize the factor on Western blots of partially- purified normal human urine, renal cell conditioned medium, and total kidney cell protein. The goal of this revised research plan is to define the potential role of CAI in human nephrolithiasis. New Specific Aims are to: 1) Utilize 2 monospecific antibodies prepared against CAI to characterize and quantitate it in the urine of normal and stone- forming individuals; 2) Study inhibition of COM, hydroxyapatite, and uric acid crystal adhesion to renal cells by CAI isolated from conditioned medium and the urine of normal and stone-forming subjects; 3) Study inhibition of COM crystal growth by CAI isolated from conditioned medium and the urine of normal and stone-forming subjects, 4) Study inhibition of COM crystal aggregation by CAI isolated from conditioned medium and the urine of normal and stone-forming individuals, 5) Utilize the monospecific antibodies prepared against CAI to isolate affinity-purified protein and study its physical-chemical properties; 6) Study the cell biology of CAI. Achieving these specific aims will provide new knowledge about mechanisms that mediate stone formation, and provide a rational basis for design of novel strategies to treat and/or prevent this disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PLASMA PURINE RATIO--A NEW BIOMARKER FOR CANCER RISK Principal Investigator & Institution: Sherley, James L.; Associate Member; Biomedical Engineering; Massachusetts Institute of Technology Room E19-750 Cambridge, Ma 02139 Timing: Fiscal Year 2002; Project Start 08-JAN-2001; Project End 31-DEC-2002 Summary: Recent advances in human cancer genetics have led to the identification of genes in which mutations in predispose to cancer. Tests for mutations in these cancer genes are becoming a part of routine clinical practice in cancer risk counseling. The benefits of cancer gene testing are countered by significant costs in emotional stress due to the inherent uncertainties of genetic risk data. Methods that provide individualized phenotypic information to reduce the degree of uncertainty in genetic test data would be beneficial to those at risk. Towards this goal, a new phenotypic marker for cancer risk assessment is presented. The new marker is based on new insights into the function of the p53 tumor suppressor gene. With high penetrance, germline p53 mutations predispose to multiple tumors or diverse tissues early in life. Recently, p53 has been shown to regulate the production of cellular guanine ribonucleotides (rGNPs). RGNPs function in growth factor signal transduction. They play a key role in regulating DNA replication and cell kinetics. Preliminary studies indicate that human germline p53 mutations are associated with a predicted increase in rGNP production. This phenotype is postulated to be an important factor in tumor development in cancer patients with germline p53 mutations. Due to related mechanisms, the same phenotype may also be at cause for cancers in patients with normal germline p53 genes. A proposal is made to develop a specific indicator of constitutional rGNP-production rate called the plasma to plasma uric acid concentration. An expanded study will be undertaken to investigate further an association detected between low PPR (indicating elevated rGNPO production) and mutant germline p53 genotype or ovarian cancer status. PPR will be evaluated retrospectively in additional members of families with inherited germline p53 mutations and in women in families at high risk for ovarian cancer, breast cancer, and other epithelial tumors. The breast cancer and ovarian cancer studies will evaluate PPR as a marker to identify women in high- risk cancer families who are at greatest risk for
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cancer. The proposed biomarker has potential as a general method to delineate individuals in clinically defined high-risk cancer populations who will benefit most from cancer prevention strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PRECLINICAL DEVELOPMENT OF URICASE-PEG 20 Principal Investigator & Institution: Bomalaski, John S.; Pharmacologics, Inc. Astecc Facility #a-217 Lexington, Ky 40506
Professor;
Phoenix
Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 31-DEC-2002 Summary: Hyperuricemia (elevated serum uric acid) results in gouty arthritis and chronic renal disease. Severe hyperuricemia can occur following cancer chemotherapy (tumor lysis syndrome) and organ transplantation (most common in heart and kidney transplant patients) which may result in acute uric acid nephropathy with resultant metabolic disorders and death. Moreover, in addition to pain, hyperuricemia can result in destructive gouty arthritis, with concomitant permanent damage to joints and connective tissue. Elevated uric acid levels (hyperuricemia) do not develop in most mammals because they have the gene which encodes urate oxidase which metabolizes the less soluble uric acid into a much more soluble metabolite, allantoin. However, in humans, the urate oxidase gene has evolved to contain a nonsense codon which results in a complete loss of enzyme activity. Many different groups of investigators have administered uricase, purified from micro organisms, to patients. Although these treatments lower plasma uric acid levels, all of the enzymes used are highly immunogenic and cause allergic reactions and anaphylaxis. Formulation of other therapeutic proteins with polyethylene glycol (PEG) has been shown to reduce their anti-genicity and prolong their circulating half-life. We have initiated Phase I clinical testing of a PEG modified uricase termed Uricase-PEG20. In this proposal we seek funding to perform the additional studies requested by the FDA in order for this drug to move into Phase 2 human clinical testing. PROPOSED COMMERCIAL APPLICATIONS: This proposal focuses on performing the additional preclinical experiments requested by the FDA in order for this drug to enter Phase 2 human testing. Although non-PEG formulated uricase is used in Europe, it has not been approved in the USA because of the high incidence of allergic reactions associated with its use. uricase-PEG 20 is formulated with polyethylene glycol (PEG), a technology known to reduce the antigenicity of heterologous proteins. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: RENAL INFLAMMATION: MECHANISMS AND CONSEQUENCES Principal Investigator & Institution: Lan, Hui; Medicine; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2003; Project Start 01-MAY-2003; Project End 30-APR-2008 Summary: (provided by applicant) The O'Brien Center for Renal Inflammation has the mission of furthering our understanding of the mechanisms involved in the initiation, maintenance, and resolution of inflammation in renal disease. Renal inflammation is recognized to have a critical role in the pathogenesis of acute renal failure, glomerulonephritis, diabetic nephropathy, hypertension, and progressive renal disease. In this Center application, we have brought together scientists with expertise in different aspects of inflammation to provide a cohesive and comprehensive investigation of the mechanisms involved in renal inflammation. The multidisciplinary approach will focus on both proinflammatory and anti-inflammatory mechanisms with an emphasis on
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molecules that have either not received much attention (e.g., uric acid) or that have only recently been identified as having a role in inflammation. The latter includes new chemokines (CXCL16), new adhesion molecules (JAM family), the recently discovered Slit/Robo family, the signaling molecule Smad7, and stanniocalcin. A pathology core that focuses on the role of these molecules in human disease will provide clinical relevance and will be a mechanism for translating basic science observations for potential future clinical research application. The Center will also train fellowship candidates for a career in academic nephrology (in concert with a T-32 training grant which is currently under review), help initiate the careers of junior investigators (via the DR/P&F program), and provide a strong interaction with the other Centers at Baylor that also focus on the inflammatory response (such as the Biology of Inflammation Center). The integrated, multidisciplinary, synergistic and comprehensive approach to study renal inflammation should provide a better understanding of the pathogenesis of renal disease and may provide new therapeutic insights. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE BIOSYNTHESIS
OF
10-FORMYLDIHYDROFOLATE
IN
PURINE
Principal Investigator & Institution: Tamura, Tsunenobu; Professor; Nutrition Sciences; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2003; Project Start 15-JUN-2003; Project End 31-MAY-2005 Summary: (provided by applicant): All folate-dependent one-carbon transfer reactions had been considered active only with the naturally occurring isomers of tetrahydrofolate (H4folate). Recently, however, in vitro and in vivo experimental evidence suggests that 10-formyldihydrofolate (10-HCO-H2folate) has physiological roles. A hypothesis is proposed that a significant portion of the carbon-2 (C2) of the purine ring originates from the formyl group of 10-HCO-H2folate. The following specific aim is proposed to test the hypothesis. To identify the folate origin of the C2 and C8 positions of the purine ring, in vivo competition experiments will be performed. Subjects will be given an oral dose of 13C-sodium formate and subsequently a dose of one of the following five formylfolates (containing a one-12C moiety); natural and unnatural isomers of 5-formyltetrahydrofolate and 5,10-methenyltetrahydrofolate and 10-HCO-H2folate. Following the oral doses of 13C-sodium formate and a formylfolate, urine samples will be collected for three days, and the 13C-enrichment pattern at the C2 and C8 positions of uric acid will be determined by mass spectrometry. At the beginning of this three-day period, an in vivo 13C-formylfolate pool will be established. The formyl carbon of 13C-formylfolates will compete with that of unlabeled formylfolates (given in a large dose) for the incorporation into the C2 and C8 positions of the purine ring. 10-HCO-H2folate will have the strongest negative effect on 13C enrichment at the C2 position and no effect on the 13C enrichment at the C8 position, since this folate is a better substrate for AICAR transformylase than is natural 10formyltetrahydrofolate. The study will provide basic knowledge of a new folate pathway involving 10-HCO-H2folate in humans. If this pathway is proven, derivatives of 10-HCO-H2folate could be used to inhibit de novo purine biosynthesis for developing new anticancer drugs. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF XANTHINE OXIDASE IN LUNG INJURY Principal Investigator & Institution: Hassoun, Paul M.; New England Medical Center Hospitals 750 Washington St Boston, Ma 021111533
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Timing: Fiscal Year 2002; Project Start 01-JUL-1993; Project End 31-AUG-2002 Summary: Hypoxia produces significant cellular perturbations in the pulmonary vasculature in lung diseases, such as the adult respiratory distress syndrome and chronic obstructive lung disease, where hypoxia is prevalent. These changes include a marked proliferation of smooth muscle cells (SMC) in the medial layer of the distal vessels and possible alterations in endothelial functions as suggested by increased platelet adhesion to the endothelium. Using cell culture systems, we have found that hypoxia produces a significant release from endothelial cell (EC) of hypoxanthine, a metabolite of ATP. This finding led us to investigate the effect of O2 tension on the enzyme xanthine oxidase/xanthine dehydrogenase (XO/XD) which catalyzes the conversion of hypoxanthine and xanthine to uric acid. Our preliminary results indicate that O2 tension might regulate the intracellular XO/XD activity of EC. Indeed, we found that intracellular XO/XD activity is absent when EC are exposed to hyperoxia and maximal (an approximate 300% increase compared to activity of EC exposed to normoxia) when EC are exposed to hypoxia or anoxia. The latter finding, combined with our previous report of an increased release of hypoxanthine from hypoxic EC, bears great significance in light of the recognized-potential for the hypoxanthine/xanthine oxidase system to produce reactive O2 species. Production of O2-based free radicals have, indeed, been shown to cause several deleterious effects on EC including cell injury and inactivation of the endothelial-derived-relaxing-factor (EDRF). We postulate that changes in the EC hypoxanthine/xanthine oxidase system in response to hypoxia may be a very early phenomenon that might be responsible for subsequent cellular changes in the pulmonary vasculature. The Specific Aims of this project are to 1) further investigate changes in EC XO/XD in relation to O2 tension using a cDNA probe that we recently developed for the enzyme; 2) assess the potential for EC to produce reactive O2 species in response to changes in O2 tension; 3) examine possible cellular regulatory mechanisms of EC XO/XD in terms of transduction mechanisms, ion transport and second messengers; 4) examine the effects of selected cytokines and some known mediators of lung injury on XO/XD activity and mRNA expression; and 5) extend our cell culture work to in vivo studies by exposing rats to hypoxia and measuring XO/XD activity and mRNA expression of lung tissue. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SORBENTS+ENGINEERED BACTERIA AS GUT-BASED UREMIA THERAPY Principal Investigator & Institution: Ranganathan, Natarajan; Kibow Biotech, Inc. University City Science Center Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-DEC-2003 Summary: End stage renal disease (ESRD) is a devastating disease with a very high cost of treatment, especially for poor patients worldwide. Our R&D goal is to progressively develop a low-cost, non-invasive gut-based treatment for efficient removal of uremic solutes in renal failure patients. We plan to develop a therapeutic oral formulation in a stepwise methodology beginning with generation I to its ultimate optimized product generation IV. This is based on a formulation of a mixture of modified sorbents plus a genetically engineered bacterium which, in the gut, would adsorb and eliminate various uremic solutes through the bowel route. Our phase I proposal is specifically directed to develop the generation I formulation consisting of zeolite based sorbent material will be replaced by a genetically engineered E. coli DH5 cells which is expected to demonstrate better urea removal capabilities. These Generation I and Generation II formulations will be investigated for their in vitro adsorption capabilities for urea, creatinine and uric acid
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removal. These phase I R&D investigations are expected to furnish data necessary to accelerate the development of the generation III and subsequently the optimized generation IV formulation for our phase II studies. PROPOSED COMMERCIAL APPLICATION: The fully developed product will have immense applications towards treatment of uremic patients from predialysis to ESRD and possibly substitute the need for dialysis, especially in developing and under- developed countries. It is equally feasible that our oral formulation may also have applications as a adjunct therapy for dialysis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ULTRASE MT12 FOR STEATORRHEA IN CYSTIC FIBROSIS Principal Investigator & Institution: Stern, Robert C.; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2002 Summary: Pancreatic replacement enzymes have been used for treatment of cystic fibrosis since shortly after the disease was first described in 1938. These enzymes were introduced into medical practice before the passage of the Food, Drug, and Cosmetics Act. In addition, because they were derived from "food" and were therefore thought to be intrinsically safe, no rigorous formal studies of efficacy and safety, such as would be needed now to fulfill the requirements of an FDA new drug application, were ever performed. The use of this class of therapeutic agents was governed by the Department of Agriculture rather than by the Food and Drug Administration. Over the first few decades of use, the only major toxicity reported was symptomatic allergy to inhaled powdered enzymes (almost always in caregivers [e.g., parents and nurses]) and a rise in serum uric acid in some patients who required high doses. Both of these problems were rare, and neither represented a clinically important threat to cause irreversible injury or death. Relatively unsupervised use of these drugs continued. In recent years, however, very high-dose enteric coated preparations were introduced. These drugs were much more effective for many patients. New technology allowed production of very high-dose capsules (each containing 25000 or more units of lipase, compared to the 4000 units in previous preparations; the amount of proteases was also increased). Some patients who took very high doses (usually >5000-10000 units/lipase per kg per meal) developed severe colonic strictures (with obstruction) and many required surgery, including some who underwent subtotal colectomy. Although the exact pathophysiology of this toxicity is not known with certainty, there is little doubt that it hss been associated with the introduction of the high-dose capsules (and usually with the consumption of large amounts of them). With this occurrence of a new major toxicity the FDA was compelled to review the status of these drugs, and ruled that the very high-dose preparation (i.e., any capsule containing more than 20000 units of lipase) be removed from the market immediately, and that all other pancreatic enzymes must be expeditiously processed as new drugs. The study proposed here is one of many which are not necessary to establish efficacy (to the standards of an FDA new drug application) of pancreatic enzymes for treatment of CF. The specific aim of the study is to compare fat and protein absorption (as determined by a 3-day stool fat and protein determination) in CF patients during a three day period of administration of pancreatic enzyme replacement (Ultrase MT12) with meals with the same patient's data during a three-day period of administration of a placebo preparation with meals. " Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: URIC ACID IN CHILDHOOD HYPERTENSION Principal Investigator & Institution: Feig, Daniel I.; Pediatrics; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-AUG-2008 Summary: (provided by applicant): An association between hyperuricemia and hypertension has been observed repeatedly since the 1870s. Generally the link was dismissed as having no causal role because of an assumption that the increase in serum uric acid was merely a surrogate for decreased glomerular filtration rate. Recently the association has been reevaluated because of results from several large clinical trials that implicate hyperuricemia as an independent risk factor for poor cardiovascular outcomes. Our own data demonstrates a close correlation between serum uric acid and primary hypertension in children. Furthermore, data from experiments using a model of mild hyperuricemia in rats reveal that the hyperuricemia alone is (1) sufficient to lead to hypertension and (2) exacerbates the progressive renal injury associated with either Cyclosporin A nephrotoxicity or surgical 5/6 nephrectomy. In the animal model, the mechanisms involved in these processes include uric acid mediated activation of cyclooxygenase-II, activation of the renin angiotensin system and down regulation of renal nitric oxide synthase. If these animal studies can be generalized to human populations, control of mild hyperuricemia will provide a new approach to management of hypertension as well as a novel therapeutic target for the prevention of progressive renal disease and cardiovascular morbidity. We propose to test whether the use of the xanthine oxidase inhibitor allopurinol, a uric acid lowering drug, will (1) ameliorate primary hypertension in children and (2) control hypertension in renal transplant recipients receiving cyclosporin or tacrolimus. We will further investigate the physiological mechanism by which serum uric acid levels are elevated in hypertensive children and the biochemical mechanisms by which elevated serum uric acid lead to increased blood pressure. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: URIC ACID IN SYSTEM AND RENAL INFLAMMATION Principal Investigator & Institution: Johnson, Richard J.; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: We have focused on the pathogenesis of essential hypertension, and have provided evidence that most forms of chronic hypertension are mediated by the development of preglomerular vascular disease with renal ischemia, generation of intrarenal oxidants and vasoconstrictive substances, and sodium retention leading to a shift in the pressure-natriuresis curve. Recently we found that hyperuricemia (which is known to predict the development of hypertension) may engage this pathway. Mild hyperuricemia in rats (created by administering a uricase inhibitor) induces preglomerular arteriolopathy, interstitial renal disease and salt-sensitive hypertension. In this application we further pursue the role of uric acid in hypertension and renal disease by hypothesizing that the arteriolopathy and renal disease induced by uric acid may be mediated by a uric acid-induced systemic and vascular inflammatory response. This hypothesis is based on preliminary studies demonstrating that uric acid can induce monocyte chemoattractant protein (MCP-1) in vascular smooth muscle cells and cytokines by leukocytes. Aim 1 will identify the pathway by which uric acid stimulates MCP-1 in vascular smooth muscle cells by examining the hypothesis that it enters via specific channels (the UAT, OAT3 and URAT1 transporter/exchangers) and that
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synthesis of MCP-1 is regulated by specific isoforms of protein kinase C and MAP kinases. In Aim 2 we will determine if hyperuricemia initiates systemic and renal inflammation in vivo. Part 1 will test the hypothesis that systemic hyperuricemia in normal rats and in rats with renal disease (remnant kidneys) causes a systemic inflammatory response and that this can be blocked by preventing the development of hyperuricemia with various agents. Part 2 will test the hypothesis that the increased MCP-1 production that occurs in vivo in hyperuricemic rats is responsible for inducing the preglomerular vascular disease and subsequent salt-sensitive hypertension. This will be addressed by blocking studies using a competitive inhibitor analog of MCP-1. These studies may provide important insights into the role of uric acid in hypertension and renal disease. The studies should also provide a potential mechanism to explain why systemic inflammation predicts and causes hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: XANTHINE OXIDASE MODULATION OF CELL OXIDANT PRODUCTION Principal Investigator & Institution: Tarpey, Margaret M.; Associate Professor; Anesthesiology; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2002; Project Start 01-FEB-2001; Project End 31-JAN-2005 Summary: (Adapted from the Applicant's Abstract): The endothelium serves as a critical component in the maintenance of vascular homeostasis. Alterations in endothelial cell production of oxidants contribute to defective vascular function and are implicated in the pathogenesis of diverse vascular diseases. However, the tissue sources of enhanced vascular cell oxidant production and the sites of oxidant action have not been determined with certainty. Recently, recognition of a) elevated plasma levels of circulating xanthine oxidase activity in diverse disease processes (sepsis, hypercholesterolemia, post- liver transplantation) and b) the ability of xanthine oxidase to specifically bind to endothelium with resultant increases in intracellular xanthine oxidase activity provide potential mechanism(s) by which non-endothelial cell-derived xanthine oxidase could contribute to endothelial oxidant production. While enhanced production of superoxide can diminish nitric oxide bioavailability by virtue of its reaction with nitric oxide and thus, concomitantly yield secondary oxidants, the potential for superoxide and other cellular oxidants to directly modify the activity of endothelial nitric oxide synthase has not been fully explored. From this foundation of understanding, it is hypothesized that increases in cell-associated xanthine oxidase modulate endothelial-dependent vascular function. To address this hypothesis, the following Specific Aims will be pursued: 1) Characterize vascular cell interactions with circulating xanthine oxidase. The kinetics of cell binding and uptake of circulating xanthine oxidase/dehydrogenase will be determined. In addition, xanthine oxidase circulating and ultimate tissue distribution will be defined in vivo. 2) Explore the impact of elevated xanthine oxidase-derived products (reactive species, uric acid) on expression and activity of endothelial nitric oxide synthase. The effects of xanthine oxidase on transcription and translation of endothelial nitric oxide synthase will be ascertained as well. The vascular functional consequences of increased xanthine oxidase activity will also be determined. Upon successful completion of the proposed aims, a) the contribution of xanthine oxidase to endothelial cell oxidant production will be better defined, b) detailed mechanistic information will be available regarding the presence, reactions and regulation of specific oxidative pathways that modulate endothelial nitric
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oxide synthase expression and activity and c) new insight will be gained for prospectively devising mechanism-directed pharmacologic strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “uric acid” (or synonyms) into the search box. This search gives you access to fulltext articles. The following is a sample of items found for uric acid in the PubMed Central database: •
A QUANTITATIVE STUDY OF RECYCLING OF ISOTOPE FROM GLYCINE-1C14,[alpha]-N15 INTO VARIOUS SUBUNITS OF THE URIC ACID MOLECULE IN A NORMAL SUBJECT. by Howell RR, Speas M, Wyngaarden JB.; 1961 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=290911
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A specific enzyme defect in gout associated with overproduction of uric acid. by Kelley WN, Rosenbloom FM, Henderson JF, Seegmiller JE.; 1967 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=224540
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Anaerobic Degradation of Uric Acid by Gut Bacteria of Termites. by Potrikus CJ, Breznak JA.; 1980 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291535
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CHANGES IN SERUM AND URINARY URIC ACID WITH THE DEVELOPMENT OF SYMPTOMATIC GOUT. by Ayvazian JH, Ayvazian LF.; 1963 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=289465
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CLOSTRIDIUM ACIDI-URIDI AND CLOSTRIDIUM CYLINDROSPORUM, ORGANISMS FERMENTING URIC ACID AND SOME OTHER PURINES. by Barker HA, Beck JV.; 1942 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=373602
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Degradation of Uric Acid by Certain Aerobic Bacteria. by Rouf MA, Lomprey RF Jr.; 1968 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=252350
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Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.
With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print.
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Effect of azlocillin on uric acid levels in serum. by Ernst JA, Sy ER.; 1983 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=185384
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EFFECT OF DIETARY ANTIBIOTICS UPON COLIFORM BACTERIA AND LACTOBACILLI IN THE INTESTINAL TRACT OF URIC ACID-FED CHICKS. by Bare LN, Wiseman RF, Abbott OJ.; 1964 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=277011
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EFFECT OF URIC ACID ON RIBOFLAVINE PRODUCTION BY INTESTINAL COLIFORM BACTERIA. by Lau HS, Wiseman RF.; 1964 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=277013
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Evidence for a Postsecretory Reabsorptive Site for Uric Acid in Man. by Diamond HS, Paolino JS.; 1973 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=302414
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Ferredoxin and Formyltetrahydrofolate Synthetase: Comparative Studies with Clostridium acidiurici, Clostridium cylindrosporum, and Newly Isolated Anaerobic Uric Acid-Fermenting Strains. by Champion AB, Rabinowitz JC.; 1977 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=235603
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Germination of Clostridium cylindrosporum Spores on Medium Containing Uric Acid. by Smith M, Sullivan C.; 1989 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=202875
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Gut bacteria recycle uric acid nitrogen in termites: A strategy for nutrient conservation. by Potrikus CJ, Breznak JA.; 1981 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=319841
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IMPAIRMENT OF URIC ACID EXCRETION IN GOUT. by Lathem W, Rodnan GP.; 1962 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291125
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INTERRELATION OF URIC ACID AND ETHANOL METABOLISM IN MAN. by Lieber CS, Jones DP, Losowsky MS, Davidson CS.; 1962 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291111
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Localization and Pyrazinamide Inhibition of Distal Transtubular Movement of Uric Acid-2-C14 with a Modified Stop-Flow Technique. by Davis BB, Field JB, Rodnan GP, Kedes LH.; 1965 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=292548
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Overproduction of Uric Acid in Hypoxanthine-Guanine Phosphoribosyltransferase Deficiency CONTRIBUTION BY IMPAIRED PURINE SALVAGE. by Edwards NL, Recker D, Fox IH.; 1979 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=372033
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Petroleum Pollution Bioremediation Using Water-Insoluble Uric Acid as the Nitrogen Source. by Koren O, Knezevic V, Ron EZ, Rosenberg E.; 2003 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=201234
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Suppression of Glycine-15N Incorporation into Urinary Uric Acid by Adenine-8-13C in Normal and Gouty Subjects. by Seegmiller JE, Klinenberg JR, Miller J, Watts RW.; 1968 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=297271
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The influence of the extracellular fluid volume on the tubular reabsorption of uric acid. by Weinman EJ, Eknoyan G, Suki WN.; 1975 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=301746
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The Kinetics of Intramolecular Distribution of 15N in Uric Acid after Administration of [15N]Glycine A REAPPRAISAL OF THE SIGNIFICANCE OF PREFERENTIAL LABELING OF N-(3 + 9) OF URIC ACID IN PRIMARY GOUT. by Sperling O, Wyngaarden JB, Starmer CF.; 1973 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=302506
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THE METABOLIC DEFECT RESPONSIBLE FOR URIC ACID STONE FORMATION. by Henneman PH, Wallach S, Dempsey EF.; 1962 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=290947
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THE RENAL EXCRETION OF URIC ACID IN GOUT. by Seegmiller JE, Grayzel AI, Howell RR, Plato C.; 1962 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291015
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Therapeutic intervention in experimental allergic encephalomyelitis by administration of uric acid precursors. by Scott GS, Spitsin SV, Kean RB, Mikheeva T, Koprowski H, Hooper DC.; 2002 Dec 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=138606
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Uric Acid CHARACTERIZATION OF ITS INTERACTION WITH HUMAN SERUM ALBUMIN. by Campion DS, Bluestone R, Klinenberg JR.; 1973 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=333043
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Uric acid degradation by Bacillus fastidiosus strains. by Bongaerts GP, Vogels GD.; 1976 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=236130
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Uric Acid Is a Genuine Metabolite of Penicillium cyclopium and Stimulates the Expression of Alkaloid Biosynthesis in This Fungus. by Helbig F, Steighardt J, Roos W.; 2002 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123850
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Uric Acid is a Major Antioxidant in Human Nasal Airway Secretions. by Peden DB, Hohman R, Brown ME, Mason RT, Berkebile C, Fales HM, Kaliner MA.; 1990 Oct 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=54803
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URIC ACID METABOLISM IN PSORIASIS. by Eisen AZ, Seegmiller JE.; 1961 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=292529
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URIC ACID PRODUCTION IN GOUT. by Seegmiller JE, Grayzel AI, Laster L, Liddle L.; 1961 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=290843
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Uric acid provides an antioxidant defense in humans against oxidant- and radicalcaused aging and cancer: a hypothesis. by Ames BN, Cathcart R, Schwiers E, Hochstein P.; 1981 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=349151
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Uric acid utilization by Mycobacterium intracellulare and Mycobacterium scrofulaceum isolates. by Falkinham JO 3rd, George KL, Parker BC, Gruft H.; 1983 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=217648
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Uric acid wit. by Duffin J.; 2001 Jan 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=80690
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Uric acid, a natural scavenger of peroxynitrite, in experimental allergic encephalomyelitis and multiple sclerosis. by Hooper DC, Spitsin S, Kean RB, Champion JM, Dickson GM, Chaudhry I, Koprowski H.; 1998 Jan 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=18479
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Uric Acid-Degrading Bacteria in Guts of Termites [Reticulitermes flavipes (Kollar)]. by Potrikus CJ, Breznak JA.; 1980 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291534
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Uricosuric agents in uremic sera. Identification of indoxyl sulfata and hippuric acid. by Boumendil-Podevin EF, Podevin RA, Richet G.; 1975 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=301867
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.
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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To generate your own bibliography of studies dealing with uric acid, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “uric acid” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for uric acid (hyperlinks lead to article summaries): •
A biomimetic phospholipid/alkanethiolate bilayer immobilizing uricase and an electron mediator on an Au electrode for amperometric determination of uric acid. Author(s): Nakaminami T, Ito S, Kuwabata S, Yoneyama H. Source: Analytical Chemistry. 1999 October 1; 71(19): 4278-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10517148
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A chemiluminescence assay detecting the antioxidative effects of glutathione and uric acid on erythrocytes and hemolysates exposed to t-butyl hydroperoxide. Author(s): Gumuslu S, Serteser M, Aydin M, Yucel G. Source: J Basic Clin Physiol Pharmacol. 1997; 8(1-2): 45-56. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9363568
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A reassessment of the peroxynitrite scavenging activity of uric acid. Author(s): Whiteman M, Ketsawatsakul U, Halliwell B. Source: Annals of the New York Academy of Sciences. 2002 May; 962: 242-59. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12076979
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A selective voltammetric method for uric acid detection at beta-cyclodextrin modified electrode incorporating carbon nanotubes. Author(s): Wang Z, Wang Y, Luo G. Source: The Analyst. 2002 October; 127(10): 1353-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12430609
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Absence of an association between serum uric acid and mortality from cardiovascular disease: NIPPON DATA 80, 1980-1994. National Integrated Projects for Prospective Observation of Non-communicable Diseases and its Trend in the Aged. Author(s): Sakata K, Hashimoto T, Ueshima H, Okayama A; NIPPON DATA 80 Research Group. Source: European Journal of Epidemiology. 2001; 17(5): 461-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11855580
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Acute uric acid nephropathy by overdosage of benziodarone in a renal transplant recipient. Author(s): Franco A, Jimenez L, Torralba J, Ortega E, Trigueros M, Olivares J. Source: Nephron. 2002; 92(3): 746-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12372973
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Adaptive stress response of glutathione and uric acid metabolism in man following controlled exercise and diet. Author(s): Svensson MB, Ekblom B, Cotgreave IA, Norman B, Sjoberg B, Ekblom O, Sjodin B, Sjodin A. Source: Acta Physiologica Scandinavica. 2002 September; 176(1): 43-56. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12193218
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Altered fractional excretion of uric acid during total parenteral nutrition. Author(s): Derus CL, Levinson DJ, Bowman B, Bengoa JM, Sitrin MD. Source: The Journal of Rheumatology. 1987 October; 14(5): 978-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3123676
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Analysis of creatinine, vanilmandelic acid, homovanillic acid and uric acid in urine by micellar electrokinetic chromatography. Author(s): Shirao MK, Suzuki S, Kobayashi J, Nakazawa H, Mochizuki E. Source: J Chromatogr B Biomed Sci Appl. 1997 June 6; 693(2): 463-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9210453
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Analysis of the relationship between fasting serum uric acid and the insulin sensitivity index in a population-based sample of 380 young healthy Caucasians. Author(s): Clausen JO, Borch-Johnsen K, Ibsen H, Pedersen O. Source: European Journal of Endocrinology / European Federation of Endocrine Societies. 1998 January; 138(1): 63-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9461318
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Antidiuretic hormone and renal clearance of uric acid. Author(s): Sheikh-Hamad D, Ayus CJ. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1998 October; 32(4): 692-3; Discussion 694-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9774136
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Antiepileptic drugs reduce serum uric acid. Author(s): Krause KH, Berlit P, Schmidt-Gayk H, Schellenberg B. Source: Epilepsy Research. 1987 September; 1(5): 306-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3143553
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Aqueous humor uric acid and ascorbic acid concentrations and outcome of trabeculectomy. Author(s): Jampel HD, Moon JI, Quigley HA, Barron Y, Lam KW. Source: Archives of Ophthalmology. 1998 March; 116(3): 281-5. Erratum In: Arch Ophthalmol 1998 May; 116(5): 597. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9514479
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Are high uric acid levels in patients with early pre-eclampsia an indication for delivery? Author(s): Odendaal HJ, Pienaar ME. Source: South African Medical Journal. Suid-Afrikaanse Tydskrif Vir Geneeskunde. 1997 February; 87(2): 213-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9180815
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Ascorbic acid and uric acid levels in lung cancer patients. Author(s): Bozkir A, Simsek B, Gungort A, Torun M. Source: Journal of Clinical Pharmacy and Therapeutics. 1999 February; 24(1): 43-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10319906
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Association between serum uric acid and cardiovascular risk factors among elderly people in Taiwan. Author(s): Lai SW, Li TC, Li CI, Tan CK, Ng KC, Lai MM, Liu CS, Lin CC. Source: Kaohsiung J Med Sci. 1999 December; 15(12): 686-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10645129
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Association of a 27-bp repeat polymorphism in intron 4 of endothelial constitutive nitric oxide synthase gene with serum uric acid levels in Chinese subjects with type 2 diabetes. Author(s): Lee YJ, Chang DM, Tsai JC. Source: Metabolism: Clinical and Experimental. 2003 November; 52(11): 1448-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14624405
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Association of GYS1 and beta(3)-AR gene with postprandial hyperglycemia and serum uric acid in type 2 diabetes mellitus. Author(s): Wang G, Li Q, Niu T, Chen C, Xu X. Source: Chinese Medical Journal. 2002 September; 115(9): 1308-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12411100
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Association of serum uric acid with all-cause and cardiovascular disease mortality and incident myocardial infarction in the MONICA Augsburg cohort. World Health Organization Monitoring Trends and Determinants in Cardiovascular Diseases. Author(s): Liese AD, Hense HW, Lowel H, Doring A, Tietze M, Keil U. Source: Epidemiology (Cambridge, Mass.). 1999 July; 10(4): 391-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10401873
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AT1 blockers and uric acid metabolism: are there relevant differences? Author(s): Puig JG, Torres R, Ruilope LM. Source: Journal of Hypertension. 2002 June; 20 Suppl 5: S29-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12184060
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Beer drinking and its effect on uric acid. Author(s): Gibson T, Rodgers AV, Simmonds HA, Toseland P. Source: British Journal of Rheumatology. 1984 August; 23(3): 203-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6743968
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Behavioural and biological correlates of serum uric acid: a study of self-defence officials in Japan. Author(s): Kono S, Shinchi K, Imanishi K, Honjo S, Todoroki I. Source: International Journal of Epidemiology. 1994 June; 23(3): 517-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7960375
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Bi-enzyme reactor for electrochemical detection of low concentrations of uric acid and glucose. Author(s): Elekes O, Moscone D, Venema K, Korf J. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 1995 August 14; 239(2): 153-65. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8542653
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Bilateral obstructing ureteral uric acid stones in an infant with hereditary renal hypouricemia. Author(s): Gofrit O, Verstandig AG, Pode D. Source: The Journal of Urology. 1993 June; 149(6): 1506-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8501797
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Bilateral ureteral obstruction due to uric acid stones in association with immune hemolytic anemia. Author(s): Schroder LE, Vilter RW. Source: Archives of Internal Medicine. 1983 May; 143(5): 1020-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6679213
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Bilirubin interference with determination of creatinine, lactate, phosphorus, and uric acid on Beckman Synchron CX7. Author(s): Beyne P, Letteron P, Herve C, Roullet JB, Delacoux E. Source: Clinical Chemistry. 1996 June; 42(6 Pt 1): 988-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8665703
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Bilirubin interference with determination of uric acid, cholesterol, and triglycerides in commercial peroxidase-coupled assays, and the effect of ferrocyanide. Author(s): Spain MA, Wu AH. Source: Clinical Chemistry. 1986 March; 32(3): 518-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3948397
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Bilirubin interference with uric acid assay in a Hycel: a look at azino uric acid. Author(s): Davidson DC, Garfield HJ, Maney F. Source: Clinical Chemistry. 1984 April; 30(4): 584-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6705210
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Bilirubin interferes with uric acid determinations involving peroxidase-mediated reactions. Author(s): Masson P, Lindahl I. Source: Clinical Chemistry. 1984 March; 30(3): 493. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6697512
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Bioassay of aldosterone antagonists in normal human subjects: a relationship between the level of plasma uric acid before treatment and apparent drug responses. Author(s): Ramsay LE, Hessian P, Tidd MJ. Source: British Journal of Clinical Pharmacology. 1975 June; 2(3): 271-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1234508
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Biochemical analysis of human seminal plasma. II. Protein, non-protein nitrogen, urea, uric acid and creatine. Author(s): Srivastava A, Chopra SK, Dasgupta PR. Source: Andrologia. 1984 May-June; 16(3): 265-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6465552
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Biochemical changes of the synovial liquid in corpses with regard to the cause of death. 1: Calcium, inorganic phosphorus, glucose, cholesterol, urea nitrogen, uric acid, proteins, and albumin. Author(s): More DS, Arroyo MC. Source: J Forensic Sci. 1985 April; 30(2): 541-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3998700
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Biochemical profile of idiopathic uric acid nephrolithiasis. Author(s): Pak CY, Sakhaee K, Peterson RD, Poindexter JR, Frawley WH. Source: Kidney International. 2001 August; 60(2): 757-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11473659
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Biorhythm in the renal excretion of electrolytes and uric acid in healthy subjects. Author(s): Grigoleit HG, Sorgel F. Source: South African Medical Journal. Suid-Afrikaanse Tydskrif Vir Geneeskunde. 1980 December 6; 58(23): 933-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7444690
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Biotransformation and uric acid lowering effect of benzbromarone in patients with liver cirrhosis - evidence for active benzbromarone metabolites? Author(s): Walter-Sack I, de Vries JX, von Bubnoff A, Pfleilschifter V, Raedsch R. Source: European Journal of Medical Research. 1995 October 16; 1(1): 16-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9392688
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Blood groups, serum cholesterol, serum uric acid, blood pressure, and obesity in adolescents. Author(s): Gillum RF. Source: Journal of the National Medical Association. 1991 August; 83(8): 682-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1956079
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Blood lipids, lipoproteins, apoproteins, and uric acid in men fed diets containing fructose or high-amylose cornstarch. Author(s): Reiser S, Powell AS, Scholfield DJ, Panda P, Ellwood KC, Canary JJ. Source: The American Journal of Clinical Nutrition. 1989 May; 49(5): 832-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2497634
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Blood uric acid as a pointer to the diagnosis of molybdenum cofactor deficiency. Author(s): Coskun T, Yetuk M, Yurdakok M, Tekinalp G. Source: Acta Paediatrica (Oslo, Norway : 1992). 1998 June; 87(6): 714-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9686674
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Blood uric acid level and IQ: a study in twin families. Author(s): Inouye E, Park KS, Asaka A. Source: Acta Genet Med Gemellol (Roma). 1984; 33(2): 237-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6540956
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Body weight, serum uric acid and lipid profile one year after spinal cord injury. Author(s): Wong PY, Wang YC, Chu NK, Tang FT, Wong MK. Source: Chang Gung Med J. 2001 September; 24(9): 569-75. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11725627
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Catalytic oxidation of uric acid at the polyglycine chemically modified electrode and its trace determination. Author(s): Yu AM, Zhang HL, Chen HY. Source: The Analyst. 1997 August; 122(8): 839-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9338990
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Cerebrospinal fluid hypoxanthine, xanthine and uric acid levels may reflect glutamate-mediated excitotoxicity in different neurological diseases. Author(s): Stover JF, Lowitzsch K, Kempski OS. Source: Neuroscience Letters. 1997 November 28; 238(1-2): 25-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9464646
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Changes in serum uric acid during treatment with antihypertensive drugs. Author(s): Pedersen OL, Krusell LR. Source: Dan Med Bull. 1987 December; 34 Suppl 1: 17-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3436169
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Changes in urinary uric acid excretion in obstructive sleep apnea before and after therapy with nasal continuous positive airway pressure. Author(s): Sahebjani H. Source: Chest. 1998 June; 113(6): 1604-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9631800
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Chemiluminescence assay for uric acid in human serum and urine using flowinjection with immobilized reagents technology. Author(s): Song ZH, Hou S. Source: Analytical and Bioanalytical Chemistry. 2002 January; 372(2): 327-32. Epub 2001 December 20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11936107
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Chemiluminescence biosensor chip based on a microreactor using carrier air flow for determination of uric acid in human serum. Author(s): Lv Y, Zhang Z, Chen F. Source: The Analyst. 2002 September; 127(9): 1176-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12375839
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Circadian relationship of serum uric acid and nitric oxide. Author(s): Kanabrocki EL, Third JL, Ryan MD, Nemchausky BA, Shirazi P, Scheving LE, McCormick JB, Hermida RC, Bremner WF, Hoppensteadt DA, Fareed J, Olwin JH. Source: Jama : the Journal of the American Medical Association. 2000 May 3; 283(17): 2240-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10807381
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Clinical and biochemical aspects of uric acid overproduction. Author(s): Garcia Puig J, Mateos FA. Source: Pharmacy World & Science : Pws. 1994 April 15; 16(2): 40-54. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8032341
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Clinical and biochemical features of uric acid nephrolithiasis. Author(s): Ito H, Kotake T, Nomura K, Masai M. Source: European Urology. 1995; 27(4): 324-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7656911
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Clinical and biochemical presentation of gouty diathesis: comparison of uric acid versus pure calcium stone formation. Author(s): Khatchadourian J, Preminger GM, Whitson PA, Adams-Huet B, Pak CY. Source: The Journal of Urology. 1995 November; 154(5): 1665-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7563316
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Close correlation between visceral fat accumulation and uric acid metabolism in healthy men. Author(s): Takahashi S, Yamamoto T, Tsutsumi Z, Moriwaki Y, Yamakita J, Higashino K. Source: Metabolism: Clinical and Experimental. 1997 October; 46(10): 1162-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9322800
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Comparative analysis of biochemical parameters for differentiation of pleural exudates from transudates Light's criteria, cholesterol, bilirubin, albumin gradient, alkaline phosphatase, creatine kinase, and uric acid. Author(s): Metintas M, Alatas O, Alatas F, Colak O, Ozdemir N, Erginel S. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 1997 August 29; 264(2): 149-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9293374
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Comparative effects of losartan and irbesartan on serum uric acid in hypertensive patients with hyperuricaemia and gout. Author(s): Wurzner G, Gerster JC, Chiolero A, Maillard M, Fallab-Stubi CL, Brunner HR, Burnier M. Source: Journal of Hypertension. 2001 October; 19(10): 1855-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11593107
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Comparative effects of losartan and irbesartan on serum uric acid in hypertensive patients with hyperuricemia and gout. Author(s): Liberopoulos E, Christides D, Elisaf M. Source: Journal of Hypertension. 2002 February; 20(2): 347. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11821722
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Concentrations of nucleotides, nucleosides, purine bases, oxypurines, uric acid, and neuron-specific enolase in the cerebrospinal fluid of children with sepsis. Author(s): Rodriguez-Nunez A, Cid E, Rodriguez-Garcia J, Camina F, Rodriguez-Segade S, Castro-Gago M. Source: Journal of Child Neurology. 2001 September; 16(9): 704-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11575617
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Correlations of serum lipids, uric acid, and albumin among mothers, offspring, and siblings in Taipei, Taiwan. Author(s): Cheng HH, Yang SH, Chen C, Chiang MS. Source: Acta Paediatr Taiwan. 1999 July-August; 40(4): 225-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10910618
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Covalent modification of glassy carbon electrode with glutamic acid for simultaneous determination of uric acid and ascorbic acid. Author(s): Zhang L, Lin X. Source: The Analyst. 2001 March; 126(3): 367-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11284341
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Creatine kinase and uric acid: early warning for metabolic imbalance resulting from disorders of fatty acid oxidation. Author(s): Marsden D, Nyhan WL, Barshop BA. Source: European Journal of Pediatrics. 2001 October; 160(10): 599-602. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11686503
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Cutaneous microdialysis of uric acid level in the dermis: modification of in vitro recovery. Author(s): Lee YS, Kim SJ, Oh JK, Chung JH, Eun HC. Source: Acta Dermato-Venereologica. 2003; 83(1): 10-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12636015
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Cyclosporine A-related proximal tubular dysfunction: impaired handling of uric acid. Author(s): Versluis DJ, Wenting GJ, Jeekel J, Weimar W. Source: Transplantation Proceedings. 1987 October; 19(5): 4029-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3313991
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Decrease in urinary uric acid concentrations after urine storage. Author(s): Moriwaki Y, Yamamoto T, Takahashi S, Yamakita J, Tsutsumi Z, Hada T. Source: Advances in Experimental Medicine and Biology. 2000; 486: 393-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11783522
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Decreased first trimester uric acid production in future preeclamptic patients. Author(s): de Jong CL, Paarlberg KM, van Geijn HP, Schipper EJ, Bast A, Kostense PJ, Dekker GA. Source: Journal of Perinatal Medicine. 1997; 25(4): 347-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9350605
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Decreased triglyceride levels with low calorie diet and increased renal excretion of uric acid in hyperuricaemic-hyperlipidaemic patients. Author(s): Tinahones FJ, Soriguer FJ, Collantes E, Perez-Lindon G, Sanchez Guijo P, Lillo JA. Source: Annals of the Rheumatic Diseases. 1995 July; 54(7): 609-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7668911
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Decreases in serum uric acid by amelioration of insulin resistance in overweight hypertensive patients: effect of a low-energy diet and an insulin-sensitizing agent. Author(s): Tsunoda S, Kamide K, Minami J, Kawano Y. Source: American Journal of Hypertension : Journal of the American Society of Hypertension. 2002 August; 15(8): 697-701. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12160192
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Definitive characterization of uric acid as an interferent in peroxidase indicator reactions and a proposed mechanism of action. Author(s): Fleming JK, Gadsden RH Sr, Kabbani I. Source: Clinical Biochemistry. 1988 January; 21(1): 27-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3345596
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Deproteinizing methods evaluated for determination of uric acid in serum by reversed-phase liquid chromatography with ultraviolet detection. Author(s): Sakuma R, Nishina T, Kitamura M. Source: Clinical Chemistry. 1987 August; 33(8): 1427-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3608161
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Determination and separation of allantoin, uric acid, hypoxanthine, and xanthine by capillary zone electrophoresis. Author(s): Pizzichini M, Arezzini L, Billarelli C, Carlucci F, Terzuoli L. Source: Advances in Experimental Medicine and Biology. 1998; 431: 797-800. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9598173
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Determination of ascorbic acid and uric acid in plasma by high-performance liquid chromatography. Author(s): Ross MA. Source: Journal of Chromatography. B, Biomedical Applications. 1994 July 1; 657(1): 197200. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7952068
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Determination of calcium oxalate (mono- and dihydrate) in mixtures with magnesium ammonium phosphate or uric acid: the use of simultaneous thermal analysis in urinary calculi. Author(s): Kaloustian J, El-Moselhy TF, Portugal H. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 2003 August; 334(1-2): 117-29. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12867282
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Determination of uric acid in human saliva by high-performance liquid chromatography with amperometric electrochemical detection. Author(s): Inoue K, Namiki T, Iwasaki Y, Yoshimura Y, Nakazawa H. Source: Journal of Chromatography. B, Analytical Technologies in the Biomedical and Life Sciences. 2003 February 25; 785(1): 57-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12535838
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Determination of uric acid in human serum by capillary electrophoresis with polarity reversal and electrochemical detection. Author(s): Boughton JL, Robinson BW, Strein TG. Source: Electrophoresis. 2002 November; 23(21): 3705-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12432532
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Determination of uric acid in scalp hair for non-invasive evaluation of uricemic controls in hyperuricemia. Author(s): Kobayashi K, Morioka Y, Isaka Y, Tozawa T. Source: Biological & Pharmaceutical Bulletin. 1998 April; 21(4): 398-400. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9586580
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Diagnostic value of uric acid to differentiate transudates and exudates. Author(s): Uzun K, Vural H, Ozer F, Imecik O. Source: Clinical Chemistry and Laboratory Medicine : Cclm / Fescc. 2000 July; 38(7): 661-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11028772
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Differentiation of uric acid from dihydroxyadenine stones. Author(s): Maddocks JL, Reed T. Source: Lancet. 1987 December 19; 2(8573): 1466. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2892026
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Discrete analysis of serum uric acid with immobilized uricase and peroxidase. Author(s): Bhargava AK, Lal H, Pundir CS. Source: Journal of Biochemical and Biophysical Methods. 1999 May 13; 39(3): 125-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10392568
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Disposition and uric acid lowering effect of oxipurinol: comparison of different oxipurinol formulations and allopurinol in healthy individuals. Author(s): Walter-Sack I, de Vries JX, Kutschker C, Ittensohn A, Voss A. Source: European Journal of Clinical Pharmacology. 1995; 49(3): 215-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8665998
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Disturbances of the excretion of uric acid in workers at high risk from lead exposure. Author(s): Karastanev I, Atanassov N, Vlaikova E, Klissourova V, Katsarova S, Mihailova Z. Source: Folia Med (Plovdiv). 1988; 30(1): 23-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3152066
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DNA breakage by uric acid and Cu(II): binding of uric acid to DNA and biological activity of the reaction. Author(s): Shamsi FA, Husain S, Hadi SM. Source: Journal of Biochemical Toxicology. 1996; 11(2): 67-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8884466
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Does industrial environment influence the prevalence of arterial hypertension, plasma cholesterol and uric acid concentration and activity of the renin-aldosterone system? Author(s): Wiecek A, Kokot F. Source: Przegl Lek. 1996; 53(4): 356-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8711191
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D-tagatose, a stereoisomer of D-fructose, increases blood uric acid concentration. Author(s): Buemann B, Toubro S, Holst JJ, Rehfeld JF, Bibby BM, Astrup A. Source: Metabolism: Clinical and Experimental. 2000 August; 49(8): 969-76. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10954012
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Editorial comment--Elevated uric acid and ischemic stroke: accumulating evidence that it is injurious and not neuroprotective. Author(s): Kanellis J, Johnson RJ. Source: Stroke; a Journal of Cerebral Circulation. 2003 August; 34(8): 1956-7. Epub 2003 July 03. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12843345
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Effect of aging on serum uric acid levels: longitudinal changes in a large Japanese population group. Author(s): Kuzuya M, Ando F, Iguchi A, Shimokata H. Source: The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 2002 October; 57(10): M660-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12242321
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Effect of atorvastatin on serum uric acid levels. Author(s): Kakafika A, Tsimihodimos V, Elisaf M. Source: Atherosclerosis. 2001 September; 158(1): 255. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11550660
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Effect of fenofibrate on serum uric acid levels. Author(s): Liamis G, Bairaktari ET, Elisaf MS. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1999 September; 34(3): 594. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10469875
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Effect of fetal number on maternal serum uric acid concentration. Author(s): Cohen SB, Kreiser D, Erez I, Kogan I, Seidman DS, Schiff E. Source: American Journal of Perinatology. 2002 August; 19(6): 291-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12357419
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Effect of losartan and furosemide on the urinary excretion of oxypurinol and uric acid. Author(s): Yamamoto T, Moriwaki Y, Takahashi S, Tsutsumi Z, Hada T. Source: Advances in Experimental Medicine and Biology. 2000; 486: 185-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11783482
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Effect of tea and coffee consumption on serum uric acid levels by liquidchromatographic and uricase methods. Author(s): Yuan SC, Wang CJ, Kuo HW, Maa MC, Hsieh YS. Source: Bulletin of Environmental Contamination and Toxicology. 2000 September; 65(3): 300-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10903352
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Effect of the angiotensin II receptor antagonist losartan on uric acid and oxypurine metabolism in healthy subjects. Author(s): Hamada T, Hisatome I, Kinugasa Y, Matsubara K, Shimizu H, Tanaka H, Furuse M, Sonoyama K, Yamamoto Y, Ohtahara A, Igawa O, Shigemasa C, Yamamoto T. Source: Intern Med. 2002 October; 41(10): 793-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12412998
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Effect of urine storage on urinary uric acid concentrations. Author(s): Yamakita J, Yamamoto T, Moriwaki Y, Takahashi S, Tsutsumi Z, Hada T. Source: Annals of Clinical Biochemistry. 2000 May; 37 ( Pt 3): 355-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10817251
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Effect of valsartan on renal handling of uric acid in healthy subjects. Author(s): Gonzalez-Ortiz M, Mora-Martinez JM, Martinez-Abundis E, Balcazar-Munoz BR. Source: Journal of Nephrology. 2000 March =april; 13(2): 126-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10858975
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Effects of combination treatment using anti-hyperuricaemic agents with fenofibrate and/or losartan on uric acid metabolism. Author(s): Takahashi S, Moriwaki Y, Yamamoto T, Tsutsumi Z, Ka T, Fukuchi M. Source: Annals of the Rheumatic Diseases. 2003 June; 62(6): 572-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12759298
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Effects of losartan/diuretic combination treatment on serum uric acid levels in hypertensive patients. Author(s): Milionis HJ, Nikas S, Elisaf MS. Source: The American Journal of Cardiology. 2001 November 1; 88(9): 1084. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11704020
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Efficacy of benzbromarone compared to allopurinol in lowering serum uric acid level in hyperuricemic patients. Author(s): Hanvivadhanakul P, Akkasilpa S, Deesomchok U. Source: J Med Assoc Thai. 2002 June; 85 Suppl 1: S40-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12188443
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Elevated serum uric acid levels are associated with diastolic dysfunction in patients with dilated cardiomyopathy. Author(s): Cicoira M, Zanolla L, Rossi A, Golia G, Franceschini L, Brighetti G, Zeni P, Zardini P. Source: American Heart Journal. 2002 June; 143(6): 1107-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12075270
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Elevated serum uric acid. Author(s): Nestler JE, Clore JN, Blackard WG. Source: Diabetologia. 1988 February; 31(2): 127. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3282954
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Elevated serum uric acid--a facet of hyperinsulinaemia. Author(s): Modan M, Halkin H, Karasik A, Lusky A. Source: Diabetologia. 1987 September; 30(9): 713-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3322912
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Estimation of plasma uric acid in pregnancy induced hypertension (PIH). Is the test still relevant? Author(s): Wakwe VC, Abudu OO. Source: Afr J Med Med Sci. 1999 September-December; 28(3-4): 155-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11205821
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Evaluation of determination of uric acid in serum and whole blood with the Reflotron. Author(s): Cattozzo G, Franzini C, Hubbuch A, Tritschler W. Source: Clinical Chemistry. 1988 February; 34(2): 414-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2830055
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Excretion of tamm-horsfall protein in patients with uric acid stones. Author(s): Bichler K, Mittermuller B, Strohmaier WL, Feil G, Eipper E. Source: Urologia Internationalis. 1999; 62(2): 87-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10461109
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Experimental meningitis in the rat: protection by uric acid at human physiological blood concentrations. Author(s): Kastenbauer S, Koedel U, Becker BF, Pfister HW. Source: European Journal of Pharmacology. 2001 August 10; 425(2): 149-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11502281
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Factor VIII related antigen/coagulant activity ratio as a predictor of fetal growth retardation: a comparison with hormone and uric acid measurements. Author(s): Whigham KA, Howie PW, Shah MM, Prentice CR. Source: British Journal of Obstetrics and Gynaecology. 1980 September; 87(9): 797-803. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6775686
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Factors influencing the serum uric acid level. A study based on a population survey in Hisayama town, Kyushu, Japan. Author(s): Okada M, Takeshita M, Ueda K, Omae T, Hirota Y. Source: J Chronic Dis. 1980; 33(10): 607-12. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7410521
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Familial hypouricaemia associated with renal tubular uricosuria and uric acid calculi: case report. Author(s): Hedley JM, Phillips PJ. Source: Journal of Clinical Pathology. 1980 October; 33(10): 971-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7430362
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Familial hypouricemia due to isolated renal tubular defect. Attenuated response of uric acid clearance to probenecid and pyrazinamide. Author(s): Benjamin D, Sperling O, Weinberger A, Pinkhas J, de Vries A. Source: Nephron. 1977; 18(4): 220-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=854144
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Familial renal hypouricaemia: two additional cases with uric acid lithiasis. Author(s): Frank M, Many M, Sperling O. Source: British Journal of Urology. 1979 April; 51(2): 88-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=465979
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Familial renal hypouricemia with intact reabsorption of uric acid. Author(s): Nakajima H, Gomi M, Iida S, Kono N, Moriwaki K, Tarui S. Source: Nephron. 1987; 45(1): 40-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3808147
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Family resemblance for serum uric acid in a Jerusalem sample of families. Author(s): Friedlander Y, Kark JD, Stein Y. Source: Human Genetics. 1988 May; 79(1): 58-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3366463
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Family resemblances in serum uric acid level. Author(s): Ahern FM, Johnson RC, Ashton GC. Source: Behavior Genetics. 1980 May; 10(3): 303-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7213306
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Fasting insulin and uric acid levels but not indices of iron metabolism are independent predictors of non-alcoholic fatty liver disease. A case-control study. Author(s): Lonardo A, Loria P, Leonardi F, Borsatti A, Neri P, Pulvirenti M, Verrone AM, Bagni A, Bertolotti M, Ganazzi D, Carulli N; POLI.ST.E.N.A. Study Group. Policentrica Steatosi Epatica Non Alcolica. Source: Dig Liver Dis. 2002 March; 34(3): 204-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11990393
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Fasting plasma glucose, uric acid, and triglycerides as predictors of the ratio of total cholesterol to HDL-C. Author(s): Philippi T, Barrett-Connor E. Source: American Journal of Clinical Pathology. 1984 September; 82(3): 329-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6465099
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Female gout. Clinical spectrum and uric acid metabolism. Author(s): Puig JG, Michan AD, Jimenez ML, Perez de Ayala C, Mateos FA, Capitan CF, de Miguel E, Gijon JB. Source: Archives of Internal Medicine. 1991 April; 151(4): 726-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2012455
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Fetal and maternal concentrations of uric acid and oxypurines during labor and post partum. Author(s): Wallenburg HC, van Kreel BK. Source: American Journal of Obstetrics and Gynecology. 1980 February 15; 136(4): 513-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7355932
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Fifteen-year experience with Magurlit in the treatment of patients with uric acid calculi. Author(s): Frang D. Source: Ther Hung. 1986; 34(1): 26-34. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3447298
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Folic acid, xanthine oxidase, and uric acid. Author(s): Flouvier B, Devulder B. Source: Annals of Internal Medicine. 1978 February; 88(2): 269. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=626464
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Four methods for determining uric acid compared with a candidate reference method. Author(s): Elin RJ, Johnson E, Chesler R. Source: Clinical Chemistry. 1982 October; 28(10): 2098-100. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7127737
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Fractional excretion of trace lithium and uric acid in acute renal failure. Author(s): Steinhauslin F, Burnier M, Magnin JL, Munafo A, Buclin T, Diezi J, Biollaz J. Source: Journal of the American Society of Nephrology : Jasn. 1994 January; 4(7): 142937. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8161725
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Fragmentation of uric acid calculi with the holmium: YAG laser produces cyanide. Author(s): Zagone RL, Waldmann TM, Conlin MJ. Source: Lasers in Surgery and Medicine. 2002; 31(4): 230-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12355566
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Free radicals, uric acid, and human disease. Author(s): Proctor PH. Source: Free Radical Biology & Medicine. 1996; 20(5): 761-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8846925
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Furosemide-induced increase in urinary and peritoneal excretion of uric acid during peritoneal dialysis in patients with chronic uremia. Author(s): Grzegorzewska A, Baczyk K. Source: Artificial Organs. 1983 February; 7(1): 147. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6838404
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Furosemide-induced increase in urinary and peritoneal excretion of uric acid during peritoneal dialysis in patients with chronic uremia. Author(s): Grzegorzewska A, Baczyk K. Source: Artificial Organs. 1982 May; 6(2): 220-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7125968
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Gender difference in the concentration of the antioxidant uric acid in human nasal lavage. Author(s): Housley DG, Eccles R, Richards RJ. Source: Acta Oto-Laryngologica. 1996 September; 116(5): 751-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8908255
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Gender differences in the relationships of serum uric acid with fasting serum insulin and plasma glucose in patients without diabetes. Author(s): Chou P, Lin KC, Lin HY, Tsai ST. Source: The Journal of Rheumatology. 2001 March; 28(3): 571-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11296961
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Genetic influence on serum creatinine, urea and uric acid. Author(s): Vij SC, Maitrya BB, Mali SL. Source: Indian J Physiol Pharmacol. 1978 July-September; 22(3): 324. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=721257
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Glycosaminoglycans, uric acid and calcium oxalate urolithiasis. Author(s): Grases F, Costa-Bauza A, March JG, Masarova L. Source: Urological Research. 1991; 19(6): 375-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1759332
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Gout and its relation to lipid metabolism. I. Serum uric acid, lipid, and lipoprotein levels in gout. Author(s): Mielants H, Veys EM, de Weerdt A. Source: Annals of the Rheumatic Diseases. 1973 November; 32(6): 501-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4357330
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Gout and its relation to lipid metabolism. II. Correlations between uric acid, lipid, and lipoprotein levels in gout. Author(s): Mielants H, Veys EM, de Weerdt A. Source: Annals of the Rheumatic Diseases. 1973 November; 32(6): 506-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4357331
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Gout and serum uric acid levels in the Cotswolds. Author(s): Badley EM, Meyrick JS, Wood PH. Source: Rheumatol Rehabil. 1978 August; 17(3): 133-142. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=705169
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Gout and uric acid excretion. Author(s): Paulsen TP. Source: American Family Physician. 1992 January; 45(1): 48, 50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1728101
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Gout and uric acid nephropathy: some new aspects in diagnosis and treatment. Author(s): Loffler W, Simmonds HA, Grobner W. Source: Klin Wochenschr. 1983 December 15; 61(24): 1233-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6689351
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Gout as a complication of Bartter's syndrome. A possible role for alkalosis in the decreased clearance of uric acid. Author(s): Meyer WJ 3rd, Gill JR Jr, Bartter FC. Source: Annals of Internal Medicine. 1975 July; 83(1): 56-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1147437
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Gout, uric acid and purine metabolism in paediatric nephrology. Author(s): Cameron JS, Moro F, Simmonds HA. Source: Pediatric Nephrology (Berlin, Germany). 1993 February; 7(1): 105-18. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8439471
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Gout, uric acid and renal disease. Author(s): Emmerson BT. Source: The Medical Journal of Australia. 1976 March 20; 1(12): 403-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1272125
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Gout, uric acid metabolism, and crystal-induced inflammation. Author(s): Weinberger A. Source: Current Opinion in Rheumatology. 1995 July; 7(4): 359-63. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7547116
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Gout, uric acid, albumin, and aging. Author(s): Seaton K. Source: Journal of the National Medical Association. 1996 August; 88(8): 473, 486. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8803426
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Gout: diet and uric acid revisited. Author(s): Snaith ML. Source: Lancet. 2001 August 18; 358(9281): 525. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11520519
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Gouty arthritis and uric acid metabolism. Author(s): Wise CM, Agudelo CA. Source: Current Opinion in Rheumatology. 1996 May; 8(3): 248-54. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8796986
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Gouty arthropathy and synovial uric acid. Author(s): Culora G, Gallagher PJ. Source: British Journal of Rheumatology. 1992 November; 31(11): 791-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1450812
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Haemodynamic correlates and prognostic significance of serum uric acid in adult patients with Eisenmenger syndrome. Author(s): Oya H, Nagaya N, Satoh T, Sakamaki F, Kyotani S, Fujita M, Nakanishi N, Miyatake K. Source: Heart (British Cardiac Society). 2000 July; 84(1): 53-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10862589
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Hepatic metabolites and uric acid excretion in fructose-1,6-diphosphatase deficiency. Author(s): Velazquez A, DeCespedes C, DeVivo DC, Costin G, Shaw KN. Source: Journal of Inherited Metabolic Disease. 1988; 11(3): 303-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3148073
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High total antioxidant activity and uric acid in tracheobronchial aspirate fluid of preterm infants during oxidative stress: an adaptive response to hyperoxia? Author(s): Vento G, Mele MC, Mordente A, Romagnoli C, Matassa PG, Zecca E, Zappacosta B, Persichilli S. Source: Acta Paediatrica (Oslo, Norway : 1992). 2000 March; 89(3): 336-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10772283
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High uric acid: a metabolic marker of coronary heart disease among alcohol abstainers. Author(s): Iribarren C, Sharp DS, Curb JD, Yano K. Source: Journal of Clinical Epidemiology. 1996 June; 49(6): 673-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8656229
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High urinary excretion of uric acid combined with high excretion of calcium links kidney stone disease to familial hypertension. Author(s): Tisler A, Pierratos A, Honey JD, Bull SB, Rosivall L, Logan AG. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 2002 February; 17(2): 253-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11812875
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High-dose methylprednisolone therapy in multiple sclerosis increases serum uric acid levels. Author(s): Toncev G, Milicic B, Toncev S, Samardzic G. Source: Clinical Chemistry and Laboratory Medicine : Cclm / Fescc. 2002 May; 40(5): 505-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12113297
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Highly sensitive flow detection of uric acid based on an intermediate regeneration of uricase. Author(s): Hasebe Y, Nawa K, Ujita S, Uchiyama S. Source: The Analyst. 1998 August; 123(8): 1775-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10071392
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High-protein diets in hyperlipidemia: effect of wheat gluten on serum lipids, uric acid, and renal function. Author(s): Jenkins DJ, Kendall CW, Vidgen E, Augustin LS, van Erk M, Geelen A, Parker T, Faulkner D, Vuksan V, Josse RG, Leiter LA, Connelly PW. Source: The American Journal of Clinical Nutrition. 2001 July; 74(1): 57-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11451718
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Hirsutism-skeletal dysplasia-mental retardation syndrome with abnormal face and a uric acid metabolism disorder. Author(s): Wiedemann HR, Oldigs HD, Oppermann HC, Oster O. Source: American Journal of Medical Genetics. 1993 June 1; 46(4): 403-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8357012
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Holmium:YAG lithotripsy of uric acid calculi. Author(s): Teichman JM, Champion PC, Wollin TA, Denstedt JD. Source: The Journal of Urology. 1998 December; 160(6 Pt 1): 2130-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9817338
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Holmium:YAG lithotripsy: photothermal mechanism converts uric acid calculi to cyanide. Author(s): Teichman JM, Vassar GJ, Glickman RD, Beserra CM, Cina SJ, Thompson IM. Source: The Journal of Urology. 1998 August; 160(2): 320-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9679869
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Hormone replacement therapy and serum uric acid. Author(s): Kashyap AS, Kashyap S. Source: Lancet. 1999 November 6; 354(9190): 1643-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10560698
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Hormone replacement therapy and serum uric acid. Author(s): Ovalle F, Bell DS. Source: Lancet. 1999 November 6; 354(9190): 1643; Author Reply 1644. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10560697
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Hyperinsulinemia and uric acid clearance. Author(s): Gaut ZN. Source: Jama : the Journal of the American Medical Association. 1992 March 18; 267(11): 1469. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1538534
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Hypertension aggregates in families of kidney stone patients with high urinary excretion of uric acid. Author(s): Tisler A, Pierratos A, Honey JD, Bull SB, Logan AG. Source: Journal of Hypertension. 1999 December; 17(12 Pt 2): 1853-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10703880
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Hyperuricemia and uric acid nephropathy. Author(s): Dykman D, Simon EE. Source: Archives of Internal Medicine. 1987 July; 147(7): 1341-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3606290
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Hypouricemia and an increased clearance of uric acid are observed in liver diseases? Author(s): Pelatti A, Quaratino CP, D'Amario C, Tentarelli R, Sforza GR, Giacomello A. Source: Advances in Experimental Medicine and Biology. 1994; 370: 57-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7660971
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Hypouricemia in severely disabled children II: influence of elemental enteral nutrition on the serum uric acid levels. Author(s): Yoshikawa H, Yamazaki S, Abe T. Source: Brain & Development. 2004 January; 26(1): 43-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14729414
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Hypoxanthine, uric acid and allantoin as indicators of in vivo free radical reactions. Description of a HPLC method and human brain microdialysis data. Author(s): Marklund N, Ostman B, Nalmo L, Persson L, Hillered L. Source: Acta Neurochirurgica. 2000; 142(10): 1135-41; Discussion 1141-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11129536
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Hypoxanthine, xanthine, and uric acid concentrations in plasma, cerebrospinal fluid, vitreous humor, and urine in piglets subjected to intermittent versus continuous hypoxemia. Author(s): Stoltenberg L, Rootwelt T, Oyasaeter S, Rognum TO, Saugstad OD. Source: Pediatric Research. 1993 December; 34(6): 767-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8108190
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Identification of a new candidate locus for uric acid nephrolithiasis. Author(s): Ombra MN, Forabosco P, Casula S, Angius A, Maestrale G, Petretto E, Casu G, Colussi G, Usai E, Melis P, Pirastu M. Source: American Journal of Human Genetics. 2001 May; 68(5): 1119-29. Epub 2001 April 17. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11309680
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Identification of a novel gene and a common variant associated with uric acid nephrolithiasis in a Sardinian genetic isolate. Author(s): Gianfrancesco F, Esposito T, Ombra MN, Forabosco P, Maninchedda G, Fattorini M, Casula S, Vaccargiu S, Casu G, Cardia F, Deiana I, Melis P, Falchi M, Pirastu M. Source: American Journal of Human Genetics. 2003 June; 72(6): 1479-91. Epub 2003 May 09. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12740763
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Identification of allantoin, uric acid, and indoxyl sulfate as biochemical indicators of filth in food packaging by LC. Author(s): Carlson M, Thompson RD. Source: J Aoac Int. 2001 May-June; 84(3): 782-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11417643
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Identification of uric acid and xanthine oxidase in atherosclerotic plaque. Author(s): Patetsios P, Song M, Shutze WP, Pappas C, Rodino W, Ramirez JA, Panetta TF. Source: The American Journal of Cardiology. 2001 July 15; 88(2): 188-91, A6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11448423
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Impaired kinetic properties of hypoxanthine-guanine phosphoribosyl transferase as a cause of uric acid nephropathy in early infancy. Author(s): Kerem E, Branski D, Gross-Kieselstein E, Hurvitz H, Abrahamov A, Pollack Y. Source: European Journal of Pediatrics. 1987 November; 146(6): 595-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3428293
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Increase in serum levels of uric acid, an endogenous antioxidant, under treatment with glatiramer acetate for multiple sclerosis. Author(s): Constantinescu CS, Freitag P, Kappos L. Source: Multiple Sclerosis (Houndmills, Basingstoke, England). 2000 December; 6(6): 378-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11212132
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Increase in serum uric acid is selectively associated with stroke in type 2 diabetes. Author(s): Seghieri G, Moruzzo D, Fascetti S, Bambini C, Anichini R, De Bellis A, Alviggi L, Franconi F. Source: Diabetes Care. 2002 June; 25(6): 1095. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12032120
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Increased expression of monocyte chemoattractant protein-1 (MCP-1) by renal epithelial cells in culture on exposure to calcium oxalate, phosphate and uric acid crystals. Author(s): Umekawa T, Chegini N, Khan SR. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 2003 April; 18(4): 664-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12637633
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Increased uric acid clearance in the syndrome of inappropriate secretion of antidiuretic hormone. Author(s): Sonnenblick M, Rosin A. Source: Isr J Med Sci. 1988 January; 24(1): 20-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3346144
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Influence of purine intake on uric acid excretion in infants fed soy infant formulas. Author(s): Kuchan MJ, Ostrom KM, Smith C, Hu PE. Source: Journal of the American College of Nutrition. 2000 February; 19(1): 16-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10682871
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Interference of the chemotherapeutic agent etoposide with the direct phosphotungstic acid method for uric acid. Author(s): Matheke ML, Kessler G, Chan KM. Source: Clinical Chemistry. 1987 November; 33(11): 2109-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3479271
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Intermittent versus continuous alkaline therapy for uric acid stones and ureteral stones of uncertain composition. Author(s): Rodman JS. Source: Urology. 2002 September; 60(3): 378-82. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12350465
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Intragastric ascorbic but not uric acid is depleted in relation with the increased pH in patients with atrophic body gastritis and H. pylori gastritis. Author(s): Capurso G, Ricci R, Panzuto F, Baccini F, Passi S, Di Giulio E, Delle Fave G, Annibale B. Source: Helicobacter. 2003 August; 8(4): 300-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12950602
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Inverse association between coffee drinking and serum uric acid concentrations in middle-aged Japanese males. Author(s): Kiyohara C, Kono S, Honjo S, Todoroki I, Sakurai Y, Nishiwaki M, Hamada H, Nishikawa H, Koga H, Ogawa S, Nakagawa K. Source: The British Journal of Nutrition. 1999 August; 82(2): 125-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10743484
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Investigation of serum calcium, phosphorus, albumine uric acid and lipid parameters in sportsmen and sedanters. Author(s): Turgut G, Genc O, Kaptanoglu B. Source: Acta Physiol Pharmacol Ther Latinoam. 1999; 49(3): 184-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10797858
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Is raised serum uric acid a cause of cardiovascular disease or death? Author(s): Dobson A. Source: Lancet. 1999 November 6; 354(9190): 1578. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10560670
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Is serum uric acid level associated with all-cause mortality in high-functioning older persons: MacArthur studies of successful aging? Author(s): Hu P, Seeman TE, Harris TB, Reuben DB. Source: Journal of the American Geriatrics Society. 2001 December; 49(12): 1679-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11844003
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Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease? Author(s): Johnson RJ, Kang DH, Feig D, Kivlighn S, Kanellis J, Watanabe S, Tuttle KR, Rodriguez-Iturbe B, Herrera-Acosta J, Mazzali M. Source: Hypertension. 2003 June; 41(6): 1183-90. Epub 2003 April 21. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12707287
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Is there a role for uric acid in an animal model of calcium phosphate nephrocalcinosis and calcium phosphate crystallization in urine of patients with idiopathic calcium urolithiasis? An orientational study. Author(s): Schwille PO, Schmiedl A, Manoharan M, Wipplinger J. Source: Journal of Endourology / Endourological Society. 1999 November; 13(9): 637-45. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10608515
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Is uric acid implicated in benign paroxysmal positional vertigo? Author(s): Ziavra NV, Bronstein AM. Source: Journal of Neurology. 2004 January; 251(1): 115. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14999502
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Ketosis, weight loss, uric acid, and nitrogen balance in obese women fed single nutrients at low caloric levels. Author(s): Bell JD, Margen S, Calloway DH. Source: Metabolism: Clinical and Experimental. 1969 March; 18(3): 193-208. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4887615
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Kidney in patients with abnormalities in uric acid metabolism. Author(s): Gonick HC. Source: Contrib Nephrol. 1977; 7: 79-96. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=891204
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Lack of effect of salt intake on urinary uric acid excretion. Author(s): Breslau NA, Pak CY. Source: The Journal of Urology. 1983 March; 129(3): 531-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6834539
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Lack of effect of warfarin on uric acid concentration. Author(s): Walker FB 4th, Becker DM, Kowal-Neeley B, Krongaard LS. Source: Clinical Chemistry. 1988 May; 34(5): 952-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3370797
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Lack of prognostic significance of early elevated serum uric acid levels in low birthweight infants. Author(s): Sysyn GD, Rozycki HJ. Source: Biology of the Neonate. 2003; 83(4): 253-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12743454
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Lactic, pyruvic, citric, and uric acid and urea content of human gastric juice. Author(s): Piper DW, Fenton BH, Goodman LR. Source: Gastroenterology. 1967 July; 53(1): 42-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6027230
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Leptin might be a regulator of serum uric acid concentrations in humans. Author(s): Bedir A, Topbas M, Tanyeri F, Alvur M, Arik N. Source: Japanese Heart Journal. 2003 July; 44(4): 527-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12906034
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Lesch-Nyhan syndrome: autopsy findings and in vitro study of incorporation of 14C8-inosine into uric acid, guanosine-monophosphate and adenosine-monophosphate in the liver. Author(s): Wada Y, Arakawa T, Koizumi K. Source: The Tohoku Journal of Experimental Medicine. 1968 July; 95(3): 253-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5707898
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Letter: Prolactin and uric acid in man. Author(s): Branch RA, Levine D, Auty R, Cole E, Ramsay L. Source: British Medical Journal. 1975 August 9; 3(5979): 369. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1156769
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Letter: Serum uric acid and coronary artery disease. Author(s): Anderson TW. Source: Can Med Assoc J. 1974 February 16; 110(4): 385. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4812830
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Letter: Serum uric acid and myocardial infarction. Author(s): Briggs MH. Source: The Medical Journal of Australia. 1974 May 18; 1(20): 812. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4852926
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Letter: Serum uric acid determination. Author(s): Emori HW, Champion GD, Bluestone R, Paulus HE. Source: Arthritis and Rheumatism. 1974 November-December; 17(6): 1058-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4433353
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Letter: Updating coninuous-flow uric acid methodology. Author(s): Moorehead WR, Kasper LM. Source: Clinical Chemistry. 1975 April; 21(4): 641. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1116307
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Letter: White cells and uric acid in alcoholism. Author(s): Goedert M, Achaeffer F, Neuberg P. Source: Lancet. 1975 January 4; 1(7897): 52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=46382
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Levels of uric acid, urea and creatinine in Iraqi children with sickle cell disease. Author(s): al-Naama LM, al-Sadoon EA, al-Sadoon TA. Source: J Pak Med Assoc. 2000 March; 50(3): 98-102. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10795471
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Limited value of uric acid to creatinine ratios in estimating uric acid excretion. Author(s): Wortmann RL, Fox IH. Source: Annals of Internal Medicine. 1980 December; 93(6): 822-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6778279
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Lipid peroxidative damage in the erythrocytes and elevation of serum LDLcholesterol, apolipoprotein-B, ferritin and uric acid with age and in coronary heart disease patients. Author(s): El-Gebali HH, Tahir SA, Haider SS, El-Fakhri MM. Source: Saudi Med J. 2000 February; 21(2): 184-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11533779
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Local chemolysis of obstructive uric acid stone with 0.1 M THAM and 0.02% chlorhexidine. Author(s): Lee YH, Chang LS, Chen MT, Huang JK. Source: Urologia Internationalis. 1993; 51(3): 147-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8249225
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Local dissolution of uric acid calculi using THAM-E. Author(s): Mills GD, Morrison ND, Walker RJ. Source: Renal Failure. 1993; 15(4): 539-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8210568
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Long-term follow-up of incorporation of 15N from glycine into uric acid in gout. Author(s): Yu TF, Roboz J. Source: The American Journal of Medicine. 1981 April; 70(4): 797-802. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7211916
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Management of uric acid renal obstruction by intravenous lactate. Author(s): Libert MH, Wart F. Source: European Urology. 1985; 11(1): 22-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3987746
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Management of uric acid stone. Author(s): Chugtai MN, Khan FA, Kaleem M, Ahmed M. Source: J Pak Med Assoc. 1992 July; 42(7): 153-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1404830
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Maternal serum uric acid as predictor of fetal acidemia. Author(s): Anceschi MM, Piazze JJ, Maranghi L, Ruozi-Berretta A, Cosmi EV. Source: International Journal of Gynaecology and Obstetrics: the Official Organ of the International Federation of Gynaecology and Obstetrics. 2002 April; 77(1): 35-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11929655
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Maternal serum uric acid levels in preeclamptic twin pregnancies. Author(s): Farina A, Barbieri M, Di Luzio L, Carinci P. Source: American Journal of Perinatology. 1998 May; 15(5): 279-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9643630
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Maternal serum uric acid levels in preeclamptic women with multiple gestations. Author(s): Hsu CD, Chung YK, Lee IS, Chou K, Copel JA. Source: American Journal of Perinatology. 1997 November; 14(10): 613-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9605248
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Maternal serum uric acid levels in twin gestations. Author(s): Fischer RL, Bianculli KW, Hediger ML, Scholl TO. Source: Obstetrics and Gynecology. 1995 January; 85(1): 60-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7800327
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Measurement of allantoin and uric acid in human body fluids. A potential index of free-radical reactions in vivo? Author(s): Grootveld M, Halliwell B. Source: The Biochemical Journal. 1987 May 1; 243(3): 803-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3663100
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Measurement of low-molecular-weight antioxidants, uric acid, tyrosine and tryptophan in plaques and white matter from patients with multiple sclerosis. Author(s): Langemann H, Kabiersch A, Newcombe J. Source: European Neurology. 1992; 32(5): 248-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1521544
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Measurement of uric acid, ascorbic acid, and related metabolites in biological fluids. Author(s): Hatch LL, Sevanian A. Source: Analytical Biochemistry. 1984 May 1; 138(2): 324-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6742409
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Mechanism of hypouricemia in Hodgkin's disease. Isolated defect in postsecretory reabsorption of uric acid. Author(s): Tykarski A. Source: Nephron. 1988; 50(3): 217-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3226456
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Metabolic effects of calcium antagonists in humans, with emphasis on carbohydrate, lipid, potassium, and uric acid homeostases. Author(s): Trost BN, Weidmann P. Source: Journal of Cardiovascular Pharmacology. 1988; 12 Suppl 6: S86-92. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2468917
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Milk- and soy-protein ingestion: acute effect on serum uric acid concentration. Author(s): Garrel DR, Verdy M, PetitClerc C, Martin C, Brule D, Hamet P. Source: The American Journal of Clinical Nutrition. 1991 March; 53(3): 665-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2000819
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Miniaturized graphite sensors doped with metal-bathophenanthroline complexes for the selective potentiometric determination of uric acid in biological fluids. Author(s): Hassan SS, Rizk NM. Source: The Analyst. 1997 August; 122(8): 815-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9338988
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Moderate alcohol consumption reduces urinary 8-hydroxydeoxyguanosine by inducing of uric acid. Author(s): Yoshida R, Shioji I, Kishida A, Ogawa Y. Source: Ind Health. 2001 October; 39(4): 322-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11758995
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Much ado about nothing, or much to do about something? The continuing controversy over the role of uric acid in cardiovascular disease. Author(s): Johnson RJ, Tuttle KR. Source: Hypertension. 2000 March; 35(3): E10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10720608
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Multilayer film analysis of serum uric acid in 2-microliter samples. Author(s): Neeley WE. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 1984 July 31; 140(3): 295-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6467616
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Myocardial malondialdehyde and uric acid release after short-lasting coronary occlusions during coronary angioplasty: potential mechanisms for free radical generation. Author(s): De Scheerder IK, van de Kraay AM, Lamers JM, Koster JF, de Jong JW, Serruys PW. Source: The American Journal of Cardiology. 1991 August 1; 68(4): 392-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1858682
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Nasal secretion of the ozone scavenger uric acid. Author(s): Peden DB, Swiersz M, Ohkubo K, Hahn B, Emery B, Kaliner MA. Source: Am Rev Respir Dis. 1993 August; 148(2): 455-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8342911
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Neuron-specific enolase, nucleotides, nucleosides, purine bases, oxypurines and uric acid concentrations in cerebrospinal fluid of children with meningitis. Author(s): Rodriguez-Nunez A, Cid E, Rodriguez-Garcia J, Camina F, Rodriguez-Segade S, Castro-Gago M. Source: Brain & Development. 2003 March; 25(2): 102-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12581805
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Neutral effect of valsartan on serum uric acid and renal function tests. Author(s): Sayin T, Doven O, Akyurek O, Dincer I. Source: Journal of Human Hypertension. 2001 June; 15(6): 435-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11439321
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New standards for uric acid excretion and evidence for an inducible transporter. Author(s): Simkin PA. Source: Arthritis and Rheumatism. 2003 October 15; 49(5): 735-6; Author Reply 736-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14558064
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Nitric oxide inhibits prooxidant actions of uric acid during copper-mediated LDL oxidation. Author(s): Sanguinetti SM, Batthyany C, Trostchansky A, Botti H, Lopez GI, Wikinski RL, Rubbo H, Schreier LE. Source: Archives of Biochemistry and Biophysics. 2004 March 15; 423(2): 302-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15001394
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Nitrogen dioxide depletes uric acid and ascorbic acid but not glutathione from lung lining fluid. Author(s): Kelly FJ, Tetley TD. Source: The Biochemical Journal. 1997 July 1; 325 ( Pt 1): 95-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9224634
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Nitrosation of uric acid by peroxynitrite. Formation of a vasoactive nitric oxide donor. Author(s): Skinner KA, White CR, Patel R, Tan S, Barnes S, Kirk M, Darley-Usmar V, Parks DA. Source: The Journal of Biological Chemistry. 1998 September 18; 273(38): 24491-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9733742
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Nitrosative stress, uric Acid, and peripheral nerve function in early type 1 diabetes. Author(s): Hoeldtke RD, Bryner KD, McNeill DR, Hobbs GR, Riggs JE, Warehime SS, Christie I, Ganser G, Van Dyke K. Source: Diabetes. 2002 September; 51(9): 2817-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12196476
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Normal uric acid concentrations in a purine nucleoside phosphorylase (PNP) deficient child presenting with severe chicken pox, possible immunodeficiency and developmental delay. Author(s): Hallett RJ, Cronin SM, Morgan G, Duley JA, Fairbanks LD, Simmonds HA. Source: Advances in Experimental Medicine and Biology. 1994; 370: 387-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7544949
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Novel, reagentless, amperometric biosensor for uric acid based on a chemically modified screen-printed carbon electrode coated with cellulose acetate and uricase. Author(s): Gilmartin MA, Hart JP. Source: The Analyst. 1994 May; 119(5): 833-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8067535
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Observations on serum uric acid levels and the risk of idiopathic Parkinson's disease. Author(s): Davis JW, Grandinetti A, Waslien CI, Ross GW, White LR, Morens DM. Source: American Journal of Epidemiology. 1996 September 1; 144(5): 480-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8781463
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Observations with Magurlit in the treatment of patients with uric acid stone. Author(s): Rosdy E, Kiss T, Torok P. Source: Ther Hung. 1984; 32(2): 82-4. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6546266
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On the significance of brain extracellular uric acid detected with in-vivo monitoring techniques: a review. Author(s): O'Neill RD, Lowry JP. Source: Behavioural Brain Research. 1995 November; 71(1-2): 33-49. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8747173
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One year follow-up of hyperuricaemic hypertensive patients treated with tienilic acid or a diuretic with or without uric acid-lowering drugs. Author(s): Waal-Manning HJ, Simpson FO. Source: Clinical Science (London, England : 1979). 1979 December; 57 Suppl 5: 379S382S. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=396085
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Oral purine loading for evaluation of uric acid excretion in patients with urinary calculi. Author(s): Zechner O, Pfluger H. Source: Invest Urol. 1980 September; 18(2): 115-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7410020
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Oral zinc therapy normalizes serum uric acid level in Wilson's disease patients. Author(s): Umeki S, Ohga R, Konishi Y, Yasuda T, Morimoto K, Terao A. Source: The American Journal of the Medical Sciences. 1986 November; 292(5): 289-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3777013
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Origin of plasma uric acid induced by l-epinephrine. Author(s): Yonetani Y, Ishii M, Yamada K, Ogawa Y. Source: Chemical & Pharmaceutical Bulletin. 1977 March; 25(3): 457-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=872279
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Overnight urinary uric acid: creatinine ratio for detection of sleep hypoxemia. Validation study in chronic obstructive pulmonary disease and obstructive sleep apnea before and after treatment with nasal continuous positive airway pressure. Author(s): Braghiroli A, Sacco C, Erbetta M, Ruga V, Donner CF. Source: Am Rev Respir Dis. 1993 July; 148(1): 173-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8317794
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Overproduction of uric acid in hypoxanthine-guanine phosphoribosyltransferase deficiency. Contribution by impaired purine salvage. Author(s): Edwards NL, Recker D, Fox IH. Source: The Journal of Clinical Investigation. 1979 May; 63(5): 922-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=447834
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Oxidation products of uric acid and ascorbic acid in preterm infants with chronic lung disease. Author(s): Ogihara T, Kim HS, Hirano K, Imanishi M, Ogihara H, Tamai H, Okamoto R, Mino M. Source: Biology of the Neonate. 1998; 73(1): 24-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9458939
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Part 1. Uric acid and losartan. Author(s): Sica DA, Schoolwerth AC. Source: Current Opinion in Nephrology and Hypertension. 2002 September; 11(5): 47582. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12187310
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Pathophysiologic basis for normouricosuric uric acid nephrolithiasis. Author(s): Sakhaee K, Adams-Huet B, Moe OW, Pak CY. Source: Kidney International. 2002 September; 62(3): 971-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12164880
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Pathophysiology of uric acid nephrolithiasis. Author(s): Moe OW, Abate N, Sakhaee K. Source: Endocrinology and Metabolism Clinics of North America. 2002 December; 31(4): 895-914. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12474637
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Phosphoribosylpyrophosphate synthetase overactivity as a cause of uric acid overproduction in a young woman. Author(s): Garcia-Pavia P, Torres RJ, Rivero M, Ahmed M, Garcia-Puig J, Becker MA. Source: Arthritis and Rheumatism. 2003 July; 48(7): 2036-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12847698
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Plasma 5'-nucleotidase activities and uric acid levels in women with pre-eclampsia. Author(s): Yoneyama Y, Suzuki S, Sawa R, Otsubo Y, Miura A, Kuwabara Y, Ishino H, Kiyokawa Y, Doi D, Yoneyama K, Kobayashi H, Araki T. Source: Gynecologic and Obstetric Investigation. 2002; 54(3): 168-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12571440
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Portable electrochemical blood uric acid meter. Author(s): Kuo CS, Hwu CM, Lin YH, Huang YH, Kao WY, Weih MJ, Hsiao LC, Kwok CF, Ho LT. Source: Journal of Clinical Laboratory Analysis. 2002; 16(2): 109-14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11948801
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Predictive value of uric acid in gastric mucosal damage in hemodialysis patients. Author(s): Tsukada K, Hasegawa T, Miyazaki T, Katoh H, Yoshikawa M, Masuda N, Ojima H, Tajima K, Fukai Y, Nakajima M, Kamiyama Y, Kuwano H, Yamamoto Y, Tsukada O. Source: Hepatogastroenterology. 2003 September-October; 50(53): 1708-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14571823
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Progesterone increases glomerular filtration rate, urinary kallikrein excretion and uric acid clearance in normal women. Author(s): Atallah AN, Guimaraes JA, Gebara M, Sustovich DR, Martinez TR, Camano L. Source: Brazilian Journal of Medical and Biological Research = Revista Brasileira De Pesquisas Medicas E Biologicas / Sociedade Brasileira De Biofisica . [et Al.]. 1988; 21(1): 71-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3179582
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Prooxidant and antioxidant properties of human serum ultrafiltrates toward LDL: important role of uric acid. Author(s): Patterson RA, Horsley ET, Leake DS. Source: Journal of Lipid Research. 2003 March; 44(3): 512-21. Epub 2002 December 16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12562831
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Protection against meningitis-associated central nervous system complications by uric acid. Author(s): Kastenbauer S, Pfister HW. Source: Medical Hypotheses. 2002 May; 58(5): 431. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12199194
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Quantification of urinary uric acid in the presence of thymol and thimerosal by highperformance liquid chromatography. Author(s): Chen Y, Pietrzyk RA, Whitson PA. Source: J Chromatogr A. 1997 February 28; 763(1-2): 187-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9129322
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Quantitation of urinary uric acid by reversed-phase liquid chromatography. Author(s): Hausen A, Fuchs D, Konig K, Wachter H. Source: Clinical Chemistry. 1981 August; 27(8): 1455-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7273411
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Quantitative estimation of uric acid, xanthine, and hypoxanthine in plasma using thin-layer chromatography. Author(s): Orsulak PJ, Haab W, Appleton MD. Source: Analytical Biochemistry. 1968 April; 23(1): 156-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5645123
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Quantitative measurements of the urinary excretion of creatinine, uric acid, hypoxanthine and xanthine, uracil, cyclic AMP, and cyclic GMP in healthy newborn infants. Author(s): Manzke H, Spreter von Kreudenstein P, Dorner K, Kruse K. Source: European Journal of Pediatrics. 1980 March; 133(2): 157-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6244960
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Quiz page. Stones in the kidney allograft and bladder. Nephrolithiasis is common after transplantation. Cyclosporine often leads to chronic hyperuricemia and the formation of uric acid stones. Author(s): Canas G. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2003 January; 41(1): Xli. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12500253
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Reaction of uric acid with peroxynitrite and implications for the mechanism of neuroprotection by uric acid. Author(s): Squadrito GL, Cueto R, Splenser AE, Valavanidis A, Zhang H, Uppu RM, Pryor WA. Source: Archives of Biochemistry and Biophysics. 2000 April 15; 376(2): 333-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10775420
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Relation between serum uric acid and plasma adenosine levels in twin pregnancies. Author(s): Suzuki S, Yoneyama Y, Sawa R, Araki T. Source: Obstetrics and Gynecology. 2000 October; 96(4): 507-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11004349
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Relation between serum uric acid and plasma adenosine levels in women with preeclampsia. Author(s): Suzuki S, Yoneyama Y, Sawa R, Otsubo Y, Takeuchi T, Araki T. Source: Gynecologic and Obstetric Investigation. 2001; 51(3): 169-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11306903
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Relation between serum uric acid and risk of cardiovascular disease in essential hypertension. The PIUMA study. Author(s): Verdecchia P, Schillaci G, Reboldi G, Santeusanio F, Porcellati C, Brunetti P. Source: Hypertension. 2000 December; 36(6): 1072-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11116127
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Relationships of serum cholesterol (total and esterified) with serum uric acid. Author(s): Saha N. Source: Singapore Med J. 1987 August; 28(4): 332-5. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3423802
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Relative associations of fitness and fatness to fibrinogen, white blood cell count, uric acid and metabolic syndrome. Author(s): Church TS, Finley CE, Earnest CP, Kampert JB, Gibbons LW, Blair SN. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 June; 26(6): 805-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12037651
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Renal disease from excess uric acid. Author(s): Maierhofer WJ. Source: Postgraduate Medicine. 1987 September 15; 82(4): 123-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3628131
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Renal handling of uric acid assessed by means of pharmacological tests in obese women. Author(s): Gonzalez-Ortiz M, Martinez-Abundis E, Mora-Martinez JM, Grover-Paez F. Source: Diabetes Nutr Metab. 2001 August; 14(4): 189-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11716287
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Renal handling of uric acid under cyclosporin A treatment. Author(s): Hoyer PF, Lee IJ, Oemar BS, Krohn HP, Offner G, Brodehl J. Source: Pediatric Nephrology (Berlin, Germany). 1988 January; 2(1): 18-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3152994
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Renal underexcretion of uric acid is present in patients with apparent high urinary uric acid output. Author(s): Perez-Ruiz F, Calabozo M, Erauskin GG, Ruibal A, Herrero-Beites AM. Source: Arthritis and Rheumatism. 2002 December 15; 47(6): 610-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12522834
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Sample preparation in patients receiving uric acid oxidase (rasburicase) therapy. Author(s): Lim E, Bennett P, Beilby J. Source: Clinical Chemistry. 2003 August; 49(8): 1417-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12881465
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Serum albumin, creatinine, uric acid and hypertensive disorders of pregnancy. Author(s): Salako BL, Odukogbe AT, Olayemi O, Adedapo KS, Aimakhu CO, Alu FE, Ola B. Source: East Afr Med J. 2003 August; 80(8): 424-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14601785
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Serum uric acid and hemorheology in borderline hypertensives and in subjects with established hypertension and left ventricular hypertrophy. Author(s): Hoieggen A, Fossum E, Reims H, Kjeldsen SE. Source: Blood Pressure. 2003; 12(2): 104-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12797630
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Serum uric acid and plasma norepinephrine concentrations predict subsequent weight gain and blood pressure elevation. Author(s): Masuo K, Kawaguchi H, Mikami H, Ogihara T, Tuck ML. Source: Hypertension. 2003 October; 42(4): 474-80. Epub 2003 September 02. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12953019
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Serum uric acid and risk for development of hypertension and impaired fasting glucose or Type II diabetes in Japanese male office workers. Author(s): Nakanishi N, Okamoto M, Yoshida H, Matsuo Y, Suzuki K, Tatara K. Source: European Journal of Epidemiology. 2003; 18(6): 523-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12908717
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Serum uric acid in hypertensive patients with and without peripheral arterial disease. Author(s): Langlois M, De Bacquer D, Duprez D, De Buyzere M, Delanghe J, Blaton V. Source: Atherosclerosis. 2003 May; 168(1): 163-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12732400
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Serum uric acid in renovascular hypertension: reduction following surgical correction. Author(s): Nunez BD, Frohlich ED, Garavaglia GE, Schmieder RE, Nunez MM. Source: The American Journal of the Medical Sciences. 1987 December; 294(6): 419-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3425590
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Serum uric acid in traditional Pacific Islanders and in Swedes. Author(s): Lindeberg S, Cordain L, Rastam L, Ahren B. Source: Journal of Internal Medicine. 2004 March; 255(3): 373-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14871461
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Structural changes and variations of uric acid in normal pregnancy. Author(s): Yatzidis A, Yatzidis H, Salamalekis E, Koutsikos D, Agroyannis B, PlemenosFrangos M, Tzanatos-Exarchou H. Source: European Journal of Obstetrics, Gynecology, and Reproductive Biology. 1987 November; 26(3): 207-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3428469
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Studies on normal and abnormal excretion patterns of uric acid in Bahawalpur. Author(s): Khan MS, Akhtar P, Majeed A. Source: J Pak Med Assoc. 1987 October; 37(10): 266-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3121881
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The ALLHAT and the cardioprotection conferred by diuretics in hypertensive patients: a connection with uric acid? Author(s): Reyes AJ, Leary WP. Source: Cardiovascular Drugs and Therapy / Sponsored by the International Society of Cardiovascular Pharmacotherapy. 2002 December; 16(6): 485-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12797357
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The effect of glucose intake on urine saturation with calcium oxalate, calcium phosphate, uric acid and sodium urate. Author(s): Gluszek J. Source: International Urology and Nephrology. 1988; 20(6): 657-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3229936
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The effect of tiaprofenic acid on uric acid excretion in man. Author(s): Sinigaglia L, Zeni S, Solazzi F, Di Minno G, Longatti S. Source: Drugs. 1988; 35 Suppl 1: 68-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3359948
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The increase in serum uric acid induced by diuretics could be beneficial to cardiovascular prognosis in hypertension: a hypothesis. Author(s): Reyes AJ, Leary WP. Source: Journal of Hypertension. 2003 September; 21(9): 1775-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12923414
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The inflammatory process in the mechanism of decreased serum uric acid concentrations during acute gouty arthritis. Author(s): Urano W, Yamanaka H, Tsutani H, Nakajima H, Matsuda Y, Taniguchi A, Hara M, Kamatani N. Source: The Journal of Rheumatology. 2002 September; 29(9): 1950-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12233891
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The renal handling of urate in acute renal failure patients with high urine uric acid/urine creatinine concentration ratio. Author(s): Tungsanga K, Kateruttanakul P, Sitprija V. Source: J Med Assoc Thai. 1988 January; 71(1): 29-32. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3361253
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The significance of serum uric acid, creatinine and urinary microprotein levels in predicting pre-eclampsia. Author(s): Weerasekera DS, Peiris H. Source: Journal of Obstetrics and Gynaecology : the Journal of the Institute of Obstetrics and Gynaecology. 2003 January; 23(1): 17-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12623475
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The treatment of uric acid calculi with extracorporeal shock wave lithotripsy. Author(s): Royce PL, Fuchs GJ, Lupu AN, Chaussy CG. Source: British Journal of Urology. 1987 July; 60(1): 6-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3620846
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Therapeutic intervention in experimental allergic encephalomyelitis by administration of uric acid precursors. Author(s): Scott GS, Spitsin SV, Kean RB, Mikheeva T, Koprowski H, Hooper DC. Source: Proceedings of the National Academy of Sciences of the United States of America. 2002 December 10; 99(25): 16303-8. Epub 2002 November 25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12451183
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Tissue hypoxia in sleep apnea syndrome assessed by uric acid and adenosine. Author(s): Saito H, Nishimura M, Shibuya E, Makita H, Tsujino I, Miyamoto K, Kawakami Y. Source: Chest. 2002 November; 122(5): 1686-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12426272
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Uric acid and diet--insights into the epidemic of cardiovascular disease. Author(s): Johnson RJ, Rideout BA. Source: The New England Journal of Medicine. 2004 March 11; 350(11): 1071-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15014177
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Uric acid and prognosis in chronic heart failure. Author(s): Kearney MT, Nolan J; UK-HEART Study Investigators. Source: Circulation. 2003 November 25; 108(21): E148. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14638530
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Uric acid and urea in human sweat. Author(s): Huang CT, Chen ML, Huang LL, Mao IF. Source: Chin J Physiol. 2002 September 30; 45(3): 109-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12817713
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Uric acid levels: a useful index of the severity of preeclampsia and perinatal prognosis. Author(s): Voto LS, Illia R, Darbon-Grosso HA, Imaz FU, Margulies M. Source: Journal of Perinatal Medicine. 1988; 16(2): 123-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3171856
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Uric acid nephrolithiasis and acute renal failure secondary to streptozotocin nephrotoxicity. Author(s): Hricik DE, Goldsmith GH. Source: The American Journal of Medicine. 1988 January; 84(1): 153-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2827466
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Uric acid reduces exercise-induced oxidative stress in healthy adults. Author(s): Waring WS, Convery A, Mishra V, Shenkin A, Webb DJ, Maxwell SR. Source: Clinical Science (London, England : 1979). 2003 October; 105(4): 425-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12801243
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Uric acid stone disease. Author(s): Moran ME. Source: Frontiers in Bioscience : a Journal and Virtual Library. 2003 September 1; 8: S1339-55. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12957851
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Uric acid transport. Author(s): Rafey MA, Lipkowitz MS, Leal-Pinto E, Abramson RG. Source: Current Opinion in Nephrology and Hypertension. 2003 September; 12(5): 511-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12920398
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Urinary glycosaminoglycans as risk factors for uric acid nephrolithiasis: case control study in a Sardinian genetic isolate. Author(s): Ombra MN, Casula S, Biino G, Maestrale G, Cardia F, Melis P, Pirastu M. Source: Urology. 2003 September; 62(3): 416-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12946738
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Urolithiasis in Okinawa, Japan: a relatively high prevalence of uric acid stones. Author(s): Hossain RZ, Ogawa Y, Hokama S, Morozumi M, Hatano T. Source: International Journal of Urology : Official Journal of the Japanese Urological Association. 2003 August; 10(8): 411-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12887361
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Value of exfoliative urinary cytology for differentiation between uric acid stone and tumor of upper urinary tract. Author(s): Rubben H, Hering F, Dahm HH, Lutzeyer W. Source: Urology. 1982 December; 20(6): 571-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7179618
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Value of the urinary uric acid to creatinine ratio in term infants with perinatal asphyxia. Author(s): Akisu M, Kultursay N. Source: Acta Paediatr Jpn. 1998 February; 40(1): 78-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9583207
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Values for uric acid in patients' sera as measured with SMAC (phosphotungstate) and AutoAnalyzer (uricase) Author(s): Robertson EA, Sliva CA, Young DS. Source: Clinical Chemistry. 1978 January; 24(1): 173-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=618654
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Variability in human parotid fluid uric acid,creatinine, total nitrogen, urea nitrogen, nonprotein nitrogen, and total protein. SAM-TR-68-8. Author(s): Shannon IL, Segreto VA. Source: Tech Rep Sam-Tr. 1968 March; : 1-13. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5303150
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Vitamin C, dehydroascorbate, and uric acid in tissues and serum: high-performance liquid chromatography. Author(s): Barja G, Hernanz A. Source: Methods Enzymol. 1994; 234: 331-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7808304
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Warfarin administration increases uric acid concentrations in plasma. Author(s): Menon RK, Mikhailidis DP, Bell JL, Kernoff PB, Dandona P. Source: Clinical Chemistry. 1986 August; 32(8): 1557-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3488142
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Warfarin and uric acid after myocardial infarction. Author(s): Smith P, Arnesen H. Source: Acta Med Scand. 1986; 220(5): 407-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3544688
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When and why a water-soluble antioxidant becomes pro-oxidant during copperinduced low-density lipoprotein oxidation: a study using uric acid. Author(s): Bagnati M, Perugini C, Cau C, Bordone R, Albano E, Bellomo G. Source: The Biochemical Journal. 1999 May 15; 340 ( Pt 1): 143-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10229669
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When, why, and how should we quantify the excretion rate of urinary uric acid? Author(s): Simkin PA. Source: The Journal of Rheumatology. 2001 June; 28(6): 1207-10. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11409110
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Xanthine interference in the Kodak “Ektachem” determination of uric acid. Author(s): Potter JL. Source: Clinical Chemistry. 1987 July; 33(7): 1265. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3594879
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X-linkage does not account for the absence of father-son similarity in plasma uric acid concentrations. Author(s): Reed DR, Price RA. Source: American Journal of Medical Genetics. 2000 May 15; 92(2): 142-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10797440
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CHAPTER 2. NUTRITION AND URIC ACID Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and uric acid.
Finding Nutrition Studies on Uric Acid 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 “uric acid” (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 “uric acid” (or a synonym): •
Dietary beta-carotene and carotenoids in young women: effects on plasma ascorbic acid and uric acid. Source: Omaye, S.T. Burri, B.J. Senh, A. Wah Choi, Y. Yeung, Y.O.A. Environ-nutrinteract. Philadelphia, PA : Taylor & Francis. Sept/December 1997. volume 1 (5/6) page 273-286. 1086-5683
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Effect of uric acid on liver injury during hemorrhagic shock. Author(s): Department of First Surgery, Gunma University School of Medicine, Showamachi Maebashi, Japan. Source: Tsukada, K Hasegawa, T Tsutsumi, S Katoh, H Kuwano, H Miyazaki, T Yamamoto, Y Surgery. 2000 April; 127(4): 439-46 0039-6060
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Is there a role for uric acid in an animal model of calcium phosphate nephrocalcinosis and calcium phosphate crystallization in urine of patients with idiopathic calcium urolithiasis? An orientational study. Author(s): Department of Surgery, University of Erlangen, Germany. Source: Schwille, P O Schmiedl, A Manoharan, M Wipplinger, J J-Endourol. 1999 November; 13(9): 637-45 0892-7790
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Oleic acid-induced injuries in the guinea-pig. Effects of allopurinol on cell dynamics, erythrocyte-catalase and uric acid plasma levels. Author(s): Department of Zoophysiology, University of Lund, Sweden. Source: Hultkvist Bengtsson, U Martensson, L Clin-Exp-Pharmacol-Physiol. 1991 Mar; 18(3): 127-30 0305-1870
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Pharmacological evidence, using in vivo dialysis, that substances additional to ascorbic acid, uric acid and homovanillic acid contribute to the voltammetric signals obtained in unrestrained rats from chronically implanted carbon paste electrodes. Author(s): MRC Brain, Behaviour and Psychiatry Group, Department of Psychology, Institute of Psychiatry, London, U.K. Source: Joseph, M H Young, A M J-Neurosci-Methods. 1991 February; 36(2-3): 209-18 0165-0270
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Protective role of uric acid against photooxidative stress in the silkworm, Bombyx mori, (Lepidoptera: Bombycidae). Author(s): Tokyo Univ. (Japan) Source: Matsuo, T. Ishikawa, Y. Applied-Entomology-and-Zoology (Japan). (November 1999). volume 34(4) page 481-484. bombyx mori photooxidation stress uric acid antioxidants 0003-6862
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Serum uric acid levels in multiple sclerosis patients correlate with activity of disease and blood-brain barrier dysfunction. Author(s): Center of Neurology, Clinical Hospital Center Kragujevac, Svetozara Markovica, Yugoslavia.
[email protected] Source: Toncev, G Milicic, B Toncev, S Samardzic, G Eur-J-Neurol. 2002 May; 9(3): 221-6 1351-5101
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The effects of personal interaction on triglyceride and uric acid levels, and coronary risk in a managerial population: a longitudinal study. Source: Howard, J.H. Cunningham, D.A. Rechnitizer, P.A. J-Hum-Stress. Washington, D.C. : Heldref Publications. Summer 1986. volume 12 (2) page 53-63. 0097-840X
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Uric acid urolithiasis and crystallization inhibitors. Author(s): Laboratory of Urolithiasis Research, Faculty of Sciences, University of Illes Balears, Palma de Mallorca, Spain.
[email protected] Source: Grases, F Ramis, M Villacampa, A I Costa Bauza, A Urol-Int. 1999; 62(4): 201-4 0042-1138
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Uric acid: an important antioxidant in acute ischaemic stroke. Author(s): Clinical Pharmacology Unit and Research Centre, The University of Edinburgh, Western General Hospital, Edinburgh, UK.
[email protected] Source: Waring, W S QJM. 2002 October; 95(10): 691-3 1460-2725
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 uric acid; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
Vitamins Vitamin B3 Source: Healthnotes, Inc.; www.healthnotes.com
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Minerals Folate Source: Prima Communications, Inc.www.personalhealthzone.com Molybdenum Source: Healthnotes, Inc.; www.healthnotes.com Quercetin Source: Integrative Medicine Communications; www.drkoop.com Sodium Bicarbonate Source: Healthnotes, Inc.; www.healthnotes.com
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Food and Diet High Cholesterol Source: Healthnotes, Inc.; www.healthnotes.com Low-Purine Diet Source: Healthnotes, Inc.; www.healthnotes.com Onions Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/foods_view/0,1523,27,00.html Variety Meats Source: Healthnotes, Inc.; www.healthnotes.com
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CHAPTER 3. ALTERNATIVE MEDICINE AND URIC ACID Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to uric acid. 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 uric acid 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 “uric acid” (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 uric acid: •
Action of biologically-relevant oxidizing species upon uric acid. Identification of uric acid oxidation products. Author(s): Kaur H, Halliwell B. Source: Chemico-Biological Interactions. 1990; 73(2-3): 235-47. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2155712
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Anaerobic degradation of uric acid via pyrimidine derivatives by selenium-starved cells of Clostridium purinolyticum. Author(s): Durre P, Andreesen JR. Source: Archives of Microbiology. 1982 May; 131(3): 255-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6808963
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Application of intensified (+) Qi Gong energy, (-) electrical field, (S) magnetic field, electrical pulses (1-2 pulses/sec), strong Shiatsu massage or acupuncture on the accurate organ representation areas of the hands to improve circulation and enhance
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drug uptake in pathological organs: clinical applications with special emphasis on the “Chlamydia-(Lyme)-uric acid syndrome” and “Chlamydia-(cytomegalovirus)-uric acid syndrome”. Author(s): Omura Y, Beckman SL. Source: Acupuncture & Electro-Therapeutics Research. 1995 January-March; 20(1): 21-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7572329 •
Blood uric acid level of Indian and western adults and its seasonal variation. Author(s): Banerjee B, Saha N. Source: J Indian Med Assoc. 1967 March 1; 48(5): 207-10. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6039391
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DNA oxidatively damaged by chromium(III) and H(2)O(2) is protected by the antioxidants melatonin, N(1)-acetyl-N(2)-formyl-5-methoxykynuramine, resveratrol and uric acid. Author(s): Burkhardt S, Reiter RJ, Tan DX, Hardeland R, Cabrera J, Karbownik M. Source: The International Journal of Biochemistry & Cell Biology. 2001 August; 33(8): 775-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11404181
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Hemodialysis for acute anuric uric acid nephropathy. Author(s): Steinberg SM, Galen MA, Lazarus JM, Lowrie EG, Hampers CL, Jaffe N. Source: Am J Dis Child. 1975 August; 129(8): 956-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1174288
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Heterogeneity in the familial aggregation of fasting serum uric acid level in five North American populations: the Lipid Research Clinics Family Study. Author(s): Rice T, Vogler GP, Perry TS, Laskarzewski PM, Province MA, Rao DC. Source: American Journal of Medical Genetics. 1990 June; 36(2): 219-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2368810
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High-protein diets in hyperlipidemia: effect of wheat gluten on serum lipids, uric acid, and renal function. Author(s): Jenkins DJ, Kendall CW, Vidgen E, Augustin LS, van Erk M, Geelen A, Parker T, Faulkner D, Vuksan V, Josse RG, Leiter LA, Connelly PW. Source: The American Journal of Clinical Nutrition. 2001 July; 74(1): 57-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11451718
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Inactivation of alpha 1-antiproteinase by hydroxyl radicals. The effect of uric acid. Author(s): Aruoma OI, Halliwell B. Source: Febs Letters. 1989 February 13; 244(1): 76-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2538353
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Interference of the chemotherapeutic agent etoposide with the direct phosphotungstic acid method for uric acid. Author(s): Matheke ML, Kessler G, Chan KM. Source: Clinical Chemistry. 1987 November; 33(11): 2109-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3479271
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Inverse association between coffee drinking and serum uric acid concentrations in middle-aged Japanese males. Author(s): Kiyohara C, Kono S, Honjo S, Todoroki I, Sakurai Y, Nishiwaki M, Hamada H, Nishikawa H, Koga H, Ogawa S, Nakagawa K. Source: The British Journal of Nutrition. 1999 August; 82(2): 125-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10743484
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Optimal conditions for the simultaneous ion-pairing HPLC determination of Lascorbic, dehydro-L-ascorbic, D-ascorbic, and uric acids with on-line ultraviolet absorbance and electrochemical detection. Author(s): Pappa- Louisi A, Pascalidou S. Source: Analytical Biochemistry. 1998 October 15; 263(2): 176-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9799529
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Parathyroid hormone, cAMP, electrolytes and uric acid after high dose CaCl2 in patients with idiopathic stone formation. Author(s): Dunzendorfer U, Schmidt-Gayk H. Source: Endokrinologie. 1981 July; 77(3): 353-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6268394
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Renal excretion of uric acid during prolonged fasting. Author(s): Fox IH, Halperin ML, Goldstein MB, Marliss ER. Source: Metabolism: Clinical and Experimental. 1976 May; 25(5): 551-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1263845
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Semimicro method for determination of serum uric acid using EDTA-hydrazine. Author(s): Patel CP. Source: Clinical Chemistry. 1968 August; 14(8): 764-75. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4970140
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The effect of a vegetarian and different omnivorous diets on urinary risk factors for uric acid stone formation. Author(s): Siener R, Hesse A. Source: European Journal of Nutrition. 2003 December; 42(6): 332-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14673606
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The influence of dietary molybdenum and copper supplementation on the contents of serum uric acid and some trace elements in cocks. Author(s): Karring M, Pohjanvirta R, Rahko T, Korpela H. Source: Acta Vet Scand. 1981; 22(3-4): 289-95. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7344523
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The stabilization of ascorbic acid by uric acid. Author(s): Hochstein P, Sevanian A, Davies KJ. Source: Advances in Experimental Medicine and Biology. 1986; 195 Pt A: 325-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3088920
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The uric acid-whewellite association in human kidney stones. Author(s): Deganello S, Chou C. Source: Scan Electron Microsc. 1985; (Pt 4): 1545-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3938066
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Uric acid and glutathione levels during short-term whole body cold exposure. Author(s): Siems WG, van Kuijk FJ, Maass R, Brenke R. Source: Free Radical Biology & Medicine. 1994 March; 16(3): 299-305. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8063192
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Uric acid and phosphorus excretion in dogs with lymphosarcoma. Author(s): Page RL, Leifer CE, Matus RE. Source: Am J Vet Res. 1986 April; 47(4): 910-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3754406
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Uric acid is closely linked to vascular nitric oxide activity. Evidence for mechanism of association with cardiovascular disease. Author(s): Maxwell AJ, Bruinsma KA. Source: Journal of the American College of Cardiology. 2001 December; 38(7): 1850-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11738284
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Uric acid is released in the zona incerta of the subthalamic region of the sheep during rumination and in response to feeding and drinking stimuli. Author(s): Kendrick KM, Baldwin BA, Cooper TR, Sharman DF. Source: Neuroscience Letters. 1986 October 8; 70(2): 272-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2430241
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Uric acid protects membranes and linolenic acid from ozone-induced oxidation. Author(s): Meadows J, Smith RC, Reeves J.
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Source: Biochemical and Biophysical Research Communications. 1986 May 29; 137(1): 536-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2872893 •
When and why a water-soluble antioxidant becomes pro-oxidant during copperinduced low-density lipoprotein oxidation: a study using uric acid. Author(s): Bagnati M, Perugini C, Cau C, Bordone R, Albano E, Bellomo G. Source: The Biochemical Journal. 1999 May 15; 340 ( Pt 1): 143-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10229669
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Yin and yang of uric acid in patients with stroke. Author(s): Chamorro A, Planas AM. Source: Stroke; a Journal of Cerebral Circulation. 2004 January; 35(1): E11-2; Author Reply E11-2.
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/
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The following is a specific Web list relating to uric acid; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
General Overview Diabetes Source: Healthnotes, Inc.; www.healthnotes.com Gout Source: Healthnotes, Inc.; www.healthnotes.com Gout Source: Integrative Medicine Communications; www.drkoop.com Gout Source: Prima Communications, Inc.www.personalhealthzone.com HIV and AIDS Support Source: Healthnotes, Inc.; www.healthnotes.com Kidney Stones Source: Integrative Medicine Communications; www.drkoop.com
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Chinese Medicine Chonglou Alternative names: Paris Root; Rhizoma Paridis Source: Chinese Materia Medica
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Herbs and Supplements Allopurinol Source: Healthnotes, Inc.; www.healthnotes.com Bromelain Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,760,00.html Celery Extract Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10014,00.html Cherry Fruit Extract Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10015,00.html
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Colchicine Source: Healthnotes, Inc.; www.healthnotes.com Cranberry Alternative names: Vaccinium macrocarpon Source: Integrative Medicine Communications; www.drkoop.com Diclofenac Source: Healthnotes, Inc.; www.healthnotes.com Equisetum Alternative names: Horsetail; Equisetum arvense L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Ginkgo Alternative names: Ginkgo biloba Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Gravel Root Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Hibiscus Alternative names: Hibiscus, Roselle; Hibiscus sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Inosine Source: Healthnotes, Inc.; www.healthnotes.com Mahonia Alternative names: Mahonia aquifolium Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Ocimum Alternative names: Basil, Albahaca; Ocimum basilicum Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Pimpinella Alternative names: Anise; Pimpinella anisum (L) Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Piper Alternative names: Kava; Piper methysticum Forst.f Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Smilax Alternative names: Sarsaparilla; Smilax glabra Roxb. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Stevia Alternative names: Sweetleaf; Stevia rebaudiana Bertoni Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
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Trigonella Alternative names: Fenugreek; Trigonella foenum graecum L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Vaccinium Macrocarpon Source: Integrative Medicine Communications; www.drkoop.com
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 4. DISSERTATIONS ON URIC ACID Overview In this chapter, we will give you a bibliography on recent dissertations relating to uric acid. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “uric acid” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on uric acid, we have not necessarily excluded non-medical dissertations in this bibliography.
Dissertations on Uric Acid ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to uric acid. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •
Excretion of uric acid in man and the dog with special reference to urine acidification by Plante, Gérard E; ADVDEG from Mcgill University (Canada), 1968 http://wwwlib.umi.com/dissertations/fullcit/NK02890
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Serum uric acid : a biochemical factor in learning by Stevens, Henry Arthur; PhD from The University of Saskatchewan (Canada), 1973 http://wwwlib.umi.com/dissertations/fullcit/NK14829
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Serum uric acid, intellect and personality by Kennett, Keith Franklin; PhD from The University of Saskatchewan (Canada), 1972 http://wwwlib.umi.com/dissertations/fullcit/NK11015
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THE RELATIONSHIP OF SERUM URIC ACID TO INTELLIGENCE, ACHIEVEMENT, AND NEED FOR ACHIEVEMENT IN U.S. ADOLESCENTS, TWELVE THROUGH SEVENTEEN YEARS OF AGE, 1966-1970. by KEEHNER, JAMES MARTIN, PHD from The Catholic University of America, 1979, 80 pages http://wwwlib.umi.com/dissertations/fullcit/7920555
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Uric acid synthesis in the blood-sucking bug Rhodnius prolixus (Stal) by Barrett, F. Michael; ADVDEG from University of Toronto (Canada), 1969 http://wwwlib.umi.com/dissertations/fullcit/NK04485
Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.
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CHAPTER 5. PATENTS ON URIC ACID 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 “uric acid” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on uric acid, we have not necessarily excluded non-medical patents in this bibliography.
Patents on Uric Acid By performing a patent search focusing on uric acid, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We
8Adapted
from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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will tell you how to obtain this information later in the chapter. The following is an example of the type of information that you can expect to obtain from a patent search on uric acid: •
Agents for intravitreal administration to treat or prevent disorders of the eye Inventor(s): Castillejos; David (Chula Vista, CA) Assignee(s): Vitreo-retinal Technologies, Inc. (irvine, Ca) Patent Number: 6,462,071 Date filed: March 2, 2000 Abstract: Methods and preparations for treating disorders of the eye and/or causing posterior vitreous disconnection or disinsertion. Preparations containing a) urea, b) urea derivatives (e.g., hydroxyurea, thiourea), c) a non-steroidal anti-inflamatory agents, d) antmetabolites, e) urea, urea derivatives, non-enzymatic proteins, nucleosides, nucleotides and their derivatives (e.g., adenine, adenosine, cytosine, cytadine, guanine, guanitadine, guanidinium, thymidine, thimitadine, uradine, uracil, cystine), uric acid, calcium acetal salicylate, ammonium sulfate or other compound capable of causing nonenzymatic dissolution of the hyaloid membrane or e) any of the possible combinations thereof, are administered to the eye in therapeutically effective amounts. Excerpt(s): The present invention relates generally to pharmaceutical preparations and medical treatment methods, and more particularly agents (i.e, urea and urea derivatives, nonsteroidal anti-inflammatory drugs (NSAIDS) and anti-metabolite drugs) used alone or in combinations with each other (or with other agents) to treat or prevent certain disorders of the eye. Neovascularization (or angiogenesis) is a process whereby new blood vessels are formed within tissues of the body. Normal neovascularization is the physiological process by which the body creates and maintains small blood vessels of the circulatory system. However, pathological or iatrogenic neovascularization is a nonphysiological process whereby abnormal networks of blood vessels are created in tissues of the body or in tumors, as a result of certain diseases, trauma or surgical procedures. Pathologcal neovasclarization occurs within tissues of the eye as a result of certain ophrbalmic disorders such as diabetic retinoparbies, proliferatve vitreoretinopathies, corneal neovascularization, iris rubeosis, and diseases that cause isctiemia of the ocalar tissues (e.g., occlusion of the central retinal vein, occlsion of the central retinal artery, certain inflammatory corldilions, etc.). Also, iatrogenic neovasculdriation can occur following certain ophthalmological surgical procedures which disrupt normal blood supply to tissues of the eye or those which cause localized proliferations of cells known as "fibroblasts". Examples of ophthalmological surgical procedures that have been associated with untoward post-surgical neovascularization include glaucoma filtration surgery and corneal transplant surgery. Web site: http://www.delphion.com/details?pn=US06462071__
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Aqueous cosmetic composition containing stably solubilized uric acid and amphoteric surfactant and method for stably solubilizing uric acid in aqueous cosmetic composition Inventor(s): Ogata; Akiko (Osaka, JP), Tomura; Kazuyo (Osaka, JP), Tsujino; Yoshio (Osaka, JP) Assignee(s): Yamahatsu Sangyo Kaisha, Ltd. (osaka-fu, Jp) Patent Number: 5,833,969 Date filed: July 30, 1997 Abstract: An aqueous cosmetic composition containing uric acid in a stably solubilized state together with 0.01 to 1.3% by weight of one or more amphoteric surfactants selected from the group consisting of (a) lauric acid amide propyl betaine, (b) alkyl carboxymethyl hydroxyethyl imidazolinium betaine, (c) coconut oil fatty acid amide propylmethylaminoacetic acid betaine, (d) sodium salt of coconut oil fatty acid acyl carboxymethyl hydroxyethyl ethylenediamine, (e) lauryl dimethylaminoacetic acid betaine and (f) coconut oil alkyl betaine, an alkali and water. The composition is adjusted to pH equal to or higher than pK.sub.1 of uric acid with the alkali to solubilize uric acid. A method for stably solubilizing uric acid in an aqueous cosmetic composition is also disclosed. Excerpt(s): The present invention relates to an aqueous cosmetic composition containing stably solubilized uric acid, a specific amphoteric surfactant, an alkali and water, and a method for stably solubilizing uric acid in an aqueous cosmetic composition. Uric acid as well as its salt and derivative (hereinafter they are simply referred to as "uric acid" altogether) are used in various cosmetic compositions as a substrate of one of oxidases, uricase, a stabilizer of a moisturizer, an ingredient for preventing skin roughness, an antidandruff ingredient and the like. For example, JP 61-118312 A discloses a keratin fiber dyeing composition of pH 4 to 10.5 which comprises uric acid, an amphoteric surfactant, a thickener and the like and a method for dyeing keratin fiber using the composition. JP 61-183204 A discloses a cosmetic composition comprising a moisturizer and uric acid as a stabilizer for the moisturizer. JP 63-246313 A (U.S. Pat. No. 4,961,925) discloses a hair cosmetic composition of pH 7.5 to 8.5 which comprises dielectron reducing oxidase, uric acid as a donor of the enzyme and the like. JP 1-275511 A discloses a topical composition for skin external use containing uric acid for preventing skin roughness. JP 1-275516 A discloses an antidandruff composition containing uric acid. JP 8-217652 (EP 0716846 A) discloses an oxidation hair dyeing composition of pH 6.7 to 9.5 which comprises uric acid, potassium hydroxide and/or monoethanolamine and the like. On the other hand, since the water-solubility of uric acid is very low such as about 0.0067%, at present, only a small amount of uric acid can be used in case of an aqueous solubilized system. In addition, in case of a dispersion system wherein uric acid is added in excess of its solubility, there are many problems such as precipitation of uric acid, limitation of containers to be used for packaging end products due to clogging of orifices thereof and the like. Web site: http://www.delphion.com/details?pn=US05833969__
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Benzofuran derivatives and use thereof for treating hyperuricemia Inventor(s): Kubota; Koichi (Nagano, JP), Tomiyama; Akira (Nagano, JP), Tomiyama; Tsuyoshi (Nagano, JP) Assignee(s): Kotobuki Seiyaku Company Limited (nagano, Jp) Patent Number: 4,797,415 Date filed: July 28, 1986 Abstract: A new series of benzofuran and benzothiophene derivatives are disclosed. These compounds have a structure which can be obtained by substituting the third position of 2-lower alkyl-benzofuran or 2-lower alkyl-benzothiophene with a substituted benzene derivative, itaconic acid derivative or a substituted phenoxymethyl tetrazole derivative. They are useful as diuretics without side effects of elevating serum uric acid levels and can be used in the treatment of hyperuricemia. Excerpt(s): It is well known that hyperuricemia and hypertension are among major risk factors of cardiovascular diseases. In long term diuretics therapy, for example, with the thiazide type diuretics, there occurs a frequent increase in serum uric acid levels. Such an increase leads to the occurrence of serious gouty arthritis. The present invention relates to diuretics without the aforesaid side effect and discloses a series of chemical compounds effective in treating hyperuricemia. Web site: http://www.delphion.com/details?pn=US04797415__
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Biological poultry litter treatment composition and its use Inventor(s): Rehberger; Thomas G. (Wauwatosa, WI) Assignee(s): AG Tech Products, Inc. (waukesha, Wi) Patent Number: 5,945,333 Date filed: August 26, 1997 Abstract: The present invention is a biological waste treatment product that utilizes the activity of scientifically selected bacteria to control the decomposition of poultry litter thereby improving litter quality. The end result is improved health and performance of the birds while also reducing the incidence of foot scabs and other lesions caused by poor litter conditions. Application of the unique combination of bacteria of the present invention results in several biochemical effects proving to be beneficial to the quality of the litter and thus the health and performance of the birds. Specially, bacteria of the present invention produce broad spectrum antimicrobial proteins active against gram (-) bacteria. The reduction of gram (-) bacteria reduces the level of microbial pathogens in the litter as well as reduces the population of gram (-) bacteria that break down uric acid into ammonia. In addition, bacteria in the present invention utilize uric acid as a substrate thus inhibiting the reduction of uric acid to ammonia. Further, bacteria of the present invention produce proteolytic enzymes which break down the protein excretion products from birds which improves the litter quality by reducing the water holding capacity of the litter. Finally, bacteria of the present invention also produce organic acids from starch fermentation which reduces the litter pH and thereby decreases the pathogenic and urilytic bacteria in the litter. Excerpt(s): Not Applicable. Controlling the condition of litter in poultry houses is essential to ensure a better environment and thus better health and performance of the birds. The condition or quality of litter can be affected by a number of factors such as
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moisture, temperature, pH, ventilation, stocking density and frequency of cleanout. Of these factors, cleaning out the built-up litter more frequently is the most effective way to control and immediately improve litter quality. Unfortunately, this method of improving litter quality is becoming less of an option for producers since litter costs have dramatically increased in recent years. Therefore, many producers have adopted the practice of reusing litter as a strategy to reduce costs. In broiler houses, litter will routinely be reused for four or more sequential flocks of birds. In turkey grow or finish houses, litter will be reused for two or more sequential flocks of birds. While the reuse of litter has reduced the immediate litter costs, the use of built-up litter necessitates implementing better management practices to maintain litter quality. Poor litter conditions lead to an increase in the populations of microbial pathogens in the litter and excessive ammonia production. Web site: http://www.delphion.com/details?pn=US05945333__ •
Color control system Inventor(s): Palmer; John L. (Philadelphia, PA), Timmerman; Marsha W. (Allentown, PA) Assignee(s): Enzymatics, Inc. (horsham, Pa) Patent Number: 5,032,506 Date filed: December 16, 1986 Abstract: An assay system useful for the determination of NAD(P)H, NAD(P), or a substrate of an enzyme which reacts with the formation or comsumption of NAD(P)H. Concentrations of organic substrates for example alcohol, cholesterol, uric acid, in a biological fluid such as saliva, blood or urine may be determined. The system includes a diaphorase which catalyzes a NAD(P)H-dependent reduction of a chromogen to cause a visible color change; this color change is indicative of the concentration sought to be determined. The system includes a chromogen which is a first substrate for the diaphorase which causes a color change when reduced by NAD(P)H, and a second substrate which is a competing substrate for the diaphorase; the competing substrate is irreversibly reduced by the diaphorase. The system is capable of measuring colorimetrically without dilution concentrations of organic compounds in biological fluids which previously could not be measured in such concentration. The system provides a convenient, practical sobriety test. The invention also provides a method for such determination and diagnostic kit. Excerpt(s): The present invention relates to a colorimetric determination of biological molecules or organic compounds that are substrates for NAD(P)-linked dehydrogenase enzymes. In addition, this invention is useful for the colorimetric determination of the levels or concentrations of NAD(P) linked dehydrogenase enzymes. This invention is also useful in the direct colorimetric measurement of NAD(P) and NAD(P)H. This invention reduces the amount of color that is generated when the substances are assayed which cause color to be generated in the presence of a chromogen. This reduction in color generation greatly expands upward the possible concentration of substance that can be measured. This makes possible the determination of the concentration of a wide variety of medical and industrial substances without dilution of the aqueous sample containing that substance to lower the concentration of the substance to be measured. This reduction in color that is generated in response to NADH production into a visible (or readable) range, is unknown in the prior art. The invention provides an improved system, devices and method for measuring
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qualitatively and quantitatively the concentration of NAD(P)H or NAD(P) using an enzyme, a diaphorase (lipoamide dehydrogenase), a chromogen which acts as a substrate (generally herein called a "first substrate") for the diaphorase, which generates color when reduced by NAD(P)H and a second substrate for the diaphorase, which substrate is irreversibly reduced but generates no color, at least not in the color range in which the chromogen generates color. Web site: http://www.delphion.com/details?pn=US05032506__ •
Composition and method for treatment and metaphylaxis of urate and mixed urate lithiasis Inventor(s): Georgiev; Georgi M. (Sofia, BG), Georgieva; Maria I. (Sofia, BG) Assignee(s): Tpo "pharmachim" (sofia, Bg) Patent Number: 4,816,483 Date filed: November 6, 1985 Abstract: A combination and method for treatment and metaphylaxis of urate and mixed urate lithiasis is disclosed. The active component of the invention is a nonionogenic surfactant of the formula R-COO(CH.sub.2 CH.sub.2 O).sub.n H, wherein R is linolic acid, linolenic acid, or oleinic acid, and n is a number from 18 to 40. The active component forms a complex water-soluble compound with uric acis, thereby dissolving urate calculi and eliminating uric acid from the urine. The invention exhibits rapid and reliable therapeutic effect, without side effects, and without reliance on maintenance of urine pH. Excerpt(s): This invention relates to a medicinal means for treatment and metaphylaxis of urate, urate-oxalate and urate-phosphate lithiasis. Nephrolithiasis is a very common urological disease characterized by the presence of renal calculi, small hard concretions of urate, oxalate, cysteine, and phosphate deposits which accumulate in the kidney. Nephrolithiasis is most often treated by surgical intervention. Pharmaceutical litholysis, the nonsurgical and medicinal dissolution of calculi, is known, but these methods are generally slow and of limited reliability for wide spread therapeutic use. Urate and mixed urate lithiasis has been treated in the past with preparations containing various salts, such as sodium and potassium citrates, bicarbonates, and citric acids. Preparation of this type include those known by the trade names Magurlite.RTM., Solurane.RTM. and another composition, Uralite.RTM., which contains certain medicinal plant extracts useful for litholysis. All of these compositions rely on the ability of the salts or extracts to maintain a pH of 7 in the urine, thus hampering the crystallization of uric acid in patients prone to renal lithogenesis. Citric acid 0.27. Web site: http://www.delphion.com/details?pn=US04816483__
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Composition of accelerating recovery of function of hematopoietic organs Inventor(s): Morishige; Fukumi (Fukuoka, JP) Assignee(s): Nissan Chemical Industries, Ltd. (tokyo, Jp) Patent Number: 4,839,172 Date filed: May 23, 1985
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Abstract: A composition for accelerating the recovery of hematopoietic function and a method of recovering the physical strength of patients by orally administering the composition are disclosed. The composition comprises a milt extract and vitamin C and/or its salt. The composition does not cause an increase of blood uric acid levels. Excerpt(s): The present invention relates to a composition for increasing the physical strength of healthy persons or for accelerating the recovery of physical strength by patients during or after medical treatment. More particularly, it relates to a composition comprising a mixture of a milt extract and vitamin C. For the purpose of accelerating the recovery of physical strength by patients during or after medical treatment, particularly by patients during or after treatment for the inhibition of nucleic acid metabolism of cancer cells, such as administration of anticancer agents and radiation, one important factor is the recovery of the hematopoietic function of bone marrow. The hematopoietic function of cancer patients, during pharmacotherapy with anticancer agents or the like or radiotherapy, is reduced. In particular, the number of blood platelets and leucocytes in the blood of such patients is significantly reduced. This reduction in hematopoietic function necessarily leads to reduced biophylaxis. For this reason, recovery of the hematopoietic function of bone marrow is contemplated to aid in the recovery of physical strength by such patients. Web site: http://www.delphion.com/details?pn=US04839172__ •
Compositions and methods of treating calcium renal stones Inventor(s): Pak; Charles Y. C. (Dallas, TX) Assignee(s): Board of Regents of the University of Texas System (austin, Tx) Patent Number: 4,888,182 Date filed: February 26, 1987 Abstract: Methods and compositions useful for the treatment and prophylaxis of calcium renal stones are disclosed. The methods involve administering potassium citrate compositions to persons afflicted with or susceptible to calcium renal stone formations. A typical dosage scheme involves administering about 30 to 120 meq potassium citrate per day in divided doses. Such treatments are effective in dissolving existing calcium stones and preventing formation of new calcium stones. Moreover, the results of a comparative clinical assay indicate the potassium citrate is superior to sodium citrate in the treatment of uric acid lithiasis. Potassium citrate therapy averts calcium renal stone formation, a complication which is often associated with sodium citrate or sodium bicarbonate alkalinization therapy. Excerpt(s): This invention is a continuation-in-part of copending U.S. patent application Ser. No. 741,715, filed June 6, 1985, now abandoned, which is a continuation of U.S. patent application Ser. No. 483,678, filed April 11, 1983, now abandoned, both of which are incorporated by reference herein. The present invention relates to methods and compositions for medical treatment; and more particularly, this invention relates to methods and compositions for the treatment and prophylaxis of calcium renal stones. Formation of stones within the urinary tract (clinically termed nephrolithiasis) represents a common health disorder. In the United States an estimated 5-10% of the population will develop urinary stones in their lifetime. Of these stones virtually all originate in the kidneys, while bladder stones are rarely encountered except in association with a foreign body. Nephrolithiasis, while usually not fatal, causes
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considerable suffering, morbidity and loss of work. Often it is a disease which recurs throughout a patient's lifetime. Web site: http://www.delphion.com/details?pn=US04888182__ •
Cyclic controlled electrolysis Inventor(s): Wolfson, Jr.; Sidney K. (Pittsburgh, PA), Yao; Shang J. (Pittsburgh, PA) Assignee(s): The Montefiore Hospital Association of Western Pennsylvania (pittsburgh, Pa) Patent Number: 4,663,006 Date filed: September 8, 1983 Abstract: Method and apparatus for cyclic control of both potential and current in electrolysis, called Cyclic, Controlled-potential, controlled current Electrolysis. The method can be used with a two-electrode cell (W and C), or a three-electrode set-up using a reference electrode R to form two half cells. The method involves supplying a controlled current, preferably a constant current, to the W and C electrodes to operate the electrolysis within well-defined upper and lower potential limits. In a first embodiment (called the constant-current, preset-voltage mode), when a predetermined voltage is reached, the current is reversed until a second predetermined voltage is reached. The cycle is then repeated continuously. In a second embodiment (called the preset-voltage, preset-time mode) the current is maintained constant until the predetermined voltage is reached. Then the voltage is maintained constant by reducing the current until a predetermined time of operation has elapsed. Then the current is reversed and the cycle repeats. In the case of both embodiments, the cell operates as above for a preset period of time after which the preset voltage and/or cycle time control is switched with respect to W and C electrodes, the role of the electrodes thus alternating over a longer time period. By this cyclic electrolysis method, improved removal in hemodialysis or peritoneal dialysis of urea, uric acid, creatinine and other wastes is achieved. Better electrode surface regeneration, which occurs sequentially while electrolysis is continuous, is obtained. Production of undersirable or toxic substances such as chloramine, hypochlorite, nitrogen oxides, cyanide, ammonia, and the like are prevented. No electrode poisoning is observed. Both in vitro and also in vivo electrolysis is achieved by the method and apparatus of the invention. Physiologic electrolyte balance can be maintained. Excerpt(s): The invention relates to apparatus and processes for Cyclic, Controlled potential, controlled current Electrolysis (CCE) employing a galvanostat (with or without a reference electrode) to monitor the potential difference between working and counter electrodes and alternately switch the current polarity so that predetermined current values i- and i+ are imposed when preset voltages, or, alternatively, voltage and time values are reached. More particularly, apparatus and process are useful in biomedical electrolysis applications, such as for removal in hemodialysis or peritoneal dialysis of urea, uric acid, creatinine, and other toxic wastes. A growing number of patients suffering from end stage renal disease are now able to survive through the use of hemodialysis and peritoneal dialysis. While hemodialysis provides life itself for these individuals, it also obligates them to a very dependent life style. Hemodialysis, generally performed at established dialysis centers, disrupts normal work schedules and severely limits travel. It may also produce a psychological burden for the patient who is time-restricted and immobilized in a center. These patients could obviously have a more pleasant, free, and productive life if treatment at home and/or office were available. The
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development of a portable or wearable regenerative hemodialysis system would certainly enhance the chance of home or office dialysis. Major efforts have been directed toward the development of a portable system. Most of the proposed portable systems are based on "closed-loop" dialysis which involves regeneration of a small volume of dialysis fluid by continuously removing the dialyzed wastes. Although a large number of toxins and wastes may be removed by passage through a charcoal bed, urea, a major metabolic waste removed by dialysis, is very poorly absorbed onto charcoal. The use of one regenerative dialysis system, Sorbsystem, has demonstrated that a urea removal device and an activated charcoal bed can provide the basis for a "closed-loop" dialysis. Sorbsystem has several problems peculiar to its urea removal method: (1) the generation of toxic ammonia; (2) the instability of the enzyme, urease, used therein; (3) the limited availability of the zirconium resins used therein; and (4) the removal of essential cations which generates an ionic imbalance. Web site: http://www.delphion.com/details?pn=US04663006__ •
Enzyme-based biosensor system for monitoring the freshness of fish Inventor(s): Luong; John H. T. (Mont-Royal, CA), Male; Keith B. (Verdun, CA), Nguyen; An L. (Dollard des Oremeaux, CA) Assignee(s): Her Majesty the Queen in Right of Canada, AS Represented by the National (ottawa, Ca) Patent Number: 5,288,613 Date filed: December 5, 1991 Abstract: The present invention relates to a method for determining the degree of freshness of raw, frozen and processed edible fish by monitoring the degradation of adenine triphosphate to inosine monophosphate, inosine and hypoxanthine. This method comprises simultaneously determining, by use of a suitable amperometric electrode such as platinum vs. silver/silver chloride polarized at 0.7 V, the amount of uric acid and hydrogen peroxide resulting from the degradation of hypoxanthine by xanthine oxidase, the degradation of inosine by the combined action of nucleoside phosphorylase and xanthine oxidase and the degradation of inosine monophosphate by the combined action of nucleotidase, nucleoside phosphorylase and xanthine oxidase. Also within the scope of this invention is a method for the immobilization of nucleotidase on the walls of a polymeric tube such as polystyrene tube and the coimmobilization of nucleoside phosphorylase and xanthine oxidase on a porous polymeric membrane such as a nylon membrane. Excerpt(s): Fish and other types of marine organisms lose their freshness very rapidly after death. Furthermore, the quality of canned salmon, tuna, crab and the like is largely dependent upon the freshness of the fish or shellfish used for processing. Freshness of fish can rarely be visually determined because it is often sold in frozen or processed form. From the standpoint of consumer protection and food hygiene, extensive research has been focused on the development of reliable and inexpensive methods of determination of fish freshness. This is urgently required in food industries since fish freshness is an important factor in the preparation of high-quality products. Indicators of fish freshness such as ammonia, amines, volatile acids, catalase activity, trimethylamine (TMA) and nucleotides have so far been proposed. Among these chemicals, nucleotides produced by adenosine triphosphate (ATP) decomposition are considered the most reliable and useful indicators. In recent years, considerable
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attention has been focused on nucleotide degradation in fish muscle as a reliable indicator of the freshness of raw fish. X is xanthine. Web site: http://www.delphion.com/details?pn=US05288613__ •
Etodolac for treatment of gout Inventor(s): Mullane; John F. (Westchester, NY) Assignee(s): American Home Products Corporation (new York, Ny) Patent Number: 4,663,345 Date filed: April 17, 1986 Abstract: A method is disclosed for lowering uric acid blood levels by administering an effective amount of etodolac. Excerpt(s): This invention relates to a novel therapeutic use of 1,8-diethyl-1,3,4,9tetrahydropyrano[3,4-b]indole-1-acetic acid whose generic name is etodolac. More specifically this invention relates to a method for lowering uric acid blood levels in humans for treatment of gout. The active agent of this invention, 1,8-diethyl-1,3,4,9tetrahydropyrano[3,4-b]indole-1-acetic acid or a therapeutically acceptable salt thereof, is disclosed in U.S. Pat. No. 3,939,178 issued Feb. 17, 1976. This active agent, hereinafter designated by its generic name etodolac, previously has been reported to be useful as an analgesic and anti-inflammatory agent. (See U.S. Pat. No. 3,939,178). I have now found unexpectedly that etodolac, either in its free acid form or in its therapeutically acceptable salt form, is useful for lowering uric acid blood levels in humans, and particularly humans suffering from gout. This finding, coupled with the fact that etodolac is a relatively safe drug, renders the method of this invention particularly useful and advantageous. Web site: http://www.delphion.com/details?pn=US04663345__
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Hair protection composition Inventor(s): Penna; Frederick J. (Ronkonkoma, NY), Smith; Walter P. (Head-Of-TheHarbor, NY) Assignee(s): Estee Lauder Inc. (new York, Ny) Patent Number: 4,786,493 Date filed: November 22, 1985 Abstract: Disclosed are a composition for protecting hair from damage caused by exposure to ultraviolet light and a method of using the composition. The composition comprises:(a) a first component selected from the group consisting of a material having superoxide dismutase activity, ascorbic acid, Cytochrome C, mixtures of nicotinamide dehydrogenase and lactate dehydrogenase, uric acid, uric acid salts, and mixtures thereof;(b) a second component selected from the group consisting of mannitol, catalase, and mixtures thereof, and(c) a third component selected from the group consisting of a disulfide, a thiol, and mixtures thereof, said disulfide and said thiol each having a molecular weight of at least about 100. Excerpt(s): The present invention relates to a composition for protecting hair from damage caused by exposure to ultraviolet light and to a method of protecting hair from
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such damage comprising applying an effective amount of the composition to the hair. Hair predominantly comprises certain polypeptide chains that are held together by disulfide bonds that link adjacent polypeptide chains. These bonds, which are formed from two cysteine amino acid residues on the adjacent keratin polypeptides, impart to the hair its mechanical strength and extensibility. Exposure to the sun tends to cause breakage of these disulfide bonds predominantly on the outer surface of the hair, including the outer surface of the hair cuticle. This results in stiffness and brittleness of the hair in dry weather and in frizziness of the hair in humid weather. It also results in the hair losing its color and luster. In addition, the breakage of the disulfide bonds of the keratin causes a protective layer of the hair to be broken down, thereby resulting in important constituents of the hair being extracted from the hair during washing. Sun damage to hair has been controlled by utilizing sunscreens which, when deposited on the hair, absorb ultraviolet light that would otherwise be absorbed by the hair itself. Sunscreen containing compositions, however, tend to be very oily, with the result that they typically are not esthetically appealing. Moreover, many commercially available sunscreens are not effective to shield the hair from all the ultraviolet light in sunlight. For example, a formulation of paraaminobenzoic acid (PABA), when it is deposited on the hair, typically might absorb only about 45 percent of the incident UVB ultraviolet radiation and virtually none of the radiation in the UVA region. Web site: http://www.delphion.com/details?pn=US04786493__ •
IL-6 as serum uric acid decreasing compound Inventor(s): Kishi; Shinji (Fukui-ken, JP), Nakamura; Toru (Kyoto, JP), Tsutani; Hiroshi (Fukui-ken, JP), Ueda; Takanori (Fukui-ken, JP), Yoshio; Nobuyuki (Fukui-ken, JP) Assignee(s): Applied Research Systems Ars Holding N.v. () Patent Number: 6,007,804 Date filed: February 23, 1998 Abstract: The present invention provides a serum uric acid decreasing agent which contains interleukin-6 (IL-6) as the active ingredient together with a pharmaceutically acceptable carrier; and a method for decreasing the serum uric acid level which comprises administering interleukin-6 (IL-6) in an effective amount to a patient. Excerpt(s): This invention relates to a serum uric acid decreasing agent and a method for decreasing serum uric acid levels. With changes in diet, gout has come to be regarded as a serious adult disease. It is known that the acute and intractable pain of gout is caused when uric acid excessively accumulates in the body and is deposited as calcium urate in the fingers and toes. Known methods for treating gout involve: 1) use of uric acid synthesis inhibitors to inhibit the accumulation of uric acid in the body; and 2) use of uric acid excretion promoters to accelerate the rapid excretion of uric acid accumulated in the body. There is only one uric acid synthesis inhibitor (i.e., allopurinol) readily available today. On the other hand, probenecid, sulfinpyrazone and benzbromarone are known as uric acid excretion promoters. However, it is known that allopurinol should be employed with caution, since it induces some problems such as systemic hypersensitivity. Similarly, uric acid excretion promoters such as benzbromarone may produce an attack of gout, when used inappropriately. Web site: http://www.delphion.com/details?pn=US06007804__
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Interference-eliminating membranes, test strips, kits and methods for use in uric acid assay Inventor(s): Chang; Tong H. (Taipei, TW), Chen; Hsueh-Fang (Taipei, TW), Ho; HungHsiu (Taipei, TW), Kuo; Ming-Yen (Taipei, TW), Lee; Tsai Yun (Taipei, TW), Lei; Yi Chih (Taipei, TW), Liu; Jiuan J. (Taipei, TW), Liu; Liahng-Yirn (Taipei, TW), Sheu; Shi-Yuan (Taipei, TW), Tsai; Yu Fen (Taipei, TW), Wu; Tai-Guang (Taipei, TW) Assignee(s): Development Center for Biotechnology (taipei, Tw) Patent Number: 6,699,720 Date filed: May 26, 2000 Abstract: The present invention relates to an interference-eliminating membrane for use in detecting uric acid in a sample, comprising a compound for inhibiting or shading uric acid interfering substances, or derivatives thereof, and a carrier having an absorption property and permeability for the sample; and a process for preparing the interferenceeliminating membrane.The present invention also provides a test strip for use in detecting uric acid in a sample, comprising a reagent reaction layer or optional interference-eliminating membranes and/or support layers; and a kit comprising the test strip of the invention. Excerpt(s): The present invention relates to an interference-eliminating membrane, test strips, kits and methods for use in detecting uric acid in a sample. The measurement of uric acid in blood serum or other body fluids is a very useful and valuable tool for diagnosing and monitoring the course of a variety of pathological conditions. For example, when uric acid is present at an abnormally high concentration in the blood, it tends to be crystallized in the body joints, which causes a very painful inflammatory condition, known as gout. High uric acid blood levels are also known to be associated with such conditions as uremia, which is characterized by an excessive destruction of white blood cell nuclei, e.g., leukemia and pneumonia. There are many substances, such as ascorbic acid, in blood serum and urine, which may be mistaken for uric acid in conventional assays. If a patient is mistakenly diagnosized as having a high level of uric acid, the patient may be erroneously subjected to a dangerous, expensive, uncomfortable, and unnecessary treatment. Therefore, the accurate determination of uric acid is not easily achieved but is essential. Web site: http://www.delphion.com/details?pn=US06699720__
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Intermediate release nicotinic acid compositions for treating hyperlipidemia having unique urinary metabolite profiles Inventor(s): Cefali; Eugenio A. (Lauderhill, FL) Assignee(s): Kos Pharmaceuticals, Inc. (miami, Fl) Patent Number: 6,406,715 Date filed: October 31, 1997 Abstract: Intermediate release nicotinic acid formulations having unique urinary metabolite profiles, which are suitable for oral administration once-a-day as a single dose during a 24 hour period for treating hyperlipidemia without causing drug-induced hepatotoxicity or drug-induced elevations in uric acid or glucose or both to levels that require the therapy to be discontinued, are disclosed.
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Excerpt(s): The present invention is directed to intermediate release nicotinic acid formulations having unique urinary metabolite profiles resulting from the absorption profiles of the nicotinic acid from the intermediate nicotinic acid formulations, which are useful for treating hyperlipidemia and methods of treating hyperlipidemia employing such compositions. Another aspect of the present invention, the nicotinic acid formulations are suitable for once a day dosing without causing drug-induced hepatotoxicity to a level which would require the therapy to be discontinued. More particularly, the present invention employs a composition of nicotinic acid, derivatives and mixtures thereof and a swelling agent to form an intermediate timed-release sustaining composition for nocturnal or evening dosing. Specifically, the present invention employs a composition of nicotinic acid and hydroxypropyl methylcellulose to treat hyperlipidemia in a once per day oral dosage form given during the evening hours that causes little if any hepatotoxicity. Nicotinic acid, 3-pyridinecarboxylic acid or niacin, is an antilipidemic agent that is marketed under, for example, the trade names Nicolar.RTM., SloNiacin.RTM., Nicobid.RTM. and Time Release Niacin.RTM. Nicotinic acid has been used for many years in the treatment of lipidemic disorders such as hyperlipidemia, hypercholesterolemia and atherosclerosis. This compound has long been known to exhibit the beneficial effects of reducing total cholesterol, low density lipoproteins or "LDL cholesterol," triglycerides and apolipoprotein a (Lp(a)) in the human body, while increasing desirable high density lipoproteins or "HDL cholesterol". The dosing regimen of IR nicotinic acid is known to provide a very beneficial effect on blood lipids as discussed in Knopp et al.; "Contrasting Effects of Unmodified and TimeRelease Forms of Niacin on Lipoproteins in Hyperlipidemic Subjects: Clues to Mechanism of Action of Niacin"; Metabolism 34/7, 1985, page 647. The chief advantage of this profile is the ability of IR nicotinic acid to decrease total cholesterol, LDL cholesterol, triglycerides and Lp(a) while increasing "HDL" particles. In fact, IR nicotinic acid has been well regarded as an effective drug in the treatment of high cholesterol since about the early 1960s. Unfortunately, IR nicotinic acid has never really become widely used because of the high incidence of flush that often occurs when an IR dose is taken. That means an individual may develop a visible, uncomfortable, hot or flushed feeling three or four times a day for about one hour following each IR dose. Web site: http://www.delphion.com/details?pn=US06406715__ •
Method and apparatus for maintaining urine specimens Inventor(s): Pak; Charles Y. C. (Dallas, TX) Assignee(s): Mission Pharmacal Company (san Antonio, Tx) Patent Number: 4,921,807 Date filed: January 26, 1988 Abstract: A urine specimen is preserved from bacterial deterioration as to relative constituents by adding thymol. To the thymol-treated specimen, lithium-solution volume-marker is added, then is divided into two (first and second) separate portions. Thereupon, using the first portion, standard conventional measurements and/or analysis is conducted for total volume, pH/acidity, uric acid, citrate, sodium, and potassium. To the second portion, there is added boric acid and hydrochloric acid, followed by standard/conventional measurement and/or analysis for ammonium ion, citrate, calcium, magnesium, phosphorus, oxalate and sulfate. Thereafter the findings are charted and compared to controls.
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Excerpt(s): It is now known that kidney stones form from a variety of metabolic, environmental and physicochemical disturbances. Metabolic factors include hypercalciuria (high urinary calcium), hyperoxaluria (high urinary oxalate), hyperuricosuria (high urinary uric acid), hypocitraturia (low urinary citrate), and unusually acid or alkaline urinary medium (Pak, Cecil Textbook of Medicine, 17th Edition, pp. 628-633, 1985). Important environmental factors are low urine volume, high urinary sodium, high urinary sulfate, high urinary phosphate, and low urinary magnesium (Pak et al. J. Urology, October, 1985, in press). Physicochemical factors indicate whether urine samples are supersaturated (therefore likely to support stone formation) with respect to stone-forming salts (calcium oxalate, brushite, sodium urate, struvite and uric acid). It is presumed that metabolic factors are due to disturbed metabolism of patients suffering from stones, whereas environmental factors originate from dietary aberrations. Physicochemical factors are dependent upon metabolic and environmental factors, since urinary saturation is calculated from various urinary excretions. Although the measurement of above stone-forming factors/risks would be very helpful in making the appropriate diagonsis and in offering proper treatment, it has been hampered by the difficulty in adequately preserving and collecting urine samples and by the lack of an easily understood way of displaying results. Web site: http://www.delphion.com/details?pn=US04921807__ •
Method and apparatus for monitoring sewage treatment efficiency and determining sewage sources Inventor(s): Braven; James (Plymouth, GB2), Brown; Leslie (Plymouth, GB2), Rhead; Michael M. (Plymouth, GB2) Assignee(s): Devon County Council (gb2) Patent Number: 4,554,077 Date filed: August 31, 1983 Abstract: A method of tracing sewage effluent is described in which samples of fluid flows are subjected to high performance liquid chromatography with respective elution systems capable of eluting different selected compounds therefrom, and the concentration of each compound in the sample is determined spectroscopically. The method is used to determine sewage flow paths in natural water bodies, such as rivers, to check for contamination by sewage, to determine possible sewage sources, the detection of uric acid, for example, being indicative of a human source; and to monitor the effluent from sewage treatment plants.A monitoring system for sewage treatment works is also described in which bromophenol blue is added to the sewage influent to the biodegradation stage as a dilution indicator and the changes in the bromophenol blue concentration and in the concentration of a biodegradable sewage component, such as uric acid, are monitored throughout the stage to give an indication of the progress of the biodegradation reaction; this information is used in controlling the operation of the plant to maximize its efficiency. Excerpt(s): The present invention relates to the qualitative and quantitative tracing of sewage flows and to the monitoring of reactions in fluids, with particular reference to biodegradation reactions in sewage treatment plants, to the monitoring of the operational efficiency of such plants and to the control thereof. The need to trace sewage effluents in environmental water bodies, such as rivers, estuaries and coastal waters is self-evident but at present various difficulties are encountered in putting it into effect. For example colored tracers, which may be added to a flow to give rapid preliminary
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information on flow paths in nonturbid flows, are generally adsorbed on to solids suspended in sewage flows and hence give anomalous results, if any, under these conditions. Constituents of the sewage itself, such as potassium and sodium chlorides, although more difficult to assess than coloured tracers, are usable in fresh water conditions but, naturally, cannot be used as tracers in salt waters. Many other sewage constituents, such as urea, also occur naturally at levels similar to those found in sewage or have until now been very difficult or time-consuming to estimate. One object of the invention is, therefore, to provide a more convenient method of tracing sewage flows than is currently available. Web site: http://www.delphion.com/details?pn=US04554077__ •
Method and system for determining bioactive substances Inventor(s): Cattaneo; Maurice V. (Outremont, CA), Luong; John H. T. (Mount Royal, CA), Male; Keith B. (Pierrfonds, CA) Assignee(s): National Research Council of Canada (ottawa, Ca) Patent Number: 5,411,866 Date filed: March 30, 1993 Abstract: An apparatus and method for measuring glutamine and glucose in certain cell cultures and body fluids in the presence of interfering endogenous compounds e.g. ascorbic acid, uric acid or glutamic acid. Prior to enzymatic degradation and amperometric detection of the products or elements resulting from the degradation, the interfering substances are retained by an anion exchanger disposed upstream of the enzymatic degradation site. The conditions of the method are controlled to utilize the difference of isoelectric points of the measured biosubstance and of the interfering compounds respectively. Excerpt(s): This invention relates to an amperometric biosensor system and method for determining certain bioactive substances, or biosubstances, particularly glutamine in cell culture samples, for example during cell cultivation processes, and glucose in urine and blood samples. More particularly, the invention provides a method and apparatus for determining glutamine or glucose using enzymatic degradation and amperometric detection, in the presence of interfering compounds. Regulation of glutamine during mammalian or insect cell culture cultivation is of vital importance for optimization of cell growth and its productivity. Cell cultivation under depleted glutamine causes severe growth limitation, whereas increasing glutamine beyond a certain limit produces ammonia at toxic levels. Therefore it is critical to regulate glutamine during the course of cultivation processes. The determination of glutamine is also of importance in a clinical laboratory. Cerebrospinal glutamine levels are used with blood ammonia determinations in diagnosis of hepatic encephalopathy. Elevated glutamine levels are reported in parenteral nutrition, meningitis and in cerebral haemorrhage. U.S. Pat. No. 4,790,191 issued Oct. 25, 1988 to Romette et al. proposes an apparatus for measuring Lglutamine in a liquid sample. The apparatus includes a membrane on which are immobilized the enzymes glutaminase and glutamate oxidase. Glutamine in the sample is acted upon by the enzymes to form an enzymatic reaction product. The membrane is associated with a sensor, e.g. an oxygen electrode, which is capable of sensing either the product or a compound or element consumed or liberated in the process. Web site: http://www.delphion.com/details?pn=US05411866__
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Method for control or calibration in a chemical analytical determination Inventor(s): Terashima; Masaaki (Saitama, JP) Assignee(s): Fuji Photo Film Co., Ltd. (kanagawa, Jp) Patent Number: 5,547,874 Date filed: April 5, 1995 Abstract: An aqueous dispersion used for control or calibration of a dry analysis element comprising at least one color producing reagent and a porous layer, which comprises water-insoluble liquid particles having a mean particle size of from about 0.01 to about 10.mu.m selected from the group consisting of phthalates, trimellitates, phosphates, benzoates, amides, phenols, aliphatic esters, hydrocarbons, halogenated hydrocarbons, adipates, sebacates and natural polymers dispersed therein and a substance which is the same as or similar to the analyte to be determined wherein said substance is selected from the group consisting of glucose, urea, uric acid, creatinine, bilirubin, hemoglobin, triolein, glycerine, cholesterol, triglyceride, (NH.sub.4).sub.2 SO.sub.4, NH.sub.4 Cl, CaCl.sub.2, Ca(NO.sub.3).sub.2, MgCl.sub.2, NaCl, KCl, K.sub.2 HPO.sub.4, (NH.sub.4).sub.2 SO.sub.4, Ca(NO.sub.3).sub.2, and NaNO.sub.3. Excerpt(s): The present invention relates to a method for chemical analytical determination using a dry analytical element and a novel aqueous dispersion for control of the precision of the analytical element or for making a calibration curve in quantitatively analyzing a target component (an analyte) in samples of organic body fluids, such as whole blood, using dry analysis materials. More specifically, it is concerned with a method which is particularly useful in quantitatively analyzing wholeblood samples with dry analysis elements. Dry analysis materials and methods for quantitative analysis of aqueous fluid sample utilizing them are described in U.S. Pat. Nos. 2,846,808, 3,016,292, 3,036,893, 3,368,872 and 3,552,928. Dry, multilayer analysis materials composed of a transparent support having thereon at least one reagent layer and a porous layer, in this order, and quantitative analysis methods of aqueous fluid samples using those materials are described, e.g., in U.S. Pat. Nos. 3,992,158, 3,983,005, 4,042,335, 4,066,403, 4,144,306, 4,132,528, 4,258,001, 4,357,363, 4,381,921 and 4,292,272 and Japanese Unexamined Patent Publication No. 24576/81, H. G. Curme et al. and R. W. Spayd et al., Clinical Chemistry, vol. 24, pp. 1,335-1,350 (1978), Bert Walter, Anal. Chem., vol. 55, No. 4, pp. 498-514 (1983) and so on. The feasibility of using not only diluted serum and blood plasma as a sample, but also non-diluted whole blood, is described. Web site: http://www.delphion.com/details?pn=US05547874__
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Method for the quantitative determination of physiological components in biological fluids Inventor(s): Hirano; Kenichi (Iwakura, JP), Kosaka; Akira (Seto, JP), Matsunaga; Kuniyoshi (Ichinomiya, JP), Murao; Sawao (Sakai, JP), Tanaka; Noriaki (Sakai, JP) Assignee(s): Amano Pharmaceutical Company Limited (jp) Patent Number: 4,554,249 Date filed: October 25, 1982 Abstract: A novel enzyme of bilirubin oxidase produced by a genus Myrothecium or genus Coprinus origin microorganism and a conventional enzyme of laccase are found, in the presence of a specific additive compound, e.g. a surface active agent, aromatic
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carboxylic acid, sulfa drug or protease, to oxidize both conjugated and unconjugated bilirubin in biological fluid to biliverdin without formation of hydrogen peroxide, such that in the case of conventional enzymatic methods of the quantitative determination of glucose, cholesterol, neutral fats, free fatty acids, phospholipids or uric acid all existing together with bilirubin in biological fluid, the usual interference with such determination, as otherwise caused by bilirubin coexisting in such fluid, can be prevented by adding such a bilirubin oxidase or laccase together with such a specific additive compound to the determinative reaction system. Excerpt(s): This invention relates to a method for the quantitative determination of physiological components in biological fluids. More particularly, it relates to a method for the quantitative determination of specific physiological components contained in biological fluids by using bilirubin oxidase either alone or together with supplemental additives. The invention relates further to the same method as above but by using laccase instead of such bilirubin oxidase. Bilirubin oxidase mentioned above is a novel enzyme, and accordingly the significance of this enzyme may be appreciated by the following detailed preliminary explanation. Bilirubin (C.sub.33 H.sub.36 N.sub.4 O.sub.6) is a pigment present in biological fluids such as blood serum, urine, etc. An enzyme present in the brain of rats or guinea pigs and an enzyme produced by a mushroom of the genus Agaricus have hitherto been reported to act on bilirubin. However, the enzymological properties of these enzymes have not been elucidated yet. Web site: http://www.delphion.com/details?pn=US04554249__ •
Method of reducing serum uric acid and/or increasing renal uric acid clearance with thromboxane synthetase inhibitor inhibitor and/or thromboxane receptor antagonist Inventor(s): Piraino; Anthony J. (Media, PA), Saris; Steven D. (Ardmore, PA) Assignee(s): Ciba-geigy Corporation (ardsley, Ny) Patent Number: 5,021,448 Date filed: February 22, 1990 Abstract: A method of reducing serum uric acid and/or increasing renal clearance of uric acid in a mammal in need thereof comprising administering to such mammal a uricosuric effective amount of a thromboxane synthetase inhibitor, a thromboxane receptor antagonist, or both in a combined uricosuric effective amount is disclosed. Compositions having one or more of the foregoing in combination with one or more known uricosurics are also set forth. Excerpt(s): The present invention relates to the field of thromboxane synthetase inhibitors, thromboxane receptor antagonists, and uric acid and disease states due to an excess thereof such as gout, gouty arthritis, etc. Uric acid is a naturally occurring metabolite of a number of typically ingested compounds, especially xanthines such theobroma (in chocolate), caffeine, etc, and is generally disposed of by the body by execretion into the urine from the blood. When uric acid production is high or its elimination from the body is low so that serum levels are at high levels for considerable periods of time, there is the risk that uric acid crystals will begin to form at various points in the body. When these crystals become large enough to become painful, clinical conditions such as gout, gouty arthritis, and uric acid stones (urinary and elsewhere) result. Such situations may result from disease states or may be drug induced, for example, serum uric acid levels are elevated with a substantial number of diuretic drugs, most notably the thiazide diuretics, and upon cytotoxic antineoplastic agent
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administration and cyclosporin A. Clinical conditions associated with elevated serum uric acid include gout, gouty arthritis, gouty nephropathy, eclampsia, and diseases that involve accelerated formation and destruction of blood cells. Upon diagnosis of the elevated serum uric acid, therapies which are begun have included dietary intervention (to reduce intake of substances which are metabolized to uric acid), intervention in the metabolic pathways leading to uric acid (i.e. allopurinol which inhibits xanthine oxidase from converting hypoxanthine and xanthine to uric acid) and uricosurics such as probenecid or sulfinpyrazone, which increase the amount of uric acid resulting in the urine by improving its passage into the urine from the blood or by interfering in its reuptake. Web site: http://www.delphion.com/details?pn=US05021448__ •
Method of testing for diabetes that reduces the effect of interfering substances Inventor(s): Bates; Harold M. (4 Barnes Ct., East Brunswick, NJ 08816), Evans; Cody A. (28 Innisbrook Ave., Las Vegas, NV 89113) Assignee(s): None Reported Patent Number: 5,571,723 Date filed: May 3, 1993 Abstract: An improved method of testing individuals for diabetes, even if they have levels of interfering substances (e.g., uric acid, bilirubin, and glutathione) that would otherwise interfere with such testing, is disclosed. The individual's protein-bound glucose level and glucose level are compared to the analogous values for a reference population to enable the risk of that individual's having diabetes to be assessed. The substances that would otherwise tend to interfere with the assay for protein-bound glucose are removed before the assay, desirably by precipitating the protein-bound glucose using uranyl acetate, which desirably leaves substantially all of the interfering substances in the supernatant, then separating the precipitate from the supernatant, redissolving the precipitate, and conducting the colorimetric assay on the resulting solution. An improved colorimetric test for protein-bound glucose using viologens as the colorimetric electron acceptors is also disclosed. Excerpt(s): This invention relates to an improved test for diabetes mellitus ("diabetes") that can be used even with a patient having levels of substances that would otherwise interfere with testing, e.g., elevated (high) uric acid/and or bilirubin levels. Broadly speaking, this invention concerns a method of testing that treats a specimen from an individual to substantially reduce or eliminate interfering substances from the specimen, assays a material derived from the treated specimen for a certain clinical value (proteinbound glucose level), obtains a second clinical variable for that individual (glucose level), and then uses those two clinical values to assess the likelihood of that individual having diabetes, e.g., by placing the individual in any one of several categories, which categories are associated with pre-established risks of having diabetes. As is well known, diabetes is a serious disease affecting a significant portion of the population. Detecting whether an individual has diabetes and monitoring diabetes therapy are some of the problems confronting medicine. An early screening test for diabetes and one that is still commonly used involves determining an individual's blood glucose level. See, e.g., U.S. Pat. Nos. 2,981,606; 3,653,841; 3,791,988; and 3,920,580 (all of the patent and other documents, including literature articles, cited or otherwise identified in this application are hereby incorporated herein in their entireties for all purposes). Glycosylated amino acids in urine have also been used to screen for diabetes. See U.S.
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Pat. No. 4,371,374. U.S. Pat. No. 4,397,956 concerns a single-reading pseudo-kinetic method for monitoring the status of control of ketoacidosis-prone diabetics by measuring the blood glucose and at least one additional indicator analyte (e.g., ketone bodies such as acetone, beta-hydroxybutyrate, and acetoacetate and fatty acid derivatives). One problem with glucose tests is that even in an individual who does not have diabetes, his or her glucose level can vary over a wide range, depending on when the test sample or specimen (e.g., blood) was taken and when and what the individual last ate. Furthermore, even if one glucose test gives a high enough reading to strongly suggest the presence of diabetes, that individual must undergo additional tests, for example, a so-called glucose tolerance test, before a diagnosis of diabetes can be confirmed. The glucose level of a diabetic taking insulin can also vary dramatically depending upon when the individual last took insulin and on the dosage. It is not unknown for individuals who have diabetes to take insulin shortly before specimens are taken from them for therapy-monitoring glucose tests, so that their glucose tests will indicate normal levels of glucose and make it appear that the individuals have been conscientiously following their prescribed regimens of insulin therapy. That makes monitoring such therapy more difficult. For all these reasons, glucose testing alone was and is known to have significant disadvantages. Web site: http://www.delphion.com/details?pn=US05571723__ •
Process for measuring the concentration of a component in body fluid such as urine or blood Inventor(s): Fujie; Shinichi (Saitama, JP), Matsuyuki; Akira (Tokyo, JP), Oshima; Nobuo (Tokyo, JP) Assignee(s): Kabushiki Kaisha Meidensha (tokyo, Jp) Patent Number: 5,055,398 Date filed: May 19, 1988 Abstract: A process for determining the concentration of a component, such as glucose, uric acid or polyamine, in a body fluid, such as urine, blood, blood serum, blood plasma, saliva or gastric juice, includes processing the body fluid with a catalase or an immobilized catalase for decomposing hydrogen peroxide included in the body fluid. When the body fluid is processed with the calalase, an inhibitor which inhibits the reaction between the catalase and the component is added to the body fluid after processing with the catalase. The process also includes processing the body fluid with a strongly basic anion exchange resin. When the concentration of polyamine in the body fluid is measured, the body fluid is processed with an acylpolyamineamido hydrolysis enzyme for converting acetylpolyamine into polyamine in the body fluid. After processing the body fluid by the these operations, hydrogen peroxide produced by the reaction between an oxidase and the component is measured. Excerpt(s): The present invention relates generally to a process for measuring the concentration of a component in a body fluid, such as blood, urine or the like. More specifically, the invention relates to a process for measuring the concentration of a component, which is able to produce hydrogen peroxide in the presence of an oxidase, in a body fluid. Further specifically, the invention relates to a process for measuring the concentration of a component, such as glucose, uric acid or polyamine, which serves as a substrate for an oxidase to produce hydrogen peroxide in the present of the oxidase, in a body fluid. As is well known, organic components, such as glucose, uric acid, polyamine or the like, exists in body fluids, such as urine, blood, blood serum, blood
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plasma, lymph, saliva, gastric juice or the like. In the case of healthy or normal organisms, the concentrations of these components are constant. On the other hand, in the case of an abnormal organism, they are changed. For the purpose of medical diagnosis, it is therefore very beneficial to be able to accurately determine the concentration of these components in body fluids. In particular, a very small amount of glucose exists in body fluids, such as blood, urine or the like. In the case of healthy or normal organisms, the glucose in the body fluids exists exists in extremely small quantity. On the other hand, in the case of an abnormal organism, such as for example, a diabetic, the concentration of glucose increases markedly. For the purpose of medical diagnosis, it is therefore very beneficial to be able to determine the concentration of glucose in body fluids. Web site: http://www.delphion.com/details?pn=US05055398__ •
Surface-modified electochemical biosensor Inventor(s): Geise; Robert J. (Piscataway, NJ), Piznik; Sylvia S. (Jackson, NJ), Reynolds; Eugene R. (Highland Park, NJ), Yacynych; Alexander M. (East Brunswick, NJ) Assignee(s): Rutgers University (new Brunswick, Nj) Patent Number: 5,286,364 Date filed: March 29, 1991 Abstract: An electrode for a biosensor (e.g., a glucose biosensor) has a layer of an electrically insulating polymer formed in situ on its operating surface by electropolymerization. For example, a diaminobenzene and a dihydroxybenzene (e.g., 1,3-diaminobenzene and resorcinol) are copolymerized on the electrode's surface by immersing the electrode in a circulating dilute solution of the monomers in deaerated phosphate buffer, and applying a small, continuously cycling voltage between that electrode and another electrode (e.g., from 0.00 V to 0.80 V) until current flow between the electrodes decreases to a minimum. Because the polymer is electrically insulating, polymerization ceases while the polymer layer is still very thin (e.g., 10 nm). An analyte sensing agent, e.g., an enzyme such as immobilized glucose oxidase, is imbedded in the polymer, but with a number of its analyte recognition sites unblocked. The polymer layer shields the electrode surface from interferrents and fouling agents such as uric acid and proteins, but it is sufficiently porous to permit smaller electroactive molecules (e.g., hydrogen peroxide) generated through contact of the enzyme with the analyte molecules to diffuse through to the electrode surface. Preferably a ferrocene compound (e.g., alpha-hydroxy-ethylferrocene or 1,1'-dimethylferrocene), which functions as an electron mediator, is applied to the polymer film, and held there by adsorption. Excerpt(s): The present invention relates to chemically modified electrodes for use as biosensors, such as have been applied in clinical chemistry testing and in other monitoring and control environments, and is more particularly directed to problems relating to electrode fouling and interference from other species present in complex matrices such as blood, serum, or fermentation broths. Biosensors are devices for sensing such substances as electrolytes, gases, proteins, enzymes, metabolites, antibodies, and antigens. They find wide application in such diverse fields as clinical chemistry testing, bioreactor monitoring and control, fermentation control, and medical research. A biosensor of the sort of interest here generally includes a base electrode and a biochemically discriminating element disposed about the electrode. Typically the biochemically discriminating element is provided by a membrane which surrounds the electrode. The biosensor is placed in contact with the sample substrate under
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investigation, and the membrane isolates and transforms the desired analyte into an electrically active species or otherwise generates an electrical potential, which is sensed and monitored by the base electrode. Familiar examples include the use of a glass membrane, which selects and traps the desired electrolyte cation, such as Na.sup.+, in the silicate matrix of the glass, thereby producing a charge separation which is sensed by the electrode, and the use of a polyvinyl chloride matrix incorporating the antibiotic molecule valinomycin for selectively extracting K.sup.+ ions. Web site: http://www.delphion.com/details?pn=US05286364__ •
Tetrazolylquinazolinones as anti-hyperuricemic agents Inventor(s): Wagner; Steven R. (Indianapolis, IN) Assignee(s): Merrell Dow Pharmaceuticals Inc. (cincinnati, Oh) Patent Number: 4,757,075 Date filed: October 14, 1986 Abstract: A method of reducing serum levels of uric acid which comprises administration of 3-(1H-tetrazol-5-yl)-4(3H)-quinazolinone or its pharmaceutically acceptable salts is described herein. Excerpt(s): Hyperuricemia, or an excess of uric acid in the blood, can lead to attacks of gout and may be a risk factor for the development of cardiovascular disease, carbohydrate intolerance, and urate-induced nephropathy. Thus, methods of lowering levels of uric acid in the blood would be useful. 3-(1H-Tetrazol-5-yl)-4(3H)quinazolinones have been described in U.S. Pat. No. 4,419,357 as useful as antiallergic agents but the patent gives no indication that the compounds would have any effect on uric acid levels in the blood. It has now been found that 3-(1H-tetrazol-5-yl)-4(3H)quinazolinone and its salts, when administered orally to humans, are useful in reducing levels of uric acid in the blood. Thus, the present invention is directed to a method of reducing levels of uric acid in the blood and, more particularly, of treating hyperuricemia by the administration of an effective amount of 3-(1H-tetrazol-5-yl)4(3H)-quinazolinone or a pharmaceutically acceptable salt thereof. Web site: http://www.delphion.com/details?pn=US04757075__
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Therapeutic combination of free-radical scavenger and tumor necrosis factor Inventor(s): Marafino, Jr.; Benedict J. (San Francisco, CA), Zimmerman; Robert (Lafayette, CA) Assignee(s): Cetus Corporation (emeryville, Ca) Patent Number: 4,985,241 Date filed: August 25, 1989 Abstract: Damage to cells, tissue and other body parts in a mammalian host may be treated by using a lymphokine or cytotoxin in conjunction with at least one biological modifier, which may be a free radical scavenger or a metabolic inhibitor. The lymphokine or cytotoxin is preferably tumor necrosis factor and the biological modifier is preferably uric acid, buthionine sulphoximine, vitamin C, aspirin, or nordihydroguaiaretic acid. Such a combination may be used to treat, for example,
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cancer, infectious diseases, and damage caused by radiation therapy, high oxygen tension, and chemotherapy. Excerpt(s): This invention relates to a composition suitable for administration to mammalian hosts as a therapeutic formulation. More particularly, this invention relates to a combination therapy for free-radical bodily damage employing a lymphokine or cytotoxin such as tumor necrosis factor (TNF) and a biological modifier consisting of either one or more free radical scavengers that protect against damage caused by freeradical generation, or that selectively increase the susceptibility of a tumor to radical damage by depleting or reducing its radical scavenging capacity, or an inhibitor of one or both of the cyclooxygenase or lipoxygenase pathways of arachidonic acid metabolism. Lymphokines and cytotoxins, such as interleukin-2, interferon-alpha, interferon-gamma, colony stimulating factor, and tumor necrosis factor, are proteins secreted by T cells and/or macrophages upon activation by antigens or lectins. Interleukin-2 (IL-2), a lymphokine which is produced by normal peripheral blood lymphocytes and induces proliferation of antigen or mitogen stimulated T cells after exposure to plant lectins, antigens, or other stimuli, was first described by Morgan, D. A., et al., Science (1976) 193:1007-1008. Then called T cell growth factor because of its ability to induce proliferation of stimulated T lymphocytes, it is now recognized that in addition to its growth factor properties it modulates a variety of functions of immune system cell in vitro and in vivo and has been renamed interleukin-2 (IL-2). IL-2 is one of several lymphocyte-produced, messenger-regulatory molecules which mediate immunocyte interactions and functions. Tumor necrosis factor (TNF) was first described by Carswell et al., Proc. Natl. Acad. Sci. USA (1975) 72:3666-3670 as an endotoxininduced serum factor which causes necrosis of chemically transformed tumor cells when growing in mice. Human TNF is known to be cytotoxic to neoplastic cells, and has been produced in recombinant form. See Pennica et al., Nature (London) (1984) 312:724-729 and Shirai et al., Nature (London) (1985) 313:803-806, Wang et al., Science (1985) 228:149154. Web site: http://www.delphion.com/details?pn=US04985241__ •
Threshold color control system Inventor(s): Palmer; John L. (Philadelphia, PA), Timmerman; Marsha W. (Allentown, PA) Assignee(s): Enzymatics, Inc. (horsham, Pa) Patent Number: 5,036,000 Date filed: July 20, 1987 Abstract: A system for quantitative colorimetric analysis of biological fluids or organic compounds, including NAD(P)H, or a substrate of an enzyme which reacts with the formation or consumption of NAD(P)H. Concentrations of organic substrates for example alcohol, cholesterol, uric acid, in a biological fluid such as saliva, blood or urine may be determined. The system gives a digital reading of the organic material the concentration which is sought to be determined; the concentration of NAD(P)H is determined by a color change or color "signal" when the NAD(P)H is above a threshold concentration and by the absence of a color signal when the concentration of NAD(P)H is below the threshold concentration. The system includes a chromogen, an electronaccepting reactant which, until exhausted, prevents a visible color change due to accumulation of reduced chromogen, and a catalyst. The system is capable of measuring
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colorimetrically without dilution concentrations of organic compounds in biological fluids which previously could not be measured in such concentration. Excerpt(s): This invention relates to systems, more particularly a device for quantitative colorimetric analysis of organic substances concentrations generally in biological fluids. The invention also relates to a method for making such analysis. The invention also relates to a system, a device and a method which involves the reduced and oxidized coenzymes nicotinamide-adenine dinucleotide (NADH, NAD+) or nicotinamideadenine dinucleotide phosphate (NADPH, NADP+) (collectively herein referred to as NAD(P)H and NAD(P)+) in a system, a device and a method for determination of NAD(P)H. The device may be disposable. The invention relates to a novel and unique analog to digital colorimetric signal system, device and method which determines the concentration of NAD(P)H or of an organic substance which generates NAD(P)H in a NAD(P)+ dependent dehydrogenase reaction where the dehydrogenase is specific to the substrate. The concentration of the NAD(P)H or of the organic substance of unknown concentration, the concentration which is determined, is ascertained by an "off"-"on" change of color, preferably quite decisive and highly distinctive, like yellow to intense blue. Web site: http://www.delphion.com/details?pn=US05036000__ •
Treatment of diseases of the central nervous system using uric acid as a scavenger of peroxynitrite Inventor(s): Farber; John L. (St. Davids, PA), Hooper; Douglas Craig (Medford, NJ), Koprowski; Hilary (Wynnewood, PA) Assignee(s): Thomas Jefferson University (philadelphia, Pa) Patent Number: 5,872,124 Date filed: July 31, 1996 Abstract: The process of treating a disease of the central nervous system with an agent from one or more of the following three classes of agents: (1) nitric oxide scavengers, (2) peroxynitrite scavengers, and (3) agents that either interfere with the synthesis of iNOS in the cell or the enzymatic activity of iNOS in the cell. Excerpt(s): The field of the invention is the treatment of diseases of the central nervous system using either a nitric oxide scavenger, a peroxynitrite scavenger, or an agent that interferes with the activity or cellular production of the enzyme, inducible nitric oxide synthase (iNOS). The overproduction in the body of nitric oxide (NO) and/or peroxynitrite (ONOO.sup.-) has been suggested by some to be a contributing factor to diseases of the central nervous system, particular those that are immune-mediated and/or inflammatory. The enzyme iNOS is responsible for the production of nitric oxide during an immune response. Nitric oxide combines with superoxide (O.sub.2.sup.-) to form peroxynitrite. Those molecular level considerations are relevant to the present inventions. Web site: http://www.delphion.com/details?pn=US05872124__
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Uricase and a method for the preparation thereof Inventor(s): Chikano; Takahide (Shizuoka, JP), Kamimura; Minoru (Yaizu, JP), Takashio; Masachika (Yaizu, JP) Assignee(s): Sapporo Breweries Limited (tokyo, Jp) Patent Number: 4,882,280 Date filed: May 22, 1986 Abstract: Different from conventional uricase products, the uricase of the present invention has outstandingly high thermal stability and is active in a wide range of pH from 5 to 10 for the oxidative decomposition of uric acid undertaken in clinical analysis. The uricase of the invention is produced microbiologically by a thermophilic microorganism belonging to the genus of Bacillus and especially named as Bacillus sp. TB-90 which is a novel species distinguishable from any of the microorganisms belonging to the genus of Bacillus. Excerpt(s): The present invention relates to a novel uricase and a method for the preparation thereof. Uricase is an enzyme useful as a reagent in the quantitative determination of uric acid and the present invention provides a novel uricase having properties quite suitable for this purpose, which can be produced by a thermophilic microorganism. Uricase (EC 1.7.3.3) is an enzyme found in the livers and kidneys of animals as well as certain microorganisms and catalyses the oxidation of uric acid in the presence of oxygen so that it is used widely in the quantitative determination of uric acid in clinical examinations. As is disclosed in Japanese Patent Kokai Koho Nos. 5581586 and 56-124381, Japanese Patent Publication No. 56-43230, uricase is widely produced by a microbiological means while one of the problems in these microbiological processes is that the culturing of the microorganism takes a considerably long time of one day to three days or even longer because the microorganism utilized in the process disclosed in each of the above mentioned patent literatures is mesophilic. Web site: http://www.delphion.com/details?pn=US04882280__
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Use of 3-(4-bromo-2-fluorobenzyl)-4-oxo-3H-phthalazin-1-ylacetic hypouricaemic agent
acid
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a
Inventor(s): Thyrum; Per T. (Wilmington, DE) Assignee(s): Ici Americas, Inc. (wilmington, De) Patent Number: 4,895,843 Date filed: February 9, 1988 Abstract: The invention concerns a novel therapeutic agent for use in reducing raised serum uric acid levels comprising 3-(4-bromo-2-fluorobenzyl)-4-oxo-3H-phthalazin-1ylacetic acid or a pharmaceutically acceptable salt thereof. Excerpt(s): This invention concerns a novel therapeutic agent and, more particularly, a novel therapeutic agent for use in lowering blood uric acid levels in man, that is a novel hypouricaemic agent. The invention also concerns the use of the therapeutic agent in the production of a novel medicament for reducing blood uric acid levels and a method of medical treatment or prophylaxis which involves reducing blood uric acid levels by administration of said therapeutic agent to man. Uric acid is the principal product of the metabolism in man of purine derivatives such as nucleic acids. The normal plasma concentration of uric acid is close to the solubility limit, beyond which crystal deposition
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tends to occur in various tissues throughout the body, leading to the disease condition known as gout and gouty arthritis. The uric acid containing deposits (also known as tophi) in such conditions may occur in cartilage, bone, bursae, tendons, connective tissue overlying bony prominences, as well as sub-cutaneously and in the area of the kidney. Elevated blood uric acid levels (hyperuricaemia) may be caused by dietary absorption of uric acid or purine derivatives and also occur in a number of disease conditions. The latter include, for example, pneumonia, blood diseases involving a large turnover of purine nucleotides (such as myeloid leukaemia, myeloid dysplasia and pernicious anaemia), psoriasis, diabetes mellitus and renal disease. In addition, hyperuricaemia may also occur following the cytotoxic chemotherapy or radiotherapy of neoplasms, after the administration of pyrazinamide or of various hypotensive agents affecting renal function, or as a result of excessive biosynthesis arising from a genetic defect. A number of therapeutic agents are known which lower blood uric acid levels (that is which possess a hypouricaemic effect). Such agents include, for example, probenecid, sulphinpyrazone and allopurinol and operate by various different mechanisms such as inhibiting uric acid formation (allopurinol) and increasing renal excretion (probenecid). However, there is a continuing need for new therapeutic agents which exert a hypouricaemic effect. Web site: http://www.delphion.com/details?pn=US04895843__ •
Use of C-5 mono-substituted barbiturates to treat disorders of uric acid metabolism Inventor(s): Warrell, Jr.; Raymond P. (New York, NY) Assignee(s): Memorial Hospital for Cancer and Allied Diseases (new York, Ny) Patent Number: 4,880,811 Date filed: June 24, 1987 Abstract: The present invention provides a method for decreasing the bodily content of uric acid in a subject which comprises administrating to the subject an effective contentdecreasing amount of a barbiturate compound mono-substituted at the carbon-5 position.The invention also provides a pharmaceutical composition and a method for treating disorders of uric acid metabolism and resulting ailments in a subject. Excerpt(s): Throughout this application various publications are referenced and citations are provided in parentheses for them. The disclosures of these publications in their entireties are hereby incorporated by reference into this application in order to more fully describe the state of the art to which this invention pertains. Disorders of uric acid metabolism are extremely common. These disorders may afflict 1% or more of human individuals (Hall, A. P., et al., Am. J. Med. 42: 27, 1967; Heine, J., Virchow's Arch. f. Path. Anat., 260: 521, 1926; Decker, J. L. et al., Arth. Rheum. 5: 144, 1962). The best known example is gout which causes a painful, chronic arthritis which can be extremely debilitating and can lead to extensive deformities (Wyngarden, J. B. and Kelly, W. N., The Metabolic Basis of Inherited Disease, 916-1010, J. B. Stanbury, J. B. Wyngarden, D. S. Fredrickson, 4th ed. McGraw-Hill: New York, 1978; Bauer, W. and Krane, S. M., Disease of Metabolism, 805-849, G. G. Duncan, 5th ed., Saunders: Philadelphia, 1964). Gout may be primary or secondary. Primary gout consists of hereditary diseases which are associated with increased serum uric acid levels (hyperuricemia). Secondary gout may occur in cancers, particularly leukemias, and in other blood disorders (e.g. polycythemia, myeloid metaplasia, etc.). There exists abundant evidence that prolonged elevations of serum uric acid are associated with the deposition of sodium urate crystals in many tissues, including kidney and joints.
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Web site: http://www.delphion.com/details?pn=US04880811__ •
Wearable, portable, light-weight artificial kidney Inventor(s): Beltz; Alex D. (956 Notre Dame St., Upland, CA 91786) Assignee(s): None Reported Patent Number: 5,284,470 Date filed: November 2, 1992 Abstract: A portable artificial kidney in the form of a self-contained unit whose size and shape is such that it is light-weight and relatively small. It can be worn or attached to a patient in such a manner that it will not interfere with normal physical activities. The artificial kidney has a blood plasma separator unit that receives impure whole blood from the body of a patient and it separates a predetermined amount of plasma therefrom and returns the remainder of the blood back to the patients body. The separated plasma is then transmitted through a chemical treatment unit where the contaminated plasma is relieved of uric acid, creatinine, phosphate, and ammonium ions. The detoxified plasma is then transmitted to a water removal unit and then the detoxified plasma is returned to the patients circulatory system. Excerpt(s): The invention relates to a blood detoxification system and more specifically to a structure in the form of a small, light-weight, wearable, artificial kidney. There are a large number of people throughout the world who have kidneys that do not function properly. The standard treatment for people when they are under medical care is to use a dialysis machine for detoxification of their blood. Some of the major drawbacks of using dialysis machines is they are very expensive, they are very large and heavy, and a patient usually has to be detoxified several times a week. A standard treatment may take four or more hours to complete and it must be done at a medical facility. Also approximately 200 to 300 liters of dialyzing fluid is needed for each dialysis treatment. The dialyzing machines utilize specialized dialyzing membranes that filter out the impurities in the blood as the combined toxic blood and dialyzing fluid are passed therethrough. More recent advances in the state of the art have been to build a structure in the form of an artificial kidney and these are basically modified versions of the dialyzing machines. Most of the research and development has been directed to the development of better dialyzing membranes, their packaging and sterilization. Some English commercial models automatically sterilize themselves after each dialyzing period. Other research and development work is concerned with a reduction of the 200300 liters of dialyzing fluid needed for each dialysis. Although there has been much done in the development of blood compatible polymers for the membranes, as yet, none has been found that will transport impure whole blood through the membrane without some undesirable effects. Web site: http://www.delphion.com/details?pn=US05284470__
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Wound therapeutic mixture containing medical grade hyaluronic acid and tissue culture grade plasma-fibronectin in a delivery system that creates a moist environment which simulates in utero healing Inventor(s): Taylor-McCord; Darlene (24666 Morningstar La., Dana Point, CA 92629) Assignee(s): None Reported Patent Number: 5,604,200 Date filed: May 2, 1994 Abstract: A wound therapeutic mixture is formulated to work alone or in combination with human growth factors, and is useful for treatment of burns, open sores, incisions, and wounds. The mixture is comprised of a medical grade hyaluronic acid (hyaluronan) and tissue culture grade plasma-fibronectin in combination with calcium, phosphate, uric acid, urea, sodium, potassium, chloride, and magnesium, all elements found in amniotic fluid. The mixture creates a moist healing environment which simulates the fetal in utero wound healing matrix. The therapeutic mixture can be sterile or contain an FDA acceptable preservative system. The compositions may be in the form of a liquid, creme, ointment, gel, hydrogel, hydrocolloid or dressing. Excerpt(s): This invention relates the treatment of burns, open sores, incisions and wounds. In particular it relates to topical wound therapeutic formulations containing a hyaluronic acid (hyaluronan) and plasma-fibronectin in combination with elements found in amniotic fluid which simulates the fetal in utero wound healing matrix. The "greying of America" is well documented. People are living longer and have expectations for a quality life as well as well as a long life. People afflicted with long term illness run the risk of getting bed sores, pressure sores and a myriad of skin irritations and chronic wounds. Web site: http://www.delphion.com/details?pn=US05604200__
Patent Applications on Uric Acid 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 uric acid: •
Agents for corneal or intrastromal administration to treat or prevent disorders of the eye Inventor(s): Carpio Aragon, Gabriel Arthuro; (Tijuana, MX), Castillejos, David; (Chula Vista, CA), Floress, Jose Luis Gutierres; (Tijuana, MX), Karageozian, Vicken H.; (Laguna Beach, CA), Park, John; (Santa Ana, CA) Correspondence: Robert D. Buyan; Stout, Uxa, Buyan & Mullins, Llp; Suite 300; 4 Venture; Irvine; CA; 92618; US Patent Application Number: 20040043082 Date filed: March 14, 2003
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This has been a common practice outside the United States prior to December 2000.
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Abstract: Methods and preparations for treating disorders of the eye and/or causing dissolution of corneal proteoglycans and organized healing of corneal stroma, softening of the cornea for non-surgical refractive correction of eyesight, removing corneal haze and opacification, inhibiting fibroblasts and preventing corneal fibrosis and scar formation, treating pterigiums and treating corneal neovascularization as well as iris neovascularization. Preparations containing a) urea, b) urea derivatives (e.g., hydroxyurea, thiourea), c) antimetabolites, e) urea, urea derivatives, non-enzymatic proteins, nucleosides, nucleotides and their derivatives (e.g., adenine, adenosine, cytosine, cytadine, guanine, guanitadine, guanidinium, guanidinium chloride, guanidinium salts, thymidine, thymitadine, uradine, uracil, cysteine), reduced thioctic acid, uric acid, calcium acetyl salicylate, ammonium sulfate, isopropyl alcohol, ethanol, polyethylene glycol, polypropylene glycol or other compound capable of causing nonenzymatic dissolution of the corneal protoeglycans or f) any of the possible combinations thereof, are administered to the eye in therapeutically effective amounts. Excerpt(s): This application claims priority to U.S. Provisional Application 60/363,979 filed on Mar. 14, 2002, which is expressly incorporated herein by reference. This application is also a continuation-in-part of copending U.S. patent application Ser. No. 10/215,680 entitled Agents for Intavitreal Administration To Treat or Prevent Disorders of the Eye filed on Aug. 9, 2002, which is a continuation of U.S. patent application Ser. No. 09/517,798 filed on Mar. 2, 2000 and now issued as U.S. Pat. No. 6,462,071 B1. The present invention relates generally to pharmaceutical preparations and medical treatment methods, and more particularly agents (i.e. Urea, Urea derivatives, nonsteroidal anti-inflammatory drugs and Anti-metabolite drugs) used alone or in combinations with each other (or with other agents) to treat or prevent certain disorders of the eye. U.S. Pat. Nos. 5,629,344 (Chariton) and 5,470,881 (Chariton) describe certain therapeutic applications of urea preparations to the eye. These prior patents specifically describe non-aqueous ointments and other non-aqueous preparations of urea for use in the eye, pointing out that aqueous solutions of urea were believed to be impractical for use in the eye. For example, these prior patents state as follows: "One of the reasons urea has not been used in treating eye disorders is that it will hydrolyze in aqueous vehicles thus producing ammonia as a byproduct. Ammonia is toxic to the eye, and thus urea in an aqueous solution would be impractical for use as an ophthalmic medicament." Thus, prior to Applicant's invention, aqueous solutions of urea or urea derivatives were thought to be unstable and potentially toxic to the eye. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Biosensing meter Inventor(s): Chen, Chao-Wang; (Taipei, TW), Ou-Yang, Xing; (Junghe City, TW), OuYang, Yao; (Junghe City, TW), Wu, Ja-Shi; (Taipei, TW), Wu, Shu-Mei; (Taipei, TW) Correspondence: Rabin & Champagne, P.C.; Suite 500; 1101 14th Street, N.W.; Washington; DC; 20005; US Patent Application Number: 20030204313 Date filed: April 26, 2002 Abstract: A biosensing meter, applicable to measure glucose, uric acid or cholesterol level in the human body, such that a user can inspect the body condition of himself/herself at any time. The biosensing meter has a slot to be plugged with a key code strip, a correction strip or an inspection strip under various conditions, so as to activate input procedure and operation parameters. Therefore, an equipment calibration
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can be performed as required. When an analyte-containing fluid (normally blood) is dripped on the inspection strip, the inspection result is obtained according to the operation procedure and parameters obtained previously, Excerpt(s): The present invention relates in general to a biosensing meter. More particularly, the present invention relates to an electrochemical glucose biosesnsor. The biosensing meter applied for detecting the substance contained in the blood to be analyzed, such as glucose or cholesterol normally employs a disposable sample strip to complete the inspection. The sample strip has a reaction well to allow blood dripped thereon. Via the combination of microprocessor/ROM, the whole operation is controlled. Further by execution various procedures, the analysis results for measurement are obtained. However, the advancement of technique continuously alters the operation procedure of measurement. To the bio-inspection field, the measurement factor is changed according to the manufacture of sample strip. However, if the hardware in the sensing meter cannot be upgraded consequently, the purchased sensing meter is then inapplicable for the new batch of sample strips. As a result, the sensing meter has to be renewed. Such method is very impractical. Another conventional sensing meter improves the above drawbacks by adding another slot on the sensing meter. According to the position for plugging the sample strip, an additional memory key is designed and inserted therein. While performing measurement, the memory key has to be inserted in the sensing meter all the time for the same batch of sample strips. According to the operation procedure and parameter provided by the memory key, a correct measurement result is obtained. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Compositions for raising uric acid levels and methods of using same Inventor(s): Sacks, Meir S.; (Pittsburgh, PA), Van Dyke, Knox; (Morgantown, WV) Correspondence: Alan G. Towner; Pietragallo, Bosick & Gordon; One Oxford Centre, 38th Floor; 301 Grant Street; Pittsburgh; PA; 15219; US Patent Application Number: 20020045580 Date filed: October 16, 2001 Abstract: Compositions for the treatment of uric acid deficiency are disclosed. The compositions generally comprise either a precursor or derivative of uric acid, which, when administered to a patient, will result in a raising of the uric acid levels in that patient. The compositions can optionally comprise one or more additional active ingredients such as antioxidants, glutathione precursors, or inhibitors of NO synthase or homocysteine. Methods for raising uric acid levels in a patient are also disclosed. These methods are useful for in the treatment of various illnesses, such as cancer, infectious disease, Alzheimer disease and neurodegenerative diseases. Use of improved solutions comprising the present compositions in organ preservation is also disclosed. Excerpt(s): This application is a continuation-in-part of U.S. application Ser. No. 09/449,037 filed Nov. 24, 1999 and a continuation-in-part of U.S. application Ser. No. 09/449,161 filed Nov. 24, 1999, both of which are continuations of Ser. No. 09/127,184 filed Jul. 31, 1998, all of which are incorporated herein by reference. The present invention relates to compositions comprising one or more uric acid precursors or uric acid derivatives. The compositions are useful in the treatment of diseases in which low levels of uric acid are observed. Accordingly, methods for treating such diseases are also within the scope of the present invention. Oxidative damage is believed to be a
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mechanism of damage in many diseases. Such damage is found, for example, in diseases such as cancer, rheumatoid arthritis, heart disease, cataracts, inflammatory diseases, artery occlusion, diabetes, neurodegenerative diseases, and age-related macular degeneration. Free radicals, a major cause of oxidative damage, may be generated by environmental radiation, air pollution, inflammation and excessive physical and mental exertion. A free radical is an atomic species having a free electron, and is typically propagated from oxygen or nitric oxide or by specific enzymatic reactions like NADPH oxidase, xanthine oxidase and NO synthase I, II or III. Peroxynitrite (OONO).sup.- is a strong oxidizer formed from superoxide [.O].sup.- and nitric oxide [.NO], which, among other things, causes tissue damage and damage to membrane lipids, DNA and RNA of cells. Peroxynitrite has 1,000 times the oxidative activity as concentration-equivalent amounts of hydrogen peroxide, and is therefore a potent oxidizer capable of causing significant damage in vivo. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method for treating gout and reducing serum uric acid Inventor(s): Burke, Steven K.; (Sudbury, MA), Holmes-Farley, Stephen Randall; (Arlington, MA) Correspondence: Hamilton, Brook, Smith & Reynolds, P.C.; 530 Virginia Road; P.O. Box 9133; Concord; MA; 01742-9133; US Patent Application Number: 20020187120 Date filed: April 17, 2002 Abstract: A method for treating gout and/or reducing serum uric acid levels in a patient is disclosed that includes administering to the patient a therapeutically effective amount of an amine polymer; for example, an aliphatic amine polymer. Examples of polymers useful in the invention are sevelamer hydrogen chloride and colesevelam. The invention includes the use of amine polymers such as a cross-linked polymer characterized by a repeat unit having the formula: 1and salts and copolymers thereof, where n is a positive integer and x is zero or an integer between 1 and about 4. Also described is a use, for the manufacture of a medicament, of a polymer that reduces serum uric acid levels in a patient. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/305,568, filed on Jul. 13, 2001, and U.S. Provisional Application No. 60/284,445, filed on Apr. 18, 2001. The entire teachings of the above application(s) are incorporated herein by reference. The prevalence of gout is approximately 1.3 to 3.7 percent of the general population. Individuals suffering from gout excrete approximately 40 percent less uric acid, the final breakdown product of purine degradation, than nongouty individuals for any given plasma urate concentrations. Hyperuricemia, a condition which precedes gout, can result from increased production or decreased excretion of uric acid, or from a combination of the two processes. In an individual with hyperuricemia, plasma and extracellular fluids are supersaturated with urate (a serum uric acid level greater than 8.5 mg/dL at baseline), and crystal deposition in tissue is likely to occur, resulting in the clinical manifestations of gout. Acute gout typically results following a prolonged period in which excessive amounts of uric acid and urate are present in serum. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods for reducing uric acid levels Inventor(s): Boyd, Marcele; (Sun Prairie, WI), Robinson, Dale; (Middlefield, CT) Correspondence: Steven J. Sarussi; Mcdonnell Boehnen Hulbert & Berghoff; 32nd Floor; 300 S. Wacker Drive; Chicago; IL; 60606; US Patent Application Number: 20010044437 Date filed: January 11, 2001 Abstract: Disclosed are methods of reducing serum uric acid levels, the methods comprising administration of substituted indolealkanoic acids to patients in need of such treatment. Also disclosed are such compounds useful in the treatment of gout and related diseases. Also disclosed are pharmaceutical compositions containing the compounds. Excerpt(s): This application claims benefit of U.S. Provisional Application Ser. No. 60/176,273, filed Jan. 14, 2000, which is incorporated herein by reference in its entirety. This invention relates to indole acetic acids and their use in pharmaceutical compositions. More specifically, it relates to substituted indole acetic acids and their use as hypouricemic agents, agents useful for lowering blood uric acid levels. Uric acid containing deposits (also known as trophi) resulting from unphysiologically elevated plasma uric acid levels tend to occur in various tissues throughout the body, leading to the disease condition known as gout and gouty arthritis. Uric acid containing deposits in such conditions may occur in cartilage, bone, bursae, tendons, connective tissue overlying bony prominences, as well as, subcutaneously and in the area of kidney. Elevated blood uric acid levels also occur in number of other disease conditions including myeloid leukemia, myeloid dysplasia, pernicious anemia, psoriasis, diabetes mellitus and renal disease. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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One-package post-foaming oxidation hair dye composition Inventor(s): Aoki, Masahiro; (Osaka, JP), Tsujino, Yoshio; (Osaka, JP) Correspondence: Henkel Corporation; 2500 Renaissance Blvd; Ste 200; Gulph Mills; PA; 19406; US Patent Application Number: 20030084517 Date filed: June 13, 2002 Abstract: A one-package post-foaming oxidation hair dye composition containing uricase, uric acid, at least one oxidation dye, and at least one post-foaming agent is provided. The oxidation hair dye composition is packaged in a single package, and foams after spreading on hair. Excerpt(s): This application is a continuation under 35 U.S.C.sctn.365(c) and 35 U.S.C.sctn.120 of international application PCT/JP99/07273, filed on Dec. 24, 1999, the international application not being published in English. The present invention relates to a one-package oxidation hair dye composition using uricase. More particularly, the present invention relates to a one-package post-foaming oxidation hair dye composition which is better in the use feeling and the handling property and which has the excellent dyeing effects to hair. In previous oxidation hair dyes, color development was performed by mixing a first solution containing an oxidation dye and a second solution containing an oxidizing agent immediately before use, and oxidation-polymerizing the
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oxidation dye. However, since the oxidizing agent greatly damages hair due to its strong oxidizing force, in order to solve such the problems, the present inventors paid attention to the mild oxidizing action of enzymes and proposed a hair dye composition which contains a dielectron transfer oxidase as an acceptor and its donor as a substrate, and utilized the oxidation of an oxidation dye by the enzymatic oxidation reaction for hair dyeing (JP-A 63-246313). When this invention is used, since an oxidation reaction occurs first by the contact of the composition with oxygen, a one-package oxidation hair dye was obtainable by blocking oxygen from the composition. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
PEG-modified uricase Inventor(s): Clark, Mike A.; (Lexington, KY), Ensor, Charles Mark; (Lexington, KY), Holtsberg, Frederick Wayne; (Nicholasville, KY) Correspondence: Gwilym John Owen Attwell; Woodcock Washburn Kurtz; Mackiewicz & Norris Llp; One Liberty Place - 46th Floor; Philadelphia; PA; 19103; US Patent Application Number: 20030082786 Date filed: August 2, 2001 Abstract: The present invention is directed to uricase modified with polyethylene glycol and to methods of treating different illnesses characterized by increased circulating uric acid levels, including but not limited to, hyperuricemia and tumor lysis syndrome. Excerpt(s): The present invention is directed to uricase modified with polyethylene glycol and to methods for treating number of different illnesses characterized by increased circulating uric acid levels. Uric acid is a product of purine metabolism in birds, reptiles, and primates, including humans. Uric acid is produced in the liver by oxidation of xanthine and hypoxanthine. Xanthine is an intermediate in the catabolism of guanine nucleotides while hypoxanthine is produced during the breakdown of adenine nucleotides. In most mammals, uric acid is further oxidized by the enzyme urate oxidase to allantoin. Allantoin, because of its lost pyrimidine ring, shows a more than 20 times greater water solubility than uric acid. Urate oxidase, also called uricase, is an enzyme of the purine degradation pathway. Uricase catalyzes the conversion of uric acid+O.sub.2 into allantoin+CO.sub.2. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Prebiotic and probiotic compositions and methods for their use in gut-based therapies Inventor(s): Dickstein, Jack; (Huntingdon Valley, PA), Mehta, Raj; (King of Prussia, PA), Ranganathan, Natarajan; (Broomall, PA) Correspondence: Licatla & Tyrrell P.C.; 66 E. Main Street; Marlton; NJ; 08053; US Patent Application Number: 20020187134 Date filed: May 15, 2001 Abstract: Microencapsulated and/or enteric coated compositions containing a mixture of probiotics, prebiotics and ammoniaphilic bacteria with high urease activity with or without sorbents with specific adsorption affinities for uremic toxins such as creatinine, uric acid, phenols, indoles, middle molecular weight molecules and inorganic
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phosphate and water absorbents are provided. Also provided are methods of alleviating symptoms of uremia in a patient which comprises administering orally to a patient suffering from uremia a microencapsulated and/or enteric-coated composition. Excerpt(s): The invention relates to pharmaceutical compositions and methods of using these compositions to treat renal, hepatic and gastrointestinal diseases by eliminating toxins and other metabolic waste products and reducing or retarding undesirable bacterial over growth. In one embodiment, the pharmaceutical composition comprises a prebiotic, a probiotic, an ammoniaphilic bacteria, and sorbents, all of which are microencapsulated and/or enteric coated. Alternatively, the probiotic, prebiotic and ammoniaphilic bacteria are administered together in a microencapsulated gelatin capsule, while the sorbents, if needed, are administered separately in a microencapsulated and/or enteric coated formulation. These pharmaceutical compositions are useful in treating renal and hepatic diseases and bacterial overgrowth in the gastrointestinal tract. Kidney disease is ranked fourth among the major diseases in the United States afflicting over 20 million Americans. More than 90,000 patients die each year because of kidney diseases. In recent years the number of chronic kidney failure patients has increased about 11 percent annually. About 80,000 Americans on dialysis die of various complications each year and more than 27,000 are on waiting lists for kidney transplants each year with only about 11,000 of these patients receiving transplants. Further, nearly 250,000 Americans suffer from end stage renal disease (ESRD), which is the final stage in chronic renal failure. In normal, healthy humans, metabolic waste nitrogen is primarily excreted via the kidneys as urea in the urine. However, in individuals with kidney disease, as well as a number of other diseases such as inborn errors in urea cycle enzyme deficit, waste nitrogen accumulates in the body thereby manifesting toxic symptoms. Hyperammonium can lead to mental retardation and, in severe cases, coma. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Thromboxane inhibitors, compositions and methods of use Inventor(s): Tejada, Inigo Saenz de; (Madrid, ES) Correspondence: Edward D Grieff; Hale & Dorr Llp; 1455 Pennsylvania Ave, NW; Washington; DC; 20004; US Patent Application Number: 20030050305 Date filed: November 1, 2002 Abstract: The present invention describes methods for treating or preventing sexual dysfunctions in males and females, and for enhancing sexual responses in males and females by administering a therapeutically effective amount of at least one thromboxane inhibitor, and, optionally, at least one compound that donates, transfers or releases nitric oxide, elevates endogenous levels of endothelium-derived relaxing factor, stimulates endogenous synthesis of nitric oxide or is a substrate for nitric oxide synthase, and/or at least one vasoactive agent. The male or female may preferably be diabetic. The present invention also provides novel compositions comprising at least one thromboxane inhibitor, and, at least one compound that donates, transfers or releases nitric oxide, elevates endogenous levels of endothelium-derived relaxing factor, stimulates endogenous synthesis of nitric oxide or is a substrate for nitric oxide synthase, and, optionally, at least one therapeutic agent, such as, vasoactive agents, nonsteroidal antiinflanmmatory compounds (NSAIDs), selective cyclooxygenase-2 (COX-2) inhibitors, anticoagulants, angiotensin converting enzymes (ACE) inhibitors,
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angiotensin II receptor antagonists, renin inhibitors, and mixtures thereof. The present invention also provides methods for treating or preventing ischemic heart disorders, myocardial infarction, angina pectoris, stroke, migraine, cerebral hemorrhage, cardiac fatalities, transient ischaemic attacks, complications following organ transplants, coronary artery bypasses, angioplasty, endarterectomy, atherosclerosis, pulmonary embolism, bronchial asthma, bronchitis, pneumonia, circulatory shock of various organs, nephritis, graft rejection, cancerous metastases, pregnancy-induced hypertension, preeclampsia, eclampsia, thrombotic and thromboembolic disorders, intrauterine growth, gastrointestinal disorders, renal diseases and disorders, disorders resulting from elevated uric acid levels and dysmenorrhea, and for inhibiting platelet aggregation or platelet adhesion or relaxing smooth muscles. Excerpt(s): This application is a continuation of PCT/US01/16318 filed May 22, 2001, which claims priority to U.S. Provisional Application No. 60/205,536 filed May 22, 2000. The present invention describes methods for treating or preventing sexual dysfunctions in males and females, and for enhancing sexual responses in males and females by administering a therapeutically effective amount of at least one thromboxaiie inhibitor, and, optionally, at least one compound that donates, transfers or releases nitric oxide, elevates endogenous levels of endothelium-derived relaxing factor, stimulates endogenous synthesis of nitric oxide or is a substrate for nitric oxide synthase, and/or at least one vasoactive agent. The male or female may preferably be diabetic. The present invention also provides novel compositions comprising at least one thromboxane inhibitor, and, at least one compound that donates, transfers or releases nitric oxide, elevates endogenous levels of endothelium-derived relaxing factor, stimulates endogenous synthesis of nitric oxide or is a substrate for nitric oxide synthase, and, optionally, at least one therapeutic agent, such as, vasoactive agents, nonsteroidal antiinflammatory compounds (NSAIDs), selective cyclooxygenase-2 (COX-2) inhibitors, anticoagulaits, angiotensin converting enzymes (ACE) inhibitors, angiotensin II receptor antagonists, renin inhibitors, and mixtures thereof. The present invention also provides methods for treating or preventing ischemic heart disorders, myocardial infarction, angina pectoris, stroke, migraine, cerebral hemorrhage, cardiac fatalities, transient ischaemic attacks, complications following organ transplants, coronary artery bypasses, angioplasty, endarterectomy, atherosclerosis, pulmonary embolism, bronchial asthma, bronchitis, pneumonia, circulatory shock of various organs, nephritis, graft rejection, cancerous metastases, pregnancy-induced hypertension, preeclampsia, eclampsia, thrombotic and thromboembolic disorders, intrauterine growth, gastrointestinal disorders, renal diseases and disorders, disorders resulting from elevated uric acid levels and dysmenorrhea, and for inhibiting platelet aggregation or platelet adhesion or relaxing smooth muscles. Adequate sexual function is a complex interaction of hormonal events and psychosocial relationships. There are four stages to sexual response as described in the International Journal of Gynecology & Obstetrics, 51(3):265277 (1995). The first stage of sexual response is desire. The second stage of sexual response is arousal. Both physical and emotional stimulation may lead to breast and genital vasodilation and clitoral engorgement (vasocongestion). In the female, dilation and engorgement of the blood vessels in the labia and tissue surrounding the vagina produce the "orgasmic platform," an area at the distal third of the vagina where blood becomes sequestered. Localized perivaginal swelling and vaginal lubrication make up the changes in this stage of sexual response. Subsequently, ballooning of the proximal portion of the vagina and elevation of the uterus occurs. In the male, vasodilation of the cavernosal arteries and closure of the venous channels that drain the penis produce an erection. The third stage of sexual response is orgasm, while the fourth stage is resolution. Interruption or absence of any of the stages of the sexual response cycle can
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result in sexual dysfunction. One study found that 35% of males and 42% of females reported some form of sexual dysfunction. Read et al, J. Public Health Med., 19(4):387391 (1997). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Treatment for cardiovascular disease Inventor(s): Johnson, Richard; (Bellaire, TX), Kivlighn, Saluh; (Doylestown, PA), Mazzali, Marilda; (Houston, TX) Correspondence: Mcdermott, Will & Emery; 600 13th Street, N.W.; Washington; DC; 20005-3096; US Patent Application Number: 20020019360 Date filed: June 28, 2001 Abstract: This invention relates to a method for treating and preventing hypertension by administering a therapeutically effective amount of an agent capable of reducing uric acid levels in a patient in need of such treatment. Additionally, the scope of the invention includes a method of treating coronary heart disease by administering a therapeutically effective amount of an agent capable of reducing uric acid levels in a patient in need of such treatment. Excerpt(s): This application claims priority from co-pending provisional application Serial No. 60/214,825 filed on Jun. 28, 2000. Uric acid is a purine metabolite that in most animals is degraded by the hepatic enzyme uricase to allantoin. However, several mutations of the gene for this enzyme occurred during early primate development with the consequence that man and other primates have relatively higher levels of serum uric acid [Wu, X., Muzny, D. M., Lee, C. C., and Caskey, C. T., Two independent mutational events resulted in the loss of urate oxidase during hominoid evolution. J Mol. Evol. 34:78-84 (1992)]. The adaptive benefit of this deletion is not known nor has the modern day consequences of these mutations been fully understood. It has been hypothesized that the loss of uricase provided a protective benefit to prehistoric man who was known to have a very low sodium diet [Eaton, S. B., Konner, and M., Paleolithic nutrition: A consideration of its nature and current implications. N Engl J Med 312: 283-289 (1985)] but in modem times these mutations resulted in the development of hypertension and other cardiovascular diseases. In most subjects, the loss of uricase appears to be of no significance, but for the 10 to 15 percent of the general population with the highest uric acid levels (>6.0 mg/dl in women and >6.5mg/dl in men), there is an increased risk for the development of hypertension, atherosclerosis, and other cardiovascular diseases. Additionally 25 to 50% of hypertensive individuals have elevated serum uric acid, based upon the current standards 7 mg/dl [Cannon, P. J., Stason, W. B., Demartini, F. E., Sommers, S. C., and Laragh, J. H., Hyperuricemia in primary and renal hypertension. N Engl J Med 275:457-464 (1966]. This invention demonstrates for the first time mechanistic evidence that uric acid is directly related to the development of increased blood pressure. An association between an elevated uric acid and an increased risk for cardiovascular disease was originally suggested by Haig in the late 1800s. Haig postulated that uric acid crystals might precipitate in the circulation and occlude the microvasculature [Haig, A., On uric acid and arterial tension. Br Med J 1:288-291 (1889)], thereby assuming that the damaging effects of uric acid were related to the formation of uric acid crystals and not to the soluble form of uric acid. Recent epidemiological studies have reported that an elevated uric acid confers an increased risk for the development of hypertension [Selby, J. V., Friedman, G. D., and Quesenberry, C. P.,
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Precursors of essential hypertension: pulmonary function, heart rate, uric acid, serum cholesterol, and other serum chemistries. Am J Epidemiol 131:1017-27 (1990); Jossa, F., et al. Serum uric acid and hypertension: the Olivetti heart study. J Hum Hypertens 8:677681 (1994); and Goldstein, H. S., and Manowitz, P., Relationship between serum uric acid and blood pressure in adolescents. Annals Hum Biol 20:423-431 (1993)], ischemic heart disease [Fang, J., and Alderman, M. H. Serum uric acid and cardiovascular mortality. The NHANES I Epidemiologic Follow-up Study, 1971-1992 JAMA 283:24042410 (2000); Bengtsson, C., Lapidus, L., Stendahl, C., and Waldenstrom, J., Hyperuricemia and risk of cardiovasular disease and overall death. Acta Med Scand 224:549-55 (1988); and Alderman, M. H., Cohen, H., Madhavan, S., Kivlighn, S. Serum uric acid and cardiovascular events in successfully treated hypertensive patients. Hypertension 34:144-150 (1999).], and stroke [Lehto, S., Niskanen, L., Ronnemaa, T., and Laakso, M., Serum uric acid is a strong predictor of stroke in patients with non-insulin dependent diabetes mellitus. Stroke 29:635-639 (1998)]. In the Worksite study an increase of 1 mg/dl of uric acid conferred the same cardiovascular risk as an increase of 10 mm Hg in systolic blood pressure or 20 mg/dl of cholesterol [Alderman, M. H., Cohen, H., Madhavan, S., and Kivlighn, S., Serum uric acid and cardiovascular events in successfully treated hypertensive patients. Hypertension 34:144-150 (1999).]. Several studies have also reported that the increased mortality associated with diuretic use can be attributed to the increase in uric acid induced by these agents [Franse, L. V., Pahor, M., and Barli, M. D., Serum uric acid, it's change with diuretic use and risk of cardiovascular events in the Systolic Hypertension in the Elderly Program (SHEP). American Society of Hypertension Annual Meeting, May 1999, New York.]. Others have shown that an increased uric acid confers increased risk for cardiovascular mortality, especially in women [Fang, J., and Alderman, M. H., Serum uric acid and cardiovascular mortality. The NHANES I Epidemiologic Follow-up Study, 1971-1992 JAMA 283:24042410 (2000); Bengtsson, C., Lapidus, L., Stendahl, C., and Waldenstrom, J., Hyperuricemia and risk of cardiovasular disease and overall death. Acta Med Scand 224:549-55 (1988); and Persky, V. W., et al. Uric acid: A risk factor for coronary heart disease? Circulation 59:969-979 (1979)]. Despite the clinical and epidemiological evidence, some authorities do not consider an elevated uric acid to be a true cardiovascular risk factor [Vaccarino, V., and Krumholz, H. M., Risk factors for cardiovascular disease: One down, many more to evaluate. Ann Int Med 131:62-63 (1999); and Wannamethee, S. G., Is serum uric acid a risk factor for coronary heart disease? J Hum Hypertens 13:153-156 (1999)]. This is because many patients with an elevated uric acid have other well-established risk factors for cardiovascular disease, such as hypertension, renal disease, obesity, dyslipidemia, and insulin resistance [Barlow, K. A., Hyperlipidemia in primary gout. Metabolism 17:289-299 (1968) and Grahame, R., and Stott, J. T., Clinical survey of 354 patients with gout. Ann Rheum Dis 29:461-468 (1970)]. Whereas some studies have found that an elevated uric acid level is an independent risk factor after controlling for the contribution of these other risk factors by multivariate analyses [Fang, J., and Alderman, M. H., Serum uric acid and cardiovascular mortality. The NHANES I Epidemiologic Follow-up Study, 1971-1992 JAMA 283:2404-2410 (2000); Bengtsson, C., Lapidus, L., Stendahl, C., and Waldenstrom, J. Hyperuricemia and risk of cardiovasular disease and overall death. Acta Med Scand 224:549-55 (1988); and Persky, V. W., et al. Uric acid: A risk factor for coronary heart disease? Circulation 59:969-979 (1979)], other studies including the recent Framingham analysis could not [Culleton, B. F., Larson, M. G., Kannel, W. B., and Levy, D., Serum uric acid and risk for cardiovascular disease and death: The Framingham Study. Ann Intern Med 131:7-13 (1999); Klein, R., et al. Serum uric acid: its relationship to coronary heart disease risk factors and cardiovascular disease. Evans County, Georgia. Arch Int Med 132:401-410 (1973); and Yano, K., Reed, D. M., and McGee, D. L., Ten year
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incidence of coronary heart disease in the Honolulu Heart Program: relationship to biologic and lifestyle characteristics. Am J Epidemiol 119:653-666 (1984).]. The lack of a mechanistic pathway by which uric acid can cause cardiovascular disease, coupled with the inconclusive clinical and epidemiological data, have left this issue unresolved. In considering this controversy, it is important to note that no animal model existed to study the effects of a mildly elevated uric acid. 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 uric acid, 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 “uric acid” (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 uric acid. You can also use this procedure to view pending patent applications concerning uric acid. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.
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CHAPTER 6. BOOKS ON URIC ACID Overview This chapter provides bibliographic book references relating to uric acid. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on uric acid 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 “uric acid” (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 uric acid: •
Disorders of the Genitourinary Tract Source: in AARP Pharmacy Service Prescription Drug Handbook, 2nd ed. Washington, DC: American Association of Retired Persons. 1992. p. 914-974. Contact: Available from Virginia Pharmacy Service. P.O. Box 13671, Richmond, VA 23225-6115. (800) 456-2277. PRICE: $12.95 plus $1 shipping and handling. Summary: This text chapter details information concerning the causes, diagnosis, and drug treatment of urinary tract infections, urinary incontinence and kidney stones. Information is included for various specific drugs for treating urinary tract infections, covering dosage form and strength, drug profile, what to know before using the drug, food-drug interactions, restrictions during daily living, possible side effects, storage instructions, and ancillary information. Also included are various urinary anti-infectives (Azo Gantanol, Azo Gantrisin, NegGRAM, Trimethoprim, Bactrim, Septra, Methenamine salts, Cipro, Floxin, Noroxin, Macrodantin) and urinary analgesics
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(Pyridium drugs). Topics under urinary incontinence include causes and types (stress, overactive bladder, overflow incontinence), diagnosis, treatment, prognosis, and detailed information on specific urinary tract stimulants (Bethanechol drugs) and antispasmodics (Ditropan, Urispas). Uric acid reducers (Allopurinol) and thiazide diuretics (Hydrochlorothiazide) used in the treatment of kidney stones also are described.
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 “uric acid” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “uric acid” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “uric acid” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •
Amino acid transport and uric acid transport : symposium, Innsbruck, June 1975, [at the Inst. of Physiology, Innsbruck, Austria, June 16-18, 1975]; ISBN: 3135380017; http://www.amazon.com/exec/obidos/ASIN/3135380017/icongroupinterna
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Gout and uric acid metabolism by John Harold Talbott; ISBN: 0913258385; http://www.amazon.com/exec/obidos/ASIN/0913258385/icongroupinterna
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Inherited biochemical disorders and uric acid metabolism by David S. Newcombe; ISBN: 0839106904; http://www.amazon.com/exec/obidos/ASIN/0839106904/icongroupinterna
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Serum uric acid values of youths 12-17 years, United States (SuDoc HE 20.6209:11/152) by U.S. Dept of Health and Human Services; ISBN: 0840600410; http://www.amazon.com/exec/obidos/ASIN/0840600410/icongroupinterna
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Uric acid; ISBN: 0387086110; http://www.amazon.com/exec/obidos/ASIN/0387086110/icongroupinterna
Chapters on Uric Acid In order to find chapters that specifically relate to uric acid, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and uric acid 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 “uric acid” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on uric acid: •
Complications of Chronic Dialysis Therapy Source: in Gutch, C.F.; Stoner, M.H.; Corea, A.L. Review of Hemodialysis for Nurses and Dialysis Personnel. 6th ed. St. Louis, MO: Mosby. 1999. p. 192-212.
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Contact: Available from Harcourt Publishers. Foots Cray High Street, Sidcup, Kent DA14 5HP UK. 02083085700. Fax 02083085702. E-mail:
[email protected]. Website: www.harcourt-international.com. PRICE: $37.95 plus shipping and handling. ISBN: 0815120990. Summary: Chronic dialysis therapy has extended the lives of hundreds of thousands of patients. The treatment, however, can be associated with significant acute and chronic complications. This chapter on the complications of chronic dialysis therapy is from a nursing text that poses questions and then answers those questions with the aim of giving a good understanding of the basic principles, basic diseases, and basic problems in the treatment of kidney patients by dialysis. Many complications in patients with end stage renal disease (ESRD) are part of the uremic syndrome and are unrelated to the dialysis treatment itself. Dialysis related complications include central nervous system (CNS) abnormalities (headache, weakness, fatigue, apathy, nausea), hypotension (low blood pressure), fluid overload (edema), hypertension (high blood pressure), congestive heart failure, arrhythmias, muscle cramping, chills and fever (febrile reactions), allergic reactions, and itching (pruritis). The author discusses medical problems associated with ESRD, including anemia and its treatment (often with erythropoietin or transfusions), the complications of blood transfusions, renal osteodystrophy (bone disease related to abnormalities of calcium and phosphorus metabolism), joint disorders (including pseudogout, which is related to elevated uric acid levels), dialysis amyloidosis, carpal tunnel syndrome (CTS), gastrointestinal problems (peptic ulcer disease, constipation, and ascites, or fluid collection in the peritoneal cavity), hepatitis, neuropathy, reproduction problems, and insomnia (inability to sleep). The authors concludes with a discussion of dialysis in the elderly, the role of exercise for dialysis patients, dialysis for people with diabetes mellitus, and the psychological consequences of long term dialysis. •
Hematuria Source: in Landau, L.; Kogan, B.A. 20 Common Problems in Urology. New York, NY: McGraw-Hill, Inc. 2001. p. 145-166. Contact: Available from McGraw-Hill, Inc. 1221 Avenue of the Americas, New York, NY 10020. (612) 832-7869. Website: www.bookstore.mcgraw-hill.com. PRICE: $45.00;plus shipping and handling. ISBN: 0070634130. Summary: Hematuria (blood in the urine) is a common problem, and its presence is usually distressing to both patient and health care provider. Hematuria may be the first sign of serious disease in the urinary tract, and is the most common presenting sign of urinary tract cancer and parenchymal (in the tissues of the organ) kidney disease. Blood in the urine is an important symptom that should prompt an appropriate evaluation to rule out or detect disease in otherwise asymptomatic patients. This chapter on hematuria is from a text on common problems in urology (written for the primary care provider). Topics include finding hematuria through dipstick urinalysis, microscopic urinalysis, and erythrocyte (red blood cell) morphology (shape and development); the importance of evaluating hematuria; the differential diagnosis considering renal (kidney) cell carcinoma, transitional cell carcinoma, renal cysts, urolithiasis (urinary tract stones), infection, exercise induced hematuria, benign prostatic hyperplasia (BPH, overgrowth of the prostate), papillary necrosis (tissue death of part of the renal tubules), Berger's disease or immunoglobulin A nephropathy (kidney disease), hematospermia (blood in the semen), and hypercalciuria (excessive calcium in the urine) and hyperuricosuria (excessive uric acid in the urine); key elements to the patient history; and the physical examination and diagnostic tests, including plain film radiography, intravenous pyelogram, ultrasound, computed tomography (CT scan), magnetic
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resonance imaging (MRI), cystogram, cystoscopy, urine cytology, renal biopsy, and nuclear renal scans. The author also notes special considerations, controversies, and emerging concepts. A patient evaluation algorithm is provided. 14 figures. 13 tables. 20 references. •
Kidney Stones: Prevention Source: in Seal, G.M. Patient's Guide to Urology: Plumbing Problems in Layman's Terms. Toledo, OH: High Oaks Publishing Company. 1995. p. 150-158. Contact: Available from bookstores and libraries and, at the wholesale level, from Baker and Taylor, (908) 722-8000. Also available in orders of 10 or more copies from High Oaks Publishing Company, Center Urology of Toledo, Inc. 3425 Executive Parkway, Suite 214, Toledo, OH 43606. (419) 531-1700. PRICE: $21.95 (cloth); $12.95 (paperback). ISBN: 0964577305 (cloth), 0964577313 (paper). Summary: In this chapter, from a patient's guide to urology, the author discusses the prevention of kidney stone disease, particularly the prevention of recurrences. The author emphasizes the need to know what type of stone has formed and to identify those factors that may lead to the formation of other stones. Topics include calcium stones and their treatment; the chance of recurrence when the patient does nothing to prevent its happening; uric acid stones; infection (struvite) stones; and cystine stones. This chapter goes hand-in-hand with two previous chapters on the treatment and physiology of kidney stones. The book concludes with a detailed glossary and brief subject index. 1 figure.
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Not All Kidney Stones Are Created Equal Source: in Rodman, J.S.; Seidman, C.; Jones, R. No More Kidney Stones. Somerset, NJ: John Wiley and Sons, Inc. 1996. p. 20-27. Contact: Available from John Wiley and Sons. One Wiley Drive, Somerset, NJ 08875. (800) 225-5945 or (732) 469-4400. Fax (732) 302-2300. E-mail:
[email protected]. Website: www.wiley.com. PRICE: $15.95 plus shipping and handling. ISBN: 0471125873. Summary: Kidney stones are composed of different substances and vary from one person to another. This chapter on the different types of kidney stones is from a book that offers readers a program designed to prevent the recurrence of kidney stones. The authors review essential lifestyle and diet changes and the latest medical research, and offer specific guidelines for both men and women. In this chapter, the authors describe calcium oxalate stones (75 percent of stones are this type), uric acid stones (10 percent), struvite or infected stones (10 percent), and cystine stones (1 percent); stones can also have a combination of these elements. For each type of stone, the authors note the causes, related diseases and medical conditions, complications (notably struvite layered on other types of stones), and risk factors (including in children). The chapter concludes with a discussion of bladder stones and the importance of stone analysis. Knowing the exact composition of a stone gives the doctor an important clue as to the reasons why the stone has formed; treatment strategies (including specific dietary modifications) can then be individualized and their success made more likely.
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How and Why Kidney Stones Form Source: in Rodman, J.S.; Seidman, C.; Jones, R. No More Kidney Stones. Somerset, NJ: John Wiley and Sons, Inc. 1996. p. 28-33.
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Contact: Available from John Wiley and Sons. One Wiley Drive, Somerset, NJ 08875. (800) 225-5945 or (732) 469-4400. Fax (732) 302-2300. E-mail:
[email protected]. Website: www.wiley.com. PRICE: $15.95 plus shipping and handling. ISBN: 0471125873. Summary: The chance of a person forming kidney stones is largely determined by their genetic makeup and by the way their diet and lifestyle interplay with this genetic inheritance. This chapter on how and why kidney stones form is from a book that offers readers a program designed to prevent the recurrence of kidney stones. The authors review essential lifestyle and diet changes and the latest medical research, and offer specific guidelines for both men and women. In this chapter, the authors stress that it is important to understand the basic factors that encourage the formation of urinary crystals. With this understanding, patients can better prevent recurrence of their kidney stone problems. Using the metaphor of making rock candy out of super saturated sugar water, the authors describe how crystals form and how to discourage their formation. Topics include the composition of kidney stones (notably calcium oxalate, a salt), the conditions that favor crystal formation, the best inhibitor of kidney stones, and how uric acid stones are formed. The authors note that there is a genetic tendency to form stones, but diet and fluid intake also make a big difference in whether or not the gene that controls stone formation can assert itself. 1 figure. •
Crystal Arthropathies Source: in Maddison, P.J.; et al., Eds. Oxford Textbook of Rheumatology. Volume 2. New York, NY: Oxford University Press, Inc. 1993. p. 983-1005. Contact: Available from Oxford University Press, Inc., New York, NY. Summary: This chapter for health professionals presents an overview of crystal arthropathies. Major clinical manifestations of gout are outlined. Epidemiological data on gouty arthritis are provided. Data on serum urate levels, hyperuricemia, uric acid metabolism, purine synthesis, and uric acid excretion are presented. The pathogenesis of hyperuricemia is explained. Biochemical aspects of inborn errors of metabolism that lead to gout are examined. The pathogenesis of crystal inflammation is described. The clinical features of gout are discussed. Conditions associated with gout are highlighted. Techniques used in the diagnosis of gout are identified. Approaches to treating gout are presented, and suggestions for long-term management and prevention are offered. The epidemiology, etiology, pathogenesis, clinical features, and treatment of calcium pyrophosphate dihydrate deposition are discussed. In addition, the role of calcium phosphate crystal deposition in various disorders is considered. 181 references, 21 figures, and 7 tables.
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Laboratory Tests Source: in Lockhart, P.B. Oral Medicine and Hospital Practice. Chicago, IL: Special Care Dentistry. 1997. p. 10.3-10.12. Contact: Available from Special Care Dentistry. 211 East Chicago Avenue, Chicago, IL 60611. (312) 440-2660. Fax (312) 440-2824. PRICE: $27.00 (member) or $30.00 (nonmember), plus shipping and handling; institutional prices and bulk orders available. ISBN: 0965719103. Summary: This chapter is from a manual designed to help dental residents, students and practitioners engaged in the care of patients in the hospital setting. This chapter presents information on common laboratory tests. The chapter describes hematology, including complete blood count (CBC), sickle cell tests, and coagulation tests; blood chemistry,
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including total protein, calcium, phosphorus, cholesterol, glucose, uric acid, creatinine, phosphatase, and transaminases; other blood determinations, including blood urea nitrogen (BUN), bilirubin, creatine phosphokinase (CPK or CK), serum iron, total iron binding capacity (TIBC), serum osmolality, glucose tolerance test (GTT), triglycerides, and electrolytes; thyroid testing, including hormones and radioactive iodine (RAI) uptake test; urinalysis, including color, odor, specific gravity, chemical examination, and microscopic examination; cerebrospinal fluid, including glucose, protein, white blood cells, and red blood cells; and arterial blood gases. For each test, the author notes the expected normal value, the significance of high or low values, and the relevant oral findings. Most information is presented in outline format, for ease of access. 1 table. •
Diet and Renal Disease Source: in Townsend, C.E. and Roth, R.A. Nutrition and Diet Therapy. 7th ed. Albany, NY: Delmar Publishers. 1999. 329-342 p. Contact: Available from Delmar Publishers. 3 Columbia Circle, Albany, NY 12212. (800) 865-5840. E-mail:
[email protected]. PRICE: $44.95 plus shipping and handling. ISBN: 0766802965. Summary: This chapter on diet and renal disease is from an undergraduate level textbook on nutrition and diet therapy. The chapter describes the work of the kidneys, explains why protein is restricted for renal patients, explains why sodium and water are sometimes restricted for renal patients, and explores why potassium and phosphorus are sometimes restricted for renal patients. The chapter covers different renal disorders, including acute kidney failure, chronic renal failure, nephritis, glomerulonephritis, nephrosclerosis, polycystic kidney disease, and nephrolithiasis. The authors then review the dietary treatment of renal disease, the use of hemodialysis and peritoneal dialysis to treat kidney disease, dietary considerations during dialysis, diet after kidney transplant, and the dietary treatment of kidney stones (including calcium oxalate, uric acid, cystine, and struvite stones). The authors stress that diet therapy for renal disorders can be extremely complex because of the multifaceted nature of the kidneys' functions. The chapter includes a section on the role of the health care professional in caring for patients with kidney disease; this section focuses on the typically chronic nature of kidney disease and the importance of a good professional patient relationship in helping patients to cope with the long term care for their disease. The chapter includes a list of recommended discussion topics, a list of suggested supplemental activities, and a section of review questions for readers to test their comprehension of the material covered. Two case studies are appended to the chapter. 2 tables.
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Nephrolithiasis Source: in Mandal, A.K. and Nahman, N.S., Jr., eds. Kidney Disease in Primary Care. Baltimore, MD: Williams and Wilkins. 1998. p. 228-234. Contact: Available from Williams and Wilkins. 351 West Camden Street, Baltimore, MD 21201-2436. (800) 638-0672 or (410) 528-4223. Fax (800) 447-8438 or (410) 528-8550. E-mail:
[email protected]. PRICE: $39.95. ISBN: 0683300571. Summary: This chapter on nephrolithiasis (kidney stones) is from a textbook that provides primary care physicians with practical approaches to common clinical problems of kidney diseases. The authors discuss the pathophysiology of kidney stones, including that of calcium oxalate, uric acid, struvite, calcium phosphate, and cystine stones; associated systemic diseases; uncommon causes of kidney stones; symptoms; diagnosis of acute renal colic; stone analysis and biochemical evaluation; differential
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diagnosis; management of an acute event; and metabolic evaluation and therapy. The chapter concludes with a discussion of the indications for referring a patient to a specialist and with the answers to a list of questions commonly asked by patients diagnosed with nephrolithiasis. The authors stress that the medical management of patients with nephrolithiasis is based on the chemical composition of the stone or, in the absence of material from the stone for analysis, 24-hour urinary chemistries. The majority of kidney stones (75 to 80 percent) are composed of calcium oxalate. Hospital admission is required for treatment of pain. Stones that do not pass within 48 hours require lithotripsy or urologic intervention. 3 tables. 7 references. •
Clinical Management of Short-Bowel Syndrome Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 479-484. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on the clinical management of short bowel syndrome is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). Short bowel syndrome generally implies either malabsorption of the necessity for specific nutrient therapies. Short bowel syndrome can occur in patients with CD who undergo multiple intestinal resections (surgical removal of a piece). Depending upon the length and health of the remaining intestine, as well as the presence or absence of the ileocecal valve or colon, such patients may require various oral supplements, intravenous fluids, or even total parenteral nutrition (TPN). Bowel length may be difficult to determine because most commonly used methods such as barium contrast studies and intraoperative measurement are imprecise. In addition, there is significant individual variation in the adaptive response to differing lengths of residual intestine. Younger individuals, especially neonates, have a much greater capacity to adapt than adults. Complications of short-bowel syndrome include dehydration (which may result in uric acid nephrolithiasis, kidney stones), generalized malnutrition, electrolyte disturbances, specific nutrient deficiencies, calcium-oxalate nephrolithia-sis, and cholelithiasis (gallstones). Those patients with significant malabsorption requiring long-term TPN are at additional risk for hepatic steatosis (fatty liver) and cholestasis (an interruption of the flow of bile) with potential progression to cirrhosis (liver scarring), either acalculous or calculous cholecystitis (inflammed gallbladder), metabolic bone disease, nephropathy (kidney disease), and central venous catheter-related problems, including infection and occlusion (thrombotic and nonthrombotic; clotting or nonclotting). 10 references.
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Are You Stone Prone? Source: in Savitz, G. and Leslie, S.W. Kidney Stones Handbook: A Patient's Guide to Hope, Cure and Prevention. 2nd ed. Roseville, CA: Four Geez Press. 1999. p. 23-37. Contact: Available from Four Geez Press. 1911 Douglas Blvd., Suite 85-131, Roseville, CA 95661. (800) 2-Kidneys. Website: www.readerndex.com/fourgeez. PRICE: $17.95 plus shipping and handling. ISBN: 0963706861. Summary: This chapter on the risk factors for kidney stones is from a patient education handbook that describes how virtually every patient who follows treatment based on
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appropriate testing, proper interpretation, and sound medical principles can substantially reduce or eliminate all future kidney stone production. The authors emphasize the need for patients to educate themselves and to take a proactive approach to preventing new stones, in many cases to the point of educating their physicians and demanding appropriate diagnostic and treatment methods. This chapter begins with statistics about kidney stones, the greater incidence of them during the summer months and in areas with soft water, the role of genetic disposition, and the likelihood of recurrence in people who have had at least one stone episode. The author then defines kidney stones and how they are formed, explaining medical concepts in nontechnical language. The author states that kidney stones are always abnormal. They form because of too much of too little of some urinary chemical and not enough water to dissolve all the minerals, compounds, and waste products the kidneys are trying to excrete. The author then discusses renal (kidney) failure, the use of creatinine to measure kidney function, the history of kidney stones, and risk factors for forming stones. The five most common kidney stone chemical risk factors are too much urinary calcium (hypercalciuria), too much urinary oxalate (hyperoxaluria), too much urinary uric acid (hyperuricosuria), too little urinary citrate (hypocitraturia), and too little urinary volume and not enough water. Other topics discussed include inadequate fluid intake, the role of urinary tract infections (UTIs), cystine, drug or chemical induced stones, and links between diet and stone formation. 1 figure. •
Chapter 52: Gout and Pseudogout Source: in Berkow, R., ed. The Merck Manual of Medical Information: Home Edition (online version). Rahway, NJ: Merck and Company, Inc. 2000. 4 p. Contact: Available online from Merck and Company, Inc. (800) 819-9456. Website: www.merck.com/pubs/mmanual_home/contents.htm. Also available from your local book store. PRICE: $29.95 plus shipping. Summary: This chapter provides the general public and people who have gout or pseudogout with information on the symptoms, diagnosis, and treatment of these disorders, which are caused by crystal deposits in the joints. Gout is characterized by sudden, recurring attacks of very painful arthritis caused by deposits of monosodium urate crystals. Gout attacks may be triggered by surgery, consumption of large quantities of alcohol or protein rich food, fatigue, emotional stress, or illness. Severe pain occurs suddenly in one or more joints, and it becomes progressively worse. The joint becomes swollen, and the skin over it appears red or purplish, tight, and shiny. Other symptoms include fever, chills, a generally sick feeling, and a rapid heartbeat. Gout most often affects the joint at the base of the big toe. Symptoms gradually disappear after a few days, and no symptoms appear until the next attack. If gout progresses, untreated attacks last longer, occur more frequently, and affect several joints. Diagnosis is made on the basis of the distinctive symptoms of gout and an examination of the joint. A high uric acid level in the blood supports the diagnosis. The identification of needle shaped urate crystals in a sample of joint fluid confirms the diagnosis. The first step in treating gout is to relieve pain by controlling the inflammation with colchicine, nonsteroidal antiinflammatory drugs (NSAIDs), and corticosteroids. The next step is to prevent recurrences. Long term drug treatment with low doses of colchicine, NSAIDs, probenecid, sulfinpyrazone, or allupurinol may be needed for people who have repeated, severe attacks. Pseudogout is characterized by intermittent attacks of painful arthritis caused by deposits of calcium pyrophosphate crystals. Symptoms vary from person to person. Diagnosis is based on the identification of calcium pyrophosphate crystals in joint fluid. X rays may support the diagnosis.
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Treatment with NSAIDs, colchicine, or corticosteroid crystal suspension can stop acute attacks and prevent new attacks but cannot prevent damage to the affected joint. •
Nephrolithiasis and Nephrocalcinosis 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. 139-158. 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 nephrolithiasis and nephrocalcinosis. After an introduction to the nature, types, and problems of management of kidney stone disease, the authors discuss calcium stones and uric acid stones in detail. A brief consideration of cystinuria and struvite stones is included. 12 figures. 13 tables. 87 references.
•
Calculi Source: in Sant, G.R., ed. Pathophysiologic Principles of Urology. Malden, MA: Blackwell Science, Inc. 1994. p. 325-356. Contact: Available from Blackwell Science, Inc. 350 Main Street, Commerce Place, Malden, MA 02148. (800) 215-1000 or (617) 388-8250. Fax (617) 388-8270. E-mail:
[email protected]. PRICE: $55.00. ISBN: 0865422214. Summary: This chapter, from a urology textbook on pathophysiology, discusses kidney and urinary calculi (stones). The authors review the normal metabolism of the compounds of interest in stone formation, then discuss the pathophysiology of stone formation and the metabolic aspects of therapy. Topics include physiochemistry; normal mineral homeostasis, including calcium, oxalate, phosphate, hydrogen ion (acid), citrate, magnesium, urate, cystine homeostasis; the pathophysiology of stone formation, including for calcium oxalate stones, hypercalciurias, hyperoxalurias, hyperuricosuric calcium oxalate stones, hypocitraturia, and calcium phosphate stones; renal tubular acidosis (RTA); uric acid stones; cystine stones; infection stones; structural abnormalities that predispose to clinical stone formation; metabolic evaluation of patients with urolithiasis; and the medical therapy recommended for the various types of stones discussed. 3 figures. 11 tables. 12 annotated references.
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Divalent Ion Metabolism Source: in Gonick, H.C., ed. Current Nephrology: Volume 17. St. Louis, MO: MosbyYear Book, Inc. 1994. p. 121-163. Contact: Available from Mosby-Year Book, Inc. 11830 Westline Industrial Drive, St. Louis, MO 63146. (800) 426-4545. PRICE: $82.95. ISBN: 0815137435. ISSN: 01485265. Summary: This chapter, from a yearbook of nephrology, covers divalent ion metabolism, with an emphasis on urinary calculi. Topics include calcium stones, idiopathic hypercalciuria, primary hyperparathyroidism, renal tubular acidosis, hyperoxaluria, cystine stones, struvite stones, uric acid stones, mechanisms of stone formation including crystallization, modifiers of crystallization and stone formation, and the control of hyperphosphatemia in patients with chronic renal failure. 10 figures. 7 tables. 168 references.
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Role of the Chemistry Laboratory in the Clinical Study of Renal Disease Source: in Barakat, A.Y. Renal Disease in Children: Clinical Evaluation and Diagnosis. Secaucus, NJ: Springer-Verlag. 1990. p. 55-90. Contact: No longer available from publisher. Summary: This chapter, from an extensive desk reference book about the clinical evaluation and diagnosis of renal disease in children, discusses the role of the chemistry laboratory in the clinical study of renal disease. Eight sections cover: recent changes in laboratory technology; reference intervals; pediatric specimens; electrolytes, fluid, and acid-base balance; other inorganic analytes; glucose and metabolites; nitrogenous compounds; and proteins. The author notes that the improved accuracy of micromethods, such as the widespread use of enzymes as diagnostic reagents for more specific measurements of substrates like glucose and uric acid, has greatly reduced potential interferences from both drugs and endogenous metabolites. Current automation allows any laboratory, whether in a children's hospital or in a facility serving both adult and pediatric patients, to perform rapid, precise microchemical determinations. 22 references.
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Urine Tests: Examining the Body's Excess Fluids Source: in Shaw, M., et al., eds. Everything You Need to Know About Medical Tests. Springhouse, PA: Springhouse Corporation. 1996. p. 549-616. Contact: Available from Springhouse Publishing. Attention: Trade and Textbook Department, 1111 Bethlehem Pike, P.O. Box 908, Springhouse, PA 19477-0908. (800) 3313170 or (215) 646-4670 or (215) 646-4671. Fax (215) 646-8716. PRICE: $24.95 (as of 1995). ISBN: 0874348234. Summary: This lengthy chapter, from a consumer handbook about medical practice and disease, presents information on urine tests used for diagnosis. Written in a question and answer format, the chapter discusses urine tests for these functions, diseases, and substances: kidney stones, kidney function, phosphate reabsorption by the kidneys, amylase, arysulfatase A, lysozyme, aldosterone, Cushing's syndrome, epinephrine, norepinephrine, dopamine, estrogens, pregnancy, placental estriol, pregnanetriol, vanillylmandelic acid, homovanillic acid, hydroxyindoleacetic acid, pregnanediol, proteins, Bence Jones protein, amino acid disorders, creatinine, creatinine clearance by the kidneys, urea clearance by the kidneys, uric acid, hemoglobin, myoglobin, porphyrins, delta-aminolevulinic acid, bilirubin, urobilinogen, sugar, glucose, ketones, vitamin B6, vitamin C, sodium, chloride, potassium, calcium, phosphates, magnesium, and iron. For each test discussed, the authors provide information about why the test is done, how the test is performed, what to do before the test, and what the results indicate.
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Medications Source: in Rodman, J.S.; Seidman, C.; Jones, R. No More Kidney Stones. Somerset, NJ: John Wiley and Sons, Inc. 1996. p. 178-184. Contact: Available from John Wiley and Sons. One Wiley Drive, Somerset, NJ 08875. (800) 225-5945 or (732) 469-4400. Fax (732) 302-2300. E-mail:
[email protected]. Website: www.wiley.com. PRICE: $15.95 plus shipping and handling. ISBN: 0471125873. Summary: Throughout medical history, people have taken a wild assortment of remedies to cure real and imagined ailments. This chapter on medications for kidney
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stones is from a book that offers readers a program designed to prevent the recurrence of kidney stones. The authors review essential lifestyle and diet changes and the latest medical research, and offer specific guidelines for both men and women. In this chapter, the authors describe the modern medications that are used to treat various kidney stone problems. The authors stress that four out of five people who present with stone problems can be managed without any medications. Medication is more likely to be prescribed for people with multiple stone episodes, difficulty in passing stones, or prior urological intervention, such as surgery or ESWL (extracorporeal shock wave lithotripsy) treatment. The authors discuss alkaline potassium salts (including potassium citrate and potassium bicarbonate), alkaline sodium salts (sodium bicarbonate), thiazide diuretics, allopurinol (which reduces the production of uric acid), triamterene, amiloride, pyridozine, magnesium oxide and other magnesium salts, thiola and penicillamine (used to treat cystinuria), acetohydroxamic acid, antibiotics and urinary antiseptics, calcium citrate and other calcium preparations, phosphates, cellulose phosphate, and aluminum hydroxide.
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CHAPTER 7. PERIODICALS AND NEWS ON URIC ACID Overview In this chapter, we suggest a number of news sources and present various periodicals that cover uric acid.
News Services and Press Releases One of the simplest ways of tracking press releases on uric acid 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 “uric acid” (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 uric acid. 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 “uric acid” (or synonyms). The following was recently listed in this archive for uric acid: •
Body weight linked to uric acid nephrolithiasis Source: Reuters Medical News Date: April 16, 2004
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Serum uric acid level predicts weight and blood pressure increases Source: Reuters Medical News Date: October 17, 2003
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Uric acid is principal mediator of immune response after tissue damage Source: Reuters Medical News Date: September 10, 2003
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Link confirmed between high uric acid, cardiovascular mortality Source: Reuters Medical News Date: May 10, 2000
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High uric acid linked to heart disease deaths Source: Reuters Health eLine Date: May 09, 2000
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Uric acid does not have a causal role in cardiovascular disease Source: Reuters Medical News Date: July 08, 1999
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Uric acid linked to heart disease risk Source: Reuters Health eLine Date: May 26, 1999
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Elevated serum uric acid predicts CVD in older patients with isolated systolic hypertension Source: Reuters Medical News Date: May 24, 1999
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Serum uric acid a marker for inflammation in patients with chronic heart failure Source: Reuters Medical News Date: January 19, 1999
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Holmium:YAG laser treatment of uric acid stones may cause cyanide poisoning Source: Reuters Medical News Date: August 03, 1998
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Uric Acid Reduces MS-Like Disease Symptoms In Mice Source: Reuters Medical News Date: January 20, 1998
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Uric Acid May Treat Multiple Sclerosis Source: Reuters Health eLine Date: January 19, 1998
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Inverse Association Between Uric Acid, Maximum Blood Flow, Reported In CHF Patients Source: Reuters Medical News Date: August 12, 1997
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High Uric Acid Levels May Lower Risk Of Idiopathic Parkinson's Disease Source: Reuters Medical News Date: September 03, 1996
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High Uric Acid Levels Risk Factor For CVD In Women Source: Reuters Medical News Date: March 19, 1996 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
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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 “uric acid” (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 “uric acid” (or synonyms). If you know the name of a company that is relevant to uric acid, 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 “uric acid” (or synonyms).
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 “uric acid” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it
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is updated every three months. The following is a typical result when searching for newsletter articles on uric acid: •
What Causes Kidney Stones Source: Columbia-Presbyterian Urology. p. 4. Fall 1996. Contact: Available from Columbia-Presbyterian Urology. Dana W. Atchley Pavilion, 11 Floor, 161 Fort Washington Avenue, New York, NY 10032-3784. (212) 305-0111. Summary: This brief newsletter article describes the causes of kidney stones. There are four factors that lead to stone formation: urine saturation, crystallization, particle retention, and matrix foundation. The author first describes who is at risk for forming kidney stones and briefly outlines the different types of stones: calcium oxalate (75 percent of patients develop these), uric acid, and struvite stones. Urine saturation occurs when urine has excessive amounts of calcium, uric acid, and oxalate crystals, which are all stone-forming substances. This saturation may occur during the day but frequently occurs after meals or during the sleeping hours or hot weather because of the lack of fluids consumed. Stone inhibiting substances include pyrophosphate, citrate, magnesium, and nephrocalcin. Freshly voided urine from most healthy individuals contains small crystals, which are flushed out of the urinary tract. However, some people have anatomic abnormalities in the kidney and or ureter, making the crystals stick to the lining of these structures. In addition to being composed of crystals, stones are also formed from an organic material called matrix. Matrix acts as the foundation for stone formation by controlling crystallization. The matrix is composed of a carbohydrate and protein. The article concludes with a section on preventing kidney stones, offering the following suggestions: increase fluid intake to lower saturation; make sure one half the fluid intake is water; produce two and a half quarts of urine in 24 hours; avoid eating grapes, berries, plums and citrus fruits; limit intake of coffee, tea and chocolate; avoid eating sardines, shrimp, and oysters; and, to prevent uric acid stones, avoid eating liver, sweet breads, and brains. Some people may require medication because they form calcium and uric acid stones even though they have adequate fluid intake and do not consume an excessive amount of dairy products. 1 figure.
•
Kidney Stones: Often Painful, But Manageable Source: Mayo Clinic Health Letter. 20(4): 6. April 2002. Contact: Available from Mayo Clinic Health Letter. Subscription Services, P.O. Box 53889, Boulder, CO 80322-3889. (800) 333-9037 or (303) 604-1465. Summary: This brief newsletter article reviews the problem of kidney stones (nephrolithiasis) and their treatment. The author first reviews the different types of kidney stones, including calcium stones, uric acid stones, struvite stones, and cystine stones. The author cautions that kidney stones often first occur between the ages of 20 and 50 and tend to recur. Small stones may pass with little or no pain. Others can be quite painful as they pass through the narrow tubes that connect each kidney to the bladder (the ureters). Drinking plenty of fluids and staying physically active can help to move a stone through the patient's system. Stones that are too large to pass or that are causing bleeding, kidney damage, or ongoing urinary tract infection (UTI) may require surgical treatment. Stone removal techniques include extracorporeal shock wave lithotripsy (ESWL), percutaneous nephrolithotomy, and ureteroscopic stone removal. One sidebar reviews strategies to prevent future stones.
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Gout: A Painful Joint Disorder Source: Mayo Clinic Health Letter. 19(11): 1-3. November 2001. Contact: Available from Mayo Clinic Health Letter. 200 First Street, SW, Rochester, MN 55905. (800) 333-9037 or (303) 604-1465. E-mail:
[email protected]. Summary: This newsletter article provides people who have gout with information on this painful joint disorder. Although gout is characterized by acute inflammation commonly affecting the big toe, it can affect the knees, ankles, and wrists. Symptoms occur when high levels of uric acid in the blood, or other triggers, cause urate crystals to form in joint spaces and other tissues. Gout occurs more frequently in men than in women, especially in men between 40 and 50 years old. Risk factors include excess weight, certain medical conditions, excessive alcohol intake or intake of foods high in purines, certain medications, surgery, and severe illness or injury. A gout attack produces intense pain, usually in one joint at a time. Symptoms typically resolve over several days. Untreated gout may result in increased pain and joint damage. Diagnosis is based on analysis of synovial fluid from the affected joint and a blood test to check for elevated uric acid levels. Nonsteroidal antiiflammatory drugs, prednisone, and colchicine may be used to treat gout. Preventive medications, such as allopurinol, probenecid, and sulfinpyrazone, may be prescribed to prevent future attacks. Lifestyle changes may also help prevent repeat gout attacks. 1 figure.
Academic Periodicals covering Uric Acid Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to uric acid. In addition to these sources, you can search for articles covering uric acid that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”
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CHAPTER 8. RESEARCHING MEDICATIONS Overview While a number of hard copy or CD-ROM resources are available for researching medications, a more flexible method is to use Internet-based databases. Broadly speaking, there are two sources of information on approved medications: public sources and private sources. We will emphasize free-to-use public sources.
U.S. Pharmacopeia Because of historical investments by various organizations and the emergence of the Internet, it has become rather simple to learn about the medications recommended for uric acid. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a non-profit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI Advice for the Patient can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with uric acid. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.). The
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following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to uric acid: Allopurinol •
Systemic - U.S. Brands: Aloprim; Zyloprim http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202021.html
Carbonic Anhydrase Inhibitors •
Systemic - U.S. Brands: Ak-Zol; Daranide; Dazamide; Diamox; Diamox Sequels; MZM; Neptazane; Storzolamide http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202114.html
Citrates •
Systemic - U.S. Brands: Bicitra; Citrolith; Oracit; Polycitra Syrup; Polycitra-K; Polycitra-K Crystals; Polycitra-LC; Urocit-K http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202144.html
Rasburicase •
Systemic - U.S. Brands: Elitek http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500425.html
Sulfinpyrazone •
Systemic - U.S. Brands: Anturane http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202538.html
Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.
Mosby’s Drug Consult Mosby’s Drug Consult database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/.
PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html.
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Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee.
Researching Orphan Drugs Although the list of orphan drugs is revised on a daily basis, you can quickly research orphan drugs that might be applicable to uric acid by using the database managed by the National Organization for Rare Disorders, Inc. (NORD), at http://www.rarediseases.org/. Scroll down the page, and on the left toolbar, click on “Orphan Drug Designation Database.” On this page (http://www.rarediseases.org/search/noddsearch.html), type “uric acid” (or synonyms) into the search box, and click “Submit Query.” When you receive your results, note that not all of the drugs may be relevant, as some may have been withdrawn from orphan status. Write down or print out the name of each drug and the relevant contact information. From there, visit the Pharmacopeia Web site and type the name of each orphan drug into the search box at http://www.nlm.nih.gov/medlineplus/druginformation.html. You may need to contact the sponsor or NORD for further information. NORD conducts “early access programs for investigational new drugs (IND) under the Food and Drug Administration’s (FDA’s) approval ‘Treatment INDs’ programs which allow for a limited number of individuals to receive investigational drugs before FDA marketing approval.” If the orphan product about which you are seeking information is approved for marketing, information on side effects can be found on the product’s label. If the product is not approved, you may need to contact the sponsor. The following is a list of orphan drugs currently listed in the NORD Orphan Drug Designation Database for uric acid: •
Potassium citrate (trade name: Urocit-K) http://www.rarediseases.org/nord/search/nodd_full?code=418
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Calcium gluconate gel 2.5% http://www.rarediseases.org/nord/search/nodd_full?code=617
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Calcium Gluconate (trade name: Calgonate) http://www.rarediseases.org/nord/search/nodd_full?code=857
If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.
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APPENDICES
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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute10: •
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
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National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
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National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
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National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
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National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
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National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
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National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
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National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
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
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National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
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National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
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National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
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National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
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National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
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National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
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National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
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National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
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National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
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National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
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National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
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National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
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Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
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National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
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National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
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Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
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Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.11 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:12 •
Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html
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HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
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NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
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Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
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Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
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Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
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Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
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Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
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Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
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Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
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MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
11
Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 12 See http://www.nlm.nih.gov/databases/databases.html.
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Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html
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Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html
The NLM Gateway13 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.14 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “uric acid” (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 19347 140 717 14 151 20369
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 “uric acid” (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/.
The Genome Project and Uric Acid In the following section, we will discuss databases and references which relate to the Genome Project and uric acid. Online Mendelian Inheritance in Man (OMIM) The Online Mendelian Inheritance in Man (OMIM) database is a catalog of human genes and genetic disorders authored and edited by Dr. Victor A. McKusick and his colleagues at Johns Hopkins and elsewhere. OMIM was developed for the World Wide Web by the National Center for Biotechnology Information (NCBI).21 The database contains textual information, pictures, and reference information. It also contains copious links to NCBI’s Entrez database of MEDLINE articles and sequence information. 18 Adapted 19
from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html.
The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 20 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process. 21 Adapted from http://www.ncbi.nlm.nih.gov/. Established in 1988 as a national resource for molecular biology information, NCBI creates public databases, conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information--all for the better understanding of molecular processes affecting human health and disease.
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To search the database, go to http://www.ncbi.nlm.nih.gov/Omim/searchomim.html. Type “uric acid” (or synonyms) into the search box, and click “Submit Search.” If too many results appear, you can narrow the search by adding the word “clinical.” Each report will have additional links to related research and databases. In particular, the option “Database Links” will search across technical databases that offer an abundance of information. The following is an example of the results you can obtain from the OMIM for uric acid: •
Uric Acid Nephrolithiasis, Susceptibility to Web site: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=605990
•
Uric Acid Urolithiasis Web site: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=191700 Genes and Disease (NCBI - Map)
The Genes and Disease database is produced by the National Center for Biotechnology Information of the National Library of Medicine at the National Institutes of Health. This Web site categorizes each disorder by system of the body. Go to http://www.ncbi.nlm.nih.gov/disease/, and browse the system pages to have a full view of important conditions linked to human genes. Since this site is regularly updated, you may wish to revisit it from time to time. The following systems and associated disorders are addressed: •
Cancer: Uncontrolled cell division. Examples: Breast and ovarian cancer, Burkitt lymphoma, chronic myeloid leukemia, colon cancer, lung cancer, malignant melanoma, multiple endocrine neoplasia, neurofibromatosis, p53 tumor suppressor, pancreatic cancer, prostate cancer, Ras oncogene, RB: retinoblastoma, von Hippel-Lindau syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Cancer.html
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Immune System: Fights invaders. Examples: Asthma, autoimmune polyglandular syndrome, Crohn’s disease, DiGeorge syndrome, familial Mediterranean fever, immunodeficiency with Hyper-IgM, severe combined immunodeficiency. Web site: http://www.ncbi.nlm.nih.gov/disease/Immune.html
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Metabolism: Food and energy. Examples: Adreno-leukodystrophy, atherosclerosis, Best disease, Gaucher disease, glucose galactose malabsorption, gyrate atrophy, juvenile-onset diabetes, obesity, paroxysmal nocturnal hemoglobinuria, phenylketonuria, Refsum disease, Tangier disease, Tay-Sachs disease. Web site: http://www.ncbi.nlm.nih.gov/disease/Metabolism.html
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Muscle and Bone: Movement and growth. Examples: Duchenne muscular dystrophy, Ellis-van Creveld syndrome, Marfan syndrome, myotonic dystrophy, spinal muscular atrophy. Web site: http://www.ncbi.nlm.nih.gov/disease/Muscle.html
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Nervous System: Mind and body. Examples: Alzheimer disease, amyotrophic lateral sclerosis, Angelman syndrome, Charcot-Marie-Tooth disease, epilepsy, essential tremor, fragile X syndrome, Friedreich’s ataxia, Huntington disease, Niemann-Pick disease, Parkinson disease, Prader-Willi syndrome, Rett syndrome, spinocerebellar atrophy, Williams syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Brain.html
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•
Signals: Cellular messages. Examples: Ataxia telangiectasia, Cockayne syndrome, glaucoma, male-patterned baldness, SRY: sex determination, tuberous sclerosis, Waardenburg syndrome, Werner syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Signals.html
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Transporters: Pumps and channels. Examples: Cystic fibrosis, deafness, diastrophic dysplasia, Hemophilia A, long-QT syndrome, Menkes syndrome, Pendred syndrome, polycystic kidney disease, sickle cell anemia, Wilson’s disease, Zellweger syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Transporters.html Entrez
Entrez is a search and retrieval system that integrates several linked databases at the National Center for Biotechnology Information (NCBI). These databases include nucleotide sequences, protein sequences, macromolecular structures, whole genomes, and MEDLINE through PubMed. Entrez provides access to the following databases: •
3D Domains: Domains from Entrez Structure, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
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Books: Online books, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=books
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Genome: Complete genome assemblies, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Genome
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NCBI’s Protein Sequence Information Survey Results: Web site: http://www.ncbi.nlm.nih.gov/About/proteinsurvey/
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Nucleotide Sequence Database (Genbank): Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Nucleotide
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OMIM: Online Mendelian Inheritance in Man, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=OMIM
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PopSet: Population study data sets, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Popset
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ProbeSet: Gene Expression Omnibus (GEO), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
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Protein Sequence Database: Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Protein
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PubMed: Biomedical literature (PubMed), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
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Structure: Three-dimensional macromolecular structures, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Structure
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Taxonomy: Organisms in GenBank, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Taxonomy
To access the Entrez system at the National Center for Biotechnology Information, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=genome, and then
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select the database that you would like to search. The databases available are listed in the drop box next to “Search.” Enter “uric acid” (or synonyms) into the search box and click “Go.” Jablonski’s Multiple Congenital Anomaly/Mental Retardation (MCA/MR) Syndromes Database22 This online resource has been developed to facilitate the identification and differentiation of syndromic entities. Special attention is given to the type of information that is usually limited or completely omitted in existing reference sources due to space limitations of the printed form. At http://www.nlm.nih.gov/mesh/jablonski/syndrome_toc/toc_a.html, you can search across syndromes using an alphabetical index. Search by keywords at http://www.nlm.nih.gov/mesh/jablonski/syndrome_db.html. The Genome Database23 Established at Johns Hopkins University in Baltimore, Maryland in 1990, the Genome Database (GDB) is the official central repository for genomic mapping data resulting from the Human Genome Initiative. In the spring of 1999, the Bioinformatics Supercomputing Centre (BiSC) at the Hospital for Sick Children in Toronto, Ontario assumed the management of GDB. The Human Genome Initiative is a worldwide research effort focusing on structural analysis of human DNA to determine the location and sequence of the estimated 100,000 human genes. In support of this project, GDB stores and curates data generated by researchers worldwide who are engaged in the mapping effort of the Human Genome Project (HGP). GDB’s mission is to provide scientists with an encyclopedia of the human genome which is continually revised and updated to reflect the current state of scientific knowledge. Although GDB has historically focused on gene mapping, its focus will broaden as the Genome Project moves from mapping to sequence, and finally, to functional analysis. To access the GDB, simply go to the following hyperlink: http://www.gdb.org/. Search “All Biological Data” by “Keyword.” Type “uric acid” (or synonyms) into the search box, and review the results. If more than one word is used in the search box, then separate each one with the word “and” or “or” (using “or” might be useful when using synonyms).
22
Adapted from the National Library of Medicine: http://www.nlm.nih.gov/mesh/jablonski/about_syndrome.html. 23 Adapted from the Genome Database: http://gdbwww.gdb.org/gdb/aboutGDB.html - mission.
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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on uric acid can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internet-based services that post them.
Patient Guideline Sources The remainder of this chapter directs you to sources which either publish or can help you find additional guidelines on topics related to uric acid. 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 uric acid. 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 “uric acid”:
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Genetic Brain Disorders http://www.nlm.nih.gov/medlineplus/geneticbraindisorders.html Gout and Pseudogout http://www.nlm.nih.gov/medlineplus/goutandpseudogout.html Kidney Stones http://www.nlm.nih.gov/medlineplus/kidneystones.html Laboratory Tests http://www.nlm.nih.gov/medlineplus/laboratorytests.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 Combined Health Information Database (CHID) CHID Online is a reference tool that maintains a database directory of thousands of journal articles and patient education guidelines on uric acid. CHID offers summaries that describe the guidelines available, including contact information and pricing. CHID’s general Web site is http://chid.nih.gov/. To search this database, go to http://chid.nih.gov/detail/detail.html. In particular, you can use the advanced search options to look up pamphlets, reports, brochures, and information kits. The following was recently posted in this archive: •
Kidney Stone Diet: Uric Acid Stones Source: Camp Hill, PA: Chek-Med Systems, Inc. 199x. [4 p.]. Contact: Available from Chek-Med Systems, Inc. 200 Grandview Avenue, Camp Hill, PA 17011-1706. (800) 451-5797 or (717) 761-0216. Fax (717) 761-0216. PRICE: $0.75 each; plus shipping and handling; bulk copies available. Booklets must be ordered in quantities of 10. Order number: D28. Summary: About 5 percent of all kidney stones are uric acid or urate kidney stones. Certain diseases, such as gout, can lead to the formation of uric acid kidney stones. Normally, urine is slightly acid. The most important factor leading to the formation of uric acid stones is the production of urine that is too acid. This booklet outlines the recommended diet for people who have been treated for uric acid stones and want to prevent recurrence of the problem. Treatment to prevent uric acid stones is usually with medication which is used to raise the pH of urine (make it less acidic) and prevent stone formation. Dietary changes may help the medication raise and maintain the alkaline level of urine. The booklet outlines five strategies that include increasing fluid intake, incorporating alkaline-ash foods in the diet, monitoring protein intake (not exceeding the RDA for protein and sometimes limiting foods high in purines), avoiding certain medications (such as aspirin), and limiting the use of alcohol (which increases uric acid production). One chart lists foods with high, moderate, and low content of purine.
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Another chart lists foods that produce acid ash or alkaline ash, and foods that are neutral; foods are listed in categories of meats, fats, milk, starches, vegetables, fruits, sweets, and beverages. A final chart offers a sample menu for patients with uric acid stone formation tendencies. 3 tables. The National Guideline Clearinghouse™ The National Guideline Clearinghouse™ offers hundreds of evidence-based clinical practice guidelines published in the United States and other countries. You can search this site located at http://www.guideline.gov/ by using the keyword “uric acid” (or synonyms). The following was recently posted: •
(1) Targeted tuberculin testing and treatment of latent tuberculosis infection Source: Centers for Disease Control and Prevention - Federal Government Agency [U.S.]; 2000 June 9 (addendum released 2003 August 8); 54 pages http://www.guideline.gov/summary/summary.aspx?doc_id=4004&nbr=3134&a mp;string=uric+AND+acid
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AACE medical guidelines for clinical practice for the diagnosis and treatment of dyslipidemia and prevention of atherogenesis Source: American Association of Clinical Endocrinologists - Medical Specialty Society; 2000 Mar-April; 52 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2199&nbr=1425&a mp;string=uric+AND+acid
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AAOS clinical guideline on osteoarthritis of the knee Source: American Academy of Orthopaedic Surgeons - Medical Specialty Society; 1996 (revised 2003); 17 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3856&nbr=3069&a mp;string=uric+AND+acid
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Chemotherapy and biotherapy: guidelines and recommendations for practice Source: Oncology Nursing Society - Professional Association; 2001; 226 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3209&nbr=2435&a mp;string=uric+AND+acid
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Chronic pain management in the long-term care setting Source: American Medical Directors Association - Professional Association; 1999; 34 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2158&nbr=1384&a mp;string=uric+AND+acid
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Diagnosis and management of hypertension in the primary care setting Source: Department of Defense - Federal Government Agency [U.S.]; 1999 May; Various pagings http://www.guideline.gov/summary/summary.aspx?doc_id=2579&nbr=1805&a mp;string=uric+AND+acid
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Disorders of the ankle and foot Source: Work Loss Data Institute - Public For Profit Organization; 2003; 76 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3798&nbr=3024&a mp;string=uric+AND+acid
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Essential hypertension Source: University of Michigan Health System - Academic Institution; 1997 (revised 2002 Aug); 14 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3539&nbr=2765&a mp;string=uric+AND+acid
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Guidelines for the diagnosis and treatment of chronic heart failure Source: European Society of Cardiology - Medical Specialty Society; 2001 September; 34 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2976&nbr=2202&a mp;string=uric+AND+acid
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Hypertension diagnosis and treatment Source: Institute for Clinical Systems Improvement - Private Nonprofit Organization; 1995 June (revised 2003 Apr); 47 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3759&nbr=2985&a mp;string=uric+AND+acid
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Lipid management in adults Source: Institute for Clinical Systems Improvement - Private Nonprofit Organization; 1997 October (revised 2002 Jul); 61 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3410&nbr=2636&a mp;string=uric+AND+acid
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Management of early rheumatoid arthritis. A national clinical guideline Source: Scottish Intercollegiate Guidelines Network - National Government Agency [Non-U.S.]; 2000 December; 44 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2914&nbr=2140&a mp;string=uric+AND+acid
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Multiple myeloma (MM) Source: Finnish Medical Society Duodecim - Professional Association; 2001 December 27; Various pagings http://www.guideline.gov/summary/summary.aspx?doc_id=3394&nbr=2620&a mp;string=uric+AND+acid
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National High Blood Pressure Education Program: Working Group report on high blood pressure in pregnancy Source: National Heart, Lung, and Blood Institute (U.S.) - Federal Government Agency [U.S.]; 1990 (revised 2000 Jul); 39 pages http://www.guideline.gov/summary/summary.aspx?doc_id=1478&nbr=704&am p;string=uric+AND+acid
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Recommendations for the use of hematopoietic colony-stimulating factors: evidencebased, clinical practice guidelines Source: American Society of Clinical Oncology - Medical Specialty Society; 1994 November (updated 2000); 37 pages http://www.guideline.gov/summary/summary.aspx?doc_id=893&nbr=44& string=uric+AND+acid
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Screening and management of lipids Source: University of Michigan Health System - Academic Institution; 2000 May (revised 2003 Apr); 13 pages http://www.guideline.gov/summary/summary.aspx?doc_id=4114&nbr=3159&a mp;string=uric+AND+acid
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Screening for hypertension in adults Source: University of Texas at Austin School of Nursing, Family Nurse Practitioner Program - Academic Institution; 2002 May; 9 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3226&nbr=2452&a mp;string=uric+AND+acid
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Smallpox vaccination and adverse reactions. Guidance for clinicians Source: Centers for Disease Control and Prevention - Federal Government Agency [U.S.]; 2003 January 24; 29 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3597&nbr=2823&a mp;string=uric+AND+acid
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Healthfinder™ Healthfinder™ is sponsored by the U.S. Department of Health and Human Services and offers links to hundreds of other sites that contain healthcare information. This Web site is located at http://www.healthfinder.gov. Again, keyword searches can be used to find guidelines. The following was recently found in this database: •
Gout Fact Sheet Summary: This online fact sheet provides basic information for consumers about gout -a painful musculoskeletal condition caused by excessive amounts of uric acid crystals settling in the joints or other Source: Arthritis Foundation http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=2216
•
Questions and Answers About Gout Summary: Gout is one of the most painful rheumatic diseases. It results from deposits of needle-like crystals of uric acid in connective tissue, in the joint space between two bones, or in both. Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6721 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 uric acid. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/specific.htm
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Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
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Med Help International: http://www.medhelp.org/HealthTopics/A.html
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Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
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Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
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WebMDHealth: http://my.webmd.com/health_topics
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Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to uric acid. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with uric acid. 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 uric acid. 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 “uric acid” (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 “uric acid”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “uric acid” (or synonyms) into the “For these words:”
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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 “uric acid” (or a synonym) into the search box, and click “Submit Query.”
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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.
Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.24
Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.
Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of
24
Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.
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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)25: •
Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/
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Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)
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Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
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California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
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California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
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California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html
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California: Gateway Health Library (Sutter Gould Medical Foundation)
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California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
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California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
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California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
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California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
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California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
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California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
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California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
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California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
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Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
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Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
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Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
25
Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
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•
Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
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Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm
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Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
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Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm
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Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp
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Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/
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Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm
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Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html
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Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/
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Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
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Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
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Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
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Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
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Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm
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Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html
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Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm
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Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
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Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
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Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
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Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
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•
Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html
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Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp
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Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp
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Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/
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Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
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Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
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Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
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Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
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Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
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Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
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Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
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Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
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Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html
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Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm
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Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
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Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
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National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
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National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/
•
National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
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Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
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New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
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New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
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New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
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New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
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New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
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New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html
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New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
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Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
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Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp
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Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/
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Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/
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Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml
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Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html
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Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html
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Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml
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Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
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Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
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Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/
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South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp
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Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/
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Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/
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Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72
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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
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MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
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Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
•
Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
•
On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
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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 uric acid: •
Basic Guidelines for Uric Acid Uric acid Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003476.htm Uric acid - urine Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003616.htm
•
Signs & Symptoms for Uric Acid Fainting Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003092.htm Leukemia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001299.htm
•
Diagnostics and Tests for Uric Acid Blood pressure Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003398.htm
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Uric acid Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003476.htm Venipuncture Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003423.htm X-ray Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003337.htm •
Nutrition for Uric Acid Ascorbic acid Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002404.htm Caffeine Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002445.htm Nicotinic acid Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002409.htm Proteins Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002467.htm Vitamin C Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002404.htm
•
Background Topics for Uric Acid Adolescent test or procedure preparation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002054.htm Amino acids Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002222.htm Bleeding Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000045.htm Exercise Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001941.htm Infant test or procedure preparation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002055.htm Lead poisoning Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002473.htm Metabolism Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002257.htm Penis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002279.htm
Online Glossaries 169
Preschooler test or procedure preparation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002057.htm Schoolage test or procedure preparation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002058.htm Toddler test or procedure preparation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002056.htm
Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •
Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical
•
MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html
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Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/
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Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
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URIC ACID 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 fat: Fat (adipose tissue) that is centrally distributed between the thorax and pelvis and that induces greater health risk. [NIH] Abdominal Pain: Sensation of discomfort, distress, or agony in the abdominal region. [NIH] Ablation: The removal of an organ by surgery. [NIH] Acatalasia: A rare autosomal recessive disorder resulting from the absence of catalase activity. Though usually asymptomatic, a syndrome of oral ulcerations and gangrene may be present. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] Accommodation: Adjustment, especially that of the eye for various distances. [EU] Acetic Acids: Acetic acid and its derivatives which may be formed by substitution reactions. Mono- and di-substituted, as well as halogenated compounds have been synthesized. [NIH] Acetone: A colorless liquid used as a solvent and an antiseptic. It is one of the ketone bodies produced during ketoacidosis. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acetylgalactosamine: The N-acetyl derivative of galactosamine. [NIH] Acetylglucosamine: The N-acetyl derivative of glucosamine. [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] Activities of Daily Living: The performance of the basic activities of self care, such as dressing, ambulation, eating, etc., in rehabilitation. [NIH] Acute renal: A condition in which the kidneys suddenly stop working. In most cases, kidneys can recover from almost complete loss of function. [NIH] Acyl: Chemical signal used by bacteria to communicate. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH]
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Adenine: A purine base and a fundamental unit of adenine nucleotides. [NIH] Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adenosine Triphosphate: Adenosine 5'-(tetrahydrogen triphosphate). An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter. [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] Adsorption: The condensation of gases, liquids, or dissolved substances on the surfaces of solids. It includes adsorptive phenomena of bacteria and viruses as well as of tissues treated with exogenous drugs and chemicals. [NIH] Adsorptive: It captures volatile compounds by binding them to agents such as activated carbon or adsorptive resins. [NIH] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [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] Affinity Chromatography: In affinity chromatography, a ligand attached to a column binds specifically to the molecule to be purified. [NIH] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]
Age of Onset: The age or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual. [NIH] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and
Dictionary 173
stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Aldehydes: Organic compounds containing a carbonyl group in the form -CHO. [NIH] 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] Aldosterone Antagonists: Compounds which inhibit or antagonize the biosynthesis or actions of aldosterone. [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] Alkaline: Having the reactions of an alkali. [EU] Alkaline Phosphatase: An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC 3.1.3.1. [NIH] Alkalinization: The process by which a substance becomes an alkali. An alkali is the opposite of an acid. [NIH] 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] Alkylating Agents: Highly reactive chemicals that introduce alkyl radicals into biologically active molecules and thereby prevent their proper functioning. Many are used as antineoplastic agents, but most are very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. They have also been used as components in poison gases. [NIH]
Allergen: An antigenic substance capable of producing immediate-type hypersensitivity (allergy). [EU] Allo: A female hormone. [NIH] Allogeneic: Taken from different individuals of the same species. [NIH] Allograft: An organ or tissue transplant between two humans. [NIH] Allopurinol: A xanthine oxidase inhibitor that decreases uric acid production. [NIH] Allylamine: Possesses an unusual and selective cytotoxicity for vascular smooth muscle cells in dogs and rats. Useful for experiments dealing with arterial injury, myocardial fibrosis or cardiac decompensation. [NIH]
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Alpha Particles: Positively charged particles composed of two protons and two neutrons, i.e., helium nuclei, emitted during disintegration of very heavy isotopes; a beam of alpha particles or an alpha ray has very strong ionizing power, but weak penetrability. [NIH] Alpha-1: A protein with the property of inactivating proteolytic enzymes such as leucocyte collagenase and elastase. [NIH] Alpha-helix: One of the secondary element of protein. [NIH] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Aluminum: A metallic element that has the atomic number 13, atomic symbol Al, and atomic weight 26.98. [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] Alveoli: Tiny air sacs at the end of the bronchioles in the lungs. [NIH] Amine: An organic compound containing nitrogen; any member of a group of chemical compounds formed from ammonia by replacement of one or more of the hydrogen atoms by organic (hydrocarbon) radicals. The amines are distinguished as primary, secondary, and tertiary, according to whether one, two, or three hydrogen atoms are replaced. The amines include allylamine, amylamine, ethylamine, methylamine, phenylamine, propylamine, and many other compounds. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Aminolevulinic Acid: A compound produced from succinyl-CoA and glycine as an intermediate in heme synthesis. [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] Ammonium Chloride: An acidifying agent that is used as an expectorant and a diuretic. [NIH]
Ammonium Sulfate: Sulfuric acid diammonium salt. It is used in fractionation of proteins. [NIH]
Amnion: The extraembryonic membrane which contains the embryo and amniotic fluid. [NIH]
Amniotic Fluid: Amniotic cavity fluid which is produced by the amnion and fetal lungs and kidneys. [NIH] Ampicillin: Semi-synthetic derivative of penicillin that functions as an orally active broadspectrum antibiotic. [NIH]
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Ampulla: A sac-like enlargement of a canal or duct. [NIH] Amylase: An enzyme that helps the body digest starches. [NIH] Amyloid: A general term for a variety of different proteins that accumulate as extracellular fibrils of 7-10 nm and have common structural features, including a beta-pleated sheet conformation and the ability to bind such dyes as Congo red and thioflavine (Kandel, Schwartz, and Jessel, Principles of Neural Science, 3rd ed). [NIH] Amyloidosis: A group of diseases in which protein is deposited in specific organs (localized amyloidosis) or throughout the body (systemic amyloidosis). Amyloidosis may be either primary (with no known cause) or secondary (caused by another disease, including some types of cancer). Generally, primary amyloidosis affects the nerves, skin, tongue, joints, heart, and liver; secondary amyloidosis often affects the spleen, kidneys, liver, and adrenal glands. [NIH] Amylose: An unbranched glucan in starch. [NIH] Anaemia: A reduction below normal in the number of erythrocytes per cu. mm., in the quantity of haemoglobin, or in the volume of packed red cells per 100 ml. of blood which occurs when the equilibrium between blood loss (through bleeding or destruction) and blood production is disturbed. [EU] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] 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] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] Analytes: A component of a test sample the presence of which has to be demonstrated. The term "analyte" includes where appropriate formed from the analyte during the analyses. [NIH]
Anaphylaxis: An acute hypersensitivity reaction due to exposure to a previously encountered antigen. The reaction may include rapidly progressing urticaria, respiratory distress, vascular collapse, systemic shock, and death. [NIH] Anaplasia: Loss of structural differentiation and useful function of neoplastic cells. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Androgens: A class of sex hormones associated with the development and maintenance of the secondary male sex characteristics, sperm induction, and sexual differentiation. In addition to increasing virility and libido, they also increase nitrogen and water retention and stimulate skeletal growth. [NIH] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anesthesia: A state characterized by loss of feeling or sensation. This depression of nerve function is usually the result of pharmacologic action and is induced to allow performance of surgery or other painful procedures. [NIH] 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]
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Aneurysm: A sac formed by the dilatation of the wall of an artery, a vein, or the heart. [NIH] Angina: Chest pain that originates in the heart. [NIH] Angina Pectoris: The symptom of paroxysmal pain consequent to myocardial ischemia usually of distinctive character, location and radiation, and provoked by a transient stressful situation during which the oxygen requirements of the myocardium exceed the capacity of the coronary circulation to supply it. [NIH] Angiogenesis: Blood vessel formation. Tumor angiogenesis is the growth of blood vessels from surrounding tissue to a solid tumor. This is caused by the release of chemicals by the tumor. [NIH] Angiopathy: Disease of the blood vessels (arteries, veins, and capillaries) that occurs when someone has diabetes for a long time. There are two types of angiopathy: macroangiopathy and microangiopathy. In macroangiopathy, fat and blood clots build up in the large blood vessels, stick to the vessel walls, and block the flow of blood. In microangiopathy, the walls of the smaller blood vessels become so thick and weak that they bleed, leak protein, and slow the flow of blood through the body. Then the cells, for example, the ones in the center of the eye, do not get enough blood and may be damaged. [NIH] Angioplasty: Endovascular reconstruction of an artery, which may include the removal of atheromatous plaque and/or the endothelial lining as well as simple dilatation. These are procedures performed by catheterization. When reconstruction of an artery is performed surgically, it is called endarterectomy. [NIH] Angiotensinogen: An alpha-globulin of which a fragment of 14 amino acids is converted by renin to angiotensin I, the inactive precursor of angiotensin II. It is a member of the serpin superfamily. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] 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] Ankle: That part of the lower limb directly above the foot. [NIH] Anoxia: Clinical manifestation of respiratory distress consisting of a relatively complete absence of oxygen. [NIH] Antagonism: Interference with, or inhibition of, the growth of a living organism by another living organism, due either to creation of unfavorable conditions (e. g. exhaustion of food supplies) or to production of a specific antibiotic substance (e. g. penicillin). [NIH] Anterior chamber: The space in front of the iris and behind the cornea. [NIH] Antiallergic: Counteracting allergy or allergic conditions. [EU] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]
Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign
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substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Antibody-Dependent Cell Cytotoxicity: The phenomenon of antibody-mediated target cell destruction by non-sensitized effector cells. The identity of the target cell varies, but it must possess surface IgG whose Fc portion is intact. The effector cell is a "killer" cell possessing Fc receptors. It may be a lymphocyte lacking conventional B- or T-cell markers, or a monocyte, macrophage, or polynuclear leukocyte, depending on the identity of the target cell. The reaction is complement-independent. [NIH] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Antidiuretic: Suppressing the rate of urine formation. [EU] Antifungal: Destructive to fungi, or suppressing their reproduction or growth; effective against fungal infections. [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] Antihypertensive: An agent that reduces high blood pressure. [EU] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] 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] Antiseptic: A substance that inhibits the growth and development of microorganisms without necessarily killing them. [EU] Antispasmodics: Medicines that help reduce or stop muscle spasms in the intestines. Examples are dicyclomine (dy-SY-klo-meen) (Bentyl) and atropine (AH-tro-peen) (Donnatal). [NIH] Antiviral: Destroying viruses or suppressing their replication. [EU] Anuria: Inability to form or excrete urine. [NIH] Anus: The opening of the rectum to the outside of the body. [NIH] Aorta: The main trunk of the systemic arteries. [NIH] Apathy: Lack of feeling or emotion; indifference. [EU] Apnea: A transient absence of spontaneous respiration. [NIH] Apolipoproteins: The protein components of lipoproteins which remain after the lipids to which the proteins are bound have been removed. They play an important role in lipid
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transport and metabolism. [NIH] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Approximate: Approximal [EU] Aqueous: Having to do with water. [NIH] Aqueous fluid: Clear, watery fluid that flows between and nourishes the lens and the cornea; secreted by the ciliary processes. [NIH] Arachidonate 12-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 12-hydroperoxyarachidonate (12-HPETE) which is itself rapidly converted by a peroxidase to 12-hydroxy-5,8,10,14-eicosatetraenoate (12-HETE). The 12-hydroperoxides are preferentially formed in platelets. EC 1.13.11.31. [NIH] Arachidonate 15-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 15-hydroperoxyarachidonate (15-HPETE) which is rapidly converted to 15-hydroxy5,8,11,13-eicosatetraenoate (15-HETE). The 15-hydroperoxides are preferentially formed in neutrophils and lymphocytes. EC 1.13.11.33. [NIH] Arachidonate Lipoxygenases: Enzymes catalyzing the oxidation of arachidonic acid to hydroperoxyarachidonates (HPETES). These products are then rapidly converted by a peroxidase to hydroxyeicosatetraenoic acids (HETES). The positional specificity of the enzyme reaction varies from tissue to tissue. The final lipoxygenase pathway leads to the leukotrienes. EC 1.13.11.- . [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Aromatic: Having a spicy odour. [EU] 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] Arteriovenous: Both arterial and venous; pertaining to or affecting an artery and a vein. [EU] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Arthritis, Gouty: Arthritis, especially of the great toe, as a result of gout. Acute gouty arthritis often is precipitated by trauma, infection, surgery, etc. The initial attacks are usually monoarticular but later attacks are often polyarticular. [NIH] Arthropathy: Any joint disease. [EU] Articular: Of or pertaining to a joint. [EU] Ascites: Accumulation or retention of free fluid within the peritoneal cavity. [NIH] Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus
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fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant. [NIH] Aspartic: The naturally occurring substance is L-aspartic acid. One of the acidic-amino-acids is obtained by the hydrolysis of proteins. [NIH] Aspartic Acid: One of the non-essential amino acids commonly occurring in the L-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter. [NIH] Asphyxia: A pathological condition caused by lack of oxygen, manifested in impending or actual cessation of life. [NIH] Aspirate: Fluid withdrawn from a lump, often a cyst, or a nipple. [NIH] Aspirin: A drug that reduces pain, fever, inflammation, and blood clotting. Aspirin belongs to the family of drugs called nonsteroidal anti-inflammatory agents. It is also being studied in cancer prevention. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Asymptomatic: Having no signs or symptoms of disease. [NIH] Ataxia: Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharnyx, larnyx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or peripheral nerve diseases. Motor ataxia may be associated with cerebellar diseases; cerebral cortex diseases; thalamic diseases; basal ganglia diseases; injury to the red nucleus; and other conditions. [NIH] Atherectomy: Endovascular procedure in which atheromatous plaque is excised by a cutting or rotating catheter. It differs from balloon and laser angioplasty procedures which enlarge vessels by dilation but frequently do not remove much plaque. If the plaque is removed by surgical excision under general anesthesia rather than by an endovascular procedure through a catheter, it is called endarterectomy. [NIH] Atrial: Pertaining to an atrium. [EU] Atrial Fibrillation: Disorder of cardiac rhythm characterized by rapid, irregular atrial impulses and ineffective atrial contractions. [NIH] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Atropine: A toxic alkaloid, originally from Atropa belladonna, but found in other plants, mainly Solanaceae. [NIH] Attenuated: Strain with weakened or reduced virulence. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autonomic: Self-controlling; functionally independent. [EU] Autopsy: Postmortem examination of the body. [NIH] Autosuggestion: Suggestion coming from the subject himself. [NIH] Axotomy: Transection or severing of an axon. This type of denervation is used often in experimental studies on neuronal physiology and neuronal death or survival, toward an understanding of nervous system disease. [NIH]
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Azlocillin: A semisynthetic ampicillin-derived acylureido penicillin. [NIH] Bacillus: A genus of Bacillaceae that are spore-forming, rod-shaped cells. Most species are saprophytic soil forms with only a few species being pathogenic. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] 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] Bacteriuria: The presence of bacteria in the urine with or without consequent urinary tract infection. Since bacteriuria is a clinical entity, the term does not preclude the use of urine/microbiology for technical discussions on the isolation and segregation of bacteria in the urine. [NIH] Barbiturate: A drug with sedative and hypnotic effects. Barbiturates have been used as sedatives and anesthetics, and they have been used to treat the convulsions associated with epilepsy. [NIH] Barium: An element of the alkaline earth group of metals. It has an atomic symbol Ba, atomic number 56, and atomic weight 138. All of its acid-soluble salts are poisonous. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Basal Ganglia Diseases: Diseases of the basal ganglia including the putamen; globus pallidus; claustrum; amygdala; and caudate nucleus. Dyskinesias (most notably involuntary movements and alterations of the rate of movement) represent the primary clinical manifestations of these disorders. Common etiologies include cerebrovascular disease; neurodegenerative diseases; and craniocerebral trauma. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Basophils: Granular leukocytes characterized by a relatively pale-staining, lobate nucleus and cytoplasm containing coarse dark-staining granules of variable size and stainable by basic dyes. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]
Benign prostatic hyperplasia: A benign (noncancerous) condition in which an overgrowth of prostate tissue pushes against the urethra and the bladder, blocking the flow of urine. Also called benign prostatic hypertrophy or BPH. [NIH] Benzbromarone: Uricosuric that acts by increasing uric acid clearance. It is used in the treatment of gout. [NIH] Benzene: Toxic, volatile, flammable liquid hydrocarbon biproduct of coal distillation. It is used as an industrial solvent in paints, varnishes, lacquer thinners, gasoline, etc. Benzene causes central nervous system damage acutely and bone marrow damage chronically and is carcinogenic. It was formerly used as parasiticide. [NIH]
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Benzoates: Salts and esters of benzoic acid that possess antibacterial and antifungal properties. They are used as preservatives in pharmaceutical formulations including oral preparations, cosmetics, and food. [NIH] Benzoic Acid: A fungistatic compound that is widely used as a food preservative. It is conjugated to glycine in the liver and excreted as hippuric acid. [NIH] Bicarbonates: Inorganic salts that contain the -HCO3 radical. They are an important factor in determining the pH of the blood and the concentration of bicarbonate ions is regulated by the kidney. Levels in the blood are an index of the alkali reserve or buffering capacity. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile Acids: Acids made by the liver that work with bile to break down fats. [NIH] Bile Acids and Salts: Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones. [NIH] Bile Ducts: Tubes that carry bile from the liver to the gallbladder for storage and to the small intestine for use in digestion. [NIH] Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [NIH] Biliary Tract: The gallbladder and its ducts. [NIH] Bilirubin: A bile pigment that is a degradation product of heme. [NIH] Bioassay: Determination of the relative effective strength of a substance (as a vitamin, hormone, or drug) by comparing its effect on a test organism with that of a standard preparation. [NIH] Bioavailability: The degree to which a drug or other substance becomes available to the target tissue after administration. [EU] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biodegradation: The series of processes by which living organisms degrade pollutant chemicals, organic wastes, pesticides, and implantable materials. [NIH] Biological response modifier: BRM. A substance that stimulates the body's response to infection and disease. [NIH] Biological therapy: Treatment to stimulate or restore the ability of the immune system to fight infection and disease. Also used to lessen side effects that may be caused by some cancer treatments. Also known as immunotherapy, biotherapy, or biological response modifier (BRM) therapy. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Biosynthesis: The building up of a chemical compound in the physiologic processes of a living organism. [EU] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and
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protein structure function analysis and prediction. [NIH] Biotransformation: The chemical alteration of an exogenous substance by or in a biological system. The alteration may inactivate the compound or it may result in the production of an active metabolite of an inactive parent compound. The alteration may be either nonsynthetic (oxidation-reduction, hydrolysis) or synthetic (glucuronide formation, sulfate conjugation, acetylation, methylation). This also includes metabolic detoxication and clearance. [NIH] Bladder: The organ that stores urine. [NIH] Blood Cell Count: A count of the number of leukocytes and erythrocytes per unit volume in a sample of venous blood. A complete blood count (CBC) also includes measurement of the hemoglobin, hematocrit, and erythrocyte indices. [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 Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such a
