Mitochondrial inhibitors and neurodegenerative disorders / (Record no. 23819)

MARC details
000 -LEADER
fixed length control field 05541cam a2200361 a 4500
001 - ACCESSION NUMBER
control field 013828893
003 - CONTROL NUMBER IDENTIFIER
control field CUTN
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20171110131947.0
008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION
fixed length control field 981218s2000 njua b 001 0 eng c
010 ## - LIBRARY OF CONGRESS CONTROL NUMBER
LC control number 98055467
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 089603805X (acidfree paper)
040 ## - CATALOGING SOURCE
Original cataloging agency DNLM/DLC
Transcribing agency DLC
Modifying agency DLC
082 00 - DEWEY DECIMAL CLASSIFICATION NUMBER
Classification number 616.8047
Edition number 21
Item number SAN
245 00 - TITLE STATEMENT
Title Mitochondrial inhibitors and neurodegenerative disorders /
Statement of responsibility, etc edited by Paul R. Sanberg, Hitoo Nishino, Cesario V. Borlongan ; foreword by Joseph T. Coyle.
260 ## - PUBLICATION, DISTRIBUTION, ETC. (IMPRINT)
Place of publication, distribution, etc Totowa, N.J. :
Name of publisher, distributor, etc Humana Press,
Date of publication, distribution, etc c2000.
300 ## - PHYSICAL DESCRIPTION
Extent xvii, 313 p. :
Other physical details ill. ;
Dimensions 24 cm.
500 ## - GENERAL NOTE
General note Mitochondria have long been the Rodney Dangerfield of cellular organelles. Believed to be the remnants of bacterial infection of eukaryotic cells eons ago, the mitochondrion evolved a symbiotic relationship in which it dutifully served as the efficient source of A TP for cell function. The extraordinary dependence of cells on the energy provided by mito- chondrial oxidative metabolism of glucose, especially through critical organs such as the heart and brain, is underlined by the fatal consequences of toxins that interfere with the mitochondrial electron transport system. Consistent with their ancestry, the mitochondria have their own DNA that encodes many but not all of their proteins. The mitochon- dria and their genes come from the mother via the ovum since sperm do not possess mitochondria. This extranuclear form of inheritance derived exclusively from the female side has proven to be a powerful tool for tracing the evolution by the number of base substitutions in mtDNA. That mitochondrial gene mutations might be a source of human dis- ease became evident a decade ago with the characterization of a group of multisystem disorders, typically involving the nervous system, which are transmitted from mother to child. Specific point mutations in mtDNA have been associated with the different syndromes.
505 ## - FORMATTED CONTENTS NOTE
Formatted contents note Part I. Mitochondrial Toxins: Symptomatology, Origin, and Chemistry. Clinical Manifestations and Mechanisms of Action of Environmental Mitochondrial Toxins, Mohammad I. Sabri, Peter S. Spencer, Safia Baggia, and Albert C. Ludolph. History of 3-Nitropropionic Acid: Occurrence and Role in Human and Animal Disease, Bradley F. Hamilton, Daniel H. Gould, and David L. Gustine. The Neurochemistry of 3-Nitropropionic Acid, Norman C. Reynolds, Jr. and Wen Lin. Part II. Mitochondrial Dysfunctions: Models of Neurodegeneration and Mechanisms of Action. In Vitro Studies of 3-Nitropropionic Acid, Gail D. Zeevalk. Cognitive and Motor Deficits Produced by Acute and Chronic Administration of 3-Nitropropionic Acid in Rats, Gary L. Dunbar, Deborah A. Shear, Jie Dong, and Kristi L. Haik-Creguer. Comparative Study on 3-Nitropropionic Acid Neurotoxicity, Cesario V. Borlongan. Mechanisms of 3-Nitropropionic Acid Neurotoxicity, James W. Geddes, Vimala Bondada, and Zhen Pang. Gender-Related Difference of the Effect of 3-Nitropropionic Acid on Striatal Artery, Keiya Nakajima, Yasunobu Shimano, Kunio Torii, and Hitoo Nishino. Variable Susceptibility to Neurotoxicity of Systemic 3-Nitropropionic Acid, Tajrena Alexi, Richard L. M. Faull, and Paul E. Hughes. The 3-Nitropropionic Acid Model of Huntington's Disease: Do Alterations in the Expression of Metabolic mRNAs Predict the Development of Striatal Pathology? Keith J. Page, Alicia Meldrum, and Stephen B. Dunnett. Mechanisms of Action of 3-Nitropropionic Acid: Dopamine Overflow and Vulnerability of the Lateral Striatal Artery, Michiko Kumazaki, Chucharin Ungsuparkorn, Shripad B. Deshpande, Atsuo Fukuda, and Hitoo Nishino. Mitochondrial Inhibition and Neuronal Death in Huntington's Disease, Maria Isabel Behrens. Effects of Brain Mitochondrial Metabolism, Aging, and Caloric Restriction on Membrance Lipids and Proteins: An Electron Paramagnetic Resonance Investigation, S. Prasad Gabbita, John M. Carney, and D. Allan Butterfield. Malonate: Profileand Mechanisms of Striatal Toxicity, Alicia Meldrum, Keith J. Page, Barry J. Everitt, and Stephen B. Dunnett. Malonic Acid and the Chronic Administration Model of Excitotoxicity, Terence J. Bazzett, Roger L. Albin, and Jill B. Becker. Sodium Azide-Induced Neurotoxicity, Yun Wang and Cesario V. Borlongan. Part III. Treatment Interventions for Mitochondrial-Induced Neurotoxicity. Neuroprotective Strategies Against Cellular Hypoxia, Matthias W. Riepe. Neuroprotective Effect of Perinatal Hypoxia Against 3-Nitropropionic Acid Neurotoxicity, Zbigniew K. Binienda and Andrew C. Scallet. Neural Transplantation and Huntington's Disease: What Can We Learn from the 3-Nitropropionic Acid Model? Cesario V. Borlongan, Christine E. Stahl, Thomas B. Freeman, Robert A. Hauser, and Paul R. Sanberg. Neuroprotective Strategies in Parkinson's Disease and Huntington's Chorea: MPTP- and 3-NPA-Induced Neurodegeneration as Models, Moussa B. H. Youdim, Gopal Krishna, and Chuang C. Chiueh. Index
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Nervous system
General subdivision Degeneration
-- Pathophysiology.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Nervous system
General subdivision Degeneration
-- Animal models.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Mitochondrial pathology.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Neurotoxic agents.
650 12 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Neurodegenerative Diseases
General subdivision chemically induced.
650 22 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Propionic Acids
General subdivision toxicity.
650 22 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Mitochondria
General subdivision metabolism.
650 22 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Neurotoxins
General subdivision toxicity.
700 1# - ADDED ENTRY--PERSONAL NAME
Personal name Sanberg, Paul R.
700 1# - ADDED ENTRY--PERSONAL NAME
Personal name Nishino, Hitoo.
700 1# - ADDED ENTRY--PERSONAL NAME
Personal name Borlongan, Cesario V.
830 #0 - SERIES ADDED ENTRY--UNIFORM TITLE
Uniform title Contemporary neuroscience
942 ## - ADDED ENTRY ELEMENTS (KOHA)
Source of classification or shelving scheme Dewey Decimal Classification
Koha item type General Books
Holdings
Date last seen Total Checkouts Full call number Barcode Price effective from Koha item type Lost status Source of classification or shelving scheme Damaged status Not for loan Collection code Withdrawn status Home library Current library Shelving location Date acquired
04/02/2020   616.8047 SAN 27583 10/11/2017 General Books   Dewey Decimal Classification     Non-fiction   CUTN Central Library CUTN Central Library Medicine, Technology & Management 10/11/2017

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