Acute Neuronal Injury (Record no. 58452)

MARC details
000 -LEADER
fixed length control field 05108nam a22005055i 4500
001 - CONTROL NUMBER
control field 978-0-387-73226-8
003 - CONTROL NUMBER IDENTIFIER
control field DE-He213
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20250710084017.0
007 - PHYSICAL DESCRIPTION FIXED FIELD--GENERAL INFORMATION
fixed length control field cr nn 008mamaa
008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION
fixed length control field 110413s2010 xxu| s |||| 0|eng d
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 9780387732268
-- 99780387732268
024 7# - OTHER STANDARD IDENTIFIER
Standard number or code 10.1007/978-0-387-73226-8
Source of number or code doi
082 04 - DEWEY DECIMAL CLASSIFICATION NUMBER
Classification number 612.8
Edition information 23
100 1# - MAIN ENTRY--PERSONAL NAME
Personal name Fujikawa, Denson G.
Relator term editor.
245 10 - TITLE STATEMENT
Title Acute Neuronal Injury
Medium [recurso electrónico] :
Remainder of title The Role of Excitotoxic Programmed Cell Death Mechanisms /
Statement of responsibility, etc. edited by Denson G. Fujikawa.
264 #1 - PRODUCTION, PUBLICATION, DISTRIBUTION, MANUFACTURE, AND COPYRIGHT NOTICE
Place of production, publication, distribution, manufacture Boston, MA :
Name of producer, publisher, distributor, manufacturer Springer US,
Date of production, publication, distribution, manufacture, or copyright notice 2010.
300 ## - PHYSICAL DESCRIPTION
Extent XI, 306p. 176 illus., 16 illus. in color. With 16 page color insert.
Other physical details online resource.
336 ## - CONTENT TYPE
Content type term text
Content type code txt
Source rdacontent
337 ## - MEDIA TYPE
Media type term computer
Media type code c
Source rdamedia
338 ## - CARRIER TYPE
Carrier type term recurso en línea
Carrier type code cr
Source rdacarrier
347 ## - DIGITAL FILE CHARACTERISTICS
File type text file
Encoding format PDF
Source rda
505 0# - FORMATTED CONTENTS NOTE
Formatted contents note Caspase-Independent Programmed Cell Death: General Considerations -- Caspase-Independent Cell Death Mechanisms in Simple Animal Models -- Programmed Necrosis: A "New" Cell Death Outcome for Injured Adult Neurons? -- Age-Dependence of Neuronal Apoptosis and of Caspase Activation -- Excitotoxic Programmed Cell Death Involves Caspase-Independent Mechanisms -- Focal Cerebral Ischemia -- Significant Role of Apoptosis-Inducing Factor (AIF) for Brain Damage Following Focal Cerebral Ischemia -- The Role of Poly(ADP-Ribose) Polymerase-1 (PARP-1) Activation in Focal Cerebral Ischemia -- Transient Global Ischemia -- Transient Global Cerebral Ischemia Produces Morphologically Necrotic, Not Apoptotic Neurons -- Apoptosis-Inducing Factor Translocation to Nuclei After Transient Global Ischemia -- Role of µ-Calpain I and Lysosomal Cathepsins in Hippocampal Neuronal Necrosis After Transient Global Ischemia in Primates -- Traumatic Central Nervous System (CNS) Injury -- Mitochondrial Damage in Traumatic CNS Injury -- Programmed Neuronal Cell Death Mechanisms in CNS Injury -- Hypoglycemic Neuronal Death -- Hypoglycemic Brain Damage -- Hypoglycemic Neuronal Death -- Seizure-Induced Neuronal Death -- Tumor Suppressor p53: A Multifunctional Protein Implicated in Seizure-Induced Neuronal Cell Death -- DNA Damage and Repair in the Brain: Implications for Seizure-Induced Neuronal Injury, Endangerment, and Neuroprotection -- Activation of Caspase-Independent Programmed Pathways in Seizure-Induced Neuronal Necrosis.
520 ## - SUMMARY, ETC.
Summary, etc. This book is the result of a convergence of scientific information regarding mechanisms that produce acute nerve cell death in the brain. Although seemingly disparate, stroke, brain and spinal cord trauma, coma from a low serum glucose concentration (hypoglycemia), and prolonged epileptic seizures have in common the inciting factor of excitotoxicity, the activation of a specific subtype of glutamate receptor by an elevated extracellular glutamate concentration that results in an excessive influx of calcium into nerve cells. The high calcium concentration in nerve cells activates several enzymes that are responsible for degradation of cytoplasmic proteins and cleavage of nuclear DNA, resulting in nerve cell death. The high calcium concentration also interferes with mitochondrial respiration, with the resultant production of free radicals that damage cellular membranes and nuclear DNA. Understanding the biochemical pathways that produce nerve cell death is the first step toward devising an effective neuroprotective strategy, the ultimate goal. Acute Neuronal Injury will be useful to neuroscientists and general cell biologists interested in cell death. The book will also be helpful to clinically oriented neuroscientists, including neurologists, neurosurgeons and psychiatrists. About the Editor: Dr. Denson Fujikawa is an Adjunct Professor of Neurology at the David Geffen School of Medicine at UCLA, a member of the Brain Research Institute at UCLA and a Staff Neurologist at the Department of Veterans Affairs Greater Los Angeles Healthcare System. His interest in mechanisms of nerve cell death in the brain began during a two-year epilepsy research fellowship with Dr. Claude Wasterlain, from 1981 to 1983. He is a Fellow of the American Academy of Neurology and is a member of the American Epilepsy Society, American Neurological Association, International Society for Cerebral Blood Flow and Metabolism, and the Society for Neuroscience.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element MEDICINE.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element NEUROSCIENCES.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element NEUROLOGY.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element PATHOLOGY.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element PSYCHIATRY.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element CYTOLOGY.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element NEUROBIOLOGY.
650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element BIOMEDICINE.
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element NEUROSCIENCES.
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element NEUROLOGY.
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element PATHOLOGY.
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element CELL BIOLOGY.
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element NEUROBIOLOGY.
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element PSYCHIATRY.
710 2# - ADDED ENTRY--CORPORATE NAME
Corporate name or jurisdiction name as entry element SpringerLink (Online service)
773 0# - HOST ITEM ENTRY
Title Springer eBooks
776 08 - ADDITIONAL PHYSICAL FORM ENTRY
Relationship information Printed edition:
International Standard Book Number 9780387732251
856 40 - ELECTRONIC LOCATION AND ACCESS
Uniform Resource Identifier <a href="http://dx.doi.org/10.1007/978-0-387-73226-8">http://dx.doi.org/10.1007/978-0-387-73226-8</a>
Public note Ver el texto completo en las instalaciones del CICY
912 ## -
-- ZDB-2-SBL
942 ## - ADDED ENTRY ELEMENTS (KOHA)
Source of classification or shelving scheme Dewey Decimal Classification
Koha item type Libros electrónicos
Holdings
Lost status Source of classification or shelving scheme Damaged status Not for loan Collection Home library Current library Shelving location Date acquired Total checkouts Full call number Date last seen Price effective from Koha item type
  Dewey Decimal Classification     Libro electrónico CICY CICY Libro electrónico 10.07.2025   612.8 10.07.2025 10.07.2025 Libros electrónicos