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Acute neuronal injurythe role of exc...
~
Fujikawa, Denson G.
Acute neuronal injurythe role of excitotoxic programmed cell death mechanisms /
Record Type:
Electronic resources : Monograph/item
Title/Author:
Acute neuronal injuryedited by Denson G. Fujikawa.
Reminder of title:
the role of excitotoxic programmed cell death mechanisms /
other author:
Fujikawa, Denson G.
Published:
Cham :Springer International Publishing :2018.
Description:
xii, 215 p. :ill., digital ;24 cm.
Contained By:
Springer eBooks
Subject:
Nervous systemDiseases
Online resource:
http://dx.doi.org/10.1007/978-3-319-77495-4
ISBN:
9783319774954$q(electronic bk.)
Acute neuronal injurythe role of excitotoxic programmed cell death mechanisms /
Acute neuronal injury
the role of excitotoxic programmed cell death mechanisms /[electronic resource] :edited by Denson G. Fujikawa. - 2nd ed. - Cham :Springer International Publishing :2018. - xii, 215 p. :ill., digital ;24 cm.
Introduction -- Excitotoxic programmed cell death involves caspase-independent mechanisms -- To survive or to die: how neurons deal with it -- Oxidative damage mechanisms in traumatic brain injury and antioxidant neuroprotective approaches -- Mitochondrial damage in traumatic CNS injury -- Neuroprotective agents target molecular mechanisms of programmed cell death after traumatic brain injury -- Involvement of apoptosis-inducing factor (AIF) in neuronal death following cerebral ischemia -- Apoptosis-inducing factor translocation to nuclei after transient global ischemia -- Necroptosis in cerebral ischemia -- Histological and elemental changes in ischemic stroke -- Hypoglycemic brain damage -- Activation of caspase-independent programmed pathways in seizure-induced neuronal necrosis -- Conclusion.
An overview of the biochemical mechanisms that produce acute nerve cell death in the brain. Covers injuries and disorders including stroke, brain and spinal cord trauma, hypoglycemic coma, and prolonged epileptic seizures. All of these lead to high concentrations of calcium in nerve cells which, in turn, causes degradation of cytoplasmic proteins, cleavage of nuclear DNA, and eventually cell death. The Second Edition contains 11 thoroughly updated chapters and 3 additional chapters that did not appear in the previous edition.
ISBN: 9783319774954$q(electronic bk.)
Standard No.: 10.1007/978-3-319-77495-4doiSubjects--Topical Terms:
455460
Nervous system
--Diseases
LC Class. No.: RC347 / .A288 2018
Dewey Class. No.: 616.807
Acute neuronal injurythe role of excitotoxic programmed cell death mechanisms /
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edited by Denson G. Fujikawa.
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Introduction -- Excitotoxic programmed cell death involves caspase-independent mechanisms -- To survive or to die: how neurons deal with it -- Oxidative damage mechanisms in traumatic brain injury and antioxidant neuroprotective approaches -- Mitochondrial damage in traumatic CNS injury -- Neuroprotective agents target molecular mechanisms of programmed cell death after traumatic brain injury -- Involvement of apoptosis-inducing factor (AIF) in neuronal death following cerebral ischemia -- Apoptosis-inducing factor translocation to nuclei after transient global ischemia -- Necroptosis in cerebral ischemia -- Histological and elemental changes in ischemic stroke -- Hypoglycemic brain damage -- Activation of caspase-independent programmed pathways in seizure-induced neuronal necrosis -- Conclusion.
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An overview of the biochemical mechanisms that produce acute nerve cell death in the brain. Covers injuries and disorders including stroke, brain and spinal cord trauma, hypoglycemic coma, and prolonged epileptic seizures. All of these lead to high concentrations of calcium in nerve cells which, in turn, causes degradation of cytoplasmic proteins, cleavage of nuclear DNA, and eventually cell death. The Second Edition contains 11 thoroughly updated chapters and 3 additional chapters that did not appear in the previous edition.
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Biomedical and Life Sciences (Springer-11642)
based on 0 review(s)
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電子館藏
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1 records • Pages 1 •
1
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000000160827
電子館藏
1圖書
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EB RC347 A189 2018 2018
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0
1 records • Pages 1 •
1
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http://dx.doi.org/10.1007/978-3-319-77495-4
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