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Acute neuronal injurythe role of exc...

Fujikawa, Denson G.

Acute neuronal injurythe role of excitotoxic programmed cell death mechanisms /

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Acute neuronal injuryedited by Denson G. Fujikawa.
其他題名:	the role of excitotoxic programmed cell death mechanisms /
其他作者:	Fujikawa, Denson G.
出版者:	Cham :Springer International Publishing :2018.
面頁冊數:	xii, 215 p. :ill., digital ;24 cm.
Contained By:	Springer eBooks
標題:	Nervous systemDiseases
電子資源:	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 injurythe 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

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505 0 $a 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.
520 $a 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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