Acute Neuronal Injury The Role of Excitotoxic Programmed Cell Death Mechanisms / edited by Denson G. Fujikawa.

সংরক্ষণ করুন:
গ্রন্থ-পঞ্জীর বিবরন
সংস্থা লেখক: SpringerLink (Online service)
অন্যান্য লেখক: Fujikawa, Denson G. (Editor)
বিন্যাস: বৈদ্যুতিন গ্রন্থ
ভাষা:English
প্রকাশিত: Cham : Springer International Publishing : Imprint: Springer, 2018.
সংস্করন:2nd ed. 2018.
মালা:Springer eBook Collection.
বিষয়গুলি:
অনলাইন ব্যবহার করুন:Click to view e-book
Holy Cross Note:Loaded electronically.
Electronic access restricted to members of the Holy Cross Community.

MARC

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245 1 0 |a Acute Neuronal Injury  |h [electronic resource] :  |b The Role of Excitotoxic Programmed Cell Death Mechanisms /  |c edited by Denson G. Fujikawa. 
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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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650 0 |a Neurosciences. 
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