LEADER 03587nam 22006495 450 001 9910298405003321 005 20200702092818.0 010 $a3-319-77495-6 024 7 $a10.1007/978-3-319-77495-4 035 $a(CKB)3850000000032741 035 $a(MiAaPQ)EBC5448095 035 $a(DE-He213)978-3-319-77495-4 035 $a(PPN)229505236 035 $a(EXLCZ)993850000000032741 100 $a20180705d2018 u| 0 101 0 $aeng 135 $aurcnu|||||||| 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 10$aAcute Neuronal Injury $eThe Role of Excitotoxic Programmed Cell Death Mechanisms /$fedited by Denson G. Fujikawa 205 $a2nd ed. 2018. 210 1$aCham :$cSpringer International Publishing :$cImprint: Springer,$d2018. 215 $a1 online resource (212 pages) 311 $a3-319-77494-8 327 $aIntroduction -- 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. 330 $aAn 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. 606 $aNeurosciences 606 $aNeurology 606 $aPathology 606 $aCytology 606 $aNeurobiology 606 $aPsychiatry 606 $aNeurosciences$3https://scigraph.springernature.com/ontologies/product-market-codes/B18006 606 $aNeurology$3https://scigraph.springernature.com/ontologies/product-market-codes/H36001 606 $aPathology$3https://scigraph.springernature.com/ontologies/product-market-codes/H4800X 606 $aCell Biology$3https://scigraph.springernature.com/ontologies/product-market-codes/L16008 606 $aNeurobiology$3https://scigraph.springernature.com/ontologies/product-market-codes/L25066 606 $aPsychiatry$3https://scigraph.springernature.com/ontologies/product-market-codes/H53003 615 0$aNeurosciences. 615 0$aNeurology. 615 0$aPathology. 615 0$aCytology. 615 0$aNeurobiology. 615 0$aPsychiatry. 615 14$aNeurosciences. 615 24$aNeurology. 615 24$aPathology. 615 24$aCell Biology. 615 24$aNeurobiology. 615 24$aPsychiatry. 676 $a616.8 702 $aFujikawa$b Denson G$4edt$4http://id.loc.gov/vocabulary/relators/edt 906 $aBOOK 912 $a9910298405003321 996 $aAcute Neuronal Injury$92522653 997 $aUNINA