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.
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.
Rezensionen
"This is an outstanding book concerning the molecular and cellular mechanisms of trauma and ischemia in the mammalian brain. ... I recommend his book to neurophysiologists, neurologists, and neurosurgeons." (Joseph J. Grenier, Amazon.com, September, 2015)
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