Maturation Phenomenon in Cerebral Ischemia IV: Apoptosis And/or Necrosis, Neuronal Recovery Vs. Death, And Protection Against Infarction by N.G. . BazanMaturation Phenomenon in Cerebral Ischemia IV: Apoptosis And/or Necrosis, Neuronal Recovery Vs. Death, And Protection Against Infarction by N.G. . Bazan

Maturation Phenomenon in Cerebral Ischemia IV: Apoptosis And/or Necrosis, Neuronal Recovery Vs…

EditorN.G. . Bazan, umeo Ito, V.L. Marcheselli

Paperback | March 27, 2001

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The maturation phenomenon, first described by Ito et al. in 1975, refers to postischemic changes that develop hours or days after an ischemic insult. The delayed neuronal death of CA1 pyramidal cells of the hippocampus is a classic example. The report of the phenomenon boosted research in the field, as it became evident that ischemic damage is not a sudden event, but a process potentially susceptible to therapeutic intervention. Since then a growing number of studies have improved our knowledge on mechanisms of cell death and recovery. This volume contains the presentations of the 4th international symposium, held in New Orleans in October/November 1999, grouped in sections covering apoptosis and/or necrosis, neuronal recovery vs. death, and protection against infarction. It outlines the present status of investigations and provides further stimulation for research in this field.
Title:Maturation Phenomenon in Cerebral Ischemia IV: Apoptosis And/or Necrosis, Neuronal Recovery Vs…Format:PaperbackDimensions:300 pages, 9.25 × 6.1 × 0 inPublished:March 27, 2001Publisher:Springer Berlin HeidelbergLanguage:English

The following ISBNs are associated with this title:

ISBN - 10:3540411070

ISBN - 13:9783540411079

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Table of Contents

The role of genetic expression and apoptosis.- Factors modulating neuronal plasticity and course of maturation phenomenon in cerebral ischemia (metabolic and inflammatory factors).- Factors and mechanisms enhancing susceptibility or tolerance (growth factors).- Ischemic infarction: threshold, experimental and clinical dynamics and therapeutic design for prevention and reduction of intensity.- Mitochondria.