List of Contributors. Preface. Chapter 1. A new perspective on ischemic brain damage (B.K. Siesjö). Section I. Temperature, Acid-Base Homeostasis, and Microcirculation. 2. Temperature modulation of ischemic brain injury - a synthesis of recent advances (M.D. Ginsberg, M.Y.-T. Globus, W. D. Dietrich, R. Busto). 3. Acidosis-related brain damage (B.K. Siesjö, K. Katsura, P. Mellergård, A. Ekholm, J. Lundgren, M.-L. Smith). 4. Cerebral ischemia: the microcirculation as trigger and target (U. Dirnagl). Section II - Free Radicals and Excitatory Amino Acids. 5. Evaluation of the concomitance of lipid peroxidation in experimental models of cerebral ischemia and stroke (B.D. Watson). 6. Role of superoxide dismutase in ischemic brain injury: reduction of edema and infarction in transgenic mice following focal cerebral ischemia (P.H. Chan, C.J. Epstein, H. Kinonchi, S. Imaizumi, E. Carlson and S.F. Chen). 7. Glutamate receptor transmission and ischemic nerve cell damage: Evidence for involvement of excitotoxic mechanisms (N.H. Diemer, E. Valente, T. Bruhn, M. Berg, M.B. Jorgenson, F.F. Johansen). 8. Antagonism of the NMDA and non-NMDA receptors in global versus focal brain ischemia (W. Pulsinelli, A. Sarokin, A. Buchan). 9. NMDA receptors and AMPA / kainate receptors mediate parallel injury in cerebral cortical cultures subjected to oxygen-glucose deprivation (D.W. Choi). Section III. Polyamine and Protein Metabolism. 10. Ischemia-induced disturbances of polyamine synthesis (W. Paschen, M. Cleef, G. Röhn, M. Müller, A.E.I. Pajunen). 11. Disturbances of cerebral protein synthesis and ischemic cell death (K.-A. Hossmann). 12. Protein phosphorylation and the regulation of mRNA translation following cerebral ischemia (T. Wieloch, K. Bergstedt, B.R. Hu). Section IV. Selective Gene Expression. 13. Stress protein and proto-oncogene expression as indicators of neuronal pathophysiology after i
In the eight years since the publication of Volume 63 of Progress in Brain Research, on this subject, developments in the research field have been very fast. For example, receptor physiology and pharmacology is now an intensively studied field, and the excitotoxic hypothesis of cell death is commonly accepted. Furthermore, it is recognized that ischemia and other insults give rise to a sustained depression of overall protein synthesis, yet lead to the expression of dormant genes and to synthesis of new proteins.
In view of this development, this volume focusses on the cellular and molecular aspects of ischemic brain damage. The book will be of great value to all those interested in the pathophysiology of ischemic and traumatic brain damage.
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- © Elsevier Science 1993
- 10th May 1993
- Elsevier Science
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Institute of Brain Diseases, Sendai, Japan
Max-Planck-Institute for Neurological Research, Cologne, Germany
University of Lund, Lund, Sweden