1995 Fiscal Year Final Research Report Summary
The mechanisms of ischemic neuronal death and its treatment.
| Project/Area Number |
05305006
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| Research Category |
Grant-in-Aid for Co-operative Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
広領域
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| Research Institution | Ehime University School of Medicine |
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Principal Investigator |
KATAOKA Kiyoshi Ehime University School of Medicine, Department of Physiology, Professor, 医学部, 教授 (20025589)
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| Co-Investigator(Kenkyū-buntansha) |
YONEDA Yukio Setsunan University, Department of Pharmacology, Associate Professor, 薬学部, 助教授 (50094454)
FUJISHIMA Masatoshi Kyusyu University School of Medicine, Department of Internal Medicine, Professor, 医学部, 教授 (80038760)
HAYAKAWA Toru Osaka University School of Medicine, Department of Neurosurgery, Professor, 医学部, 教授 (20135700)
TAMURA Akira Teikyo University School of Medicine, Department of Neurosurgery, Professor, 医学部, 教授 (80111532)
KIRINO Takaaki Tokyo University School of Medicine, Department of Neurosurgery, Professor, 医学部, 教授 (90126045)
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| Project Period (FY) |
1993 – 1995
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| Keywords | Ischemic neuronal death / Excitotoxicity / Remote effects / Resistance to ischemia / Mild hypothermia / Glial cells / Red cell deformability / Transcription factor |
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| Research Abstract |
Following the early process in ischemic neurons, a glutamate surge and a subsequent calcium mobilization, proceed further complicated intracellular cascade reactions, being tangled with environmental changes including glial responses, which eventually lead to irreversible neuronal damage. The present project intended to posturate these patho-physiological entity on different aspects and by different methods. Examples of means to protect ischmic neurons against damage were also demonstrated.
As experimental models, primary culture systems of cells and also of slices were newly developed along with forebrain or regional ischemic models (Hayakawa and others). As the very early phase of ischemia, glutamate release and calcium mobilization, and suppressive effects of mild hypothermia thereto were demonstrated (Kataoka and others). Mechanisms of intracellular calcium dischage were studied by newly synthesized inositol polyphosphoric acids ; and dantrolene derivatives were studied on their neu
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roprotective activities (Ozaki and others). As the cascade reactions, an ischemia-induced enhancement of the binding activity of a transcription factor, AP1, was posturated with a speculation of its relation to neuronal survival (Yoneda and others). Dysfunction of protein metabolism and special synthetic response to ischemia were studid by the use of heat shock protein or ubiquitin (Kirino and others). Apoptotic mechanisms were proposed to be involved in ischemic damage through the studies of related genes and analysis of phospholipids (Tamura and others). Specific resistance to ischemia and the importance of glucose were demonstrated in neurons of new born animals (Okada and others). On the other hand, regional cerebral blood flow were found lowered in neurons of aged animals along with elevated stress responses (Fujishima and others). A device for analysis of red cell deformability was newly developed and an enhancement of the deformability was shown in red cells from spontaneously hypertensive rats (Uyesaka and others). Less
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