| Project/Area Number |
08457189
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Osaka University |
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Principal Investigator |
YANAGIHARA Takehiko Osaka University Hospital, Professor, 医学部・附属病院, 教授 (70243201)
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| Co-Investigator(Kenkyū-buntansha) |
KITAGAWA Kazuo Medical School, Assistant Professor, 医学部, 助手
UEDA Hirokazu Medical School, Assistant Professor, 医学部, 助手 (10294117)
MATSUMOTO Masayasu Medical School, Lecturer, 医学部, 講師 (20192346)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 1997: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1996: ¥4,400,000 (Direct Cost: ¥4,400,000)
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| Keywords | Ischemic tolerance / HSP72 / Neuronal death / Gerbil / near-infrared spectroscopy / Bifemelane hydrochloride / 脳虚血 / ストレス蛋白質 |
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| Research Abstract |
Involvement of heat shock protein 72 (HSP72) in ischemic tolerance in gerbil brain was examined by using (1) hemispheric ischemia model and (2) conditions to enhance tolerance. Oxygen metabolism under acquisition of ischemic tolerance was also examined by using a near-infrared spectroscopy. A moderate degree of ischemic pretreatment for 10 min to one hemisphere was reversible but strong enough to produce HSP72. The treatment given two days earlier induced neuronal protection in the caudoputamen after ischemia for 30 min (Brain Res.716 : 39-46 : 1996). We then successfully induced augmentation of tolerance by repetitive ischemic pretreatment (Neuroscience 81 : 989-998 : 1997) and by administartion of a neuroprotective agent, bifemelane hydrochloride (Life Sci.59 : 979-985 : 1996). However, the increase in HSP72 after augmentation of tolerance was not significantey more in comparison with a single ischemic pretreatment. The study for intracerebral oxygenation states with a near-infrared spectroscopy showed that ischemic pretreatment could induce improvement of oxygen metabolism during subsequent ischemia (Stroke 28 : 1451-1457 : 1997). These data suggested that (1) ischemic tolerance could be observed in focal cerebral ischemia, (2) involvement of HSP72 in ischemic tolerance was likely present but HSP72 was not a sole molecule responsible for ischemic tolerance and might not be the primary molecule, and (3) improvement in oxygen metabolism might be related to acquisition of ischemic tolerance.
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