| Project/Area Number |
05671185
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Teikyo University School of Med. |
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Principal Investigator |
NAKAGOMI Tadayoshi Teikyo Univ., School of Medicine, Associate Professor, 医学部, 助教授 (90198052)
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| Co-Investigator(Kenkyū-buntansha) |
KANEMITSU Hideaki Teikyo Univ., School of Medicine, Assistant Professor, 医学部, 講師 (10129992)
TAMURA Akira Teikyo Univ., School of Medicine, Professor, 医学部, 教授 (80111532)
戸向 則子 帝京大学, 医学部, 教務職 (30192214)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1994: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1993: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | neuronal death / protein synthesis / ischmic tolerance / stress protein / gerbil / ウエスタンブロット / 蛋白合成阻害剤 / 砂ネズミ / 熱ショック蛋白 / 脳虚血 |
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| Research Abstract |
Following brief cerebral ischemia, tolerance to subsequent ischemia is induced in the hippocampal neurons. The aim of this study was to investigate the relationship between ischemic tolerance phenomenon and protein synthesis. First, recovery of protein synthesis was studied autoradiographically in gerbils with induced tolerance. To observe the effect of tolerance acquisition, double forebrain ischemia, 2-min ischemia followed by 5 min-ischemia, was induced 2 days later. In this group, recovery of protein synthesis in the CAI sector was rapid. At 1 day of recirculation, protein synthesis returned near normal. On the other hand, protein synthesis in the 5-min ischemia group was severely suppressed and never returned to the normal level. The present study revealed an early recovery of protein synthesis in the hippocampal neurons in the gerbil with induced tolerance. Secondly, possible differences in electrophoresis pattern of the brain protein between tolerance-induce animals and animals injected with protein synthesis inhibitor. There was no differences in the pattern of the protein between these two groups. Thirdly, we investigated whether multiple sublethal ishemia can enhance the ability of tolerance induction or prolong the period of tolerance. At 1 month after the multiple exposure to sublethal 2-min ischemia, animals did not acquire ischemic tolerance to 4-min lethal ischemia. To clarify the mechanism of ischemic tolerance, further studies are needed.
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