| Project/Area Number |
10470351
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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 |
Otorhinolaryngology
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| Research Institution | University of Tsukuba |
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Principal Investigator |
HARA Akira University of Tsukuba, Inst.of Clinical Medicine, Otolaryngology, Associate Professor, 臨床医学系, 助教授 (10156474)
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| Co-Investigator(Kenkyū-buntansha) |
SENARITA Masamitsu University of Tsukuba, Inst.of Clinical Medicine, Otolaryngology, Assistant Professor, 臨床医学系, 講師 (60282357)
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| Project Period (FY) |
1998 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2001: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2000: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Cochlear dysfunction / Free radicals / Hydrnxyl radicals / NO / Transient ischemia / Steroid hormone / Iron chelator / Acoustic trauma / アスフィキシア / フリーラジカルスカベンジャー / ヒドロモシルラジカル / NOS阻害薬 / 鉄 / 虚血 / マンニトール |
|---|
| Research Abstract |
Metallic elements : Concentration of free iron transiently increased after local ischemia or asphyxia. The depression of DPOAE after local ischemia was improved by cochlear perfusion of an iron chelator.
Hydroxyl radicals : The generation of hydroxyl radicals was recognized in the perilymph after local ischemia, and was continued for 2 hours or more after reperfusion. The threshold shift of CAP after ischemia was significantly reduced by administration of scavengers to hydroxyl radicals.
Steroid hormones : The high level glucocorticoid receptor mRNA was revealed in the cochlea of the guinea pig. The level of glucocorticoid receptor mRNA significantly decreased immediately after exposure to the acoustic overstimulation. The concentration of glucocorticoid was high and maintained for a long period in the cochlea.
Nitric oxide (NO) : Significant increase of NO concentration was recognized after reperfusion. NO inhibitors alleviated the CAP threshold shift after local ischemia.
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