| Project/Area Number |
09470294
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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 |
Cerebral neurosurgery
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| Research Institution | Mie University |
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Principal Investigator |
KANAMARU Kenji Mie University School of Medicine, Neurosurgery, Associate Professor, 医学部, 助教授 (70185908)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUSHIMA Satoshi Mie University School of Medicine, Neurosurgery, Assistant Professor, 医学部・附属病院, 講師 (50252367)
久我 純弘 三重大学, 医学部・附属病院, 助手 (70221926)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥10,600,000 (Direct Cost: ¥10,600,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1998: ¥8,000,000 (Direct Cost: ¥8,000,000)
Fiscal Year 1997: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | calcium / cerebral ischemia / rat / thromboembolism / fra-2AM / Rose Bengal / chemiluminescence / ischemic penumbra / カルシウムイオン / 神経細胞死 / 光誘導血栓症モデル / クモ膜下出血 / 平滑筋収縮反応 / ラットモデル / heme oxygenases / endothelin / 脳血栓症 |
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| Research Abstract |
The increase in intracellular calcium ion plays a pivotal in processing vital function. Both necrosis and apoptosis are triggered by the influx of calcium ion via plasma membrane. The stimuli, such as ischemia and trauma, enhance permeability of calcium ion through plasma membrane. The elevation of intracellular calcium ion activates various proteolytic enzymes and caspases. If the calcium ion level reaches high enough to cause cell dysfunction, either apoptosis or necrosis may be programmed. One can surmise that cell death may be prevented by the inhibition of calcium overload. However, distribution of calcium signals during cerebral ischemia has not yet been demonstrated. We developed a novel method to detect calcium signals in the rat cerebral cortex after thromboembolic ischemia. Exposed rat cerebral cortex was preloaded with fra-2 AM, then Rose Bengal was injected intravenously. The proximal middle cerebral artery was irradiated producing thrombosis with 540 nm wavelength green light. Thereafter, ischemic cerebral cortex was alternatively irradiated with 340 and 380 nm light to emit chemiluminescence. The intensity of chemiluminescence took a peak at 60 minutes after the alternative irradiation. The highest calcium signals occurred in ischemic core which was proved by the pathological examination. In ischemic penumbra calcium signal was moderate. No calcium signal was demonstrated in normal cortex. The region of ischemic penumbra deemed a therapeutic target of rescue from cell death. In conclusion, we demonstrated for the first time calcium signals in the ischemic cerebral cortex in vivo.
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