| Project/Area Number |
15591548
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 | Kyorin University |
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Principal Investigator |
KURITA Hiroki Kyorin University, School of Medicine, Assistant Professor, 医学部, 講師 (70262003)
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| Co-Investigator(Kenkyū-buntansha) |
SHIOKAWA Yoshiaki Kyorin University, School of Medicine, Professor, 医学部, 教授 (20245450)
坪川 民治 杏林大学, 医学部, 助手 (30360100)
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| Project Period (FY) |
2003 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2006: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2005: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2004: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | radiosurgery / oligodendroglia / apoptosis / demyelination / radiation necrosis / p53 knockout mouse / oligodendroglia / Radiosurgery / oilgodendrocyte / rasiation necrosis / aminosteroid / optic chiasm / Radiation / Apoptosis / Optic chiasm |
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| Research Abstract |
The adverse effect of radiosurgery (single, high-dose irradiation) to the central nervous system remains to be elucidated.
The purpose of this study was to characterize the apoptotic death of oligodendrocyte immediately after the irradiation, and to investigate the relationship between the acute cell loss and delayed demyelinating encephalopathy or radiation necrosis of the brain.
The extent of acute oligodendroglial cell loss several hours after the radiation was well correlated with the extent of delayed encephalopathy in rat radiosurgery model. The radioprotectant drugs, such as aminosteroids and corticosteroids did not block the acute cell death.
Single high-dose irradiation also resulted in vasculopathy of the microvessels of the brain, which caused cyst formation or repetitive bleeding within the irradiated brain. Immunohistopathological investigation confirmed the destruction of tight gap junction of endothelium and exudation to the surrounding tissues.
In conclusion, acute oligodendroglial loss and endothelial damage play a significant role for delayed radiation necrosis in the central nervous system
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