Project/Area Number |
08457371
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Cerebral neurosurgery
|
Research Institution | Nagoya City University |
Principal Investigator |
AIHARA Noritaka (1998) Nagoya City University, Neurosurgery, Lecturer, 医学部, 助手 (00264739)
神谷 健 (1996-1997) 名古屋市立大学, 医学部, 助教授 (70137115)
|
Co-Investigator(Kenkyū-buntansha) |
IWATA Akira Nagoya City University, Neurosurgery, Lecturer, 医学部, 助手 (90275131)
YAMASHITA Nobuko Nagoya City University, Neurosurgery, Lecturer, 医学部, 助手 (80220341)
YAMADA Kazuo Nagoya City University, Neurosurgery, Professor, 医学部, 教授 (90150341)
|
Project Period (FY) |
1996 – 1998
|
Project Status |
Completed (Fiscal Year 1998)
|
Budget Amount *help |
¥7,900,000 (Direct Cost: ¥7,900,000)
Fiscal Year 1998: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1997: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1996: ¥3,900,000 (Direct Cost: ¥3,900,000)
|
Keywords | SAH / apoptosis / immediate early gene / CA1 / hypothermia / bax / bcl-2 / アポトーシス / 脳血管萎縮 / Subarachnoid hemorrhege / rat / vasospasm / Delayad Nearoncl Death |
Research Abstract |
We have detected c-fos and c-jun mRNA in cerebral cortex, hippocampus and dentate gyrus in the penetrated side after subarachnoid hemorrhage (SAH). mRNA coding for hsp7O was induced in the cerebral cortex, hippocampus, thalamus, hypothalamus, and caudoputamen in the penetrated side and extended to the contralateral side. In the TUNEL.method, only CAl neurons in the penetrated side showed apoptosis-like changes 48hr after SAH.The genes for bax and p53 were induced fairly in the CAl with peak between l2hr and 48hr which might cause apoptosis, although bcl-2 was also upregulated during the same period. The regulation of bax/bcl-2 ratio through p53 might influence apoptotic cell death. We investigated the effect of hypothermia on brain exposed to SAH.Mild hypothermia depressed hsp7O mRNA expression in the cortex, thalamus and hippocampus. The c-jun mRNA expression was also reduced with hypothermia in the cortex, thalamus and CA1. In the future, we indicated that hypothermia therapy might be one of the procedures to treat SAH.
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