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Ischemic neuronal cell damage and iron metaoblism

Research Project

Project/Area Number 06671421
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Cerebral neurosurgery
Research InstitutionTeikyo Univ.School of Med.

Principal Investigator

KANEMITSU Hitdeaki  Teikyo Univ.School of Med., Dept.of Neurosurgery, Assistant Prof., 医学部, 講師 (10129992)

Co-Investigator(Kenkyū-buntansha) TAMURA Akira  Teikyo Univ.School of Med., Dept.of Neurosurgery, Professor, 医学部, 教授 (80111532)
川合 謙介  帝京大学, 医学部, 助手 (70260924)
Project Period (FY) 1994 – 1996
Project Status Completed (Fiscal Year 1996)
Budget Amount *help
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1996: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1994: ¥800,000 (Direct Cost: ¥800,000)
Keywordscerebral ischemia / rat / gerbil / iron / clathrin / transferrin / transferrin receptor / home oxygenase / 免疫組織化学 / in situ hybridization / 脳虚血 / 全脳虚血 / 鉄染色
Research Abstract

We have studied the distribution and the metabolism of iron in rat and gerbil brains following three kinds of cerebral ischemia. One was the focal cerebral ischemia which occluded middle cerebral artery in the rat. Second was the whole cerebral ischemia which was induced by cardiac arrest in the rat. Third was the forebrain ischemia which occulded bilateral common carotid arteries in the gerbil. The methods for the distribution and the metabolism of iron were carried out by Perls' and Gomori methods for iron deposition, immunohistochemistry for clathrin, transferrin and transferrin receptor, and in situ hibridization or in situ reverse transcriptase-polymerase chain reaction (RT-PCR) hybridization for home oxygenase 1 and 2. We could not detect iron deposition in the ischemic group as well as in the normal group. We could not recognized the significant difference between in the ischemic group and in the normal group regarding the immunohistochemistry for clathrin, transferrin and transferrin receptor, and in situ hybridization or in situ RT-PCR hybridization for home oxygnase 1 and 2. These results suggest that the deposition and the metabolism of iron do not plays a direct role of neuronal death following cerebral ischemia.

Report

(4 results)
  • 1996 Annual Research Report   Final Research Report Summary
  • 1995 Annual Research Report
  • 1994 Annual Research Report

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Published: 1994-04-01   Modified: 2016-04-21  

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