| Project/Area Number |
12470262
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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 |
Digestive surgery
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| Research Institution | HYOGO COLLEGE OF MEDICINE (2001)
Kyoto University (2000) |
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Principal Investigator |
IIMURO Yuji Hyogo College of Medicine,1st Surgery,Professor, 医学部, 助教授 (30252018)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIMOTO Jiro Hyogo College of Medicine, 1st Surgery, Professor, 医学部, 教授 (90199373)
山本 雄造 京都大学, 医学研究科, 講師 (70281730)
嶌原 康行 京都大学, 医学研究科, 助教授 (30196498)
山岡 義生 京都大学, 医学研究科, 教授 (90089102)
山本 成尚 京都大学, 医学研究科, 助手 (30253298)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥14,000,000 (Direct Cost: ¥14,000,000)
Fiscal Year 2001: ¥5,800,000 (Direct Cost: ¥5,800,000)
Fiscal Year 2000: ¥8,200,000 (Direct Cost: ¥8,200,000)
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| Keywords | liver regeneration / shear stress / partial hepatectomy / Racl / ischemia / reperfusion / 虚血再灌流 / 肝虚血再灌流障害 / 遺伝子導入 |
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| Research Abstract |
Change in portal blood flow after partial resection of the liver followed by increased "shear stress" has been proposed to play a critical role in initiation of liver regeneration. In the present study, we tried to investigate whether stretching mechanical stress resembling "shear stress" affect cell-proliferation of liver cells in vitro, and whether small GTPase Racl may participate in this process. Moreover, we analysed the effect of Racl-inactivation in the liver on regeneration-process after partial hepatectomy. To confirm that Racl activity was really inactivated in the liver with the method used in this study, we investigated another animal model. In a hepatic ischemia/reperfusion model, inactivation of Racl almost totally blocked hepatic injury after reperfusion. Therefore, we concluded that the method inactivating Racl activity used in this study t> was effective. After 70% partial hepatectomy, inactivation of Racl disturbed normal liver regeneration and activation of NFKB. From these results, we can speculate that Racl plays an important role in liver regeneration. Now we are investigating the effect of Racl-inactivation on cell proliferation of primary-cultured liver cells in vitro in a cell-stretching system, and trying to elucidate interaction among "shear stress", cell proliferation, and liver regeneration.
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