1995 Fiscal Year Final Research Report Summary
Experimental Research for Regeneration of damaged Liver
| Project/Area Number |
06454366
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General surgery
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
UEMOTO Shinji Kyoto University, Faculty of Medicine, Assistant, 医学研究科, 助手 (40252449)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAOKA Yoshio Kyoto University, Faculty of Medicine, Professor, 医学研究科, 教授 (90089102)
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| Project Period (FY) |
1994 – 1995
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| Keywords | lymphicyte beta2-adrenoreceptor / receptor binding capacity / hepatic resection / liver regeneration / hypexia / EGF receptor / sigual transduction / acute rejtction |
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| Research Abstract |
1.In the hepatectomized patients, binding capacity of lymphocyte beta2-adrenoreceptor was assayd in relation to changes in arterial blood ketone body ratio (AKBR) presenting mitochondrial redox potential. In the low post-operative AKBR group, postoperative maximum biding capacity of lymphocyte beta2-adrenoreceptor (Bmax) decreased more that in the high AKBR group. It was suggested that the surgical stress produced by hepatectomy may influence the ligand-receptor binding capacity, and that AKBR can indicate the magnitude of surgical stress.
2.The effects of extracellular FK binding protein 12 (FKBP12) were studied in vitro and in patients received liver transplantation. FKBP12 inhibited the ability of FK506 (immuno-suppressive agent) to suppress phytohem-agglutinin-induced proliferative response of human peripheral blood mono-nuclear cells. Clinically, the rapid increase in plasma level of FKBP12 may contribute to the occurrence and progress of acute cellular rejection, probably due to inhibition of the immunosuppressive activity of FK506.
3.The effects of transient non-lethal hypoxia on epidermal growth factor (EGF) -induced DNA synthesis of rat hepatocytes were investigated. Transient hypoxia decreased intracellular ATP content, but reoxygenation restored the decrease in ATP.Such a hypoxia decreased the number of available EGF receptors without affecting the receptor protein expression, and inhibited the EGF-induced DNA aynthesis of rat hepatocytes through reversible changes in the EGF receptor molecule.
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