| Project/Area Number |
07671246
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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 |
Kidney internal medicine
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| Research Institution | Hamamatsu university School of Medicine |
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Principal Investigator |
HISHIDA Akira Hamamatsu University School of Medicine, Department of Medicine, Associate Professor, 医学部附属病院, 助教授 (70111812)
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| Co-Investigator(Kenkyū-buntansha) |
YAMASHITA Fuyuki Hamamatsu university School of Medicine, Senior Resident, 医学部附属病院, 医員
FUJIGAKI Yosihide Hamamatsu university School of Medicine, Research Associate, 医学部, 助手 (20283351)
大石 和久 浜松医科大学, 医学部・附属病院, 助手 (90211094)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1995: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | acute renal failure / ischemia / uranyl acetate / apoptosis / tubular regeneration / uninephrectomy / rechallenged injury / 細胞増殖 / 虚血性腎障害 |
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| Research Abstract |
The aim of this study was to evaluate the roles of apoptosis and tubular regeneration in the development of ischemic and nephrotoxic acute renal failure. Ischemic acute renal failure was provoked by a 60-min left renal artery occlusion in right nephrectomized (Nx) and sham-nephretomized (sham-Nx)rats. Apoptotic cells characterized by apoptotic body and DNA fragmentation were observed in both groups, suggesting the induction of apoptosis in ischemic tubular cells. Ischemic tubular injury was significantly less in Nx rats than sham-Nx animals. Less tubular injury was associated with less apoptotic tubular cells. Nephrotoxic acute renal failure was induced by the injection of uranyl acetate (UA). UA-induce increase in plasma creatinine and the histological tubular injury peaked on day 5 following UA and returned to basal level on day 14. The re-administration of UA on day 14 to rats recovered from previous acute renal failure induced less increase in plasma creatinine and less tubular damage compared with the first US.Less tubular damage in rechallenged rats was associated with the less apoptotic tubular cells. These findngs suggest the role of apoptosis in the development of ischemic and nephrotoxic acute renal failure. The increased tubular regeneration evaluated with the number of PCNA positive cells was associated with the less tubular damage in ischemic ARF.In contrast, the less tubular damage in UA-induced ARF was associated with the less number of mitotic cells evaluated with positive BrdU.The discrepancy between ischemic and nephrotoxic ARF might be caused by the difference of insult or the difference of the method to evaluate the regeneration of tubular cells.
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