| Project/Area Number |
09670824
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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 |
Pediatrics
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| Research Institution | Fukushima Medical University School of Medicine |
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Principal Investigator |
SUZUKI Junzo Fukushima Medical University, Pediatrics, Associate Professor, 医学部, 助教授 (20171217)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Shigeo Fukushima Medical University, Pediatrics, Research Associate, 医学部, 助手 (00274960)
SUZUKI Hitoshi Fukushima Medical University, Pediatrics, Professor, 医学部, 教授 (80045682)
久米 一成 福島県立医科大学, 医学部, 講師 (40254023)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 1999: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1998: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1997: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | GTP-binding protein / PI turnover / TXAィイD22ィエD2 / PGEィイD22ィエD2 / nephrotic syndrome / PAF / platelet / calcium / GTP結合蛋白質 / トロンボキサンA_2 |
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| Research Abstract |
(2) The blood 11-dehydro-TXBィイD22ィエD2 level in the onset group was significantly higher than those in the remission and control groups.
We investigated the changes of prostanoid metabolites, platelet calcium ion concentrations by STAィイD22ィエD2 (TXAィイD22ィエD2 agonist) and platelet activating factor (PAF) stimulation and the distribution of GTP-binding protein in the kidney with nephrotic syndrome. The following results were obtained:
(1) Urinary TXBィイD22ィエD2 and 11-dehydro-TXBィイD22ィエD2 excretion were significantly higher in the onset and relapse groups compared to the remission and control groups.
(3) Platelet calcium concentration due to STAィイD22ィエD2 stimulation were significantly increased in the onset, relaps and remission groups compared to the control group.
(4) Platelet calcium concentration due to PAF stimulation were significantly increase in the onset, relaps and remission groups compared to the control group.
(5) Distribution of GTP-binding protein was showed renal medullary collecting tubule cells in rat, but not glomeruli, and the distinction of the distribution of GTP-binding protein seems to be made between nephrotic and normal rat kidney.
(6) Enhanced phophatidylinositol turnover of the glomerus was observed in the state of nephrosis.
(7) Sensitivity of the PI turnover system to PGEィイD22ィエD2 was accentuated.
These findings suggest that the changes of intracellular signal-transducting GTP-binding protein in platelets of patients with nephrotic syndrome is deeply involved in the pathophysiology of nephrosis.
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