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Approach to elucidate the pathogenesis of multiple organ disfunction syndrome in critically ill patients

Research Project

Project/Area Number 22592014
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Emergency medicine
Research InstitutionShiga University of Medical Science

Principal Investigator

TABATA Takahisa  滋賀医科大学, 医学部, 講師 (90278200)

Co-Investigator(Kenkyū-buntansha) MATSUMURA Kazuhiro  滋賀医科大学, 医学部, 准教授 (50378486)
FUJINO Kazunori  滋賀医科大学, 医学部, 助教 (70402716)
Project Period (FY) 2010 – 2012
Project Status Completed (Fiscal Year 2012)
Budget Amount *help
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Keywords多臓器不全 / インスリン / 骨髄細胞 / 多臟器不全 / インスリン治療
Research Abstract

On the aspect that the pathogenesis of multiple organ dysfunction syndromes (MODS) is resembles to that of end-stage diabetes mellitus (DM) patients, we investigated the mechanism of MODS by referring the results of recent advance of DM research. In patients who died by MODS, we found the proinsulin positive cells in both kidney and liver. These cells were also TNF-alpha positive in confocal study. These results suggest that the high glucose induces proinsulin positive cells in bone marrow, and those cells invade to visceral organs, release a TNF-alpha, and resulted in MODS.

Report

(4 results)
  • 2012 Annual Research Report   Final Research Report ( PDF )
  • 2011 Annual Research Report
  • 2010 Annual Research Report

URL: 

Published: 2010-08-23   Modified: 2019-07-29  

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