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A new therapeutic strategy by suppression of F-actin/DNGR-1 signal in a rat model of crush injury

Research Project

Project/Area Number 26861521
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Emergency medicine
Research InstitutionOsaka University

Principal Investigator

Matsumoto Hisatake  大阪大学, 医学部附属病院, 医員 (70644003)

Project Period (FY) 2014-04-01 – 2016-03-31
Project Status Completed (Fiscal Year 2015)
Budget Amount *help
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Keywordsクラッシュ症候群 / Fアクチン / DNGR1受容体 / DAMPs / Fアクチン / DNGR1受容体 / DAMPs / DNGR1
Outline of Final Research Achievements

The purposes of this study are as follows.①To investigate the F-actin/DNGR-1 signal in the context of systemic acute inflammation following crush injury and to assess the therapeutic effects of anti- F-actin antibody in a rat model of crush injury. ②To evaluate the F-actin/DNGR-1 signal in the patients with systemic inflammation (Trauma and Sepsis). In this study, the administration of anti-Factin antibody did not improve the 7-day survival rate of crush injury rat model. The circulating F-actin levels significantly increased in the patients with sepsis, suggesting that the signal play a role in the pathogenesis of sepsis.

Report

(3 results)
  • 2015 Annual Research Report   Final Research Report ( PDF )
  • 2014 Research-status Report

URL: 

Published: 2014-04-04   Modified: 2017-05-10  

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