Mechanism and control of inflammation and organ failure in crush syndrome.
Project/Area Number |
24791941
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Emergency medicine
|
Research Institution | Osaka University |
Principal Investigator |
SHIMAZAKI Junya 大阪大学, 医学(系)研究科(研究院), 研究員 (40528767)
|
Project Period (FY) |
2012-04-01 – 2014-03-31
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | クラッシュ症候群 / 全身性炎症反応症候群 / RAGE / HMGB1 / DAMPs |
Research Abstract |
Patients with crush injury often present systemic inflammatory response syndrome and fall into multiple organ failure, but the mechanism is still unclear. We focused on RAGE. (1)In Rat model of crush injury, administration of anti-RAGE antibody reduced inflammatory reaction and improved survival. (2)Patient with SIRS, serum soluble RAGE increased significantly than normal. Soluble RAGE was related to serum HMGB1 or acute DIC score. Expression of RAGE reflect to serum soluble RAGE. In patients with SIRS, RAGE expression may be increased. These results indicate blocking of RAGE such as anti-RAGE antibody may become a promising novel therapy against crush syndrome or SIRS.
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Report
(3 results)
Research Products
(6 results)