The establishment of a control system for HIF1alpha activation pathway in post-cardiac arrest syndrome.
| Project/Area Number |
25861736
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Emergency medicine
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| Research Institution | Hokkaido University |
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Principal Investigator |
WADA TAKESHI 北海道大学, 大学病院, 助教 (30455646)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 生体侵襲 / 臓器不全 / 凝固線溶系 / VEGF / Angiopoietin / 心停止後症候群 / 播種性血管内凝固症候群 / DIC |
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| Outline of Final Research Achievements |
I investigated the important role of fibrinolysis which are involved in neutrophil elastase and plasmin, which is affected by plasminogen activator inhibitor-1 (PAI-1), which is induced by Hypoxia inducible factor-1α (HIF1α) in post-cardiac arrest syndrome (PCAS). The results indicated that fibrinolytic shutdown plays important roles in the development of organ dysfunction in PCAS patients. Neutrophil elastase-mediated fibrinolysis cannot overcome the fibrinolytic shutdown that occurs in DIC patients with PCAS, thus resulting in the development of multiple organ dysfunction.
In addition, I studied the relationship between the serum levels of HIF1α and the development of DIC or organ dysfunction in sepsis, severe trauma, and PCAS patients. These studies showed no significant results. This can be explained by the fact that HIF1α acts inside the cell.
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Report
(3 results)
Research Products
(10 results)
