Bone marrow stromal cells and thymosin beta 4 attenuate septic organ failure
| Project/Area Number |
23592688
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Emergency medicine
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| Research Institution | Fujita Health University |
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Principal Investigator |
KANO Hideki 藤田保健衛生大学, 医学部, 准教授 (90340231)
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| Co-Investigator(Kenkyū-buntansha) |
TAKEYAMA Naoshi 藤田保健衛生大学, 医学部救命救急医学講座, 教授 (00155053)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 骨随前駆細胞 / VEGF / CXCL8 / 敗血症 / NETs / 免疫染色 / cell-free DNA / 間葉系幹細胞 / thymosin 4 |
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| Research Abstract |
Recent evidence suggests that vascular maintenance during sepsis is thought to important mechanisms to repair endothelial damage. This repair is mediated by recruitment from bone marrow of endothelial progenitor cells (EPCs). Therefore we were interested in whether EPCs, measured by FACS, are mobilized during sepsis and if this mobilization is related to clinical outcome. We showed that the appearance of CD34+ cells in the blood of patients with sepsis reduced compared to healthy controls. Plasma levels of growth factor VEGF and chemokine CXCL8 are significantly higher in septic patients compared to healthy volunteers. These results suggest that sepsis would induce bone marrow hypo-responsiveness to cytokines.
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Report
(4 results)
Research Products
(19 results)
