Detection of Circulating Endothelial Cells in Severe Sepsis
Project/Area Number |
21390482
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Emergency medicine
|
Research Institution | Kyoto University |
Principal Investigator |
KOIKE Kaoru 京都大学, 医学研究科, 教授 (10267164)
|
Co-Investigator(Kenkyū-buntansha) |
MATSUDA Naoyuki 名古屋大学, 医学研究科, 教授 (50332466)
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥18,200,000 (Direct Cost: ¥14,000,000、Indirect Cost: ¥4,200,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2010: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2009: ¥12,610,000 (Direct Cost: ¥9,700,000、Indirect Cost: ¥2,910,000)
|
Keywords | 敗血症 / 遊離型血管内皮細胞 / CEC / AP-1 / TAK-1 / NF-κB / 播種性血管愛凝固症候群 / DIC / 血管内皮細胞 / アポトーシス / ショック / 遺伝子核酸治療 / マウス / Death受容体 |
Research Abstract |
Sepsis is a severe disorder as systemic inflammation with infection. In this illness, vascular endothelial damage proceeds to induce disseminated intravascular coagulation(DIC). This study revealed that circulating endothelial cell(CEC) was increased and plasma platelet count was decreased in the time dependent manner after sepsis induction by cecal ligation and puncture in male BALB-C mice. Nuclear factor-kappaB decoy oligonucleotides more strongly decreased CEC count than inactivation of FADD, TAK-1, and activator protein-1. The CEC count could be a reliable marker to evaluate DIC and dysfunction of vascular endothelium.
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Report
(4 results)
Research Products
(2 results)