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To elucidate the pathophysiology of sepsis-associated organ dysfunction involving the Ang/Tie2 signaling pathway

To elucidate the pathophysiology of sepsis-associated organ dysfunction involving the Ang/Tie2 signaling pathway
阐明涉及 Ang/Tie2 信号通路的脓毒症相关器官功能障碍的病理生理学
批准号:
23792091
负责人:
WADA Takeshi
金额:
$2.66万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Young Scientists (B)
财政年份:
2011
资助国家:
日本
项目状态:
已结题
起止时间:
2011 至 2012

项目摘要

项目成果

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中文摘要
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英文摘要
The aim of this study was to elucidate the pathophysiology of sepsis-associated organ dysfunction involving the Ang/Tie2 signaling pathway and to establish a new therapeutic strategy for treating critical illnesses, such as sepsis, severe trauma and post-cardiac arrest syndrome. I examined the relationship between organ dysfunction associated with critical illness and angiogenic factors, including VEGF, Ang and their receptors and found that Ang2 plays a pivotal role in the development of organ dysfunction due to coagulofibrinolytic abnormalities. The findings of this study have been presented at six domestic and four international conferences and have also been published by four peerreview articles.
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会议论文
外傷患者における血管新生関連因子と凝固線溶反応
创伤患者血管生成相关因素及凝血纤溶反应
DOI: --
发表时间: 2011
期刊:
影响因子: --
作者: [和田剛志, ジェスミン・サブリナ, 丸藤哲, 横田裕行]
通讯作者: 横田裕行
Time-dependent expression of endothelin-1 in lungs and the effects of TNF-α blocking peptide on acute lung injury in an endotoxemia rat model
肺内皮素-1的时间依赖性表达及TNF-α阻断肽对内毒素血症大鼠模型急性肺损伤的影响
DOI: --
发表时间: 2011
期刊:
影响因子: --
作者: [S. Jesmin, T. Wada, S. Zaedi, S.N. Sultana,N. Yamaguchi, Y. Iwashima, A. Sawamura, S. Gando]
通讯作者: S. Gando
Angiogenic factors and their soluble receptors in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) in critically ill patients
危重患者急性肺损伤(ALI)/急性呼吸窘迫综合征(ARDS)中的血管生成因子及其可溶性受体
DOI: --
发表时间: 2012
期刊:
影响因子: --
作者: [Takeshi Wada, Subrina Jesmin, Satoshi Gando, Yuichiro Yanagida, Asumi Mizugaki, Hiroyuki Yokota]
通讯作者: Hiroyuki Yokota
外傷患者におけるVEGF発現と凝固線溶反応
创伤患者VEGF表达与凝血纤溶反应
DOI: --
发表时间: 2011
期刊:
影响因子: --
作者: [和田剛志, 丸藤哲]
通讯作者: 丸藤哲
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      17K17068
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    • 资助金额:
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      26860808
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