| Project/Area Number |
17K17075
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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 | Kurume University |
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Principal Investigator |
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| Research Collaborator |
TAKASU osamu
HIRAYU nobuhisa
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | CLPモデル / バイオインピーダンス法 / HMGB1 / CLP / HMGB-1 / 臨床 |
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| Outline of Final Research Achievements |
Alarmins, such as HMGB1, etc., has been suggested to contribute to vascular hyperpermeability in patients with severe sepsis. The extracellular water in CLP mice with cecal ischemia was higher than that of sham operation mice at the point of 36 hours after operation. The concentration of HMGB1 in plasma was also higher than that of sham operation mice. However, there was no relationship between delta-ECW% and HMGB1 concentration. In vitro experiments using cultured cells, an addition of plasma of CLP mice with cecal ischemia to the cultured fluid showed decreasing of TEER and disruption of cells after 10 hours later. This reaction was one of a typical difference between CLP mice without cecal ischemia and with cecal ischemia. The addition of EVs isolated from plasma to the cell cultured fluid showed a similar pattern of impairments. These facts show the necessity for further investigations about EVs, particularly in the relation to Alarmin.
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| Academic Significance and Societal Importance of the Research Achievements |
敗血症をはじめとする高度侵襲下に生じる血管透過性亢進は、臓器障害の一因と考えられる。ひとたび血管透過性亢進が制御困難になれば、臓器障害の進行から致死的となるため、この制御メカニズムを検討し、あらたな知見から新規治療アプローチを探索することが重要である。本研究では、血管透過性亢進を制御する対象として、血漿中のHMGB1との関係を検討したが、むしろ、血漿中に存在する細胞外小胞とHMGB1等のAlarminの関係、さらには血漿中に存在するEVsの機能を抑制しうる物質など、血管透過性亢進を制御するための新たなアプローチと検討すべき方向性を得る事ができた。
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