Identification of main factor of pressure ulcer formation, and prevention by phsical agents
| Project/Area Number |
23700602
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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 |
Rehabilitation science/Welfare engineering
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| Research Institution | Hiroshima University |
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Principal Investigator |
KUROSE Tomoyuki 広島大学, 医歯薬保健学研究院, 助教 (20363054)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 褥瘡 / 血流 / トマトレクチン / 炎症性サイトカイン / Real-Time PCR / Western Blot / 磁石 / 圧迫 / ウェスタンブロット / 血管開通率 / ラット / 皮膚温 / 酸化ストレス |
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| Research Abstract |
We produced the experimental pressure ulcer model rat to clear the mechanism of pressure ulcers. Repeated compression at 50mmHg for 4 hours did not cause the macroscopic and microscopic alteration. But, repeated compression at 100mmHg for 4 hours induces the destruction of skin and ulcer formation. Expression of IL-1beta, which is an inflammatory cytokine, was not changed at 50mmHg compression. Compression at 100mmHg cause high expression of IL-1beta, and increased with compression times. TNF-alpha was not changed at 50mmHg compression ,and slightly increased at 100mmHg compression.
Inhibition of inflammatory cytokine may have possibility to prevent the pressure ulcers.
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Report
(4 results)
Research Products
(30 results)
