| Project/Area Number |
26461157
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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 |
Respiratory organ internal medicine
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| Research Institution | Niigata University |
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Principal Investigator |
Moro Hiroshi 新潟大学, 医歯学総合病院, 助教 (40509452)
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| Co-Investigator(Kenkyū-buntansha) |
高田 俊範 新潟大学, 医歯学総合病院, 特任教授 (40361919)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 肺MAC症 / 鉄 / Hepcidin / 鉄代謝 / IP-10 |
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| Outline of Final Research Achievements |
Patients with fibrocavitary MAC lung disease tend to have elevated inflammatory markers, poor nutritional status and deterioration of iron status, and long-term management is necessary. Serum IP-10 levels were significantly increased in the cavitary form, and it is significantly correlated with CRP, Fe, pre-Alb. With prolonged pro-inflammatory state of pulmonary MAC disease, IP-10 might associated with comorbid poor nutritional status and deterioration of iron status, and it might reflect the disease forms and severity of pulmonary MAC disease, as well as pulmonary tuberculosis.
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