| Project/Area Number |
21591584
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Radiation science
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| Research Institution | Kurume University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TONAN Tatsuyuki 久留米大学, 医学部, 講師 (40268892)
KAWAGUCHI Atsushi 久留米大学, バイオ統計センター, 講師 (60389319)
KAWAHARA Akihiro 久留米大学, 大学病院, 臨床検査技師 (00469347)
HAYABUCHI Naofumi 久留米大学, 医学部, 教授 (20108731)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | SPIO造影MRI / 非アルコール性脂肪肝炎(NASH) / 単純性脂肪肝 / Kupffer機能 / CD14抗体 / 非アルコール性脂肪肝炎 / MRI / CD14 / CD68 / Kupffer細胞 / 病理像 / NASH / Kuffer機能 / SPIO |
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| Research Abstract |
Kupffer cell(KC) function and CD14 expression contributes to pathogenesis of non-alcoholic steatohepatitis(NASH), but these relationships remain unclear. This retrospective study included 32 patients(24 with NASH and eight with simple steatosis) who had previously undergone superparamagnetic iron oxide-enhanced magnetic resonance imaging(SPIO-MRI). All subjects were diagnosed pathologically and were evaluated for Brunt classification(necroinflammation grade and fibrosis stage), and number of CD14-positive KCs. There were statistically significant differences in percent reduction of liver-to-muscle signal intensity ratio(reduction-% LMR), as a surrogate parameter of KC function, and number of CD14-positive KCs between NASH and simple steatosis patients. A high correlation was seen between number of CD14-positive KCs and reduction-% LMR. KC phagocytic function evaluated with SPIO-MRI correlated with histopathological severity and number of CD14-positive KCs. These results support the concept that KC phagocytic dysfunction contributes to the pathogenesis of NASH.
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