| Project/Area Number |
15K19578
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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 |
Collagenous pathology/Allergology
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| Research Institution | Yokohama City University |
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Principal Investigator |
Minegishi Kaoru 横浜市立大学, 附属市民総合医療センター, 助教 (40616877)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 骨修復 / NaF-PET / 骨破壊 / 関節リウマチ / 骨代謝 |
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| Outline of Final Research Achievements |
We assessed rheumatoid arthritis (RA) patients using FDG-PET and NaF-PET/CT. NaF and FDG signals were mainly located in the bone and the surrounding soft tissues, respectively. Co-existing PET signals of FDG and NaF in the affected joints suggest that inflammation is coupled with upregulated bone turnover, leading to joint destruction. Furthermore, bone repair was more frequently occurred in early-stage RA patients who have achieved sustained good clinical response.
On the other hand, reducing inflammation and bone destraction by heme oxygenase 1 (HO-1) induction was shown in Bach1-deficient mice of collagen-induced arthritis model. Inhibition of Bach1 activity may be worthy of consideration as a target for treatment of inflammatory bone loss in RA.
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