| Project/Area Number |
26860369
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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 |
Laboratory medicine
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| Research Institution | Osaka University |
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Principal Investigator |
Inoue Naoya 大阪大学, 医学部附属病院, 臨床検査技師 (80710269)
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| Research Collaborator |
IWATANI Yoshinori 大阪大学, 大学院 医学系研究科 保健学専攻 生体情報科学講座, 教授
WATANABE Mikio 大阪大学, 大学院 医学系研究科 保健学専攻 生体情報科学講座, 准教授
HIDAKA Yoh 大阪大学, 医学部附属病院臨床検査部
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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 |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | TLR / 遺伝子多型 / 発現解析 / 検査法 / TLR7 / TLR9 / 自己免疫性甲状腺疾患 / 臨床検査 / polymorphism / 臨床検査法の開発 |
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| Outline of Final Research Achievements |
In the TLR4 rs41426344 polymorphism, GC + CC genotypes and C allele were more frequent in the mild HD group compared to the severe HD group.The ratio of intracellular TLR7 and intracellular TLR9 intensities in B cells was lower in patients with GD in remission than in patients with intractable GD.In conclusion, the GC + CC genotypes of the TLR4 rs41426344 polymorphism protect against thyroid destruction and are less prone to hypothyroidism.The ratio of intracellular TLR7 and intracellular TLR9 intensities in B cells was associated with the development and intractability of GD and UNC93B1 polymorphisms were associated with the development of GD.
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