Project/Area Number |
15H04780
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Hygiene and public health
|
Research Institution | Hokkaido University |
Principal Investigator |
Atsuko Araki 北海道大学, 環境健康科学研究教育センター, 准教授 (00619885)
|
Co-Investigator(Kenkyū-buntansha) |
小島 弘幸 北海道立衛生研究所, その他部局等, 主幹 (10414286)
乃村 俊史 北海道大学, 大学病院, 講師 (50399911)
宮下 ちひろ 北海道大学, 環境健康科学研究教育センター, 特任准教授 (70632389)
岸 玲子 北海道大学, 環境健康科学研究教育センター, センター特別招へい教授 (80112449)
|
Co-Investigator(Renkei-kenkyūsha) |
SHIMIZU Hiroshi 北海道大学, 医学研究院, 教授 (00146672)
KOBAYASHI Sumitaka 北海道大学, 環境健康科学研究教育センター, 特任講師 (10733371)
MINATOYA Machiko 北海道大学, 環境健康科学研究教育センター, 特任講師 (50733367)
|
Research Collaborator |
AIT BAMAI Yu
ITO Sachiko
TAKEUCHI Shinji
URAMARU Naoto
OKUDA Katsuhiro
TAKEDA Mai
KAWAI Toshio
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥16,380,000 (Direct Cost: ¥12,600,000、Indirect Cost: ¥3,780,000)
Fiscal Year 2017: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2015: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
|
Keywords | 環境化学物質 / アトピー性皮膚炎 / 遺伝子 / ハウスダスト / 酸化ストレスマーカー / フィラグリン / 遺伝子発現 / バイオマーカー / 環境 / 衛生 |
Outline of Final Research Achievements |
Association between environmental chemicals exposure on asthma and allergies and oxidative stress marker, 8-OHdG, and existence of FLG mutation were examined among 7 years old children. There was no difference on proportion of with or without FLG mutation between allergic cases and controls. When DINP levels in dust was higher, the risk of eczema increased, only those without FLG mutation. There was no significant association between FLG mutation, environmental chemicals and asthma and allergies, and 8-OHdG did not show any modifier effect on exposure and allergies. Studies of in vitro and in silico of DEHP and its 6 metabolites activation on PPARα/γ and PXR showed that DEHP and its metabolites have activities that differ from those of the parent compound. The results obtained from the microarray analysis suggest that DEHP and MEHP might affect the gene expression of THP-1 cells via PPARα and PXR.
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