2009 Fiscal Year Final Research Report
Mechanism of rituximab therapy for refractory nephritic syndrome in children
| Project/Area Number |
20790762
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pediatrics
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| Research Institution | National Research Institute for Child Health and Development |
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Principal Investigator |
MAKIKO Nakayama National Research Institute for Child Health and Development, 腎臓科, 客員臨床研究員 (80469999)
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| Project Period (FY) |
2008 – 2009
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| Keywords | 小児難治性ネフローゼ / リツキシマブ / B細胞 |
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| Research Abstract |
Potentiated generation of reactive oxygen spices (ROS) from neutrophil Nox2 by TNF-α was reported to contribute to ICAM-1 expression in vascular endothelial cells (VEC), which plays a key role in neutrophil extravasation and following aneurysm formation. However, this possibility was only concluded by indirect studies using reducing agents or inhibitors against Nox. In order to get a definite answer, we produced a mouse model of Kawasaki disease using LCWE, and then inspected it with Nox2-KO mice. The inspection studies clearly demonstrated that TNF-α induces ICAM-1 expression, directly affecting VEC without the aid of ROS from neutrophil Nox2.
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[Presentation] メサンギウム領域にC1qが沈着した腎低形成の1例2009
Author(s)
岩城拓磨, 大橋育子, 阿部多恵, 伊地知園子, 小西行彦, 岩瀬孝志, 難波正則, 西田智子, 今井正, 磯部健一, 伊藤進, 中山真紀子, 長田道夫
Organizer
第4 4回日本小児腎臓病学会学術集会
Year and Date
2009-06-27
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