Project/Area Number |
09671810
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Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Ophthalmology
|
Research Institution | NAGOYA CITY UNIVERSITY |
Principal Investigator |
OZEKI Hironori (1998) NAGOYA CITY UNIVERSITY,MEDICAL SCHOOL,ASSISTANT PROFESSOR, 医学部, 講師 (60254299)
白井 正一郎 (1997) 名古屋市立大学, 医学部, 助教授 (30080063)
|
Co-Investigator(Kenkyū-buntansha) |
NOZAKI Miho NAGOYA CITY UNIVERSITY,MEDICAL SCHOOL,INSTRUCTOR, 医学部, 助手 (00295601)
MIZUNO Shinichi NAGOYA CITY UNIVERSITY,MEDICAL SCHOOL,INSTRUCTOR, 医学部, 助手 (90281261)
宇野 真 名古屋市立大学, 医学部, 助手 (50264726)
尾関 年則 名古屋市立大学, 医学部, 助手 (60254299)
|
Project Period (FY) |
1997 – 1998
|
Project Status |
Completed (Fiscal Year 1998)
|
Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1998: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1997: ¥1,600,000 (Direct Cost: ¥1,600,000)
|
Keywords | developmental eye abnormalities / neural crest cells / retinoic acid / mouse fetuses / congenital anomalies / critical period / 臨床的検討 / 組織学的 / 組織化学的 |
Research Abstract |
Using retinoic acid as a teratogenic factor, we made experimental models in mouse fetuses for various human ocular anomalies, including persistent hyperplastic primary vitreous, uveal coloboma. Axenfeld-Rieger syndrome, and Peters' anomaly. And we elucidated that these ocular anomalies are caused by the abnormal neural crest cell migration. In addition, we determined their critical periods in mice ; from day 7 through day 11 of gestation. Based on the results, we inferred corresponding periods in human ; from 2.5 weeks through 7 weeks of gestation. We believe that these results lead to the prevention of human ocular congenital anomalies. We also clarified the role of hialuronic acid in the developmental process of the eyelids. We also found the delay in changes of main glycosaminoglycans in the eyelids of spontaneous small eye mice. Clinically, we reviewed cases with Axenfeld-Rieger syndrome, Peters' anomaly and uveal coloboma encountered at our hospital. We warned that these ocular anomalies frequently accompanied other anomalies in the tissues derived from neural crest cells. To prevent ocular anomalies, we are to investigate the role of programmed cell death and growth factors in the developmental process of the normal and malformed eye.
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