| Project/Area Number |
04404063
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Urology
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| Research Institution | Osaka University |
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Principal Investigator |
OKUYAMA Akihiko Osaka University, Dept.of Urology, Professor, 医学部, 教授 (20093388)
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| Co-Investigator(Kenkyū-buntansha) |
YOKOKAWA Kiyoshi Osaka University, Dept.of Urology, Assistant, 医学部, 助手 (40220545)
YOSHIOKA Toshiaki Osaka University, Dept.of Urology, Assistant, 医学部, 助手 (30191547)
NAMIKI Mikio Osaka University, Dept.of Urology, Assistant Professor, 医学部, 講師 (70155985)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥10,500,000 (Direct Cost: ¥10,500,000)
Fiscal Year 1993: ¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 1992: ¥6,500,000 (Direct Cost: ¥6,500,000)
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| Keywords | testis / sertoli cell / activin / FSH / LH / androgen / receptor / male infertility / 器官培養 / 停留精巣 / androgen受容体 / growth factor / inhibin |
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| Research Abstract |
It is very important for diagnosis and treatment of human testicula disorders such as male inferfility to clarify the control mechanism of human testicular function. In the present research, the following results were obtained by experiments with molecular biological techniques using human testis.
1. Syntheses of androgen binding protein, plasminoger activator and transferrin in cultured sertoli cells were increaed by FSH, LH, EGF and activir, but not change by pasmlin.
2. Same results as above were obtained by in vivo experiments using biopsied human testes.
3. Expression of AR or RNA was increased by a small amount of androgen, but decreased by an excess amount of androgen.
One-point mutation AR gene were found in all four cases with testicular feminization syndrome and 2 out of 20 cases with idropathic male infertility.
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