| Project/Area Number |
10557194
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Surgical dentistry
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| Research Institution | Aichi-Gakuin University |
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Principal Investigator |
NATSUME Nagato Aichi-Gakuin University, The 2nd Department of Oral & Maxillofacial Surgery, Professor, 歯学部, 特殊診療科教授 (90183532)
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| Co-Investigator(Kenkyū-buntansha) |
NIIMI Teruyuki Aichi-Gakuin University, The 2nd Department of Oral & Maxillofacial Surgery, Assistant Professor, 歯学部, 助手 (60291762)
FURUKAWA Hiroo Aichi-Gakuin University, The 2nd Department of Oral & Maxillofacial Surgery, Assistant Professor, 歯学部, 助手 (70291763)
KAWAI Tsuyoshi Aichi-Gakuin University, The 2nd Department of Oral & Maxillofacial Surgery, Professor, 歯学部, 名誉教授 (50064788)
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| Project Period (FY) |
1998 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥4,700,000 (Direct Cost: ¥4,700,000)
Fiscal Year 2001: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | genetic engineering / cleft lip / cleft palate / A / J mouse / reprodctive function / CCC mouse / 生殖細胞 |
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| Research Abstract |
The purpose of this study is to make clear the cause of cleft lip and/or palate (CL/P) occurring in CL/P-prone A/J strain mouse. Incidence of CL/P in A/J mice obviously higher than in other strains and they inherit this characteristic for generations. Therefore, we studied about the causes of CL/P from genetic factor and maternal environmental factor respectively.
We crossbred CL/P-resistant mice and CL/P-prone mice. Then observing embryos in the uteri, we studied about genetic and environmental factors. As a result, the number of placenta in CL/P-prone mice was low and that m CL/P-resistant mice was high regardless embryo's gene type. Also the rate of stillbirth and absorption was higher among embryos raised in the uteri of CL/P-prone mice. It was made clear that raising embryos in the uteri of CL/P-prone mice was more difficult than in CL/P-resistant mice. However, as there were no F1 embryos with CL/P raised in the uteri of CL/P-prone mice, it was suggested that maternal environmental factors were the cause of CL/P.
Furthermore, by transplanting fertilized ova of CL/P-prone mice to uteri of CL/P-resistant mice, we observed the occurring of CL/P. As a result, CL/P occurred in embryos of CL/P-prone mice raised in the uteri of CL/P-resistant mice. This result suggested that genetic factor was the cause of CL/P rather than the environmental factor.
In order to observe genetic factor experimentally, we put inherited gene of CL/P-prone mice into CL/P-resistant mice for generations to raise genetic ratio and observed the change of incidence. As a result, as genetic ratio of CL/P-prone mice raised, incidence raised. This result suggests that CL/P gene is transmitted to CL/P-resistant mice from CL/P-prone mice. At the same time, this mouse was admitted as a newly established CL/P model mouse, CCC to meet international standard.
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