| Project/Area Number |
11671395
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Cerebral neurosurgery
|
|---|
| Research Institution | The Jikei University School of Medicine |
|---|
Principal Investigator |
TAKAHASI Koichi The Jikei University School of Medicine Department of Neurosurgery Assistant, 脳神経外科, 助手 (90246413)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
NAKAZAKI Hiromichi The Jikei University School of Medicine Department of Neurosurgery Assistant, 脳神経外科, 助手 (40266656)
TANAKA Hideaki The Jikei University School of Medicine Department of Neurosurgery Assistant, 脳神経外科, 助手 (70227164)
NAKAHARA Shigehiro Meitokukai Sato First Hospital Vice-Director, 脳神経外科, 副院長
|
|---|
| Project Period (FY) |
1999 – 2000
|
| Project Status |
Completed (Fiscal Year 2000)
|
| Budget Amount *help |
¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2000: ¥900,000 (Direct Cost: ¥900,000)
|
|---|
| Keywords | Chiari H malformation / Splotch Delayed Mouse / GFAP / NFP / Vimentin / Splotch delayed mouse / Immunohistochemical analysis / apoptosis |
|---|
| Research Abstract |
It has been widely recognized that Chiari II malformation is often complicated with myeloschisis or other brain anomalies. The pathogenesis of these congenital anomalies is still controversial. We studied a localization and a quantitative measurement of Glial fibrillary acidic protein (GFAP), Neurofilament protein (NFP) and Vimentin in the brain of Splotch Delayed mice (Spd/Spd) that developed the myeloschisis, and more specifically the pathogenesis of brain anomalies associated with Chiari II malformation.
Result : There were no significant difference for localization of GFAP, NFP, and Vimentin between the Spd/Spd mice with myeloschisis and normal mice on 12, 14, 16, 18 and 19 days of gestation. No statistically significant differences were detected on these filaments between these two groups by Western blot methods. However, GFAP tend to exist more in normal mice than in Spd/Spd mice with myeloschisis on gestation day 19.
Conclusion : We couldn't prove that the pathogenesis of brain anomalies are associated with Chiari II malformation. One of the reasons being that we could study Spd/Spd mice with myeloschisis only in their fetal days because they can only survive in utero. Further investigations are needed.
|
