Study of the pathogenesis of fetal brain damage due to lack of thyroid hormone.
| Project/Area Number |
19591228
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Pediatrics
|
|---|
| Research Institution | Kanazawa Medical University |
|---|
Principal Investigator |
ITOH Masatsune (2009) Kanazawa Medical University, 医学部, 講師 (60367472)
柿沼 宏明 (2007-2008) Kanazawa Medical University, 看護学部, 教授 (60271376)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SATO Hitoshi 金沢医科大学, 医学部, 助教 (20303224)
伊藤 順庸 金沢医科大学, 医学部, 助教 (60367472)
|
|---|
| Project Period (FY) |
2007 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2009: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2008: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2007: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Keywords | 甲状腺ホルモン輸送体(MCT8) / 胎児脳発達 / 甲状腺ホルモン / 乳酸 / ピルビン酸 |
|---|
| Research Abstract |
We studied the effect of thyroid hormone in fetal brain. Thyroid hormone transporter (MCT8) was cloned and plasmid was created based on cloning MCT8. For a normal fetal brain development, it was suggested that thyroid hormone is necessary equivalent amount of wild-type. MCT8 deficiency showed high levels of serum lactic acid in early infancy, it was suggested to be useful as a diagnostic marker. To confirm the localization of MCT8 protein in the brain, we immunized the rabbit with a synthetic peptide derived from human MCT8 and an antibody was purified from rabbit serum.
|
Report
(4 results)
Research Products
(6 results)
