Grant-in-Aid for Scientific Research (A)
|Allocation Type||Single-year Grants |
Pathological medical chemistry
|Research Institution||Kagawa Medical University |
NAGAO Seigo (1997-1998) Kagawa Medical University, Faculty of Medicine, Professor, 医学部, 教授 (60100947)
入野 昭三 (1996) 香川医科大学, 事務局, 学長 (50033056)
TOKUDA Masaaki Kagawa Medical University, Faculty of Medicine, Associate Professor, 医学部, 助教授 (10163974)
KOBAYASHI Ryoji Kagawa Medical University, Faculty of Medicine, Professor, 医学部, 教授 (00020917)
HIRASHIMA Mitsuomi Kagawa Medical University, Faculty of Medicine, Professor, 医学部, 教授 (70109700)
SAKAMOTO Haruhiko Kagawa Medical University, Faculty of Medicine, Professor, 医学部, 教授 (60106549)
TAKEUCHI Yoshiki Kagawa Medical University, Faculty of Medicine, Professor, 医学部, 教授 (20116619)
高原 二郎 香川医科大学, 医学部, 教授 (00033085)
板野 俊文 香川医科大学, 医学部, 教授 (60145042)
畠瀬 修 香川医科大学, 医学部, 教授 (50033220)
|Project Period (FY)
1996 – 1998
Completed (Fiscal Year 1998)
|Budget Amount *help
¥34,400,000 (Direct Cost: ¥34,400,000)
Fiscal Year 1998: ¥5,400,000 (Direct Cost: ¥5,400,000)
Fiscal Year 1997: ¥5,900,000 (Direct Cost: ¥5,900,000)
Fiscal Year 1996: ¥23,100,000 (Direct Cost: ¥23,100,000)
|Keywords||calcium / Cdk5 / p35 / neuronal cell / calbrain / kindlling / ischemic neuronal death / ecalectin / calmodulin-dependent enzyme / 成長ホルモン / 脳血管関門 / 老化促進モデルマウス / RU-51599 / リンホカイン / カルモジュリン依存性リン酸化酵素 / 長期記憶増強 / Calbrain / タウ / 網膜|
1. Anti-allergic drugs such as amlexanox and cromolyn bound to S-100, visin-like protein, and 14-3-3, and inhibited their functions.
2. During the developmental processes of rat brain, the expression level of cyclin-dependent kinase 5 (Cdk5) did not alter, and its activaot, p35, did.
3. Calmodulin-dependent protein kinases (CaMK) I and IV were involved in the formation of long-term potentiation using rat hippocampal slices. A novel calcium-binding protein, calbrain, inhibited CaMK II.
4. Using a calcineurin-specific inhibitor, FK506, calcineurin was shown to be involved in the epileptogenesis of the kindled rats.
5. By the study using SAM (Senescence-Accelerated Mouse), the impairment of blood-brain barrier was shown to occur during the aging processes.
6. The hypothermic treatment worked effectively to protect the delayed neuronal death after the brain ischemia. It was important to raise the body temperature to the normal level as slow as possible after this therapy.
7. Neuronal transplantation of fetal hippocampal cells induced the recovery of the memory and learning impaired rats.
8. Transcription and translation of growth hormone was enhanced by the inhibition of calcineurin using immunosuppressive drugs (FK506 and cyclosporin A).