| Project/Area Number |
04454362
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Okayama University Medical School |
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Principal Investigator |
MORI Akitane Okayama Univ.Med.Sch.Dept.of Neuroscience, Professor, 医学部, 教授 (20028434)
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| Co-Investigator(Kenkyū-buntansha) |
TSUTSUI Kimiko Okayama Univ.Med.Sch.Dept.of Anatomy, Assistant, 医学部, 助手 (70144748)
MIZUKAWA Kiminao Okayama Univ.Med.Sch.Dept.of Anatomy, Instructor, 医学部, 講師 (40137154)
OHMOTO Takashi Okayama Univ.Med.Sch.Dept.of Neuroscience, Professor, 医学部, 教授 (60032900)
YOKOI Isao Okayama Univ.Med.Sch.Dept.of Neuroscience, Assistant, 医学部, 助手 (80150366)
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥5,600,000 (Direct Cost: ¥5,600,000)
Fiscal Year 1994: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1993: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1992: ¥3,800,000 (Direct Cost: ¥3,800,000)
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| Keywords | posttraumatic epilepsy / iron-iduced epileptogenic focus / superoxide / hydroxyl radical / nitric oxide / superoxide dismutase / alpha-guanidinoglutaric acid / adnosine / スパーオキシド / 遷移金属 / エピガロカエキン / ドーパミンニューロン / 酸化窒素ラジカル / 硝酸イオン / 亜硝酸イオン / 活性酸素種 / フローインジェクション法 / セカンドメッセンジャー / 血管拡張因子 |
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| Research Abstract |
1. The normal brain was found to scavenge both superoxide (O^-_2) and hydroxyl radicals (・OH) . However brain damage can be induced by excess reactive oxygen species (ROS) since they are known to react virtually with any type of molecule such as nucleic acid, membran lipids, and protein in the brian, and may result in an epileptogenic focus formation.
2. An injection of iron ion into the rat brain decreased nitric oxide (NO) from arginine by nitric oxide synthase (NOS). Generally, No is thougt to play an inhibitory role in the seizure mechanism. Therefore, decreased NO may accelerate the seizure procedure induced by iron ion. alpha-Guanidinoglutaric acid, an endogenous convulsant, could induced seizures by inhibiting NOS activity.
3. Oxygen inhalation for 3 weeks accelerated the formation of ・OH,・ R and methylguanidine, an endogenous convulsant. We proposed that oxygen inhalation is a clinical first aid for patients with severe head injury, but the clinical beneficial concentration and period for treatment should be reexamined carefully from the veiw point of oxygen intoxication.
4. Superoxide dismutase (SOD) was induced in the iron induced epileptogenic focus in the rat brian. It may be a defense mechanism against excess O^-_2 induced by iron ion in the brian.
5. Antioxidants or free radical scavengers, e.g., epigallocatechin and its derivatives, adenosine and chlor-adenosin could be a possible rational treatment for post-traumatic epilepsy. As well, probcol, TJ960 (a Japanese herbal medicine) , baicalein (an effective component of TJ960) , and Bio-normalizer (a natural healthy food) may be effective for it, as they are found to be effective free radical scavengers.
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