On the genesis of sudden infant death syndrome : the determination of muscular cytochrome c oxidase by the 4th derivative absorption spectroscopy
Project/Area Number |
61570468
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
Pediatrics
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Research Institution | Keio University |
Principal Investigator |
NOBUTAKE Matsuo Keio University Medical School Associate Professor of Pediatrics, 医学部小児科学教室, 助教授 (50173802)
|
Co-Investigator(Kenkyū-buntansha) |
YOKO Tanaka Keio University Medical School Instructor of Pediatrics, 医学部小児科学教室, 助手 (30138052)
YUZURU Ishimura Keio University Medical School Professor of Biochemistry, 医学部医化学教室, 教授 (40025599)
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Project Period (FY) |
1986 – 1989
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Project Status |
Completed (Fiscal Year 1988)
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Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1988: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1987: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1986: ¥1,100,000 (Direct Cost: ¥1,100,000)
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Keywords | SIDS / 4th derivative absorption spectroscopy / cytochrome c oxidase / muscular mitochondria / 電子伝達系 / 筋肉ミトコンドリア / 乳幼児突然死症候群 / 針筋生検 / 大腿四頭筋 |
Research Abstract |
The pathogenesis of sudden infant death syndrome (SIDS) remains nabulous despite extensive research. In 1981, we proposed a hypothesis that inberent defect in motochondrial oxidative mechanism may be associated with SIDS. In order ot further test the above hypothesis, we developed a sensitive method for the measurement of the muscular cytochrome c oxidase by the 4th derivative absorption spectroscopy. Ten controls and i near-miss SIDS were studied for the diopsied muscle specimens. The cytochrome c oxidase content nanged from 2.07 to 5.43 pmole/mg wet weight for the former and was 2.08 0.29 p mole/mg wet weight for the latter. The size and site of the specimens and coexistent other biological pigments did not affect the results of the measurement. We conclude that the technique can be clinically applicable to the study of mitochondrial oxidative enzymes in SIDS. The role of defective motochondrial oxidation in the pathogenesis of SIDS remains to be studied.
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Report
(4 results)
Research Products
(19 results)