| Project/Area Number |
15590573
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Legal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
SHINTANI Kaori The University of Tokyo, Graduate School of Medicine, Research Associate, 大学院・医学系研究科, 助手 (50345047)
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| Co-Investigator(Kenkyū-buntansha) |
UEMURA Koichi The University of Tokyo, Graduate School of Medicine, Research Associate, 大学院・医学系研究科, 助手 (30244586)
YOSHIDA Ken-ichi The University of Tokyo, Graduate School of Medicine, Professor, 大学院・医学系研究科, 教授 (40166947)
KIMURA Hiroko Juntendo University, School of Medicine, Lecturer, 医学部, 講師 (00053299)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2004: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2003: ¥3,200,000 (Direct Cost: ¥3,200,000)
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| Keywords | Surfactant / Cardiogenic pulmonary edema / Myocardial infarction / サイトカイン |
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| Research Abstract |
1.Forensic autopsy cases
SP-A1 and SP-A2 mRNA levels in lung tissue derived from forensic autopsy were determined using a real-time RT-PCR method. The ratio of SP-A1 to SP-A2 mRNA (SP-A1/SP-A2 ratio) was high in not only asphyxia and drowning cases but also in most cases of acute myocardial infarction. The higher SP-A1/SP-A2 ratio, the smaller the amount of SP-A1 or SP-A2 mRNA. The decrease of SP-A2 mRNA was larger than that of SP-A1. There results indicated that the decrease of SP-A mRNA in survival period causes the increase of SP-A1/SP-A2 ratio.
2.Rat model
The left anterior descending coronary artery (LAD) of the rat was occluded with a nylon ligature as a model of myocardial infarction. After the occlusion for 24 hours, the lung weight was measured for an evaluation of pulmonary edema. The weight significantly increased in myocardial infarction as compared with that in sham operation. Ischemic preconditioning, consisted of three cycles of 4 minute occlusion and 4 minute-reperfusion, limited the infarct size and abolished the increase of lung weight.
There were not SP-A1 and SP-A2 alleles on the SP-A gene locus of rodents, and thus the amount of SP-A mRNA was investigated instead of SP-A1/SP-A2 ratio. The SP-A mRNA in myocardial infarction was quantified by a real-time RT-PCR method. The amount of SP-A mRNA in myocardial infarction significantly decreased as compared with that in sham, and IP procedure followed by myocardial infarction suppressed the decrease of SP-A mRNA level. Although the amount of TNF-α mRNA was also measured in myocardial infarction, there was no difference between sham, myocardial infarction and IP groups.
In conclusion, the pulmonary edema and the decrease of SP-A mRNA in rat model indicate that the alteration of SP-A mRNA in myocardial infarction may affect the respiratory dysfunction.
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