| Project/Area Number |
10671023
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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 |
Embryonic/Neonatal medicine
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| Research Institution | Saitama Medical School |
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Principal Investigator |
SHIMIZU Hiroshi Saitama Medical School, Associate Professor, 医学部, 助教授 (90260843)
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| Co-Investigator(Kenkyū-buntansha) |
IGARASHI Yoko Saitama Medical School, Assistant, 医学部, 助手 (00301466)
OBATA Makoto Saitama Medical School, Assistant, 医学部, 助手 (70286045)
KAKINUMA Ryota Saitama Medical School, Assistant, 医学部, 助手 (30281306)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Pulmonary surfactant / Surfactant convertase / Surface area cycling |
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| Research Abstract |
We studied the effect of surfactant inhibitors (meconium, neutrophil elastase, and serum) on the rate of surfactant subtype conversion from surface-active large surfactant aggregates to inactive small surfactant aggregates using the in vitro surface area cycling method. Each surfactant inhibitor was added to a suspension of large surfactant aggregates, and the mixture was cycled in a capped polystyrene tube. The conversion rate from large to small surfactant aggregates depended on the amount of the surfactant inhibitor added. The effect of surfactant inhibitors on subtype conversion was reduced in the presence of diisopropyl fluorophosphate (DFP) and α1-antitrypsin, but not in the presence of urinastatin, human urinary trypsin inhibitor. Further studies with radioactive DFP showed that meconium contained a DFP-binding protein with an apparent molecular mass of 3OkD.These results suggest that surfactant inhibitors exhibit surfactant conversion activity, or activates "surfactant convertase" already present in large surfactant aggregates. The increased rate of conversion caused by surfactant inhibitors may be responsible for surfactant dysfunction that occurs with lung injuries.
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