| Project/Area Number |
12670800
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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 |
Pediatrics
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| Research Institution | University of Occupational and Environmental Health |
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Principal Investigator |
SHIRAHATA Akira University of Occupational and Environmental Health, School of Medicine, Professor, 医学部, 教授 (10081712)
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| Co-Investigator(Kenkyū-buntansha) |
KANIZONO Junji University of Occupational and Environmental Health, School of Medicine, Research Associate, 医学部, 助手 (50299616)
SAKAI Michio University of Occupational and Environmental Health, School of Medicine, Research Associate, 医学部, 助手 (10279333)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2001: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2000: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Kawasaki desease / polymorphism / tissue plasminogen activator / plasminogen activator / cardiac complication / プラスミノゲン・アクチベーター・インヒビター |
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| Research Abstract |
1.Time course of fibrinolytic system in patients with Kawasaki disease (KD) during acute phase.
To determine whether the fibrinolytic system is related to the occurrence of cardiac ccmplication in KD, we measured tissue plasminogen activator (1PA), plasminogen activator inhibitor-1 (PAI-1), and related factors in the plasma of children with KD. TPA and PAI-1 were increased in acute phase. Ch the other hand, TPA/lPAI-1 ratio was lower in the cardiac complication group than in the no ccmplication group throughout the observation period These results indicate that a low fibrinolytic activity may be related to the occurrence of cardiac Duplication in KD.
2.Polymorphism in PAI-1 in KD
PAI-1 polymorphismwas investigated in patients with KD and controls. Genotype (4G, 5G allele of PAI-1gene) was determined, using PCR assays based on published method The distribution of 4G/4G, 4G/5G and 5G/5G genotype was similar in KD and control. On the other hand, weak association of homozygote of 4G with no cardiac ccmplication were observed in KD. These results provide preliminary evidence that polymorphism in PAI-1 does not contribute to occurrence of KD and cardiac complication in KD.
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