Studies on the molecular markers of coagulation, fibrinolysis and vascular endothelial cells in children

儿童凝血、纤溶及血管内皮细胞分子标志物研究

• 批准号: 09670857
• 负责人: SHIRAHATA Akira
• 金额: $ 1.86万
• 依托单位: University of Occupational and Environmental Health
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1997
• 资助国家: 日本
• 起止时间: 1997 至 1999
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09670857/
• 关键词: Child; Life style-related disease; Obesity; Diabetes mellitus; Kawasaki disease; PAI-1; TPA; Spontaneously thrombogenic rats; 新生児; TPA; トロンボモジュリン; 組織因子; アスベスト

We examined the molecular markers of coagulation, fibrinolysis and vascular endothelial cells in children with simple obesity, diabetes mellitus or Kawasaki disease in order to clarify the prognostic risk factors for the progression of atherosclerosis in these children. Main data obtained from this research project were as follows.(1) Plasma levels of plasminogen activator inhibitor 1 ( PAI-1 ) were significantly higher in children with moderate or severe obesity than in age-matched control. On the other hand, plasma levels of tissue plasminogen activator ( TPA ) were significantly lower in children with severe obesity than in those with moderate obesity.(2) In children with past histories of Kawasaki disease, plasma PAI-1 levels were significantly higher compared with age-matched control Furthermore, these levels were significantly higher in children suffered from Kawasaki disease with histories of persistent or transient coronary artery lesions than in children suffered from Kawasaki disease without those complications.Those results indicate that suppression of fibrinolytic system may be responsible for the progression of atherosclerosis in children with life style-related disease.

我们检测了单纯性肥胖、糖尿病或川崎病儿童的凝血、纤溶和血管内皮细胞的分子标志物，以阐明这些儿童动脉粥样硬化进展的预后危险因素。本研究项目获得的主要数据如下：(1)中度或重度肥胖儿童血浆纤溶酶原激活物抑制剂1 （PAI-1）水平明显高于同龄对照组。另一方面，重度肥胖儿童血浆组织纤溶酶原激活物（TPA）水平明显低于中度肥胖儿童。(2)有川崎病病史的患儿血浆PAI-1水平明显高于同龄对照组，且有持续或短暂冠状动脉病变史的川崎病患儿血浆PAI-1水平明显高于无这些并发症的川崎病患儿。这些结果表明，纤维蛋白溶解系统的抑制可能与生活方式相关疾病儿童动脉粥样硬化的进展有关。

项目成果

Karas Ki Y. Shirahata A et al.: "Increase in DNA and protein synthesis in human umbilical Vein endothelial cell treated with asbestos"J. Occup Health. 40. 302-306 (1998)

Karas Ki Y. Shirahata A 等人：“用石棉处理的人脐静脉内皮细胞中 DNA 和蛋白质合成的增加”J。

Miyata T,Shirahata A et al: "Genetic analysis of protein C deficiency in nineteen gapanese families:Five recurrent defects can explain half of the deficioncies" Thrombosis Research. 92. 181-187 (1998)

Miyata T，Shirahata A等人：“十九个gapanese家族中蛋白C缺乏症的基因分析：五种复发性缺陷可以解释一半的缺陷”血栓形成研究。

Yoshimura Y, Shirahata A et al: "No directeffects on Shiga toxin 1 and 2 on the aggregation of human platelets in vivo."Thromb Haemost. 80. 529-530 (1998)

Yoshimura Y、Shirahata A 等人：“志贺毒素 1 和 2 对人体内血小板聚集没有直接影响。”Thromb Haemost。

Shrakawa Y, Shirahata A et al: "The difference in reactivity of prothrombin families, protein C and osteocalcin to vitamin K administration."Seminars in Thrombosis and Hemostasis. (in press).

Shrakawa Y、Shirahata A 等人：“凝血酶原家族、蛋白 C 和骨钙素对维生素 K 给药的反应性差异。”血栓形成和止血研讨会。

Karasaki Y,Shirahata A.et al: "Increases in DNA and protein synthesis in human umbilical vein endothelial cell treated with asbestos" J Occup Health. 40. 302-306 (1998)

Karasaki Y、Shirahata A.等人：“石棉处理后人脐静脉内皮细胞 DNA 和蛋白质合成增加”J Occup Health。