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The study aimed to analyze the circulating levels of thrombotic and haemostatic components; tissue factor, tissue factor pathway inhibitor, tissue plasminogen activator and plasminogen activator inhibitor-1 in patients with acute myocardial infarction at presentation (Group 1, n=49), unstable angina and Non-ST elevated MI after treatment (Group 2, n=22), stable angina (Group 3, n=18) and healthy individuals (Group 4, n=31). Significant finding was increase in tissue factor not only in Group 1 (2.0 fold, P=0.001), Group 2 (2.2 fold, P=0.015) but also in Group 3 (1.8 fold, P=0.018) as compared to controls. In Group 1 Plasminogen activator inhibitor-1 increased significantly (35.8%, P=0.02). Tissue factor pathway inhibitor and tissue plasminogen activator demonstrated increase in Group 1 of age<40 years while insignificant changes in elder patients. Increased thrombotic and decreased fibrinolytic conditions in acute myocardial infarction patients were observed. Increase TF in stable angina demonstrates procoagulant status in these patients as well.  相似文献   
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Matrix metalloproteinases (MMPs) play important role in the pathogenesis of coronary artery disease (CAD). 5A allele of -1612 5A/6A polymorphism of MMP-3 is associated with two fold higher activity than 6A allele. Present study was designed to analyse the association of this polymorphism with CAD in Indian population. Subjects included in the study were patients with stable angina (n=35), unstable angina (n=53), patients with recent event of myocardial infarction (MI) (MI Group-1, n=56) and patients at presentation of the acute MI (MI Group-2, n=49). Controls were healthy individuals (n=99). Genotyping of MMP-3 5A/6A polymorphism was carried out by PCR-based restriction digestion method. The genotype distribution of patient groups did not deviate from controls. Serum MMP-3 levels were significantly elevated at presentation of the acute MI by 36.8% (P=0.031) as compared to controls and more associated with 6A genotype suggesting discrepancy between in vitro transfection experiment and peripheral MMP-3 levels.  相似文献   
3.
验证收缩骨骼肌细胞葡萄糖转运蛋白4（GLUT4）基因的表达在转录水平上是否受转录抑制子Ⅱ型HDAC5蛋白（简写为HDAC5）的调节。研究运用运动模拟信号5-氨基-4-甲酰胺咪唑核糖核苷酸（AICAR）和HDACs抑制剂SCRIPTAID孵育骨骼肌细胞。用蛋白印迹技术测定HDAC5蛋白表达,定量RT-PCR法检测GLUT4 mRNA表达。与无AICAR的对照组相比,AICAR组骨骼肌细胞内HDAC5减少了29%,并伴随有124% GLUT4 mRNA的增加,但肌细胞内HDAC5的蛋白总量无变化;使用HDACs抑制剂SCRIPTAID刺激骨骼肌细胞能够明显增加核心组蛋白乙酰化水平和上调GLUT4基因的表达。这些结果提示,通过AICAR和SCRIPTAID分别减少或抑制核HDAC5均能上调骨骼肌细胞GLUT4基因的转录,HDAC5可能在转录水平上对肌肉收缩引起的GLUT4基因的表达起着重要的调节作用。  相似文献   
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Platelet-endothelial cell adhesion molecule-1 (PECAM-1) has role in atherosclerotic plaque development as well as in thrombosis leading to myocardial infarction (MI). Present study was aimed to analyse the association of PECAM-1 Leu125Val gene polymorphism with MI in Indian population. Subjects included healthy individuals as control (N = 116) and MI patients (N = 100) divided into two groups; MI patients at presentation of the acute event (MI-Group-1, N = 46) and patients with recent event of MI stabilized with treatment 4.5 days from their symptoms (MI-Group-2, N = 54). The difference in the distribution of Leu125Val genotype frequencies of controls and patients did not reach statistical significance. However Leu allele frequency (0.57) was more associated with MI patients as compared to control (0.504). sPECAM-1 levels were significantly elevated in patients at acute event of MI (MI-Group-1) by 44.1% (P = 0.009) as compared to controls and by 95.2% (P = 0.001) as compared to stabilized MI patients (MI-Group-2).  相似文献   
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