Conclusions: The study shows platelet activity of cerebral infarction patients increases. The elevation of β-TG, PF4 may be the ACI patients in 6-72h, only the increase in plasma PF4 may be multi-focus cerebral infarction.
Conclusions The study shows platelet activity of cerebrel infarction patients increases. Theelevation of β-TG、PF_4 may be the ACI patients in 6-72h,only the increase in plasma PF_4 may be multi-fo-cus cerebral infarction.
Methods Twenty one centenarians were tested for PAgT, TXB2, 6 acetone-PGF1α, GMP-140, t-PA:Ag, PAI:A in compare with 30 healthy elders. The changes of platelet activity and plasminogen activity were investigated.
Conclusion Patients with acute PTE show evidence of enhanced platelet activation and endothelial cell disturbance,which relates to pathological process of PTE.
In order to investigate the platelet activation of diabetics and the relationship with thepathogenesis of microangiopathy in diabetics, plasma levels of β -thromboglobulin (β TG) and plateletfactor 4 (PF_4) in 10 normal controls and 48 NIDDM patients were studied in the present study using theenzyme linked immunosorbent assay (ELISA).
The marker P-selectin and β-TG of platelets activation and the marker vWF and ET-1 of endothelial cell disturbance were determined before and after treatment.
观察治疗前后血小板活性标志物P选择素、血浆 β 血栓球蛋白和内皮功能受损标志物血浆血管性假性血友病因子 (vWF)、血管内皮受损指标内皮素 (ET 1)的变化。
The parameters of the platelet activity and aggregation indicated the absence of age-related changes in the structure and functions of platelets in response to inducers, including epinephrine, collagen, and ristocetin.
On average, statins improve lipid profiles and have been shown to have ancillary beneficial effects on inflammation, platelet activity, and endothelial function.
Evidence is emerging that aspirin resistance, as defined by residual platelet activity, merely reflects an individual's enhanced basal platelet function and suggests a hereditary component.
The characteristic features of the propagation phase are: almost quantitative prothrombin activation at a high rate, completion of platelet activation, and solid clot formation.
Thrombin production and platelet activation also initiate the process of wound healing requiring thrombin-dependent cell activation and platelet-dependent formation of new blood vessels (angiogenesis).
Failure to localize and adequately regulate thrombin production and/or platelet activation can have pathological consequences, including the development and propagation of atherosclerosis and enhancement of tumor development.
In vitro human platelet prostaglandin synthesis has been studied from added radioactive arachidonic acid (i) as function of substrate concentration, (ii) as function of platelet concentration and (iii) as function of pH.
These results suggest that the function of platelet fibrinogen receptor is impaired in patients with stable angina pectoris and that PTCA and CABG surgery activates platelets.