Platelet-dependent thrombin level is enhanced in smokers, even when not smoking, when compared with non-smokers and increases immediately after smoking. Increases in nicotine and cotinine levels caused by smoking induced a prothrombotic state in smokers via increased platelet-dependent thrombogenesis.

Hypercholesterolemia, but not hypertriglyceridemia, was associated with increased platelet-dependent thrombin generation. Pravastatin normalized the generation of thrombin.

Coagulability is evidently enhanced in patients with non-insulin-dependent diabetes mellitus compared with that in healthy normal subjects on the basis of assessments of the platelet-dependent thrombin generation, and good glycemic control may help to correct a hypercoagulable state in diabetic patients.

Abstract. Erythropoietin is known to be effective for the treatment of anemia in chronic renal failure, but the efficacy of erythropoietin for anemia in other diseases is not so great. Insulin exerts a growth promoting activity in various kinds of cells. In the present study, the effects of insulin on erythroid progenitors (colony forming units-erythroid, CFU-E; and burst forming units-erythroid, BFU-E) in human bone marrow were examined at various concentrations of recombinant human erythropoietin (rh-Epo) to clarify the relationship between erythropoietin and insulin. Human insulin stimulated the formation of CFU-E and BFU-E in the presence of three concentrations (0.25, 5, and 100 Ulml) of rh-Epo. Stimulatory effects of human insulin on CFU-E and BFU-E were also observed in the nonphagocytic and nonadherent bone marrow fraction (NP-NA fraction) and in the NP-NA and T cell-depleted fraction at each concentration of rh-Epo. Human insulin further stimulated the CFU-E and BFU-E growth in CD34' separated bone marrow cells. These results indicate that the enhancing effect of human insulin on erythroid progenitors is not mediated through monocytes and macrophages or T cells, suggesting a direct action on erythroid progenitors.

SummaryBackground: Shear stress generated in stenosed arteries promotes platelet thrombi formation at the stenosed sites by accelerating the binding of von Willebrand factor (vWF) to platelets. Shear-induced platelet aggregation (SIPA) has been studied in acute coronary syndromes, but not in chronic coronary disease.Hypothesis: We investigated the effect of both the site and severity of coronary stenosis on SIPA in patients with chronic coronary artery disease.Methods: Shear-induced platelet aggregation was measured using platelet-rich plasma in 49 patients (41 men and 8 women; mean age 61 ± 10 years) with coronary artery disease to evaluate the association between the extent of SIPA and coronary angiographic findings. Stenoses > 75% were considered severe. In all, 62 healthy individuals (54 men and 18 women; mean age 45 ± 7 years) served as controls. The correlation between SIPA and the site and severity of the coronary lesion, and parameters of coagulation and fibrinolysis were evaluated.Results: Shear-induced platelet aggregation was increased in the stenosis group (69.0 ± 10.6%) compared with the controls (57.7 ± 10.3%, p < 0.0001). Patients with severe stenosis in the proximal segments had significantly increased SIPA (p< 0.0001) and vWF larger multimer concentration (p < 0.0001) compared with the control group. A significant correlation existed between SIPA and the vWF larger multimer concentration in all subjects studied (r = 0.422, p < 0.0001).