Hepatitis C virus nonstructural protein NS3 binds to Sm-D1, a small nuclear ribonucleoprotein associated with autoimmune disease.

Hepatitis C virus (HCV) causes a persistent infection, chronic hepatitis, and leads to hepatocellular carcinoma. Nonstructural protein 3 (NS3) of HCV possesses protease, nucleoside triphosphatase, and helicase activities. Using the yeast two hybrid assay, we identified Sm-D1, a host protein that binds to NS3.

Shear-induced platelet aggregation increases in patients with proximal and severe coronary artery stenosis.

Background: 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.

Platelet-dependent thrombin generation in patients with unstable angina pectoris.

Platelet-dependent thrombin generation was assessed during both unstable and stable periods in 59 patients with unstable angina and at rest in 31 healthy controls. Thrombin generation during the unstable period was significantly greater than that at rest in the healthy control group (p < 0.0001) and that during the stable period (p < 0.

Acute effects of cigarette smoking on platelet-dependent thrombin generation.

Aims: Thrombin is an important factor in the pathogenesis of thrombotic diseases. To clarify whether smoking has an effect in platelet-dependent thrombogenesis, we studied the acute effects of smoking on platelet-dependent thrombin level in smokers.

Methods And Results: Subjects consisted of ten smokers and nine non-smokers.

Human platelet activation by thrombolytic agents: effects of tissue-type plasminogen activator and urokinase on platelet surface P-selectin expression.

The mechanisms that underlie reocclusion during thrombolytic therapy have not yet been clarified. The purpose of this study was to investigate the activating effects of tissue-type plasminogen activator and urokinase and the inhibitory effects of acetylsalicylic acid by measuring platelet surface P-selectin as a marker of platelet activation. After addition of urokinase (final concentration 192 U/ml, 1920 U/ml, or 19,200 U/ml) or tissue-type plasminogen activator (final concentration 120 U/ml, 1200 U/ml, or 12,000 U/ml) to platelet-rich plasma from 12 healthy persons, platelet surface P-selectin expression was measured by means of flow cytometry with an anti-CD62 monoclonal antibody.