Calcium-Dependent Src Phosphorylation and Reactive Oxygen Species Generation Are Implicated in the Activation of Human Platelet Induced by Thromboxane A2 Analogs.

The thromboxane (TX) A elicits TP-dependent different platelet responses. Low amounts activate Src kinases and the Rho-Rho kinase pathway independently of integrin αβ and ADP secretion and synergize with epinephrine to induce aggregation. Aim of the present study was to investigate the role Src kinases and the interplay with calcium signals in reactive oxygen species (ROS) generation in the activatory pathways engaged by TXA in human platelets.

Non-alcoholic fatty liver disease and increased risk of all-cause mortality in elderly patients admitted for acute heart failure.

Background: Nonalcoholic fatty liver disease (NAFLD) is an emerging risk factor for incident heart failure (HF). It is currently unknown whether NAFLD predicts all-cause mortality in patients admitted for acute HF. We aimed to assess whether NAFLD and its severity (diagnosed by ultrasonography and non-invasive fibrosis biomarkers) were associated with increased all-cause mortality in this particularly high-risk patient population.

Reduced platelet count, but no major platelet function abnormalities, are associated with loss-of-function ATP-binding cassette-1 gene mutations.

Loss-of-function mutations of the the ATP-binding cassette-1 () gene are the cause of Tangier disease (TD) in homozygous subjects and familial HDL deficiency (FHD) in heterozygous subjects. These disorders are characterized by reduced plasma HDL-cholesterol (HDL-C) and altered efflux of cholesterol from cells. Previous studies in TD patients and murine models reported defects in platelet count, morphology, and function, but the issue is still controversial.

Antiplatelet Agents Inhibit the Generation of Platelet-Derived Microparticles.

Platelet microparticles (PMPs) contribute to thrombogenesis but the effects of antiplatelet drugs on PMPs generation is undefined. The present study investigated the cellular events regulating PMPs shedding, testing platelet agonists and inhibitors. Platelet-rich plasma from healthy subjects was stimulated with arachidonic acid (AA), U46619, collagen type-I (10 and 1.

Henoch-Schönlein purpura and Crohn's disease in a family.

A 16-year-old female who underwent an appendicectomy had terminal segmental ileitis, and developed Henoch-Schonlein purpura (HSP) a few days later. Her brother had suffered from post-infection HSP, while her mother has suffered from Crohn's disease. Human leukocyte antigen (HLA) typing in the patient disclosed the DRB1*11 allele, which has been reported to be associated with HSP, but the brother proved negative, suggesting that this allele was irrelevant to the HSP pathogenesis.