1,721,060 research outputs found
Iron, platelet function, and coronary heart disease. A possible link?
Full text linkSalonen et al. have recently reported an interesting study in which they suggest that iron may be an independent predictor of myocardial infarction (MI) in a Finnish population
Free radical-mediated platelet activation by hemoglobin released from red blood cells.
No full textIt is known that the rate of thrombus formation depends on interaction between platelets and erythrocytes, but the mechanism of this process has remained obscure. We here show that nanomolar levels of hemoglobin released from damaged red blood cells can induce platelet aggregation. The molecular mechanism is not receptor-based, but involves oxidation of oxyhemoglobin by platelet-derived hydrogen peroxide, with subsequent generation of a small unknown free radical species, detected by ESR spectroscopy. Methemoglobin and carbon monoxide-treated hemoglobin are unable to cause platelet activation or radical formation. The aggregation of platelets induced by hemoglobin is completely blocked by catalase or radical scavengers. These findings indicate a role for a novel extracellular free radical second messenger in the activation of platelets
Evidence of non reproducibility. Human basophil histamine release is not triggered by very diluted anti-IgE. Letter
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Selective killing of hepatitis B envelope antigen-specific B cells by class I-restricted, exogenous antigen-specific T lymphocytes.
No full textA simple method for evaluating platelet superoxide dismutase.
No full textA simple and rapid spectrophotometric method for evaluating platelet superoxide dismutase is reported. Platelets prepared avoiding erythrocyte and leucocyte contamination were lysated and tested in a Tris-cacodylic buffer containing pyrogallol. Platelet superoxide dismutase was calculated by evaluating the degree of the pyrogallol autoxidation inhibition induced by platelet lysate. Possible interferences of hydrogen peroxide, peroxidases and reducing substances were excluded. Platelet superoxide dismutase content was studied in 38 healthy subjects and was 19.1 +/- 4.1 U/10(8) platelets or 35 +/- 7.8 U/mg protein
Dipyridamole potentiates the inhibition of platelet aggregation by aspirin (in human platelet rich plasma and whole blood).
No full textThis study investigates the influence of dipyridamole on platelet aggregation as evaluated by a single agonist or a pair of agonists in human platelet rich plasma and whole blood. Dipyridamole up to 30 microM was not found to influence the platelet aggregation of platelet rich plasma or whole blood; aspirin (100 microM), on the contrary, did inhibit platelet aggregation. The inhibition of platelet aggregation by aspirin could be reversed by using high concentrations of agonists or pairs of agonists. In this model dipyridamole inhibited platelet aggregation in both platelet rich plasma and whole blood in a dose-dependent fashion. Thromboxane A2 was less than 10% of controls in aspirin-treated PRP stimulated with low or high concentrations of collagen or with a pair of agonists. This study suggests that dipyridamole has direct antiplatelet activity in platelet rich plasma and whole blood when the cyclooxygenase pathway is blocked by aspirin
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