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The objective is to describe and quantify levels of platelet reactivity in three different cohorts of patients taking thienopyridine: patients who report nuisance bleeding, patients who report alarming bleeding, and patients who report no nuisance or alarming bleeding. The investigators hypothesize that patients with nuisance or alarming bleeding events on maintenance thienopyridine therapy will have lower levels of platelet reactivity than patients without nuisance or alarming bleeding on thienopyridine therapy.
Observational Model: Case Control, Time Perspective: Retrospective
Washington Hospital Center
District of Columbia
Medstar Research Institute
Published on BioPortfolio: 2014-08-27T03:12:36-0400
The purpose of this study is to see if there is a racial and/or gender difference in platelet aggregation.
The purpose of the study was to determine the influence of fluvastatin and atorvastatin on platelet aggregation in patients treated with aspirin and plavix after coronary stenting. We hypo...
Nonsteroidal antiinflammatory drugs such as diclofenac or naproxen may interfere with the inhibition of platelet aggregation by aspirin, because they all interact with the platelet cycloox...
The purpose of this study is to determine whether shear-induced platelet aggregation is able to discriminate first acute coronary syndrome (ACS) from recurrent ACS
The purpose of this study is to compare the effects of repeat doses of SB-659032 with placebo on platelet aggregation in subjects.
Thrombosis is a hallmark of the fatal fungal infection mucormycosis. Yet, the platelet activation pathway in response to mucormycetes is unknown. In this study we determined the platelet aggregation p...
Neuromedin U (NmU) is a pleiotropic hypothalamic neuropeptide involved in the gut-brain axis. It acts via both a Gαq/11-coupled receptor (NMUR1) and a Gαi-coupled receptor (NMUR2) in different cell ...
Coronary artery disease (CAD) remains a major cause of mortality and morbidity worldwide. The aggregation of activated platelets on a ruptured atherosclerotic plaque is a critical step in most acute c...
A series of 2-oxo-2-phenylethylidene linked 2-oxo-benzo[1,4]oxazine analogues 17a-x and 18a-o, incorporated with a variety of electron-withdrawing as well as electron-donating groups at ring A and rin...
OBJECTIVE To assess the effect of decreased platelet and WBC counts on platelet aggregation as measured by a multiple-electrode impedance aggregometer in dogs. ANIMALS 24 healthy dogs. PROCEDURES From...
Drugs or agents which antagonize or impair any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system.
Surface glycoproteins on platelets which have a key role in hemostasis and thrombosis such as platelet adhesion and aggregation. Many of these are receptors.
Platelet membrane glycoprotein complex important for platelet adhesion and aggregation. It is an integrin complex containing INTEGRIN ALPHAIIB and INTEGRIN BETA3 which recognizes the arginine-glycine-aspartic acid (RGD) sequence present on several adhesive proteins. As such, it is a receptor for FIBRINOGEN; VON WILLEBRAND FACTOR; FIBRONECTIN; VITRONECTIN; and THROMBOSPONDINS. A deficiency of GPIIb-IIIa results in GLANZMANN THROMBASTHENIA.
A congenital bleeding disorder with prolonged bleeding time, absence of aggregation of platelets in response to most agents, especially ADP, and impaired or absent clot retraction. Platelet membranes are deficient in or have a defect in the glycoprotein IIb-IIIa complex (PLATELET GLYCOPROTEIN GPIIB-IIIA COMPLEX).
A phosphodiesterase inhibitor which inhibits platelet aggregation. Formerly used as an antineoplastic.