6 results match your criteria: "The Netherlands. Electronic address: jwm.heemskerk@maastrichtuniversity.nl.[Affiliation]"

Introduction: Current developments to assess qualitative and quantitative platelet traits in flowed whole-blood are based on microfluidic devices that mostly operate at room temperature. However, operation at physiological temperature (37 °C) may increase the assay's sensitivity, and facilitates the comparison to other platelet function tests of the diagnostic laboratory.

Materials And Methods: We adapted the conventional microspot-based microfluidic device with a simple thermo-coupled pre-heating module.

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Platelet populations and priming in hematological diseases.

Blood Rev

November 2017

Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands. Electronic address:

In healthy subjects and patients with hematological diseases, platelet populations can be distinguished with different response spectra in hemostatic and vascular processes. These populations partly overlap, and are less distinct than those of leukocytes. The platelet heterogeneity is linked to structural properties, and is enforced by inequalities in the environment.

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Platelets and coagulation in thrombus formation: aberrations in the Scott syndrome.

Thromb Res

May 2016

Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Centre, Maastricht, The Netherlands. Electronic address:

Platelets play key roles in thrombosis and hemostasis by forming aggregates and providing a procoagulant surface, at which thrombin is generated and fibrin fibers are formed. Here we present an overview of the different mechanisms how platelets orchestrate coagulation processes in thrombus formation in thrombosis and hemostasis. Parts of these are via Ca(2+)-dependent activation responses, leading to phosphatidylserine exposure; swelling to form balloons with increased binding of coagulation factors; and calpain-mediated integrin αIIbβ3 cleavage and inactivation.

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Normal platelet activation profile in patients with peripheral arterial disease on aspirin.

Thromb Res

March 2015

Departments of Biochemistry and Internal Medicine, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Centre, Maastricht, The Netherlands. Electronic address:

Background: Peripheral arterial disease (PAD) is a progressive vascular disease associated with a high risk of cardiovascular morbidity and death. Antithrombotic prevention is usually applied by prescribing the antiplatelet agent aspirin. However, in patients with PAD aspirin fails to provide protection against myocardial infarction and death, only reducing the risk of ischemic stroke.

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Insights into platelet-based control of coagulation.

Thromb Res

May 2014

Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands. Electronic address:

The coagulation process is activated by tight control mechanisms, in which platelets play prominent and unique roles. In thrombosis and hemostasis, activated platelets regulate the coagulation system in various ways: by exposing a phosphatidylserine surface for thrombin formation, by supporting fibrin formation, and by regulating the retraction of a fibrin clot. In this review we discuss the involvement of platelet receptors, other membrane proteins, downstream signaling proteins, cytoskeleton-linked proteins and plasma proteins in these procoagulant functions.

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In this review, we presume that the process of thrombus formation, as assessed in whole blood flow studies and in experimental (murine) thrombosis studies, reflects the platelet responses in human haemostasis and thrombosis. Following this concept, we give an up-to-date overview of the main platelet receptors and signalling pathways that contribute to thrombus formation and are used as targets in (pre)clinical intervention studies to prevent cardiovascular disease. Discussed are receptors for thrombin, thromboxane, ADP, ATP, prostaglandins, von Willebrand factor, collagen, CLEC-2 ligand, fibrinogen and laminin.

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