A5080485297- Platelet Disorders and Treatments
- Antiplatelet Therapy and Cardiovascular Diseases
- Venous Thromboembolism Diagnosis and Management
- Blood Coagulation and Thrombosis Mechanisms
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Blood properties and coagulation
- Cell Adhesion Molecules Research
- Receptor Mechanisms and Signaling
- Heparin-Induced Thrombocytopenia and Thrombosis
- Adenosine and Purinergic Signaling
- World Trade Organization Law
- Diverse Musicological Studies
- Manufacturing Process and Optimization
- Private Equity and Venture Capital
- DNA Repair Mechanisms
- Autoimmune Bullous Skin Diseases
- Monoclonal and Polyclonal Antibodies Research
- Nanoparticle-Based Drug Delivery
- Carcinogens and Genotoxicity Assessment
- Blood disorders and treatments
- Blood groups and transfusion
- Advanced Manufacturing and Logistics Optimization
- Extracellular vesicles in disease
- Immune Cell Function and Interaction
- Bayesian Methods and Mixture Models
University of Maryland, Baltimore
2025
Beth Israel Deaconess Medical Center
2006-2012
Harvard University
2006-2010
University of Birmingham
2005-2008
Parsons (United States)
2005
NIHR Birmingham Biomedical Research Centre
2005
University of Vienna
2003
Medical University of Vienna
2003
University of Oxford
2001-2003
The role of Rac family proteins in platelet spreading on matrix under static and flow conditions has been investigated by using Rac-deficient platelets. Murine platelets form filopodia undergo limited fibrinogen independent Rac1 Rac2. In the presence thrombin, marked lamellipodia formation is observed fibrinogen, which abrogated absence Rac1. However, not required for thrombin-induced aggregation or elevation F-actin levels. Formation collagen laminin also Rac1-dependent. Analysis adhesion...
Summary The major activation-inducing collagen receptor glycoprotein VI (GPVI) has been cloned within the last two years. It is a member of Ig superfamily proteins and constitutively associated with ITAM-bearing Fc γ-chain (FcR γ-chain). GPVI signals through pathway that involves several used by Fc, B- T-lymphocyte receptors which takes place in glycolipid-enriched membrane domains plasma known as GEMs. Responses to are regulated PECAM-1 (CD31) possibly other ITIM-bearing receptors. Despite...
Various platelet membrane glycoproteins have been proposed as receptors for collagen, in some cases specific collagen types. In this study we compared the ability of a range types to activate platelets. Bovine I–V, native equine tendon fibrils and collagen‐related peptide (CRP) all induced aggregation shape change. Responses were abolished FcRγ chain‐deficient platelets, which also lack GPVI, indicating critical dependence on GPVI/FcRγ chain complex. collagens unaffected CD36‐deficient A...
Summary Plasma microparticles (MPs, <1·5 μm) originate from platelet and cell membrane lipid rafts possibly regulate inflammatory responses thrombogenesis. These actions are mediated through their phospholipid‐rich surfaces associated cell‐derived surface molecules. The ectonucleotidase CD39/ecto‐nucleoside triphosphate diphosphohydrolase1 (E‐NTPDase1) modulates purinergic signalling pericellular ATP ADP phosphohydrolysis is localized within in the membranes of endothelial‐ immune cells....
We have investigated the role of secretion and intracellular signalling events in aggregation induced by glycoprotein (GP)VI-selective snake venom toxin convulxin collagen. demonstrate that threshold concentrations undergoes synergy with ADP acting via P2Y12 receptor whereas there is no P2Y1 or thromboxanes. On other hand, apyrase, antagonist, AR-C67085, indomethacin only marginally inhibit convulxin. In comparison, these inhibitors severely attenuate response to order investigate whether...
Activation of human platelets by thrombin is mediated the proteolytic cleavage two G‐protein coupled protease‐activated receptors, PAR‐1 and PAR‐4. However, also binds specifically to platelet surface glycoprotein GPIb. It has been claimed that can induce aggregation via a novel GPIb‐mediated pathway, which independent PAR activation fibrinogen binding α IIb β 3 integrin, but dependent upon polymerizing fibrin generation intracellular signals. In presence both receptor antagonist lotrafiban,...
We have investigated the function of p110delta catalytic subunit phosphoinositide 3-kinase (PI 3-kinase) in platelets using knock-out (p110delta(-/-)) mice and knock-in (p110delta(D910A/D910A)) mice, which express a catalytically inactive form enzyme. Aggregation to threshold concentrations GPVI-specific agonist, CRP, was partially reduced p110delta(-/-) p110delta(D910A/D910A) platelets. This inhibition overcome by higher CRP. The degree considerably weaker than that induced LY294002...
ABSTRACT Objective : The role of collagen receptor complex GPVI‐FcR γ‐chain, PLCγ2 and LAT in laser‐induced thrombosis is unclear. Controversy surrounds whether exposed this model or dependent on thrombin. This study hypothesized that exposure plays a critical thrombus formation model, which was tested by investigating contributions FcR LAT, Methods Thrombi were monitored using intravital microscopy anesthetized wild‐type knockout mice. Hirudin (thrombin inhibitor) administered to γ‐chain...
Integrated life, vibration and performance monitoring/diagnostics capable of detecting classifying developing engine faults is critical to reducing operating maintenance costs while optimizing the life “hot section” components (Troudet Merrill, 1990). Advanced fault pattern recognition classification techniques utilizing complex finite-element empirical models structural related areas can now be accessed in a real-time monitoring environment (Dietz et al., 1989). Integration implementation...
Although it is well established that G(q)- and G(i)-coupled receptors can combine to mediate platelet aggregation, the signalling events underlying synergy are not fully characterised. This study has used calcium ionophore, A23187, phorbol ester, PMA, investigate this question. We show aggregation submaximal but maximal concentrations of ionophore partially inhibited by antagonism P2Y(12) ADP receptor or PKC blockade. However, a full response be restored under these conditions addition PMA...