A5022448402- Platelet Disorders and Treatments
- Antiplatelet Therapy and Cardiovascular Diseases
- Complement system in diseases
- Cell Adhesion Molecules Research
- Heparin-Induced Thrombocytopenia and Thrombosis
- Blood groups and transfusion
- Monoclonal and Polyclonal Antibodies Research
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Blood Coagulation and Thrombosis Mechanisms
- Blood properties and coagulation
- Inflammatory mediators and NSAID effects
- Blood disorders and treatments
- Venous Thromboembolism Diagnosis and Management
- Glycosylation and Glycoproteins Research
- Protease and Inhibitor Mechanisms
- Peptidase Inhibition and Analysis
- Immunodeficiency and Autoimmune Disorders
- Eicosanoids and Hypertension Pharmacology
- Autoimmune Bullous Skin Diseases
- Protein purification and stability
- Synthesis of β-Lactam Compounds
- Transplantation: Methods and Outcomes
- Nitric Oxide and Endothelin Effects
- Xenotransplantation and immune response
- Protein Kinase Regulation and GTPase Signaling
KU Leuven
2012-2021
Research Institute for Chromatography
2012-2021
Max Delbrück Center
2017
Justus-Liebig-Universität Gießen
2003-2015
University of Maryland, Baltimore
2015
University of Würzburg
2010
Deutsche Forschungsgemeinschaft
2010
University Medical Center Utrecht
2006-2008
Vlaams Instituut voor Biotechnologie
2006-2008
Baruch College
2007
Neutrophil extracellular traps (NETs) have been shown to promote thrombus formation. Little is known about the exact composition of thrombi that cause ischemic stroke. In particular, no information yet available on presence NETs in cerebral occlusions. Such is, however, essential improve current thrombolytic therapy with tissue plasminogen activator (t-PA). This study aimed at investigating neutrophils and more specifically stroke thrombi.Sixty-eight retrieved from patients undergoing...
Ischemic stroke is caused by a thromboembolic occlusion of cerebral arteries. Treatment focused on fast and efficient removal the occluding thrombus, either via intravenous thrombolysis or endovascular thrombectomy. Recanalization, however, not always successful factors contributing to failure are completely understood. Although thrombus primary target acute treatment, little known about its internal organization composition. The aim this study, therefore, was better understand ischemic...
Objective: The inability to regulate the inflammatory response initiated upon infection leads severe sepsis, characterized by widespread microvascular injury and thrombosis, organ ischemia, dysfunction. A disintegrin-like metalloprotease with thrombospondin type 1 repeats (ADAMTS)-13 regulates primary hemostasis proteolyzing von Willebrand factor (VWF). Decreased ADAMTS-13 has been reported in disseminated intravascular coagulation due sepsis. present study investigates whether...
Abstract TGF-β1, β2 and β3 bind a common receptor to exert vastly diverse effects in cancer, supporting either tumor progression by favoring metastases inhibiting anti-tumor immunity, or suppression malignant cell proliferation. Global TGF-β inhibition thus bears the risk of undesired tumor-promoting effects. We show that selective blockade TGF-β1 production Tregs with antibodies against GARP:TGF-β1 complexes induces regressions mouse tumors otherwise resistant anti-PD-1 immunotherapy....
BACKGROUND Fibrinogen-dependent cross-linking of glycoprotein (GP) IIb/IIIa on activated platelets is the final mechanism leading to platelet aggregation. Inhibition this may result in a novel antithrombotic agent. We studied activity MK-383 (L-700,462), new, nonpeptide GPIIb/IIIa antagonist, vitro and vivo, man. METHODS AND RESULTS MK-383, tyrosine derivative, dose-dependently inhibited fibrinogen-dependent aggregation, vitro. Binding 125I-labeled fibrinogen was prevented competitive manner...
BACKGROUND RGD-containing peptides are able to prevent binding of ligands certain integrins such as alpha IIb beta 3 (glycoprotein IIb/IIIa) and v inhibitors for platelet aggregation smooth muscle cell migration, both which involved in neointima formation. METHODS AND RESULTS Hamster carotid arteries were damaged, formation was determined at different time points. G4120, a cyclic peptide, administered continuously intravenously by an implanted osmotic pump. Neointima inhibited dose...
Atherosclerotic plaque develops at sites of disturbed flow. We previously showed that flow activates endothelial cell integrins, which then bind to the subendothelial extracellular matrix (ECM), and, in cells on fibronectin or fibrinogen, trigger nuclear factor-kappaB activation. Additionally, and fibrinogen are deposited into ECM atherosclerosis-prone early times. now show ECM-specific signals establish patterns integrin dominance. Flow induced alpha2beta1 activation collagen, but not...
Summary The plasma metalloprotease ADAMTS13 (A Disintegrin And Metalloprotease with ThromboSpondin type 1 motif 13) cleaves prothrombotic ultralarge multimers of the platelet‐adhesive protein von Willebrand factor (ULVWF) into less active that promote haemostasis in injured blood vessels. When enzyme is dysfunctional or undetectable, circulating ULVWF may cause massive intravascular aggregation platelets and thrombotic thrombocytopenic purpura. This study compared antigen activity a large...
Dipyridamole possesses antithrombotic properties in the animal and man but it does not inhibit platelet aggregation plasma. We evaluated effect of dipyridamole ex vivo vitro on induced by collagen adenosine-5'-diphosphate (ADP) human whole blood with an impedance aggregometer. Two hundred mg a significant inhibition both ADP- collagen-induced samples taken 2 hr after oral drug intake. Administration for four days, 400 mg/day, further increased antiplatelet effect. A negative correlation was...
MK-383 (L-tyrosine, N-n-butylsulfonyl)-O-[4-butyl(4-piperidinyl)], monohydrochloride monohydrate) is a potent and specific platelet fibrinogen receptor antagonist that may be useful in preventing processes lead to occlusive thrombus formation the lumen of blood vessel. Two placebo-controlled phase I trials were completed 56 healthy volunteers investigate safety, tolerability, pharmacokinetics, pharmacodynamics administered as 1- 4-hour infusions presence absence aspirin. When male subjects...
Soluble von Willebrand factor (VWF) has a low affinity for platelet glycoprotein (GP) Ibalpha and needs immobilization and/or high shear stress to enable binding of its A1 domain the receptor. The previously described anti-VWF monoclonal antibody 1C1E7 enhances VWF/GPIbalpha recognizes an epitope in amino acids 764-1035 region N-terminal D'D3 domains. In this study we demonstrated that negatively modulates VWF/GPIb-IX-V interaction; (i) deletion VWF augmented GPIbalpha, suggesting inhibitory...