- Platelet Disorders and Treatments
- Blood Coagulation and Thrombosis Mechanisms
- Blood groups and transfusion
- Antiplatelet Therapy and Cardiovascular Diseases
- Cell Adhesion Molecules Research
- Heparin-Induced Thrombocytopenia and Thrombosis
- Blood properties and coagulation
- Blood disorders and treatments
- Complement system in diseases
- Hemophilia Treatment and Research
- Venous Thromboembolism Diagnosis and Management
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Monoclonal and Polyclonal Antibodies Research
- Biochemical and Structural Characterization
- Immune Cell Function and Interaction
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Hepatitis B Virus Studies
- Angiogenesis and VEGF in Cancer
- Immunodeficiency and Autoimmune Disorders
- Viral Infections and Outbreaks Research
- Autoimmune Bullous Skin Diseases
- Cardiovascular Disease and Adiposity
- Atrial Fibrillation Management and Outcomes
- Adenosine and Purinergic Signaling
- Glycosylation and Glycoproteins Research
Scripps Research Institute
2015-2024
Scripps (United States)
2023
Scripps Institution of Oceanography
2023
Center for Vascular Biology Research
2018
University Medical Center Hamburg-Eppendorf
2017
University of California, San Diego
2017
Johannes Gutenberg University Mainz
2017
University Medical Center of the Johannes Gutenberg University Mainz
2017
Universität Hamburg
2017
Bloodworks Northwest
2015
Metastasis is the primary cause of death in human breast cancer. to bone, lungs, liver, and brain involves dissemination cancer cells via bloodstream requires adhesion within vasculature. Blood cell vasculature depends on integrins, a family transmembrane receptors, regulated by integrin activation. Here we show that αvβ3 supports attachment under blood flow conditions an activation-dependent manner. Integrin was found two distinct functional states cells. The activated, but not...
We have examined the multimeric composition of factor VIII/von Willebrand in plasma and platelet lysates by means sodium dodecyl sulfate agarose electrophoresis followed staining with (125)I-labeled affinity-purified antibody. In normal lysates, displayed 10 distinct multimers that ranged apparent molecular weight from 0.86 to 9.9 x 10(6). The difference between adjacent bands was 0.8-1.1 Larger material, not resolved into discrete bands, also present an average M(r) 14.5 Though dimer...
The binding of 125I-von Willebrand factor (125I-vWF) to platelets stimulated by thrombin, ADP, and a combination ADP + epinephrine (EPI) is specific, saturable, reversible. Active platelet metabolism divalent cations are required for induced these stimuli, but not ristocetin, suggesting the existence different mechanisms involved in vWF-platelet interaction. A monoclonal antibody directed against an epitope membrane glycoprotein (GP) Ib had no effect on 125I-vWF normal thrombin or EPI,...
The form of von Willebrand's disease characterized by a qualitative abnormality Factor VIII/von Willebrand factor (FVIII/vWF) in plasma has been designated as Type II. We have now identified 20 persons from five families whose qualitatively abnormal FVIII/vWF shows heightened responsiveness to ristocetin. classified this the IIB and reclassified IIA previously described II, which interaction with platelets is decreased or absent presence enhanced reactivity was evident studies...
Proteolytic cleavage of the von Willebrand factor subunit may be important for processing and/or function molecule and is altered in certain subtypes disease. It results generation two main fragments with apparent molecular masses 140 kDa 176 from 225-kDa subunit. We have now obtained chemical evidence to locate protease-sensitive bond between residues Tyr-842 Met-843, a site that appears reflect specificity calcium-dependent neutral proteases (calpains). Antibodies were raised against four...
Platelets contain both pro- and antiangiogenic factors, but their regulatory role in angiogenesis is poorly understood. Although previous studies showed that platelets stimulate vitro , the of vivo largely uncharacterized. To address this topic, we used two approaches, cornea micropocket assay Matrigel model, four animal models: thrombocytopenic, Lyst bg (platelet storage pool deficiency), glycoprotein (GP) Ibα/IL4R transgenic (lacking extracellular GPIbα, receptor for von Willebrand factor...
Thermal inkjet printing technology has been applied successfully to cell printing. However, there are concerns that process may cause damages or death. We conducted a comprehensive study of thermal printed Chinese hamster ovary (CHO) cells by evaluating viability and apoptosis, possible membrane damages. Additionally, we studied the concentration bio-ink found optimum concentrations around 8 million per mL. Printed was 89% only 3.5% apoptotic were observed after Transient pores developed in...
Chronic infection with hepatitis B virus (HBV) is a major risk factor for the development of hepatocellular carcinoma (HCC). The pathogenesis HBV-associated HCC involves both viral and host factors. latter include functionally inefficient CD8 + T-cell response that fails to clear from liver but sustains chronic necroinflammatory process contributes HCC. According this scenario, amelioration immune-mediated injury may prevent Because platelets facilitate by promoting hepatic accumulation...
The functions of platelets depend on their ability to interest with surface exposed at sites tissue damage and then one another after activation, thus aggregating into thrombi. This complex process, normally beneficial arrest bleeding during hemostasis, may become a cause catastrophic disease when it leads thrombotic occlusion atherosclerotic vessels curtailing arterial blood flow vital organs. Fluid dynamic conditions modulate all aspects platelet response vascular injury. At higher levels...
Introduction The reader will find here a concise summary of established notions on the structure and function von Willebrand factor (vWF), followed by brief discussion selected recent advances that illustrate how this molecule supports platelet in hemostasis thrombosis. A comprehensive review topic is beyond scope chapter may be found elsewhere.1-3
We have found that the form of glycoprotein (GP) IIb-IIIa (integrin alpha IIb beta 3) expressed on nonstimulated platelets is a functional receptor mediates selective and irreversible adhesion to immobilized fibrinogen. This occurs even in presence elevated intracellular cAMP levels induced by prostaglandin E1 or after inhibition protein kinase C activity sphingosine. In absence inhibitors, adhering fibrinogen through GP become fully activated aggregate with one another. Immobilized von...