Publications by authors named "J Cosemans"

Article Synopsis
  • This study analyzes how different platelet collagen receptors (GPVI, α2β1, and GPIb-IX-V) interact with various sources of collagen, impacting platelet activation and thrombus formation.
  • Ethical collagens tested include type I collagen from equine tendon, rat tail, and acid-soluble collagen from human umbilical cord.
  • The results show varied reliance on receptors for platelet aggregation depending on the collagen type, with GPVI playing a crucial role in reducing thrombus parameters when inhibited, demonstrating that collective receptor interactions influence platelet behavior on different collagen surfaces.
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Heart failure with preserved ejection fraction (HFpEF) is characterized by a lack of a specific targeted treatment and a complex, partially unexplored pathophysiology. Common comorbidities associated with HFpEF are hypertension, atrial fibrillation, obesity and diabetes. These comorbidities, combined with advanced age, play a crucial role in the initiation and development of the disease through the promotion of systemic inflammation and consequent changes in cardiac phenotype.

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Endothelialized in vitro models for cardiovascular disease have contributed greatly to our current understanding of the complex molecular mechanisms underlying thrombosis. To further elucidate these mechanisms, it is important to consider which fundamental aspects to incorporate into an in vitro model. In this review, we will focus on the design of in vitro endothelialized models of thrombosis.

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Background: Platelets and neutrophils are the first blood cells accumulating at sites of arterial thrombus formation, and both cell types contribute to the pathology of thrombotic events. We aimed to identify key interaction mechanisms between these cells using microfluidic approaches.

Methods: Whole-blood perfusion was performed over a collagen surface at arterial shear rate.

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All irreversible Bruton tyrosine kinase (Btk) inhibitors including ibrutinib and acalabrutinib induce platelet dysfunction and increased bleeding risk. New reversible Btk inhibitors were developed, like MK-1026. The mechanism underlying increased bleeding tendency with Btk inhibitors remains unclear.

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