Antithrombin and tissue factor pathway inhibitor (TFPI) provide different anticoagulant mechanisms. Having established a potent anticoagulant role of cultured human umbilical vein endothelial cells in vessel-on-a-chip microfluidic models, we now investigated how these cells modulated thrombin generation under stasis through antithrombin and TFPI pathways. We observed that endothelial monolayers in 96 well-plates strongly delayed and suppressed the thrombin generation process induced by tissue factor, regardless of the presence of whole blood, platelet-rich plasma or platelet-free plasma.
View Article and Find Full Text PDFAgonist-induced rises in cytosolic Ca control most platelet responses in thrombosis and hemostasis. In human platelets, we earlier demonstrated that the ORAI1-STIM1 pathway is a major component of extracellular Ca entry, in particular when induced via the ITAM-linked collagen receptor, glycoprotein VI (GPVI). In the present article, using functionally defective platelets from patients with a loss-of-function mutation in ORAI1 or STIM1, we show that Ca entry induced by the endoplasmic reticulum ATPase inhibitor, thapsigargin, fully relies on this pathway.
View Article and Find Full Text PDFBackground: Metallic artefacts caused by metal implants, are a common problem in computed tomography (CT) imaging, degrading image quality and diagnostic accuracy. With advancements in artificial intelligence, novel deep learning (DL)-based metal artefact reduction (MAR) algorithms are entering clinical practice.
Objective: This systematic review provides an overview of the performance of the current supervised DL-based MAR algorithms for CT, focusing on three different domains: sinogram, image, and dual domain.
Introduction: The CC chemokine ligand 18 (CCL18) is a chemokine highly expressed in chronic inflammation in humans. Recent observations of elevated CCL18 plasma levels in patients with acute cardiovascular syndromes prompted an investigation into the role of CCL18 in the pathogenesis of human and mouse atherosclerosis.
Methods And Results: CCL18 was profoundly upregulated in ruptured human atherosclerotic plaque, particularly within macrophages.