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    Home Page Banner Membership-2024-2400×350 Specialist Directory This directory is a valuable SVM Member benefit, that allows patients and referring physicians to search for a “Vascular Specialist”. We…

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    • RT @SVM_tweets: Learn more from @DGlaucomflecken about what vascular medicine physicians and SVM can do: https://t.co/O66DCHkmDj @RKolluri…

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    Thrombosis is the most feared complication and a major pathomechanism of three major cardiovascular disorders, ischemic heart disease, stroke, and venous thromboembolism, which are leading causes of mortality among adults worldwide (1). The current concept of hemostasis proposes that vessel damage and exposure of subendothelial tissue factor (TF) generate trace amounts of thrombin, which has…

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    • Thanks @jclinicalinvest for highlighting our work! 👇 @BidmcCvi @HemeThrombBIDMC & thanks to János G. Filep for the thoughtful commentary https://t.co/yFcasSjhKs https://t.co/4IgFg468Ar

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    ResearchIn-Press PreviewHematologyVascular biology Open Access | 10.1172/JCI163808 Papa F. Anderson,1 Siyu M. Chen,2 Emale El-Darzi,1 Ivan Aivasovsky,2 Milan P. Kaushik,1 Kelsey D. Sack,1 H. Criss Hartzell,3 Samir M. Parikh,4 Robert Flaumenhaft,1 and Sol Schulman1 1Department of Medicine, Beth Israel…

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    • Extremely excited to have our work published: TMEM16E regulates endothelial cell procoagulant activity and thrombosis https://t.co/sjyClSMInR https://t.co/6A6qVJp3y9

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    Abstract Endothelial dysfunction accompanies the microvascular thrombosis commonly observed in severe COVID-19. Constitutively, the endothelial surface is anticoagulant, a property maintained at least in part via signaling through the Tie2 receptor. During inflammation, the Tie2 antagonist angiopoietin-2 (Angpt-2) is released from endothelial cells and inhibits Tie2, promoting a…

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    • Tie2 activation decreases endothelial procoagulant activity 🧫🐁Excited to see trials targeting Tie2 to improve outcomes in #COVID19 💉💊 https://t.co/2C7tmqgW5n https://t.co/QomblDMR6C https://t.co/haChklCk3H

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    Lethal COVID-19 is associated with respiratory failure that is thought to be caused by acute respiratory distress syndrome (ARDS) secondary to pulmonary infection. To date, the cellular pathogenesis has been inferred from studies describing the expression of ACE2, a transmembrane protein required for SARS-CoV-2 infection, and detection of viral RNA or protein in infected humans, model animals,…

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    • Novel hACE2🐁 model supports this: Genetic ablation of hACE2 in lung➡️no SARS-CoV2 lung infection➡️🐁 still die after SARS-CoV2 exposure I repeat: No SARS-CoV2 replicating in lung but still lethal #COVID19...with lung pathology (microthrombi, etc) https://t.co/UHRRDQZtrJ https://t.co/09SSmYmtWY