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10.1016/j.bcmd.2022.102653 http://scihub22266oqcxt.onion/10.1016/j.bcmd.2022.102653 35180460!8832951!35180460     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=35180460&cmd=llinks): Failed to open stream: HTTP request failed! 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Upregulation of cytokine signalling in platelets increases risk of thrombophilia in severe COVID-19 patients |pdf=|usr=}}{{35180460}} gab.com Text Upregulation of cytokine signalling in platelets increases risk of thrombophilia in severe COVID-19 patients JO: Blood Cells Mol Dis http://www.kidney.de/pget.php?&tw=1&pmid=35180460 #FOAvip Abnormal coagulation dynamics, including disseminated intravascular coagulopathy, pulmonary embolism, venous thromboembolism and risk of thrombosis are often associated with the severity of COVID-19. However, very little is known about the contribution of platelets in above pathogenesis. In order to decipher the pathophysiology of thrombophilia in COVID-19, we recruited severely ill patients from ICU, based on the above symptoms and higher D-dimer levels, and compared these parameters with their asymptomatic counterparts. Elevated levels of platelet-derived microparticles and platelet-leukocyte aggregates suggested the hyperactivation of platelets in ICU patients. Strikingly, platelet transcriptome analysis showed a greater association of IL-6 and TNF signalling pathways in ICU patients along with higher plasma levels of IL-6 and TNFalpha. In addition, upregulation of pathways like blood coagulation and hemostasis, as well as inflammation coexisted in platelets of these patients. Further, the increment of necrotic pathway and ROS-metabolic processes in platelets was suggestive of its procoagulant phenotype in ICU patients. This study suggests that higher plasma IL-6 and TNFalpha may trigger platelet activation and coagulation, and in turn aggravate thrombosis and hypercoagulation in severe COVID-19 patients. Therefore, the elevated IL-6 and TNFalpha, may serve as potential risk factors for platelet activation and thrombophilia in these patients. Twit Text FOAVip Upregulation of cytokine signalling in platelets increases risk of thrombophilia in severe COVID-19 patients ????Blood Cells Mol Dis http://www.kidney.de/pget.php?&tw=1&pmid=35180460 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35180460 #FOAvip English Wikipedia <ref>{{Cite pmid|35180460}}</ref> Upregulation of cytokine signalling in platelets increases risk of thrombophilia in severe COVID-19 patients #MMPMID35180460 Kaur S; Singh A; Kaur J; Verma N; Pandey AK; Das S; Bhattacharyya S; Guchhait P Blood Cells Mol Dis 2022[May]; 94 (ä): 102653 PMID35180460show ga Abnormal coagulation dynamics, including disseminated intravascular coagulopathy, pulmonary embolism, venous thromboembolism and risk of thrombosis are often associated with the severity of COVID-19. However, very little is known about the contribution of platelets in above pathogenesis. In order to decipher the pathophysiology of thrombophilia in COVID-19, we recruited severely ill patients from ICU, based on the above symptoms and higher D-dimer levels, and compared these parameters with their asymptomatic counterparts. Elevated levels of platelet-derived microparticles and platelet-leukocyte aggregates suggested the hyperactivation of platelets in ICU patients. Strikingly, platelet transcriptome analysis showed a greater association of IL-6 and TNF signalling pathways in ICU patients along with higher plasma levels of IL-6 and TNFalpha. In addition, upregulation of pathways like blood coagulation and hemostasis, as well as inflammation coexisted in platelets of these patients. Further, the increment of necrotic pathway and ROS-metabolic processes in platelets was suggestive of its procoagulant phenotype in ICU patients. This study suggests that higher plasma IL-6 and TNFalpha may trigger platelet activation and coagulation, and in turn aggravate thrombosis and hypercoagulation in severe COVID-19 patients. Therefore, the elevated IL-6 and TNFalpha, may serve as potential risk factors for platelet activation and thrombophilia in these patients. |*COVID-19/complications[MESH] |*Cell-Derived Microparticles/metabolism[MESH] |*Thrombophilia/complications[MESH] |Blood Platelets/metabolism[MESH] |Cytokines/metabolism[MESH] |Humans[MESH] |SARS-CoV-2[MESH]Upregulation of cytokine signalling in platelets increases risk of thr(epmc).pdf DeepDyve Pubget Overpricing