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10.1002/art.39938 http://scihub22266oqcxt.onion/10.1002/art.39938 C5329054!5329054!27696751     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Arthritis+Rheumatol 2017 ; 69 (3): 655-67 Nephropedia Template TP {{tp|p=27696751|t=2017. In vivo role of neutrophil extracellular traps in antiphospholipid antibody-mediated venous thrombosis |pdf=|usr=}}{{27696751}} gab.com Text In vivo role of neutrophil extracellular traps in antiphospholipid antibody-mediated venous thrombosis JO: Arthritis Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=27696751 #FOAvip Objective: Antiphospholipid syndrome (APS) is a leading acquired cause of thrombotic events. While antiphospholipid antibodies have been shown to promote thrombosis in mice, the role of neutrophils has not been explicitly studied. Here, we characterized neutrophils in the context of a new model of antiphospholipid antibody-mediated venous thrombosis. Methods: Mice were administered IgG fractions prepared from patients with APS. At the same time, flow through the inferior vena cava was reduced by a standard stenosis. Resulting thrombi were characterized for size and neutrophil content. Circulating factors and the vessel wall were also assessed. Results: As measured by both thrombus weight and thrombosis frequency, mice treated with IgG from patients with APS demonstrated exaggerated thrombosis as compared with controls. APS thrombi were enriched for citrullinated histone H3 (a marker of neutrophil extracellular traps/NETs). APS mice also demonstrated elevated levels of circulating cell-free DNA and human IgG bound to the neutrophil surface. In contrast, circulating neutrophil numbers and markers of vessel wall activation were not appreciably different between APS and control mice. Regarding therapy, treatment with either deoxyribonuclease (which dissolves NETs) or a neutrophil-depleting antibody reduced thrombosis in APS mice to the level seen in controls. Conclusion: These data support a mechanism whereby circulating neutrophils are primed by antiphospholipid antibodies to accelerate thrombosis. This line of investigation suggests new, immunomodulatory approaches for the treatment of APS. Twit Text FOAVip In vivo role of neutrophil extracellular traps in antiphospholipid antibody-mediated venous thrombosis ????Arthritis Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=27696751 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27696751 #FOAvip English Wikipedia <ref>{{Cite pmid|27696751}}</ref> In vivo role of neutrophil extracellular traps in antiphospholipid antibody-mediated venous thrombosis #MMPMID27696751 Meng H; Yalavarthi S; Kanthi Y; Mazza LF; Elfline MA; Luke CE; Pinsky DJ; Henke PK; Knight JS Arthritis Rheumatol 2017[Mar]; 69 (3): 655-67 PMID27696751show ga Objective: Antiphospholipid syndrome (APS) is a leading acquired cause of thrombotic events. While antiphospholipid antibodies have been shown to promote thrombosis in mice, the role of neutrophils has not been explicitly studied. Here, we characterized neutrophils in the context of a new model of antiphospholipid antibody-mediated venous thrombosis. Methods: Mice were administered IgG fractions prepared from patients with APS. At the same time, flow through the inferior vena cava was reduced by a standard stenosis. Resulting thrombi were characterized for size and neutrophil content. Circulating factors and the vessel wall were also assessed. Results: As measured by both thrombus weight and thrombosis frequency, mice treated with IgG from patients with APS demonstrated exaggerated thrombosis as compared with controls. APS thrombi were enriched for citrullinated histone H3 (a marker of neutrophil extracellular traps/NETs). APS mice also demonstrated elevated levels of circulating cell-free DNA and human IgG bound to the neutrophil surface. In contrast, circulating neutrophil numbers and markers of vessel wall activation were not appreciably different between APS and control mice. Regarding therapy, treatment with either deoxyribonuclease (which dissolves NETs) or a neutrophil-depleting antibody reduced thrombosis in APS mice to the level seen in controls. Conclusion: These data support a mechanism whereby circulating neutrophils are primed by antiphospholipid antibodies to accelerate thrombosis. This line of investigation suggests new, immunomodulatory approaches for the treatment of APS. äIn vivo role of neutrophil extracellular traps in antiphospholipid ant(epmc).pdf DeepDyve Pubget Overpricing