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10.1097/MOH.0000000000000271 http://scihub22266oqcxt.onion/10.1097/MOH.0000000000000271 C5148823!5148823 !27380557     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27380557 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Curr+Opin+Hematol 2016 ; 23 (5 ): 445-52 Nephropedia Template TP {{tp|p=27380557 |t=2016. Antithrombotic potential of the contact activation pathway |pdf=|usr=}}{{27380557 }} gab.com Text Antithrombotic potential of the contact activation pathway JO: Curr Opin Hematol http://www.kidney.de/pget.php?&tw=1&pmid=27380557 #FOAvip PURPOSE OF REVIEW: This report examines the mechanism(s) by which each protein of the contact activation system - factor XII (FXII), high-molecular-weight kininogen, and prekallikrein - influences thrombosis risk. RECENT FINDINGS: FXII generates thrombin through contact activation via interaction with artificial surfaces as on medical instruments such as indwelling catheters, mechanical valves, stents, and ventricular assist devices. Inhibition of FXIIa-mediated contact activation prevents thrombosis under contact activation circumstances without affecting hemostasis. Current studies suggest that high-molecular-weight kininogen deficiency parallels that of FXII and inhibits contact activation. Prekallikrein inhibition contributes to thrombosis prevention by contact activation inhibition in the nylon monofilament model of transient middle cerebral artery occlusion. However, in arterial thrombosis models where reactive oxygen species are generated, prekallikrein deficiency results in downregulation of vessel wall tissue factor generation with reduced thrombin generation. Exploiting this latter prekallikrein pathway for thrombosis risk reduction provides a general, overall reduced tissue factor, antithrombotic pathway without risk for bleeding. SUMMARY: These investigations indicate that the proteins of the contact activation and kallikrein/kinin systems influence thrombosis risk by several mechanisms and understanding of these pathway provides insight into several novel targets to prevent thrombosis without increase in bleeding risk. Twit Text FOAVip Antithrombotic potential of the contact activation pathway ????Curr Opin Hematol http://www.kidney.de/pget.php?&tw=1&pmid=27380557 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27380557 #FOAvip English Wikipedia <ref>{{Cite pmid|27380557 }}</ref> Antithrombotic potential of the contact activation pathway #MMPMID27380557 Schmaier AH Curr Opin Hematol 2016[Sep]; 23 (5 ): 445-52 PMID27380557 show ga PURPOSE OF REVIEW: This report examines the mechanism(s) by which each protein of the contact activation system - factor XII (FXII), high-molecular-weight kininogen, and prekallikrein - influences thrombosis risk. RECENT FINDINGS: FXII generates thrombin through contact activation via interaction with artificial surfaces as on medical instruments such as indwelling catheters, mechanical valves, stents, and ventricular assist devices. Inhibition of FXIIa-mediated contact activation prevents thrombosis under contact activation circumstances without affecting hemostasis. Current studies suggest that high-molecular-weight kininogen deficiency parallels that of FXII and inhibits contact activation. Prekallikrein inhibition contributes to thrombosis prevention by contact activation inhibition in the nylon monofilament model of transient middle cerebral artery occlusion. However, in arterial thrombosis models where reactive oxygen species are generated, prekallikrein deficiency results in downregulation of vessel wall tissue factor generation with reduced thrombin generation. Exploiting this latter prekallikrein pathway for thrombosis risk reduction provides a general, overall reduced tissue factor, antithrombotic pathway without risk for bleeding. SUMMARY: These investigations indicate that the proteins of the contact activation and kallikrein/kinin systems influence thrombosis risk by several mechanisms and understanding of these pathway provides insight into several novel targets to prevent thrombosis without increase in bleeding risk. |*Blood Coagulation [MESH] |*Signal Transduction [MESH] |Animals [MESH] |Biomarkers [MESH] |Enzyme Activation [MESH] |Factor XII/antagonists & inhibitors/genetics/metabolism [MESH] |Humans [MESH] |Kininogen, High-Molecular-Weight/genetics/metabolism [MESH] |Leukocytes/metabolism [MESH] |Prekallikrein/genetics/metabolism [MESH] |Protein Binding [MESH]Antithrombotic potential of the contact activation pathway (epmc).pdf DeepDyve Pubget Overpricing