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10.18632/oncotarget.16205 http://scihub22266oqcxt.onion/10.18632/oncotarget.16205 C5482616!5482616!28415757     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 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       Oncotarget 2017 ; 8 (22): 35776-82 Nephropedia Template TP {{tp|p=28415757|t=2017. An absence of platelet activation following thalidomide treatment in vitro or in vivo |pdf=|usr=}}{{28415757}} gab.com Text An absence of platelet activation following thalidomide treatment in vitro or in vivo JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28415757 #FOAvip Increased risk of thromboembolism and platelet hyperreactivity has been reported in patients receiving thalidomide therapy. Whether thalidomide induces platelet activation directly or through other factors remains unclear. The aim of this study was to evaluate the effect of thalidomide on platelet activation under resting conditions in vitro and in vivo. Isolated human or mouse platelets were treated with different concentrations of thalidomide (10, 50 and 100 ?g/ml) for 60 min at 37°C followed by analysis of platelet surface expression of platelet receptors GPIb?, GPVI, ?IIb?3 and P-selectin, and PAC-1 or fibrinogen binding, by flow cytometry and collagen- or ADP-induced platelet aggregation. In addition, thalidomide (200 mg/kg) was intraperitoneally injected into mice for analysis of the effect of thalidomide on platelet activation in vivo. No increased expression of P-selectin, PAC-1 or fibrinogen binding was observed in either human and mouse platelets after thalidomide treatment in vitro for 60 min at 37°C. Thalidomide treatment also did not affect expression of GPIb?, GPVI or ?IIb?3, nor did it affect collagen- or ADP-induced platelet aggregation at threshold concentrations. However, while mice injected with thalidomide displayed no increased surface expression of platelet P-selectin or ?IIb?3, there was a significantly shortened tail bleeding time, thrombin time, prothrombin time together with higher levels of Factor IX and fibrinogen. In conclusion, thalidomide at therapeutic doses does not directly induce platelet activation under resting conditions in vitro or in vivo, but results in increased procoagulant activity, which could explain the thalidomide-dependent prothrombotic tendency in patients. Twit Text FOAVip An absence of platelet activation following thalidomide treatment in vitro or in vivo ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28415757 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28415757 #FOAvip English Wikipedia <ref>{{Cite pmid|28415757}}</ref> An absence of platelet activation following thalidomide treatment in vitro or in vivo #MMPMID28415757 Qiao J; Wu Y; Wu X; Liu Y; Li X; Ju W; Qi K; Li D; Gardiner EE; Andrews RK; Zeng L; Xu K Oncotarget 2017[May]; 8 (22): 35776-82 PMID28415757show ga Increased risk of thromboembolism and platelet hyperreactivity has been reported in patients receiving thalidomide therapy. Whether thalidomide induces platelet activation directly or through other factors remains unclear. The aim of this study was to evaluate the effect of thalidomide on platelet activation under resting conditions in vitro and in vivo. Isolated human or mouse platelets were treated with different concentrations of thalidomide (10, 50 and 100 ?g/ml) for 60 min at 37°C followed by analysis of platelet surface expression of platelet receptors GPIb?, GPVI, ?IIb?3 and P-selectin, and PAC-1 or fibrinogen binding, by flow cytometry and collagen- or ADP-induced platelet aggregation. In addition, thalidomide (200 mg/kg) was intraperitoneally injected into mice for analysis of the effect of thalidomide on platelet activation in vivo. No increased expression of P-selectin, PAC-1 or fibrinogen binding was observed in either human and mouse platelets after thalidomide treatment in vitro for 60 min at 37°C. Thalidomide treatment also did not affect expression of GPIb?, GPVI or ?IIb?3, nor did it affect collagen- or ADP-induced platelet aggregation at threshold concentrations. However, while mice injected with thalidomide displayed no increased surface expression of platelet P-selectin or ?IIb?3, there was a significantly shortened tail bleeding time, thrombin time, prothrombin time together with higher levels of Factor IX and fibrinogen. In conclusion, thalidomide at therapeutic doses does not directly induce platelet activation under resting conditions in vitro or in vivo, but results in increased procoagulant activity, which could explain the thalidomide-dependent prothrombotic tendency in patients. äAn absence of platelet activation following thalidomide treatment in v(epmc).pdf DeepDyve Pubget Overpricing