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10.1186/s13045-017-0496-x http://scihub22266oqcxt.onion/10.1186/s13045-017-0496-x C5477256!5477256!28629435     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Hematol+Oncol 2017 ; 10 (ä): ä Nephropedia Template TP {{tp|p=28629435|t=2017. Eculizumab treatment: stochastic occurrence of C3 binding to individual PNH erythrocytes |pdf=|usr=}}{{28629435}} gab.com Text Eculizumab treatment: stochastic occurrence of C3 binding to individual PNH erythrocytes JO: J Hematol Oncol http://www.kidney.de/pget.php?&tw=1&pmid=28629435 #FOAvip Background: C5 blockade by eculizumab prevents complement-mediated intravascular hemolysis in paroxysmal nocturnal hemoglobinuria (PNH). However, C3-bound PNH red blood cells (RBCs), arising in almost all treated patients, may undergo extravascular hemolysis reducing clinical benefits. Despite the uniform deficiency of CD55 and of CD59, there are always two distinct populations of PNH RBCs, with (C3+) and without (C3?) C3 binding. Methods: To investigate this paradox, the phenomenon has been modeled in vitro by incubating RBCs from eculizumab untreated PNH patients with compatible sera containing eculizumab, and by assessing the C3 binding after activation of complement alternative pathway. Results: When RBCs from untreated patients were exposed in vitro to activated complement in the context of C5-blockade, there was the prompt appearance of a distinct C3+ PNH RBC population whose size increased with time and also with the rate of complement activation. Eventually, all PNH RBCs become C3+ to the same extent, without differences between old and young (reticulocytes) PNH RBCs. Conclusions: This study indicates that the distinct (C3+ and C3?) PNH RBC populations are not intrinsically different; rather, they result from a stochastic all-or-nothing phenomenon linked to the time-dependent cumulative probability of each individual PNH red cell to be exposed to levels of complement activation able to trigger C3 binding. These findings may envision novel approaches to reduce C3 opsonization and the subsequent extravascular hemolysis in PNH patients on eculizumab. Electronic supplementary material: The online version of this article (doi:10.1186/s13045-017-0496-x) contains supplementary material, which is available to authorized users. Twit Text FOAVip Eculizumab treatment: stochastic occurrence of C3 binding to individual PNH erythrocytes ????J Hematol Oncol http://www.kidney.de/pget.php?&tw=1&pmid=28629435 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28629435 #FOAvip English Wikipedia <ref>{{Cite pmid|28629435}}</ref> Eculizumab treatment: stochastic occurrence of C3 binding to individual PNH erythrocytes #MMPMID28629435 Sica M; Rondelli T; Ricci P; De Angioletti M; Risitano AM; Notaro R J Hematol Oncol 2017[]; 10 (ä): ä PMID28629435show ga Background: C5 blockade by eculizumab prevents complement-mediated intravascular hemolysis in paroxysmal nocturnal hemoglobinuria (PNH). However, C3-bound PNH red blood cells (RBCs), arising in almost all treated patients, may undergo extravascular hemolysis reducing clinical benefits. Despite the uniform deficiency of CD55 and of CD59, there are always two distinct populations of PNH RBCs, with (C3+) and without (C3?) C3 binding. Methods: To investigate this paradox, the phenomenon has been modeled in vitro by incubating RBCs from eculizumab untreated PNH patients with compatible sera containing eculizumab, and by assessing the C3 binding after activation of complement alternative pathway. Results: When RBCs from untreated patients were exposed in vitro to activated complement in the context of C5-blockade, there was the prompt appearance of a distinct C3+ PNH RBC population whose size increased with time and also with the rate of complement activation. Eventually, all PNH RBCs become C3+ to the same extent, without differences between old and young (reticulocytes) PNH RBCs. Conclusions: This study indicates that the distinct (C3+ and C3?) PNH RBC populations are not intrinsically different; rather, they result from a stochastic all-or-nothing phenomenon linked to the time-dependent cumulative probability of each individual PNH red cell to be exposed to levels of complement activation able to trigger C3 binding. These findings may envision novel approaches to reduce C3 opsonization and the subsequent extravascular hemolysis in PNH patients on eculizumab. Electronic supplementary material: The online version of this article (doi:10.1186/s13045-017-0496-x) contains supplementary material, which is available to authorized users. äEculizumab treatment: stochastic occurrence of C3 binding to individua(epmc).pdf DeepDyve Pubget Overpricing