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10.1016/j.ekir.2016.08.015 http://scihub22266oqcxt.onion/10.1016/j.ekir.2016.08.015 C5678626!5678626!29142942     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29142942&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Kidney+Int+Rep 2017 ; 2 (1): 66-75 Nephropedia Template TP {{tp|p=29142942|t=2017. Complement Activation Induces Neutrophil Adhesion and Neutrophil-Platelet Aggregate Formation on Vascular Endothelial Cells |pdf=|usr=}}{{29142942}} gab.com Text Complement Activation Induces Neutrophil Adhesion and Neutrophil-Platelet Aggregate Formation on Vascular Endothelial Cells JO: Kidney Int Rep http://www.kidney.de/pget.php?&tw=1&pmid=29142942 #FOAvip Introduction: Atypical hemolytic uremic syndrome is a thrombotic microangiopathy, which is linked to hereditary or autoimmune defects in complement activators or regulators present in blood and on vascular endothelial cells. Acute thrombotic microangiopathy episodes are typically preceded by infections, which by themselves would not be expected to manifest HUS. Thus, it is possible that the host immune response contributes to the precipitation of aHUS. However, the mechanisms involved are not fully understood. We hypothesized that neutrophils trigger aHUS via initiating platelet aggregate formation on complement-activated endothelial cells. Methods: We investigated neutrophil adhesion to complement-activated endothelial cells under static and flow conditions in vitro and ex vivo. Results: Our results show that complement activation on endothelial cells promotes neutrophil adhesion, which is significantly reduced when the complement terminal pathway is blocked. When neutrophils and platelets are perfused simultaneously, neutrophils adhering to endothelial cells also induce the formation of platelet-neutrophil aggregates on these cells. Sera from patients with aHUS recapitulated these results. Discussion: Therefore, our findings of (i) neutrophils adhering to complement-activated endothelial cells, (ii) the formation of neutrophil-platelet aggregates on endothelial cells, and (iii) the ability of aHUS serum to induce similar effects identify a possible role for neutrophils in aHUS manifestation. Twit Text FOAVip Complement Activation Induces Neutrophil Adhesion and Neutrophil-Platelet Aggregate Formation on Vascular Endothelial Cells ????Kidney Int Rep http://www.kidney.de/pget.php?&tw=1&pmid=29142942 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29142942 #FOAvip English Wikipedia <ref>{{Cite pmid|29142942}}</ref> Complement Activation Induces Neutrophil Adhesion and Neutrophil-Platelet Aggregate Formation on Vascular Endothelial Cells #MMPMID29142942 Riedl M; Noone DG; Khan MA; Pluthero FG; Kahr WH; Palaniyar N; Licht C Kidney Int Rep 2017[Jan]; 2 (1): 66-75 PMID29142942show ga Introduction: Atypical hemolytic uremic syndrome is a thrombotic microangiopathy, which is linked to hereditary or autoimmune defects in complement activators or regulators present in blood and on vascular endothelial cells. Acute thrombotic microangiopathy episodes are typically preceded by infections, which by themselves would not be expected to manifest HUS. Thus, it is possible that the host immune response contributes to the precipitation of aHUS. However, the mechanisms involved are not fully understood. We hypothesized that neutrophils trigger aHUS via initiating platelet aggregate formation on complement-activated endothelial cells. Methods: We investigated neutrophil adhesion to complement-activated endothelial cells under static and flow conditions in vitro and ex vivo. Results: Our results show that complement activation on endothelial cells promotes neutrophil adhesion, which is significantly reduced when the complement terminal pathway is blocked. When neutrophils and platelets are perfused simultaneously, neutrophils adhering to endothelial cells also induce the formation of platelet-neutrophil aggregates on these cells. Sera from patients with aHUS recapitulated these results. Discussion: Therefore, our findings of (i) neutrophils adhering to complement-activated endothelial cells, (ii) the formation of neutrophil-platelet aggregates on endothelial cells, and (iii) the ability of aHUS serum to induce similar effects identify a possible role for neutrophils in aHUS manifestation. äComplement Activation Induces Neutrophil Adhesion and Neutrophil-Plate(epmc).pdf DeepDyve Pubget Overpricing