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10.1165/rcmb.2010-0444OC http://scihub22266oqcxt.onion/10.1165/rcmb.2010-0444OC C5460894!5460894!21421909     free     free     free 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       Am+J+Respir+Cell+Mol+Biol 2011 ; 45 (4): 834-42 Nephropedia Template TP {{tp|p=21421909|t=2011. Complement Inhibition Alleviates Paraquat-Induced Acute Lung Injury |pdf=|usr=}}{{21421909}} gab.com Text Complement Inhibition Alleviates Paraquat-Induced Acute Lung Injury JO: Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=21421909 #FOAvip The widely used herbicide, paraquat (PQ), is highly toxic and claims thousands of lives from both accidental and voluntary ingestion. The pathological mechanisms of PQ poisoning?induced acute lung injury (ALI) are not well understood, and the role of complement in PQ-induced ALI has not been elucidated. We developed and characterized a mouse model of PQ-induced ALI and studied the role of complement in the pathogenesis of PQ poisoning. Intraperitoneal administration of PQ caused dose- and time-dependent lung damage and mortality, with associated inflammatory response. Within 24 hours of PQ-induced ALI, there was significantly increased expression of the complement proteins, C1q and C3, in the lung. Expression of the anaphylatoxin receptors, C3aR and C5aR, was also increased. Compared with wild-type mice, C3-deficient mice survived significantly longer and displayed significantly reduced lung inflammation and pathology after PQ treatment. Similar reductions in PQ-induced inflammation, pathology, and mortality were recorded in mice treated with the C3 inhibitors, CR2-Crry, and alternative pathway specific CR2-fH. A similar therapeutic effect was also observed by treatment with either C3a receptor antagonist or a blocking C5a receptor monoclonal antibody. Together, these studies indicate that PQ-induced ALI is mediated through receptor signaling by the C3a and C5a complement activation products that are generated via the alternative complement pathway, and that complement inhibition may be an effective clinical intervention for postexposure treatment of PQ-induced ALI. Twit Text FOAVip Complement Inhibition Alleviates Paraquat-Induced Acute Lung Injury ????Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=21421909 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21421909 #FOAvip English Wikipedia <ref>{{Cite pmid|21421909}}</ref> Complement Inhibition Alleviates Paraquat-Induced Acute Lung Injury #MMPMID21421909 Sun S; Wang H; Zhao G; An Y; Guo Y; Du L; Song H; Qiao F; Yu H; Wu X; Atkinson C; Jiang S; Tomlinson S; Zhou Y Am J Respir Cell Mol Biol 2011[Oct]; 45 (4): 834-42 PMID21421909show ga The widely used herbicide, paraquat (PQ), is highly toxic and claims thousands of lives from both accidental and voluntary ingestion. The pathological mechanisms of PQ poisoning?induced acute lung injury (ALI) are not well understood, and the role of complement in PQ-induced ALI has not been elucidated. We developed and characterized a mouse model of PQ-induced ALI and studied the role of complement in the pathogenesis of PQ poisoning. Intraperitoneal administration of PQ caused dose- and time-dependent lung damage and mortality, with associated inflammatory response. Within 24 hours of PQ-induced ALI, there was significantly increased expression of the complement proteins, C1q and C3, in the lung. Expression of the anaphylatoxin receptors, C3aR and C5aR, was also increased. Compared with wild-type mice, C3-deficient mice survived significantly longer and displayed significantly reduced lung inflammation and pathology after PQ treatment. Similar reductions in PQ-induced inflammation, pathology, and mortality were recorded in mice treated with the C3 inhibitors, CR2-Crry, and alternative pathway specific CR2-fH. A similar therapeutic effect was also observed by treatment with either C3a receptor antagonist or a blocking C5a receptor monoclonal antibody. Together, these studies indicate that PQ-induced ALI is mediated through receptor signaling by the C3a and C5a complement activation products that are generated via the alternative complement pathway, and that complement inhibition may be an effective clinical intervention for postexposure treatment of PQ-induced ALI. äComplement Inhibition Alleviates Paraquat-Induced Acute Lung Injury (epmc).pdf DeepDyve Pubget Overpricing