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10.1016/j.ymthe.2018.05.017 http://scihub22266oqcxt.onion/10.1016/j.ymthe.2018.05.017 29910176!6094359!29910176     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Ther 2018 ; 26 (8): 2060-2069 Nephropedia Template TP {{tp|p=29910176|t=2018. EMAPII Monoclonal Antibody Ameliorates Influenza A Virus-Induced Lung Injury |pdf=|usr=}}{{29910176}} gab.com Text EMAPII Monoclonal Antibody Ameliorates Influenza A Virus-Induced Lung Injury JO: Mol Ther http://www.kidney.de/pget.php?&tw=1&pmid=29910176 #FOAvip Influenza A virus (IAV) remains a major worldwide health threat, especially to high-risk populations, including the young and elderly. There is an unmet clinical need for therapy that will protect the lungs from damage caused by lower respiratory infection. Here, we analyzed the role of EMAPII, a stress- and virus-induced pro-inflammatory and pro-apoptotic factor, in IAV-induced lung injury. First, we demonstrated that IAV induces EMAPII surface translocation, release, and apoptosis in cultured endothelial and epithelial cells. Next, we showed that IAV induces EMAPII surface translocation and release to bronchoalveolar lavage fluid (BALF) in mouse lungs, concomitant with increases in caspase 3 activity. Injection of monoclonal antibody (mAb) against EMAPII attenuated IAV-induced EMAPII levels, weight loss, reduction of blood oxygenation, lung edema, and increase of the pro-inflammatory cytokine TNF alpha. In accordance with the pro-apoptotic properties of EMAPII, levels of caspase 3 activity in BALF were also decreased by mAb treatment. Moreover, we detected EMAPII mAb-induced increase in lung levels of M2-like macrophage markers YM1 and CD206. All together, these data strongly suggest that EMAPII mAb ameliorates IAV-induced lung injury by limiting lung cell apoptosis and shifting the host inflammatory setting toward resolution of inflammation. Twit Text FOAVip EMAPII Monoclonal Antibody Ameliorates Influenza A Virus-Induced Lung Injury ????Mol Ther http://www.kidney.de/pget.php?&tw=1&pmid=29910176 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29910176 #FOAvip English Wikipedia <ref>{{Cite pmid|29910176}}</ref> EMAPII Monoclonal Antibody Ameliorates Influenza A Virus-Induced Lung Injury #MMPMID29910176 Lu H; Chelvanambi S; Poirier C; Saliba J; March KL; Clauss M; Bogatcheva NV Mol Ther 2018[Aug]; 26 (8): 2060-2069 PMID29910176show ga Influenza A virus (IAV) remains a major worldwide health threat, especially to high-risk populations, including the young and elderly. There is an unmet clinical need for therapy that will protect the lungs from damage caused by lower respiratory infection. Here, we analyzed the role of EMAPII, a stress- and virus-induced pro-inflammatory and pro-apoptotic factor, in IAV-induced lung injury. First, we demonstrated that IAV induces EMAPII surface translocation, release, and apoptosis in cultured endothelial and epithelial cells. Next, we showed that IAV induces EMAPII surface translocation and release to bronchoalveolar lavage fluid (BALF) in mouse lungs, concomitant with increases in caspase 3 activity. Injection of monoclonal antibody (mAb) against EMAPII attenuated IAV-induced EMAPII levels, weight loss, reduction of blood oxygenation, lung edema, and increase of the pro-inflammatory cytokine TNF alpha. In accordance with the pro-apoptotic properties of EMAPII, levels of caspase 3 activity in BALF were also decreased by mAb treatment. Moreover, we detected EMAPII mAb-induced increase in lung levels of M2-like macrophage markers YM1 and CD206. All together, these data strongly suggest that EMAPII mAb ameliorates IAV-induced lung injury by limiting lung cell apoptosis and shifting the host inflammatory setting toward resolution of inflammation. |Animals[MESH] |Antibodies, Monoclonal/*administration & dosage/pharmacology[MESH] |Bronchoalveolar Lavage Fluid/chemistry/virology[MESH] |Caspase 3[MESH] |Cell Line[MESH] |Disease Models, Animal[MESH] |Humans[MESH] |Influenza A virus/drug effects[MESH] |Influenza, Human/*drug therapy/metabolism[MESH] |Injections[MESH] |Lung Injury/drug therapy/metabolism/*virology[MESH] |Mice[MESH] |Microtubule-Associated Proteins/*metabolism[MESH] |Protein Transport/drug effects[MESH] |Treatment Outcome[MESH]EMAPII Monoclonal Antibody Ameliorates Influenza A Virus-Induced Lung (epmc).pdf DeepDyve Pubget Overpricing