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10.1093/infdis/jit062 http://scihub22266oqcxt.onion/10.1093/infdis/jit062 23420903!ä!23420903 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Infect+Dis 2013 ; 207 (10): 1576-84 Nephropedia Template TP {{tp|p=23420903|t=2013. Inducible nitric oxide contributes to viral pathogenesis following highly pathogenic influenza virus infection in mice |pdf=|usr=}}{{23420903}} gab.com Text Inducible nitric oxide contributes to viral pathogenesis following highly pathogenic influenza virus infection in mice JO: J Infect Dis http://www.kidney.de/pget.php?&tw=1&pmid=23420903 #FOAvip Highly pathogenic influenza A viruses, including avian H5N1 viruses and the 1918 pandemic virus, cause severe respiratory disease in humans and animals. Virus infection is followed by intense pulmonary congestion due to an extensive influx of macrophages and neutrophils, which can release large quantities of reactive oxygen species potentially contributing to the pathogenesis of lung disease. Here, the role of nitric oxide (NO), a potent signaling molecule in inflammation, was evaluated following highly pathogenic influenza virus challenge in mice. We observed higher levels of NO in mice infected with H5N1 and 1918 viruses as compared to a seasonal H1N1 virus. Mice deficient in inducible NO synthase (NOS2(-/-)) exhibited reduced morbidity, reduced mortality, and diminished cytokine production in lung tissue following H5N1 and 1918-virus challenge, compared with wild-type control mice. Furthermore, systemic treatment of mice with the NOS inhibitor NG-monomethyl-l-arginine delayed weight loss and death among 1918 virus infected mice compared to untreated control animals. This study demonstrates that NO contributes to the pathogenic outcome of H5N1 and 1918 viral infections in the mouse model. Twit Text FOAVip Inducible nitric oxide contributes to viral pathogenesis following highly pathogenic influenza virus infection in mice ????J Infect Dis http://www.kidney.de/pget.php?&tw=1&pmid=23420903 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23420903 #FOAvip English Wikipedia <ref>{{Cite pmid|23420903}}</ref> Inducible nitric oxide contributes to viral pathogenesis following highly pathogenic influenza virus infection in mice #MMPMID23420903 Perrone LA; Belser JA; Wadford DA; Katz JM; Tumpey TM J Infect Dis 2013[May]; 207 (10): 1576-84 PMID23420903show ga Highly pathogenic influenza A viruses, including avian H5N1 viruses and the 1918 pandemic virus, cause severe respiratory disease in humans and animals. Virus infection is followed by intense pulmonary congestion due to an extensive influx of macrophages and neutrophils, which can release large quantities of reactive oxygen species potentially contributing to the pathogenesis of lung disease. Here, the role of nitric oxide (NO), a potent signaling molecule in inflammation, was evaluated following highly pathogenic influenza virus challenge in mice. We observed higher levels of NO in mice infected with H5N1 and 1918 viruses as compared to a seasonal H1N1 virus. Mice deficient in inducible NO synthase (NOS2(-/-)) exhibited reduced morbidity, reduced mortality, and diminished cytokine production in lung tissue following H5N1 and 1918-virus challenge, compared with wild-type control mice. Furthermore, systemic treatment of mice with the NOS inhibitor NG-monomethyl-l-arginine delayed weight loss and death among 1918 virus infected mice compared to untreated control animals. This study demonstrates that NO contributes to the pathogenic outcome of H5N1 and 1918 viral infections in the mouse model. |Animals[MESH] |Chemokines/blood[MESH] |Cytokines/blood[MESH] |Disease Models, Animal[MESH] |Female[MESH] |Influenza A Virus, H1N1 Subtype/*pathogenicity[MESH] |Influenza A Virus, H5N1 Subtype/*pathogenicity[MESH] |Lung/pathology/virology[MESH] |Macrophages/immunology[MESH] |Mice[MESH] |Mice, Inbred BALB C[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Neutrophils/cytology/immunology[MESH] |Nitric Oxide Synthase Type II/genetics/*metabolism[MESH] |Nitric Oxide/*metabolism[MESH] |Orthomyxoviridae Infections/*pathology/virology[MESH] |Pandemics[MESH]Inducible nitric oxide contributes to viral pathogenesis following hig(epmc).pdf DeepDyve Pubget Overpricing