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10.1002/path.4638 http://scihub22266oqcxt.onion/10.1002/path.4638 C4789761!4789761!26383585     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26383585&cmd=llinks): Failed to open stream: HTTP request failed! 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Coinfected mice exhibited markedly more severe disease, shortened survival time and more severe lung pathology, including widespread thrombi. Transcriptional profiling revealed activation of coagulation only in coinfected mice, consistent with the extensive thrombogenesis observed. Immunohistochemistry showed extensive expression of tissue factor (F3) and prominent deposition of neutrophil elastase on endothelial and epithelial cells in coinfected mice. Lung sections of SP-positive 1918 autopsy cases showed extensive thrombi and prominent staining for F3 in alveolar macrophages, monocytes, neutrophils, endothelial and epithelial cells, in contrast to coinfection-positive 2009 pandemic H1N1 autopsy cases. This study reveals that a distinctive feature of 1918 influenza virus and SP coinfection in mice and humans is extensive expression of tissue factor and activation of the extrinsic coagulation pathway leading to widespread pulmonary thrombosis. Twit Text FOAVip 1918 pandemic influenza virus and Streptococcus pneumoniae coinfection results in activation of coagulation and widespread pulmonary thrombosis in mice and humans ????J Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26383585 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26383585 #FOAvip English Wikipedia <ref>{{Cite pmid|26383585}}</ref> 1918 pandemic influenza virus and Streptococcus pneumoniae coinfection results in activation of coagulation and widespread pulmonary thrombosis in mice and humans #MMPMID26383585 Walters KA; D'Agnillo F; Sheng ZM; Kindrachuk J; Schwartzman LM; Keustner RE; Chertow DS; Golding BT; Taubenberger JK; Kash JC J Pathol 2016[Jan]; 238 (1): 85-97 PMID26383585show ga To study bacterial coinfection following 1918 H1N1 influenza virus infection, mice were inoculated with the 1918 influenza virus followed by Streptococcus pneumoniae 72 h later. Coinfected mice exhibited markedly more severe disease, shortened survival time and more severe lung pathology, including widespread thrombi. Transcriptional profiling revealed activation of coagulation only in coinfected mice, consistent with the extensive thrombogenesis observed. Immunohistochemistry showed extensive expression of tissue factor (F3) and prominent deposition of neutrophil elastase on endothelial and epithelial cells in coinfected mice. Lung sections of SP-positive 1918 autopsy cases showed extensive thrombi and prominent staining for F3 in alveolar macrophages, monocytes, neutrophils, endothelial and epithelial cells, in contrast to coinfection-positive 2009 pandemic H1N1 autopsy cases. This study reveals that a distinctive feature of 1918 influenza virus and SP coinfection in mice and humans is extensive expression of tissue factor and activation of the extrinsic coagulation pathway leading to widespread pulmonary thrombosis. ä1918 pandemic influenza virus and Streptococcus pneumoniae coinfection(epmc).pdf DeepDyve Pubget Overpricing