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10.1513/AnnalsATS.201502-088AW http://scihub22266oqcxt.onion/10.1513/AnnalsATS.201502-088AW C4722834!4722834!26595738     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Ann+Am+Thorac+Soc 2015 ; 12 (Suppl 2): S186-92 Nephropedia Template TP {{tp|p=26595738|t=2015. Viruses in Idiopathic Pulmonary Fibrosis Etiology and Exacerbation |pdf=|usr=}}{{26595738}} gab.com Text Viruses in Idiopathic Pulmonary Fibrosis Etiology and Exacerbation JO: Ann Am Thorac Soc http://www.kidney.de/pget.php?&tw=1&pmid=26595738 #FOAvip Viral infections are important contributors to exacerbation of asthma and chronic obstructive pulmonary disease; however, the role of viruses in the pathogenesis of idiopathic pulmonary fibrosis (IPF) is less clear. This likely reflects that fact that IPF acute exacerbations are defined clinically as ?noninfectious,? and little attention has been paid to the outcomes of patients with IPF with diagnosed infections. However, accumulating evidence suggests that infections (both bacterial and viral) may influence disease outcomes either as exacerbating agents or initiators of disease. Support for a viral role in disease initiation comes from studies demonstrating the presence of herpesviral DNA and epithelial cell stress in the lungs of asymptomatic relatives at risk for developing familial IPF. In addition, the number of studies that can associate viral (especially herpesviral) signatures in the lung with the development of IPF is steadily growing, and activated leukocyte signatures in patients with IPF provide further support for infectious processes driving IPF progression. Animal modeling has been used to better understand how a gamma herpesvirus infection can modulate the pathogenesis of lung fibrosis and has demonstrated that preceding infections appear to reprogram lung epithelial cells during latency to produce profibrotic factors, making the lung more susceptible to subsequent fibrotic insult, whereas exacerbations of existing fibrosis, or infections in susceptible hosts, involve active viral replication and are influenced by antiviral therapy. In addition, there is new evidence that bacterial burden in the lungs of patients with IPF may predict a poor prognosis. Twit Text FOAVip Viruses in Idiopathic Pulmonary Fibrosis Etiology and Exacerbation ????Ann Am Thorac Soc http://www.kidney.de/pget.php?&tw=1&pmid=26595738 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26595738 #FOAvip English Wikipedia <ref>{{Cite pmid|26595738}}</ref> Viruses in Idiopathic Pulmonary Fibrosis Etiology and Exacerbation #MMPMID26595738 Moore BB; Moore TA Ann Am Thorac Soc 2015[Nov]; 12 (Suppl 2): S186-92 PMID26595738show ga Viral infections are important contributors to exacerbation of asthma and chronic obstructive pulmonary disease; however, the role of viruses in the pathogenesis of idiopathic pulmonary fibrosis (IPF) is less clear. This likely reflects that fact that IPF acute exacerbations are defined clinically as ?noninfectious,? and little attention has been paid to the outcomes of patients with IPF with diagnosed infections. However, accumulating evidence suggests that infections (both bacterial and viral) may influence disease outcomes either as exacerbating agents or initiators of disease. Support for a viral role in disease initiation comes from studies demonstrating the presence of herpesviral DNA and epithelial cell stress in the lungs of asymptomatic relatives at risk for developing familial IPF. In addition, the number of studies that can associate viral (especially herpesviral) signatures in the lung with the development of IPF is steadily growing, and activated leukocyte signatures in patients with IPF provide further support for infectious processes driving IPF progression. Animal modeling has been used to better understand how a gamma herpesvirus infection can modulate the pathogenesis of lung fibrosis and has demonstrated that preceding infections appear to reprogram lung epithelial cells during latency to produce profibrotic factors, making the lung more susceptible to subsequent fibrotic insult, whereas exacerbations of existing fibrosis, or infections in susceptible hosts, involve active viral replication and are influenced by antiviral therapy. In addition, there is new evidence that bacterial burden in the lungs of patients with IPF may predict a poor prognosis. äViruses in Idiopathic Pulmonary Fibrosis Etiology and Exacerbation (epmc).pdf DeepDyve Pubget Overpricing