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10.1152/ajplung.00283.2015 http://scihub22266oqcxt.onion/10.1152/ajplung.00283.2015 C4652148!4652148!26408556     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       Am+J+Physiol+Lung+Cell+Mol+Physiol 2015 ; 309 (10): L1041-6 Nephropedia Template TP {{tp|p=26408556|t=2015. Influenza lung injury: mechanisms and therapeutic opportunities |pdf=|usr=}}{{26408556}} gab.com Text Influenza lung injury: mechanisms and therapeutic opportunities JO: Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26408556 #FOAvip In this Perspectives, we discuss some recent developments in the pathogenesis of acute lung injury following influenza infection, with an emphasis on promising therapeutic leads. Damage to the alveolar-capillary barrier has been quantified in mice, and agents have been identified that can help to preserve barrier integrity, such as vasculotide, angiopoietin-like 4 neutralization, and sphingosine 1-phosphate mimics. Results from studies using mesenchymal stem cells have been disappointing, despite promising data in other types of lung injury. The roles of fatty acid binding protein 5, prostaglandin E2, and the interplay between IFN-? and STAT1 in epithelial signaling during infection have been addressed in vitro. Finally, we discuss the role of autophagy in inflammatory cytokine production and the viral life cycle and the opportunities this presents for intervention. Twit Text FOAVip Influenza lung injury: mechanisms and therapeutic opportunities ????Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26408556 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26408556 #FOAvip English Wikipedia <ref>{{Cite pmid|26408556}}</ref> Influenza lung injury: mechanisms and therapeutic opportunities #MMPMID26408556 Gregory DJ; Kobzik L Am J Physiol Lung Cell Mol Physiol 2015[Nov]; 309 (10): L1041-6 PMID26408556show ga In this Perspectives, we discuss some recent developments in the pathogenesis of acute lung injury following influenza infection, with an emphasis on promising therapeutic leads. Damage to the alveolar-capillary barrier has been quantified in mice, and agents have been identified that can help to preserve barrier integrity, such as vasculotide, angiopoietin-like 4 neutralization, and sphingosine 1-phosphate mimics. Results from studies using mesenchymal stem cells have been disappointing, despite promising data in other types of lung injury. The roles of fatty acid binding protein 5, prostaglandin E2, and the interplay between IFN-? and STAT1 in epithelial signaling during infection have been addressed in vitro. Finally, we discuss the role of autophagy in inflammatory cytokine production and the viral life cycle and the opportunities this presents for intervention. äInfluenza lung injury: mechanisms and therapeutic opportunities (epmc).pdf DeepDyve Pubget Overpricing