Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1165/rcmb.2012-0462OC http://scihub22266oqcxt.onion/10.1165/rcmb.2012-0462OC C5459549!5459549!23848293     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 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Respir+Cell+Mol+Biol 2013 ; 49 (6): 1029-37 Nephropedia Template TP {{tp|p=23848293|t=2013. Pulmonary Antifibrotic Mechanisms Aspirin-Triggered Lipoxin A4 Synthetic Analog |pdf=|usr=}}{{23848293}} gab.com Text Pulmonary Antifibrotic Mechanisms Aspirin-Triggered Lipoxin A4 Synthetic Analog JO: Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=23848293 #FOAvip No successful therapies are available for pulmonary fibrosis, indicating the need for new treatments. Lipoxins and their 15-epimers, aspirin-triggered lipoxins (ATL), present potent antiinflammatory and proresolution effects (Martins et al., J Immunol 2009;182:5374?5381). We show that ATLa, an ATL synthetic analog, therapeutically reversed a well-established pulmonary fibrotic process induced by bleomycin (BLM) in mice. We investigated the mechanisms involved in its effect and found that systemic treatment with ATLa 1 week after BLM instillation considerably reversed the inflammatory response, total collagen and collagen type 1 deposition, vascular endothelial growth factor, and transforming growth factor (TGF)-? expression in the lung and restored surfactant protein C expression levels. ATLa also inhibited BLM-induced apoptosis and cellular accumulation in bronchoalveolar lavage fluid and in the lung parenchyma as evaluated by light microscopy and flow cytometry (Ly6G+, F4/80+, CD11c+, CD4+, and B220+ cells) assays. Moreover, ATLa inhibited the lung production of IL-1?, IL-17, TNF-?, and TGF-? induced by BLM-challenged mice. ATLa restored the balance of inducible nitric oxide synthase?positive and arginase-positive cells in the lungs, suggesting a prevalence of M2 versus M1 macrophages. Together, these effects improved pulmonary mechanics because ATLa treatment brought to normal levels lung resistance and elastance, which were clearly altered at 7 days after BLM challenge. Our findings support ATLa as a promising therapeutic agent to treat lung fibrosis. Twit Text FOAVip Pulmonary Antifibrotic Mechanisms Aspirin-Triggered Lipoxin A4 Synthetic Analog ????Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=23848293 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23848293 #FOAvip English Wikipedia <ref>{{Cite pmid|23848293}}</ref> Pulmonary Antifibrotic Mechanisms Aspirin-Triggered Lipoxin A4 Synthetic Analog #MMPMID23848293 Guilherme RF; Xisto DG; Kunkel SL; Freire-de-Lima CG; Rocco PR; Neves JS; Fierro IM; Canetti C; Benjamim CF Am J Respir Cell Mol Biol 2013[Dec]; 49 (6): 1029-37 PMID23848293show ga No successful therapies are available for pulmonary fibrosis, indicating the need for new treatments. Lipoxins and their 15-epimers, aspirin-triggered lipoxins (ATL), present potent antiinflammatory and proresolution effects (Martins et al., J Immunol 2009;182:5374?5381). We show that ATLa, an ATL synthetic analog, therapeutically reversed a well-established pulmonary fibrotic process induced by bleomycin (BLM) in mice. We investigated the mechanisms involved in its effect and found that systemic treatment with ATLa 1 week after BLM instillation considerably reversed the inflammatory response, total collagen and collagen type 1 deposition, vascular endothelial growth factor, and transforming growth factor (TGF)-? expression in the lung and restored surfactant protein C expression levels. ATLa also inhibited BLM-induced apoptosis and cellular accumulation in bronchoalveolar lavage fluid and in the lung parenchyma as evaluated by light microscopy and flow cytometry (Ly6G+, F4/80+, CD11c+, CD4+, and B220+ cells) assays. Moreover, ATLa inhibited the lung production of IL-1?, IL-17, TNF-?, and TGF-? induced by BLM-challenged mice. ATLa restored the balance of inducible nitric oxide synthase?positive and arginase-positive cells in the lungs, suggesting a prevalence of M2 versus M1 macrophages. Together, these effects improved pulmonary mechanics because ATLa treatment brought to normal levels lung resistance and elastance, which were clearly altered at 7 days after BLM challenge. Our findings support ATLa as a promising therapeutic agent to treat lung fibrosis. äPulmonary Antifibrotic Mechanisms Aspirin-Triggered Lipoxin A4 Synthet(epmc).pdf DeepDyve Pubget Overpricing