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10.1513/AnnalsATS.201502-082OC http://scihub22266oqcxt.onion/10.1513/AnnalsATS.201502-082OC C5467092!5467092!26230374     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 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 (9): 1302-9 Nephropedia Template TP {{tp|p=26230374|t=2015. Airway Inflammation after Bronchial Thermoplasty for Severe Asthma |pdf=|usr=}}{{26230374}} gab.com Text Airway Inflammation after Bronchial Thermoplasty for Severe Asthma JO: Ann Am Thorac Soc http://www.kidney.de/pget.php?&tw=1&pmid=26230374 #FOAvip Rationale: Bronchial thermoplasty is an alternative treatment for patients with severe, uncontrolled asthma in which the airway smooth muscle is eliminated using radioablation. Although this emerging therapy shows promising outcomes, little is known about its effects on airway inflammation.Objectives: We examined the presence of bronchoalveolar lavage cytokines and expression of smooth muscle actin in patients with severe asthma before and in the weeks after bronchial thermoplasty.Methods: Endobronchial biopsies and bronchoalveolar lavage samples from 11 patients with severe asthma were collected from the right lower lobe before and 3 and 6 weeks after initial bronchial thermoplasty. Samples were analyzed for cell proportions and cytokine concentrations in bronchoalveolar lavage and for the presence of ?-SMA in endobronchial biopsies.Measurements and Main Results: ?-SMA expression was decreased in endobronchial biopsies of 7 of 11 subjects by Week 6. In bronchoalveolar lavage fluid, both transforming growth factor-?1 and regulated upon activation, normal T-cell expressed and secreted (RANTES)/CCL5 were substantially decreased 3 and 6 weeks post bronchial thermoplasty in all patients. The cytokine tumor-necrosis-factor?related apoptosis-inducing ligand (TRAIL), which induces apoptosis in several cell types, was increased in concentration both 3 and 6 weeks post bronchial thermoplasty.Conclusions: Clinical improvement and reduction in ?-SMA after bronchial thermoplasty in severe, uncontrolled asthma is associated with substantial changes in key mediators of inflammation. These data confirm the substantial elimination of airway smooth muscle post thermoplasty in the human asthmatic airway and represent the first characterization of significant changes in airway inflammation in the first weeks after thermoplasty. Twit Text FOAVip Airway Inflammation after Bronchial Thermoplasty for Severe Asthma ????Ann Am Thorac Soc http://www.kidney.de/pget.php?&tw=1&pmid=26230374 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26230374 #FOAvip English Wikipedia <ref>{{Cite pmid|26230374}}</ref> Airway Inflammation after Bronchial Thermoplasty for Severe Asthma #MMPMID26230374 Denner DR; Doeing DC; Hogarth DK; Dugan K; Naureckas ET; White SR Ann Am Thorac Soc 2015[Sep]; 12 (9): 1302-9 PMID26230374show ga Rationale: Bronchial thermoplasty is an alternative treatment for patients with severe, uncontrolled asthma in which the airway smooth muscle is eliminated using radioablation. Although this emerging therapy shows promising outcomes, little is known about its effects on airway inflammation.Objectives: We examined the presence of bronchoalveolar lavage cytokines and expression of smooth muscle actin in patients with severe asthma before and in the weeks after bronchial thermoplasty.Methods: Endobronchial biopsies and bronchoalveolar lavage samples from 11 patients with severe asthma were collected from the right lower lobe before and 3 and 6 weeks after initial bronchial thermoplasty. Samples were analyzed for cell proportions and cytokine concentrations in bronchoalveolar lavage and for the presence of ?-SMA in endobronchial biopsies.Measurements and Main Results: ?-SMA expression was decreased in endobronchial biopsies of 7 of 11 subjects by Week 6. In bronchoalveolar lavage fluid, both transforming growth factor-?1 and regulated upon activation, normal T-cell expressed and secreted (RANTES)/CCL5 were substantially decreased 3 and 6 weeks post bronchial thermoplasty in all patients. The cytokine tumor-necrosis-factor?related apoptosis-inducing ligand (TRAIL), which induces apoptosis in several cell types, was increased in concentration both 3 and 6 weeks post bronchial thermoplasty.Conclusions: Clinical improvement and reduction in ?-SMA after bronchial thermoplasty in severe, uncontrolled asthma is associated with substantial changes in key mediators of inflammation. These data confirm the substantial elimination of airway smooth muscle post thermoplasty in the human asthmatic airway and represent the first characterization of significant changes in airway inflammation in the first weeks after thermoplasty. äAirway Inflammation after Bronchial Thermoplasty for Severe Asthma (epmc).pdf DeepDyve Pubget Overpricing