Within the next few weeks, the National Institute for Health and Care Excellence (NICE) is expected to release guidance recommending the use of nitric oxide breath tests to help diagnose and manage asthma.
This study compares the effect of heliox-driven to that of air-driven bronchodilator therapy on the pulmonary function test (PFT) in patients with different levels of asthma severity.
METHODS: One-hundred thirty-two participants were included in the study. Participants underwent spirometry twice with bronchodilator testing on two consecutive days. Air-driven nebulization was used one day and heliox-driven nebulization the other day in random order crossover design. After a baseline PFT, each participant received 2.5 mg of albuterol sulfate nebulized with the randomized driving gas. Post bronchodilator PFT was repeated after 30 min. The next day, the exact same protocol was repeated, except that the other driving gas was used to nebulize the drug. Participants were subgrouped and analyzed according to their baseline FEV1 on day 1: Group I, FEV1 ≥80 %; Group II, 80 % > FEV1 > 50 %; Group III, FEV1 ≤50 %. The proportion of participants with greater than 12 % and 200-mL increases from their baseline FEV1 and the changes from baseline in PFT variables were compared between heliox-driven versus air-driven bronchodilation therapy.
RESULTS: The proportion of participants with >12 % and 200-mL increases from their baseline FEV1 with air- or heliox-driven bronchodilation was not different with respect to the proportion of participants with baseline FEV1 ≥80 % (20 vs. 18 %, respectively) and 80 % > FEV1 > 50 % (36 vs. 43 %, respectively), but it was significantly greater with heliox-driven bronchodilation in participants with FEV1 ≤50 % (43 vs. 73 %, respectively; p = 0.01). Changes from baseline FVC, FEV1, FEV1/FVC, FEF25-75 %, FEFmax, FEF25 %, FEF50 %, and FEF75 % were significantly larger with heliox-driven versus air-driven bronchodilation in participants with baseline FEV1 ≤50 %.
CONCLUSION: Improvements in PFT variables are more frequent and profound with heliox-driven compared to air-driven bronchodilator therapy only in asthmatic patients with baseline FEV1 ≤50 %.
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Idiopathic Pulmonary Fibrosis (IPF) is a chronic, progressive, and high lethality fibrotic lung disease characterized by excessive fibroblasts proliferation and extracellular matrix accumulation and, ultimately, loss of lung function. Although dysregulation of some miRNAs has been shown to play important roles in the pathophysiological processes of IPF, the role of miRNAs in fibrotic lung diseases is not well understood.
In this study, we found the downregulation of miR-26a in the lungs of mice with experimental pulmonary fibrosis and in IPF, which resulted in post-transcriptional derepression of CTGF, and induced collagen production. More importantly, inhibition of miR-26a in the lungs caused pulmonary fibrosis in vivo, whereas over-expression of miR-26a repressed TGF-ß1-induced fibrogenesis in MRC-5 cells and attenuated experimental pulmonary fibrosis in mice. Our study showed that miR-26a was downregulated by TGF-ß1-mediated phosphorylation of Smad3. Moreover, miR-26a inhibited the nuclear translocation of p-Smad3 through directly targeting Smad4 which determines the nuclear translocation of p-Smad2/Smad3.
Taken together, our experiments demonstrated the anti-fibrotic effects for miR-26a in fibrotic lung diseases and suggested a new strategy for the prevention and treatment of IPF using miR-26a.
The present study also uncovered a novel positive feedback loop between miR-26a and p-Smad3, which is involved in pulmonary fibrosis.Molecular Therapy (2014); doi:10.1038/mt.2014.42.
DNA-based microbiological studies are moving beyond studying healthy human microbiota to investigate diverse infectious diseases, including chronic respiratory infections such as those in the airways of people with cystic fibrosis (CF) and non-CF bronchiectasis (BE).
The species identified in the respiratory secretion microbiota from such patients can be classified into those that are common and abundant among similar subjects (core) versus those that are infrequent and rare (satellite).
This categorization provides a vital foundation for investigating disease pathogenesis and improving therapy. However, whether the core microbiota of people with different respiratory diseases, which are traditionally associated with specific culturable pathogens, are unique or shared with other chronic infections of the lower airways is not well studied. Little is also known about how these chronic infection microbiota change from childhood into adulthood. Objectives: We sought to compare the core microbiota in respiratory specimens from children and adults with different chronic lung infections.
Methods: We used bacterial 16S rRNA gene pyrosequencing, phylogenetic analysis, and ecological statistical tools to compare the core microbiota in respiratory samples from three cohorts of symptomatic children with clinically distinct airway diseases (protracted bacterial bronchitis, BE, CF), and from four healthy children. We then compared the core pediatric respiratory microbiota with those in samples from adults with BE and CF. Measurements and Main
Results: All three pediatric disease cohorts shared strikingly similar core respiratory microbiota that differed from adult CF and BE microbiota. The most common species in pediatric disease cohort samples were also detected in those from healthy children. The adult CF and BE microbiota also differed from each other, suggesting common early infection airway microbiota that diverge by adulthood. The shared core pediatric microbiota included both traditional pathogens and many species not routinely identified by standard culture.
Conclusions: Our results indicate that these clinically distinct chronic airway infections share common early core microbiota, which are likely shaped by natural aspiration and impaired clearance of the same airway microbes, but that disease-specific characteristics select for divergent microbiota by adulthood. Longitudinal and interventional studies will be required to define the relationships between microbiota, treatments, and disease progression.
Chronic obstructive pulmonary disease (COPD) is a common chronic inflammatory disease of the lung with a high mortality and morbidity rate. Some of the inflammatory markers such as C-reactive protein (CRP), leukocyte count are associated with COPD.
In this study, we aimed to evaluate the role of neutrophil-to-lymphocyte ratio (NLR) in COPD patients comparing with the other well-known inflammatory markers.
We retrospectively enrolled the laboratory results of 269 COPD patients of which 178 patients at stable period and 91 patients during acute exacerbation and 50 sex- and age- matched healthy controls.
We found that NLR values of the stable COPD patients were significantly higher than those of the controls (P < 0.001). During acute exacerbation of the disease there was a further increase compared to stable period (P < 0.001). NLR values were also positively correlated with serum CRP levels and red cell distribution width (RDW) and negatively correlated with mean platelet volume (MPV) in both COPD groups.
In conclusion, NLR could be considered as a new inflammatory marker for assessment of inflammation in COPD patients with its quick, cheap, easily measurable property with routine complete blood count analysis.