The latest medical research on Respiratory Medicine

The research magnet gathers the latest research from around the web, based on your specialty area. Below you will find a sample of some of the most recent articles from reputable medical journals about respiratory medicine gathered by our medical AI research bot.

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Sputum transcriptomics implicates increased p38 signalling activity in severe asthma.

Respirology

Severe asthma is responsible for a disproportionate burden of illness and healthcare costs spent on asthma. This study analyses sputum transcriptomics to investigate the mechanisms and novel treatment targets of severe asthma.

Induced sputum samples were collected in a cross-sectional study from participants with severe asthma (n = 12, defined as per GINA criteria), non-severe uncontrolled (n = 21) and controlled asthma (n = 21) and healthy controls (n = 15). Sputum RNA was extracted and transcriptomic profiles were generated (Illumina HumanRef-8 V2) and analysed (GeneSpring). Sputum protein lysates were analysed for p38 activation in a validation study (n = 24 asthma, n = 8 healthy) by western blotting.

There were 2166 genes differentially expressed between the four groups. In severe asthma, the expression of 1875, 1308 and 563 genes was altered compared to healthy controls, controlled and uncontrolled asthma, respectively. Of the 1875 genes significantly different to healthy controls, 123 were >2-fold change from which four networks were identified. Thirty genes (>2-fold change) were significantly different in severe asthma compared to both controlled asthma and healthy controls. There was enrichment of genes in the p38 signalling pathway that were associated with severe asthma. Phosphorylation of p38 was increased in a subset of severe asthma samples, correlating with neutrophilic airway inflammation.

Severe asthma is associated with substantial differences in sputum gene expression that underlie unique cellular mechanisms. The p38 signalling pathway may be important in the pathogenesis of severe asthma, and future investigations into p38 inhibition are warranted as a 'non-Th2' therapeutic option.

MUC1 intracellular bioactivation mediates lung fibrosis.

Thorax

Serum KL6/mucin 1 (MUC1) has been identified as a potential biomarker in idiopathic pulmonary fibrosis (IPF), but the role of MUC1 intracellular bioactivation in IPF is unknown.

To characterise MUC1 intracellular bioactivation in IPF.

The expression and phosphorylation of Thr41 and Tyr46 on the intracellular MUC1-cytoplasmic tail (CT) was increased in patients with IPF (n=22) compared with healthy subjects (n=21) and localised to fibroblasts and hyperplastic alveolar type II cells. Transforming growth factor (TGF)-β1 phosphorylated SMAD3 and thereby increased the phosphorylation of MUC1-CT Thr41 and Tyr46 in lung fibroblasts and alveolar type II cells, activating β-catenin to form a phospho-Smad3/MUC1-CT and MUC1-CT/β-catenin nuclear complex. This nuclear complex promoted alveolar epithelial type II and fibroblast to myofibroblast transitions, as well as cell senescence and fibroblast proliferation. The inhibition of MUC1-CT nuclear translocation using the inhibitor, GO-201 or silencing MUC1 by siRNA, reduced myofibroblast transition, senescence and proliferation in vitro. Bleomycin-induced lung fibrosis was reduced in mice treated with GO-201 and in MUC1-knockout mice. The profibrotic lectin, galectin-3, directly activated MUC1-CT and served as a bridge between the TGF-β receptor and the MUC1-C domain, indicating TGF-β1-dependent and TGF-β1-independent intracellular bioactivation of MUC1.

MUC1 intracellular bioactivation is enhanced in IPF and promotes fibrotic processes that could represent potential druggable targets for IPF.

Prospective development of practical screening strategies for diagnosis of asthma-COPD overlap.

Respirology

ACO is a syndrome with high prevalence. However, a pragmatic diagnostic criterion to differentiate ACO is non-existent. We aimed to establish an effective model for screening ACO.

A multicentre survey was developed to assess the clinical criteria considered important and applicable by pulmonologists for screening ACO. These experts were asked to take the surveys twice. The expert grading method, analytic hierarchy process and ROC curve were used to establish the model, which was then validated by a cross-sectional study of 1066 patients. The GINA/GOLD document was the gold standard in assessing this model.

Increased variability of symptoms, paroxysmal wheezing, dyspnoea, historical diagnosis of COPD or asthma, allergic constitution, exposure to risk factors, the FEV1 /FVC < 70% and a positive BDT were important for screening ACO. According to the weight of each criterion, we confirmed that patients meeting six or more of these eight criteria should be considered to have ACO. We called this Chinese screening model for ACO 'CSMA'. It differentiated patients with ACO with a sensitivity of 83.33%, while the sensitivity of clinician-driven diagnosis had a sensitivity of only 42.73%.

CSMA is a workable model for screening ACO and provides a simple tool for clinicians to efficiently diagnose ACO.

Impact of newborn screening on outcomes and social inequalities in cystic fibrosis: a UK CF registry-based study.

Thorax

Newborn bloodspot screening (NBS) for cystic fibrosis (CF) was introduced across the UK in 2007 but the impact on clinical outcomes and health inequalities for children with CF is unclear.

We undertook longitudinal analyses of UK CF registry data on over 3000 children with CF born between 2000 and 2015. Clinical outcomes were the trajectories of percent predicted forced expiratory volume in one second (%FEV1) from age 5, weight for age and body mass index (BMI) SD-scores from age one, and time to chronic Pseudomonas aeruginosa (cPA) infection. Using mixed effects and time-to-event models we assessed the association of NBS with outcomes and potential interactions with childhood socioeconomic conditions, while adjusting for confounders.

NBS was associated with higher average lung function trajectory (+1.56 FEV1 percentage points 95% CI 0.1 to 3.02, n=2216), delayed onset of cPA, and higher average weight trajectory intercept at age one (+0.16 SD; 95% CI 0.07 to 0.26, n=3267) but negative rate of weight change thereafter (-0.02 SD per year; 95% CI -0.03 to -0.00). We found no significant association of NBS with BMI or rate of change of lung function. There was no clear evidence of an impact of NBS on health inequalities early in life.

Children diagnosed with CF by NBS in the UK have better lung function and increased early weight but NBS does not appear to have narrowed early health inequalities.

Analysis of fibroblast migration dynamics in idiopathic pulmonary fibrosis using image-based scaffolds of the lung extracellular matrix.

Am J Physiol

Idiopathic pulmonary fibrosis (IPF) is characterized by a profound remodeling of the collagen in the extracellular matrix (ECM), where the fibers b...

Tissue traction microscopy to quantify muscle contraction within precision-cut lung slices.

Am J Physiol

In asthma, acute bronchospasm is driven by contractile forces of airway smooth muscle (ASM). These forces can be imaged in the cultured ASM cell, o...

Indwelling Tunneled Pleural Catheters

ATS ICU

American Journal of Respiratory and Critical Care Medicine, Volume 200, Issue 11, Page P20-P21, December 1, 2019.

Reply to Bogaard et al.: Emphysema Is—at the Most—Only a Mild Phenotype in the Sugen/Hypoxia Rat Model of Pulmonary Arterial Hypertension

ATS ICU

American Journal of Respiratory and Critical Care Medicine, Volume 200, Issue 11, Page 1450-1452, December 1, 2019.

Emphysema Is—at the Most—Only a Mild Phenotype in the Sugen/Hypoxia Rat Model of Pulmonary Arterial Hypertension

ATS ICU

American Journal of Respiratory and Critical Care Medicine, Volume 200, Issue 11, Page 1447-1450, December 1, 2019.

Reply to Puxeddu et al.: CD71− Alveolar Macrophages in Idiopathic Pulmonary Fibrosis: A Look beyond the Borders of the Disease

ATS ICU

American Journal of Respiratory and Critical Care Medicine, Volume 200, Issue 11, Page 1446-1447, December 1, 2019.

CD71− Alveolar Macrophages in Idiopathic Pulmonary Fibrosis: A Look beyond the Borders of the Disease

ATS ICU

American Journal of Respiratory and Critical Care Medicine, Volume 200, Issue 11, Page 1444-1446, December 1, 2019.

Reply to Moy: Not All Home-based Exercise Programs Are Home-based Pulmonary Rehabilitation Programs

ATS ICU

American Journal of Respiratory and Critical Care Medicine, Volume 200, Issue 11, Page 1443-1444, December 1, 2019.