Background and objectives Intradialytic hypoxemia has been recognized for decades, but its associations with outcomes have not yet been assessed in a large patient cohort.Design, setting, participants, & measurements Our retrospective cohort study was conducted between January of 2012 and January of 2015. We recorded blood oxygen saturation every minute during hemodialysis in patients with arteriovenous access. A 6-month baseline period with at least 10 treatments with oxygen saturation measurements preceded a 12-month follow-up. Patients were stratified by the presence or absence of prolonged intradialytic hypoxemia defined as oxygen saturation ,90% for at least one third of the treatment time. Demographic, laboratory, and treatment data and hospitalization and mortality rates were compared between the groups. Multivariate Cox regression analysis was used to assess baseline predictors of all-cause mortality during follow-up.Results In total, 100 (10%) of 983 patients had prolonged intradialytic hypoxemia. These patients were older (+3.6 years; 95% confidence interval, 0.8 to 6.3), had longer dialysis vintage (+1.2 years; 95% confidence interval, 0.3 to 2.1), and had higher prevalence of congestive heart failure (+10.8%; 95% confidence interval, 1.6 to 20.7) and chronic obstructive pulmonary disease (+13%; 95% confidence interval, 5 to 21.2). They also resembled an inflammatory phenotype, with lower serum albumin levels (20.1 g/dl; 95% confidence interval, 20.2 to 0) and higher neutrophil-to-lymphocyte ratios (+1; 95% confidence interval, 0.5 to 1.6). They had lower hemoglobin levels (20.2 g/dl; 95% confidence interval, 20.4 to 0) and required more erythropoietin (+1374 U per hemodialysis treatment; 95% confidence interval, 343 to 2405). During follow-up, all-cause hospitalization (1113 hospitalizations; univariate hazard ratio, 1.46; 95% confidence interval, 1.22 to 1.73) and mortality (89 deaths; adjusted hazard ratio, 1.98; 95% confidence interval, 1.14 to 3.43) were higher in patients with prolonged intradialytic hypoxemia.Conclusions Prolonged intradialytic hypoxemia was associated with laboratory indicators of inflammation, higher erythropoietin requirements, and higher all-cause hospitalization and mortality.

Background The effect of high-flow nasal cannula (HFNC) therapy in patients after planned extubation remains inconclusive. We aimed to perform a rigorous and comprehensive systematic meta-analysis to robustly quantify the benefits of HFNC for patients after planned extubation by investigating postextubation respiratory failure and other outcomes. Method We searched MEDLINE, EMBASE, Web of Science, and the Cochrane Library from inception to August 2018. Two researchers screened studies and collected the data independently. Randomized controlled trials (RCTs) and crossover studies were included. The main outcome was postextubation respiratory failure. Results Ten studies (seven RCTs and three crossover studies; HFNC group: 856 patients; Conventional oxygen therapy (COT) group: 852 patients) were included. Compared with COT, HFNC may significantly reduce postextubation respiratory failure (RR, 0.61; 95% CI, 0.41, 0.92; z = 2.38; P = 0.02) and respiratory rates (standardized mean differences (SMD), − 0.70; 95% CI, − 1.16, − 0.25; z = 3.03; P = 0.002) and increase PaO 2 (SMD, 0.30; 95% CI, 0.04, 0.56; z = 2.23; P = 0.03). There were no significant differences in reintubation rate, length of ICU and hospital stay, comfort score, PaCO 2 , mortality in ICU and hospital, and severe adverse events between HFNC and COT group. Conclusions Our meta-analysis demonstrated that compared with COT, HFNC may significantly reduce postextubation respiratory failure and respiratory rates, increase PaO 2 , and be safely administered in patients after planned extubation. Further large-scale, multicenter studies are needed to confirm our results. Electronic supplementary material The online version of this article (10.1186/s13054-019-2465-y) contains supplementary material, which is available to authorized users.

The in-plane optical anisotropies of a series of GaAs/Al x Ga 1Ϫx As single-quantum-well structures have been observed at room temperature by reflectance difference spectroscopy. The measured degree of polarization of the excitonic transitions is inversely proportional to the well width. Numerical calculations based on the envelope function approximation incorporating the effect of C 2v -interface symmetry have been performed to analyze the origin of the optical anisotropy. Good agreement with the experimental data is obtained when the optical anisotropy is attributed to anisotropic-interface structures. The fitted interface potential parameters are consistent with predicted values.

No abstract

The subepithelial fibrosis component of airway remodeling in asthma is mediated through induction of transforming growth factor-beta1 (TGF-beta1) expression with consequent activation of myofibroblasts to produce extracellular matrix proteins. The number of myofibroblasts is increased in the asthmatic airway and is significantly correlated with the thickness of lamina reticularis. However, much is still unknown regarding the origin of bronchial myofibroblasts. Emerging evidence suggests that myofibroblasts can derive from epithelial cells by an epithelial-to-mesenchymal transition (EMT). In this study we investigated whether TGF-beta1 could induce bronchial epithelial EMT in the human bronchial epithelial cell. Cultured human bronchial epithelial cells, 16HBE-14o, were stimulated with 10 ng/ml TGF-beta1. Morphologic changes were observed and stress fiber by actin reorganization was detected by indirect immunostaining. The expression of alpha-SMA (alpha-smooth muscle actin) and the epithelial cell marker E-cadherin were detected in those 16HBE-14o cells after TGF-beta1 stimulation for 72 h, using immunostaining and RT-PCR. The contents of collagen I were determined by radioimmunoassay, and the levels of endogenous TGF-beta1 were measured with ELISA. Human bronchial epithelial cells stimulated with TGF-beta1 were converted from a "cobblestone" epithelial structure into an elongated fibroblast-like shape. Incubation of human bronchial epithelial cells with TGF-beta1 induced de novo expression of alpha-SMA, increased formation of stress fiber by F-actin reorganization, and loss of epithelial marker E-cadherin. Moreover, a significant increase in the levels of collagen I and endogenous TGF-beta1 released from bronchial epithelial cells stimulated with TGF-beta1 were observed. These results suggested that human bronchial epithelial cells, under stimulation of TGF-beta1, underwent transdifferentiation into myofibroblasts.