Background. Cardiac magnetic resonance imaging (CMR) is an effective technique for the diagnosis of cardiac sarcoidosis (CS). The efficacy of CMR versus the Japanese Ministry of Health and Welfare (JMHW) guidelines considered as standard criterion for the diagnosis of CS remains to be elucidated.Methods. In this systematic review and meta-analysis, we aimed at assessing the diagnostic accuracy of CMR in cardiac sarcoidosis. We searched on PubMed from January 1, 1980, to March 28, 2018, on Embase from January 1, 1980, to March 29, 2018, and on the Cochrane Library from January 1, 1980, to April 1, 2018, using a strategy based on the search terms (sarcoidosis and magnetic resonance imaging) independently. We analyzed the data obtained with Revman 5.3 and Stata 14.0 software.Results. Eight studies with a total of 649 participants met the inclusion criteria, and data were extracted. CMR had an overall sensitivity of 0.93 (95% confidence interval (CI), 0.87–0.97) and specificity of 0.85 (95% CI, 0.68–0.94) for the diagnosis of cardiac sarcoidosis. The area under the summary receiver operating characteristic (SROC) curve was 0.95 (95% CI, 0.93–0.97). The subgroup analysis via public year showed that studies between 2011 and 2017 had an overall sensitivity of 0.95 (95% CI, 0.88–0.98) and specificity of 0.92 (95% CI, 0.49–0.99), with an area under the SROC curve being 0.96.Conclusions. The results of this meta-analysis suggest that CMR could be used for the diagnosis of cardiac sarcoidosis and screening of patients suspected of CS. With the improvement of the technique, the diagnostic accuracy of MRI has improved.

Background: Soluble Epoxide Hydrolase (sEH) metabolizes anti-inflammatory epoxyeicosatrienoic acids and critically affects airway inflammation in chronic obstructive pulmonary disease (COPD). Considering the excessive endoplasmic reticulum stress is associated with the earlier onset of COPD. The role of sEH and endoplasmic reticulum stress in the pathogenesis of COPD remains unknown. Method: 16 weeks of cigarette-exposed mice were used to detect the relationship between sEH and endoplasmic reticulum stress in COPD. Human epithelial cells were used in vitro to determine the regulation mechanism of sEH in endoplasmic reticulum stress induced by cigarette smoke. Results: sEH deficiency helps reduce emphysema formation after smoke exposure by alleviating endoplasmic reticulum stress response. sEH deficiency effectively reverses the upregulation of phosphorylation IRE1α and JNK and the nuclear expression of AP-1, alleviating the secretion of inflammatory factors induced by cigarette smoke extract. Furthermore, the treatment with endoplasmic reticulum stress and IRE1α inhibitor downregulated cigarette smoke extract-induced sEH expression and the secretion of inflammatory factors. Conclusion: sEH probably alleviates airway inflammatory response and endoplasmic reticulum stress via the IRE1α/JNK/AP-1 pathway, which might attenuate lung injury caused by long-term smoking and provide a new pharmacological target for preventing and treating COPD.

Background: Increasing evidence has demonstrated that there was a strong correlation between COVID-19 and idiopathic pulmonary fibrosis (IPF). However, the studies are limited, and the real biological mechanisms behind the IPF progression were still uncleared.Methods: GSE70866 and GSE 157103 datasets were downloaded. The weight gene co-expression network analysis (WGCNA) algorithms were conducted to identify the most correlated gene module with COVID-19. Then the genes were extracted to construct a risk signature in IPF patients by performing Univariate and Lasso Cox Regression analysis. Univariate and Multivariate Cox Regression analyses were used to identify the independent value for predicting the prognosis of IPF patients. What’s more, the Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Ontology (GO), and gene set enrichment analysis (GSEA) were conducted to unveil the potential biological pathways. CIBERSORT algorithms were performed to calculate the correlation between the risk score and immune cells infiltrating levels.Results: Two hundred thirty three differentially expressed genes were calculated as the hub genes in COVID-19. Fourteen of these genes were identified as the prognostic differentially expressed genes in IPF. Three (MET, UCHL1, and IGF1) of the fourteen genes were chosen to construct the risk signature. The risk signature can greatly predict the prognosis of high-risk and low-risk groups based on the calculated risk score. The functional pathway enrichment analysis and immune infiltrating analysis showed that the risk signature may regulate the immune-related pathways and immune cells.Conclusion: We identified prognostic differentially expressed hub genes related to COVID-19 in IPF. A risk signature was constructed based on those genes and showed great value for predicting the prognosis in IPF patients. What’s more, three genes in the risk signature may be clinically valuable as potential targets for treating IPF patients and IPF patients with COVID-19.

Background: Ventilatory inefficiency contributes to exercise intolerance in chronic obstructive pulmonary disease (COPD). The intercept of the minute ventilation (V^̇ _E) vs. carbon dioxide output (V^̇ CO₂) plot is a key ventilatory inefficiency parameter. However, its relationships with lung hyperinflation (LH) and airflow limitation are not known. This study aimed to evaluate correlations between the V^̇ _E/V^̇ CO₂ intercept and LH and airflow limitation to determine its physiological interpretation as an index of functional impairment in COPD. Methods: We conducted a retrospective analysis of data from 53 COPD patients and 14 healthy controls who performed incremental cardiopulmonary exercise tests (CPETs) and resting pulmonary function assessment. Ventilatory inefficiency was represented by parameters reflecting the V^̇ _E/V^̇ CO₂ nadir and slope (linear region) and the intercept of V^̇ _E/V^̇ CO₂ plot. Their correlations with measures of LH and airflow limitation were evaluated. Results: Compared to control, the slope (30.58±3.62, P<0.001) and intercept (4.85±1.11 L/min, P<0.05) were higher in COPD_stages1-2, leading to a higher nadir (31.47±4.47, P<0.01). Despite an even higher intercept in COPD_stages3-4 (7.16±1.41, P<0.001), the slope diminished with disease progression (from 30.58±3.62 in COPD_stages1-2 to 26.84±4.96 in COPD_stages3-4, P<0.01). There was no difference in nadir among COPD groups and higher intercepts across all stages. The intercept was correlated with peak V^̇ _E/maximal voluntary ventilation (MVV) (r=0.489, P<0.001) and peak V^̇ O₂/Watt (r=0.354, P=0.003). The intercept was positively correlated with residual volume (RV) % predicted (r=0.571, P<0.001), RV/total lung capacity (TLC) (r=0.588, P<0.001), peak tidal volume (V_T)/FEV₁ (r=0.482, P<0.001) and negatively correlated with rest inspiratory capacity (IC)/TLC (r=−0.574, P<0.001), peak V_T/TLC (r=−0.585, P<0.001), airflow limitation forced expiratory volume in 1 s (FEV₁) % predicted (r=−0.606, P<0.001), and FEV₁/forced vital capacity (FVC) (r=−0.629, P<0.001). Conclusions: V^̇ _E/V^̇ CO₂ intercept was consistently correlated with worsening static and dynamic LH, pulmonary gas exchange, and airflow limitation in COPD. The V^̇ _E/V^̇ CO₂ intercept emerged as a useful index of ventilatory inefficiency in COPD patients.

Dynamic pulmonary hyperinflation and abnormal air exchange are the primary causes of the exercise limitation of chronic obstructive pulmonary disease (COPD) patients. During exercise, COPD sufferers’ lungs are dynamically hyperinflated. Increased inefficient ventilation reduces ventilation efficiency and causes a mismatch between ventilation volume and blood flow. The ventilatory equivalent for CO₂ (VeqCO₂) is a physiological parameter that can be measured using cardiopulmonary exercise testing. Therefore, the aim of this exploratory study was to perform cardiopulmonary exercise testing on people with COPD, investigate the impact of static pulmonary function on ventilation efficiency under the exercise state, and screen the predictive indicators of ventilation efficiency. Subject. The aim of this study was to look at the factors that influence the exercise ventilation efficiency of people with COPD. Method. A total of 76 people with COPD were recruited during the stable period. Age, gender, body height, body mass, and other basic information were recorded. The body mass index (BMI) was determined, and forced vital capacity (FVC), forced expiratory volume in one second (FEV1), residual volume/total lung capacity (RV/TLC), diffusing capacity of the lung for carbon monoxide (DLCO), and DLCO divided by the alveolar volume (DLCO/VA) were measured. The ventilatory equivalent for carbon dioxide (VE/VCO2) under the rest state (EqCO₂rest), anaerobic threshold (EqCO₂at), and maximum exercise state (EqCO₂ max) were calculated to investigate the influencing factors for ventilation efficiency of people with COPD. Results. FEV1% was negatively correlated with EqCO₂rest (r = −0.277, value <0.05); FEV1/FVC % was negatively correlated with EqCO2rest and EqCO2at (r = −0.311, −0.287, value <0.05); DLCO% was negatively correlated with EqCO₂rest, EqCO₂at, and EqCO₂max (r = −0.408, −0.462, and −0.285, value <0.05); DLCO/VA% was negatively correlated with EqCO₂rest, EqCO₂at, and EqCO₂max (r = −0.390, −0.392, and −0.245, value <0.05); RV/TLC was positively correlated with EqCO2rest and EqCO2at (r = 0.289, 0.258, -value <0.05). The prediction equation from the multivariable regression analysis equation was Y = 40.04–0.075X (Y = EqCO₂, X = DLCO/VA%). Conclusions. As the degree of ventilatory obstruction increased, the ventilation efficiency of the stable people with COPD under the exercise state showed a progressive decrease; the ventilation efficiency of the people with COPD decreased significantly under the maximum exercise state, and the ventilation capacity and diffusion capacity were the significant factors that affected the exercise ventilation efficiency. The diffusion function may predict the maximum ventilation efficiency and enable primary hospitals without exercise test equipment in developing countries to predict and screen patients at risk for current exercise based on limited information.

Background: Recent research has increasingly underscored a significant correlation between gut microbiota and obstructive sleep apnea (OSA). Probiotics have emerged as promising adjunctive interventions for OSA. Metabolites and their related biochemical pathways have emerged as important contributors to the development of OSA. This study aimed to estimate the causal association between gut microbiota and OSA and to quantify the mediating effects of metabolites. Methods: We employed two-step, two-sample Mendelian randomization techniques, utilizing single nucleotide polymorphisms as genetic instruments for exposures and mediators. Summary statistics were obtained from genome-wide association studies of gut microbiota (the Dutch Microbiome Project, n=7,738), plasma metabolites (the Canadian Longitudinal Study on Aging cohort, n=8,299), and OSA (FinnGen database, n=410,385). To ensure the robustness of our findings, sensitivity analyses and heterogeneity tests were systematically conducted. Results: In the Dutch Microbiome Project, species Parabacteroides merdae, genus Faecalibacterium, species Faecalibacterium prausnitzii and species Bifidobacterium longum demonstrated a potential protective association with OSA. We included the top 10 metabolites with potential biological significance as candidate mediators. Among them, only 2-hydroxypalmitate was associated with a reduced risk of OSA. 2-hydroxypalmitate partially mediated the association between species Parabacteroides merdae and OSA, with a mediation proportion of 20.53%. Conclusion: The study highlighted the protective effect of species Parabacteroides merdae against OSA. It also revealed the mediating role of 2-hydroxypalmitate in the relationship between species Parabacteroides merdae and OSA.