Liuzijue is a traditional Qigong exercise that is commonly performed in China. However, the treatment effects of Liuzijue Qigong are controversial. The aim of this systematic review was to evaluate the efficacy of Liuzijue Qigong in patients with chronic obstructive pulmonary disease (COPD). Randomised controlled trials were identified by searching several English and Chinese databases from inception to August 8, 2020. Study selection and data extraction were independently performed by two investigators. Data synthesis and analysis were carried out with Review Manager software 5.2. Quality assessment for each study was based on the modified Jadad scale. Forty studies with 3137 participants were included. Significant improvements were observed in the following outcomes (mean difference, 95% confidence interval): forced expiratory volume in 1 s (0.17, 0.09-0.25) and its percent predicted normal value (6.04, 3.43-8.65), forced expiratory volume in 1 s to forced volume capacity ratio (6.95, 3.06-10.83), 6-min walking distance (33.06, 23.73-42.38), 30-s sit-to-stand test (2.65, 0.98-4.32), COPD assessment test score (- 2.04, - 2.77 to - 1.30), modified Medical Research Council dyspnea scale (- 0.34, - 0.48 to - 0.20), Medical Research Council dyspnea scale (- 0.37, - 0.57 to - 0.18), Traditional Chinese Medicine syndrome score (- 1.85, - 2.86 to - 0.85), Hamilton Anxiety Scale (- 2.31, - 3.04 to - 1.59), Hamilton Depression Scale (- 2.08, - 2.45 to - 1.71) and St. George's Respiratory Questionnaire (- 6.94, - 9.20 to - 4.67). Liuzijue Qigong may be an effective adjuvant therapy for the improvement of lung function, exercise capacity, health status, mental status and quality of life in patients with COPD.

Objectives Patients with pulmonary embolism (PE) have a higher red cell distribution width (RDW), which may complicate the interpretation of the prognosis of PE. We aim to evaluate the diagnostic utility of the RDW in patients with PE. Methods Eligible studies were identified by searching PubMed and EMBASE from inception to December 23, 2018. The data were pooled using Stata 12 to evaluate the prognostic value. The sources of heterogeneity were detected. Results For the analysis of prognosis, 7 studies with 2146 patients were included, with median RDW values ranging from 13.4% to 15.7% and a median cut-off point of 18.27%. A total of 247 patients (11.5% mortality) among the 2146 participants died. Overall, RDW was positively associated with the prognosis of PE in the overall analysis (HR = 1.19, 95% CI = 1.10-1.29,I-2 = 73.4%;P = 0.000). Subgroup analyses by study design, sex and follow-up time indicated that they were not sources of heterogeneity. Conclusions An elevated RDW has the potential to be a biomarker for prognosis in PE patients.

Objective: To determine the association of serum cardiac troponin (cTn) with the mortality of pulmonary hypertension (PH) patients via a meta‐analysis.Date Source: We searched PubMed and EMBASE from inception to October 25, 2017.Study Selection: The reference lists of the retrieved articles were also consulted. The Q test and I² test were used for to assess heterogeneity. The relationship between cTn elevation and mortality was analysed. Studies were stratified according to type of troponin (cTnT vs cTnI), region (Europe vs America) and follow‐up length (≤3 years vs >3 years).Results: Eight studies with 739 patients were included in the meta‐analysis. Cardiac troponin elevation ranged from 14.3% to 94.5%. Overall, 48.8% (39/80) of patients with elevated cTn died compared to 18.6% (45/242) of patients with normal cTn levels. These findings showed cTn elevation was significantly related to an increased mortality risk in PH patients [hazard ratio (HR) = 3.05, 95% confidence interval (95% CI) = 2.16‐4.32, I² = 24.9%]. cTnI was better at predicting mortality than cTnT (HR = 3.37, 95%CI = 2.05‐5.55 vs HR = 2.80, 95%CI = 1.97‐3.98, respectively). American populations had increased mortality compared to European populations (HR = 4.23, 95%CI = 2.29‐7.80 vs HR = 2.70, 95% CI = 1.95‐3.74, respectively). This finding was independent of the follow‐up length of the studies (≤3 years: HR = 2.36, 95%CI = 1.65‐3.38; >3 years: HR = 4.55, 95%CI = 2.80‐7.39).Conclusions: Although different studies detected the expression cTnT or cTnI by various methods, the mortality in the cTn‐positive group was higher than that in the cTn‐negative group. Serum cTn elevation emerged as an independent predictor of increased risk of mortality in PH patients.

Background: Airway neutrophilia has been associated with asthma severity and asthma exacerbations. This study attempted to identify biomarkers, pathogenesis, and therapeutic molecular targets for severe asthma in neutrophils using bioinformatics analysis. Methods: Fifteen healthy controls and 3 patients with neutrophilic severe asthma were screened from the Gene Expression Omnibus (GEO) database. Based on the analysis of differentially expressed genes (DEGs), functional and pathway enrichment analyses, gene set enrichment analysis, protein–protein interaction network construction, and analysis were performed. Moreover, small-molecule drug candidates have also been identified. Results: Three hundred and three upregulated and 59 downregulated genes were identified. Gene ontology function enrichment analyses were primarily related to inflammatory response, immune response, leukocyte migration, neutrophil chemotaxis, mitogen-activated protein kinase cascade, Jun N-terminal kinase cascade, I-kappaB kinase/nuclear factor-κB, and MyD88-dependent toll-like receptor signaling pathway. Pathway enrichment analyses and gene set enrichment analysis were mainly involved in cytokine-cytokine receptor interaction, the TNF signaling pathway, leukocyte transendothelial migration, and the NOD-like receptor signaling pathway. Furthermore, 1 important module and 10 hub genes (CXCL8, TLR2, CXCL1, ICAM1, CXCR4, FPR2, SELL, PTEN, TREM1, and LEP) were identified in the protein–protein interaction network. Moreover, indoprofen, mimosine, STOCK1N-35874, trapidil, iloprost, aminoglutethimide, ajmaline, levobunolol, ethionamide, cefaclor, dimenhydrinate, and bethanechol are potential drugs for the treatment of neutrophil-predominant severe asthma. Conclusion: This study identified potential biomarkers, pathogenesis, and therapeutic molecular targets for neutrophil-predominant severe asthma.