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.

The current outbreak of coronavirus disease 2019 (COVID-19) has affected people around the world. Typically, COVID-19 originates in the lung, but lately it can extend to other organs and lead to tissue injury and multiorgan failure in severe patients, such as acute respiratory distress syndrome (ARDS), kidney failure and sepsis or systemic inflammation. Given that COVID-19 has been detected in a range of other organs, the COVID-19-associated disease is an alert of aberrant activation of host immune response which drives un-controlled inflammation that affects multiple organs. Complement is a vital component of innate immunity where it forms the first line of defense against potentially harmful microbes, but its role in COVID-19 is still not clear. Notably, the abnormal activation and continuous deposits of complement components were identified in the pre-clinical samples from COVID-19 patients, which have been confirmed in animal models. Recent evidence has revealed that the administration of complement inhibitors leads to relieve inflammatory response in ARDS. Hence, we speculate that the targeting complement system could be a potential treatment option for organ damage in COVID-19 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.

Severe neutrophilic asthma is often characterized by persistent airway inflammation and irreversible airway remodeling, which are overstimulated by the high-mobility group box protein 1 (HMGB1). Although wogonin, an O-methylated flavone, has been widely used to treat inflammatory and allergic diseases, its therapeutic effects and potential mechanisms on severe neutrophilic asthma remain elusive. To evaluate whether wogonin alleviates airway neutrophilia through inducing neutrophil apoptosis and attenuates airway smooth muscle cells (ASMCs) proliferation and migration. The effect of wogonin on reducing neutrophilic airway inflammation, including neutrophil infiltration and inflammatory mediators, was examined in a mouse model of severe neutrophilic asthma sensitized with ovalbumin and lipopolysaccharide. Also, the effect of wogonin on inducing human neutrophil apoptosis was manifested using cellular morphology, flow cytometry, and caspase inhibition assays. Furthermore, the effect of wogonin on inhibiting HMGB1-mediated ASMCs proliferation and migration was determined. Wogonin reduced the frequency of neutrophils and inhibited the production of multiple inflammatory mediators, including ovalbumin-specific IgE, tumor necrosis factor-α, interleukin-6, and HMGB1, in bronchoalveolar lavage fluid and lung tissues of the neutrophilic asthmatic mouse model. These data strongly support a significantly suppressed neutrophilic airway inflammation, functionally consistent to the relieved airway hyperresponsiveness by wogonin in vivo. Wogonin induced human neutrophil apoptosis in a dose-dependent manner by activating caspase-8 and caspase-3 in vitro. Wogonin pretreatment abolished HMGB1-induced ASMCs proliferation and migration, which can be explained by the inhibition of phosphorylation in the mitogen-activated protein kinase (MAPK) /Akt singling pathways. Our findings demonstrate that wogonin augments caspase-dependent apoptosis in neutrophils to alleviate neutrophilic inflammatory responses and regulates intracellular signaling to inhibit HMGB1-mediated ASMCs activation, providing a promising therapeutic agent for severe neutrophilic asthma.

Background: Lung cancer is one of the most prevalent cancers and the leading cause of cancer-related deaths worldwide; non-small cell lung cancer (NSCLC) comprises approximately 80% of all lung cancer cases. This study aimed to construct a competing endogenous RNA (ceRNA) network and identify prognostic signatures in elderly patients with NSCLC. Methods: We extracted data from elderly patients with NSCLC from The Cancer Genome Atlas and identified differentially expressed (DE) messenger RNAs (mRNAs), microRNAs (miRNAs), and long non-coding RNAs (lncRNAs). Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses were performed to investigate the functions of DEmRNAs. The interactions between RNAs were predicted using starBase, TargetScan, miRTarBase, and miRanda. Cytoscape version 3.0 was used to construct and visualize the lncRNA-miRNA-mRNA ceRNA network. The association between the expression levels of DERNAs in the constructed ceRNA network and overall survival was determined using the survival package in R software. Furthermore, another Gene Expression Omnibus cohort was studied to externally validate the ceRNA network. Results: In total, 2865 DEmRNAs, 62 DEmiRNAs, and 131 DElncRNAs were identified. Dysregulated mRNAs are enriched in cancer-related processes and pathways. A ceRNA network was constructed using 38 miRNAs, 61 lncRNAs, and 164 mRNAs. Of these, 3 lncRNAs, 3 miRNAs, and 16 mRNAs were closely related to overall survival. The MIR99AHG-hsa-miR-31-5p-PRKCE axis has been identified as a potential ceRNA network involved in the development of NSCLC in elderly individuals. External validation of the MIR99AHG-hsa-miR-31-5p-PRKCE axis in the GSE19804 cohort showed that PRKCE was downregulated and that MIR99AHG was upregulated in the tumor tissues of elderly patients with NSCLC compared with normal lung tissues. Conclusions: This study provides novel insights into the lncRNA-miRNA-mRNA ceRNA network and reveals potential biomarkers for the diagnosis and prognosis of elderly patients with NSCLC.