Aim of Study: Four hundred million people live at high altitude worldwide. Prevalence and risk factors for COPD in these populations are poorly documented. We examined the prevalence and risk factors for COPD in residents living at an altitude of 2,100–4,700 m.Methods: We performed a cross-sectional survey in Xinjiang and Tibet autonomous region. A multistage stratified sampling procedure was used to select a representative population aged 15 years or older from eight high altitude regions. All participants underwent pre- and post-bronchodilator measurement of forced expiratory volumes. COPD was diagnosed according to 2019 Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria.Results: Between June, 2015 and August 2016, 4,967 subjects were included. Median age was 38.0 years (range: 15–91 years; inter-quartile range: 28–49 years); 51.4% participants were female. Overall prevalence of spirometry-defined COPD was 8.2% (95% CI 7.4–8.9%): 9.3% in male (95% CI 8.2–10.4%), and 7.1% in female (95% CI 6.1–8.2%). By multivariable logistic regression analysis, COPD was significantly associated with being aged ≥40 years (odds ratio: 2.25 [95% CI 1.72–2.95], P < 0.0001), exposure to household air pollution (OR: 1.34 [95% CI 1.01–1.79], P = 0.043), and a history of tuberculosis (OR: 1.79 [95% CI 1.23–2.61], P = 0.030), while living at a higher altitude (OR: 0.45 [95% CI 0.33–0.61], P < 0.0001) and having a higher educational level (OR: 0.64 [95% CI 0.43–0.95], P = 0.025) were associated with a lower prevalence of COPD.Conclusions: Our results show that the spirometry-defined COPD is a considerable health problem for residents living at high altitudes and COPD prevalence was inversely correlated with altitude. Preventing exposure to household air pollution and reducing the incidence of tuberculosis should be public health priorities for high altitude residents.

Background Studies report high in-hospital mortality of acute exacerbation of chronic obstructive pulmonary disease (AECOPD) especially for those requiring admission to an intensive care unit. Recognizing factors associated with mortality in these patients could reduce health care costs and improve end-of-life care. Methods This retrospective study included AECOPD patients admitted to the respiratory intensive care unit of a tertiary hospital in Beijing from Jan 1, 2011 to Dec 31, 2018. Patients demographic characteristics, blood test results and comorbidities were extracted from the electronic medical record system and compared between survivors and non-survivors. Results We finally enrolled 384 AECOPD patients: 44 (11.5%) patients died in hospital and 340 (88.5%) were discharged. The most common comorbidity was respiratory failure (294 (76.6%)), followed by hypertension (214 (55.7%)), coronary heart disease (115 (29.9%)) and chronic heart failure (76 (19.8%)). Multiple logistic regression analysis revealed that independent risk factors associated with in-hospital mortality included lymphocytopenia, leukopenia, chronic heart failure and requirement for invasive mechanical ventilation. Conclusions The in-hospital mortality of patients with acute COPD exacerbation requiring RICU admission is high. Lymphocytes < 0.8 × 109/L, leukopenia, requirement for invasive mechanical ventilation, and chronic heart failure were identified as risk factors associated with increased mortality rates.

ObjectivesPulmonary function impairment and chronic respiratory symptoms after tuberculosis are relatively common in low-income and middle-income countries. We aimed to estimate the impact of post-tuberculosis (post-TB) on pulmonary function.MethodsThis large cross-sectional, population-based study included subjects aged 15 years or older with technically acceptable postbronchodilator spirometry measurements. Post-TB was diagnosed on the basis of radiological evidence and/or medical history. Airflow obstruction was defined as a postbronchodilator forced expiratory volume in 1 s/forced vital capacity ratio below the lower limit of normal of Global Lung Function Initiative (GLI) lung function equations. Small airway dysfunction was diagnosed if at least two of the following indicators were less than 65% of predicted: maximal mid-expiratory flow, forced expiratory flow (FEF) 50% or FEF 75%.ResultsIn this population sample (N=8680, mean age: 40.1 years), 610 (7.0% (95% CI 6.5 to 7.6) participants were post-TB. Post-TB subjects had more frequent respiratory symptoms (46.8% vs 28.3%). Among post-TB subjects, 130 (21.3% (95% CI 18.1 to 24.8)) had airflow obstruction; OR of airflow obstruction was significantly associated with post-TB after adjustment for other confounding factors (OR 1.31, 95% CI 1.05 to 1.62). Post-TB was also associated with small airway dysfunction (OR 1.28, 95% CI1.07 to 1.53), which was present in 297 (48.9% (95% CI 33.9 to 53.0)) post-TB subjects.ConclusionsOur findings support existing knowledge that post-TB is positively associated with pulmonary function impairment and make for frequent respiratory symptoms. Post-TB should be considered as a potentially important cause of airflow obstruction and respiratory symptoms in patients originating from countries with a high burden of tuberculosis.

Aims/IntroductionAdiponectin has been proposed to have an essential role in the regulation of insulin sensitivity and metabolism, but previous studies on levels of adiponectin in prediabetes remain inconsistent. The present study aimed to assess the differences of adiponectin levels between prediabetes patients and healthy controls by carrying out a meta-analysis.Materials and MethodsWe carried out a systematic literature search of PubMed, EMBASE, and other databases for case–control studies and cohort studies measuring adiponectin levels in serum or plasma from prediabetes patients and healthy controls. The pooled weighted mean difference (WMD) and 95% confidence interval (CI) were used to estimate the association between adiponectin levels and prediabetes.ResultsThree cohort studies and 15 case–control studies with a total of 41,841 participants were included in the meta-analysis. The results showed that circulating adiponectin levels in prediabetes patients were significantly lower than that of healthy controls (WMD –1.694 μg/mL; 95% CI –2.151, –1.237; P < 0.001). Subgroup analysis showed more significant differences between prediabetes patients and healthy controls when the ratio of the homeostatic model assessment of insulin resistance was >2.12 (WMD −2.95 μg/mL; 95% CI –4.103, –1.806; P < 0.001) and average age was >60 years (WMD −2.20 μg/mL; 95% CI –3.207, –1.201; P < 0.001). Additionally, WMD in adiponectin showed a trend of direct correlation in subgroups of homeostatic model assessment of insulin resistance ratio, body mass index and age.ConclusionsThe present meta-analysis supports adiponectin levels in prediabetes patients being lower than that of healthy controls,indicating that the level of circulating adiponectin decreases before the onset of diabetes.

Background: Chronic obstructive pulmonary disease (COPD) is a public health challenge globally. The burden of COPD is high in never-smokers but little is known about its causes. We aimed to find the prevalence and correlates of COPD in never-smokers, with a special focus on solid fuel exposure.Methods: We conducted a cross-sectional study in Western China. COPD was defined by FEV1/FVC &lt; lower limits of normal (LLN). Descriptive statistics and multivariable logistic regression were used for analyses.Results: Six thousand two hundred and seventy one patients were enrolled between June 2015 and August 2016. The prevalence of COPD in never-smokers was 15.0% (95% confidence interval 14.1–15.9). The common independent predictors of COPD in never-smokers included age ≥60 years, exposure to solid fuel, living in a rural area and a history of tuberculosis. Participants with solid fuel exposure were 69% more likely to have COPD (adjusted odds ratio 1.69, 95% CI 1.41–2.04) than those without such exposure. In addition, we found a positive association between small airway dysfunction and solid fuel exposure (OR 1.35, 95% CI 1.18–1.53).Conclusions: This study confirmed the substantial burden of COPD among never-smokers and also defined the risk factors for COPD in never-smokers. Furthermore, we found a positive association between solid fuel exposure and COPD or small airway dysfunction.

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Tetrandrine (Tet), a traditional Chinese herbal medicine extract, exhibits anti‐cancer effect on many types of cancer. Nonetheless, the action mechanism of Tet in gastric cancer (GC) is still largely unclear. In the current study, proliferation, invasion, and migration of the BGC‐823 and MKN‐45 cells were effectively suppressed by Tet treatment in a dose‐dependent manner. Moreover, Tet suppressed expression of the proliferation‐associated protein PCNA, the interstitial cell phenotype N‐cadherin, and the extracellular matrix‐associated MMP‐2 and MMP‐9 in BGC‐823 and MKN‐45 cells in a dose‐dependent manner. PI3K/AKT/mTOR, a cancer promoting signaling, was inactivated by Tet in a dose‐dependent manner in BGC‐823 and MKN‐45 cells. Furthermore, our results demonstrated that the inhibition of Tet to PCNA, N‐cadherin, MMP‐2, and MMP‐9 expression was partly rescuedby AKT inhibitor or mTOR inhibitor. In animal experiments, tumor growth was inhibited by Tet administration in a dose‐dependent manner. In conclusion, the current data indicated that Tet had a critical effect on inhibiting BGC‐823 and MKN‐45 cells proliferation, migration, invasion, and tumor growth via regulating PI3K/AKT/mTOR signaling pathway, suggesting that Tet might be a potential treatment for GC.

Fungal hydrophobins have many important physiological functions, such as maintaining hydrophobicity and affecting virulence, growth, and development. In Ganoderma lucidum, the molecular regulation mechanisms of hydrophobins in mushroom are unclear. In this study, we investigated a hydrophobin protein 1 (Hyd1) in G. lucidum, which belongs to the fungal Class I hydrophobins. The hyd1 gene was highly expressed during the formation of primordia, and expression was the lowest in fruiting bodies. Through the construction of hyd1 silenced strains, we found that primordia formation was not initiated in these strains. This finding indicated that Hyd1 played an important role in the development of G. lucidum. Second, AreA, a key transcription factor in nitrogen metabolism, negatively regulated the expression of hyd1. In an areA silenced strain, the expression of hyd1 increased by approximately 14-fold compared with that of the wild-type (WT) strain. Electrophoretic mobility shift assays (EMSA) indicated binding of AreA to the promoter of hyd1. Additionally, expression of hyd1 was determined in the presence of different nitrogen sources. Compared with that in the ammonia nitrogen source, the expression of hyd1 in nitrate nitrogen source significantly increased. Finally, we found that hyd1 plays important roles not only in nitrogen regulation but also in the resistance to other abiotic stresses. After silencing of hyd1, the resistance to heat, cell wall, and salt stresses decreased. Our findings reveal the important roles of Hyd1 in the development and resistance to abiotic stresses in G. lucidum and provide insights into the nitrogen regulation mechanism of hydrophobins in higher basidiomycetes.