Purpose: The sit-to-stand test (STST) has been used to evaluate the exercise tolerance of patients with COPD. However, mutual comparisons to predict poor exercise tolerance have been hindered by the variety of STST modes used in previous studies, which also did not consider patients’ subjective perceptions of different STST modes. Our aim was to compare the five-repetition sit-to-stand test (5STS) with the 30-second sit-to-stand test (30STS) for predicting poor performance in the six-minute walking test and to evaluate patients’ subjective perceptions to determine the optimal mode for clinical practice. Patients and methods: Patients with stable COPD performed 5STS, 30STS and the 6MWT and then evaluated their feelings about the two STST modes by Borg dyspnea score and a questionnaire. Moreover, we collected data through the pulmonary function test, mMRC dyspnea score, COPD assessment test and quadriceps muscle strength (QMS). A receiver operating characteristic curve analysis of the 5STS and 30STS results was used to predict 6-minute walk distance (6MWD) <350 m. Results: The final analysis included 128 patients. Similar moderate correlations were observed between 6MWT and 5STS (r=-0.508, P<0.001) and between 6MWT and 30STS (r=0.528, P<0.001), and there were similar correlations between QMS and 5STS (r=-0.401, P<0.001) and between QMS and 30STS (r=0.398, P<0.001). The 5STS and 30STS score cutoffs produced sensitivity, specificity and positive and negative predictive values of 76.0%, 62.8%, 56.7% and 80.3% (5STS) and 62.0%, 75.0%, 62.0% and 75.0% (30STS), respectively, for predicting poor 6MWT performance. The 5STS exhibited obvious superiority in terms of the completion rate and the subjective feelings of the participants. Conclusion: As a primary screening test for predicting poor 6MWD, the 5STS is similar to the 30STS in terms of sensitivity and specificity, but the 5STS has a better patient experience.

Short-term exposures to air pollution are associated with acute effects on respiratory health. This study aimed to describe 10-year temporal trends in respiratory mortality in the urban areas of Shenyang, China, according to gender and age and estimate the effects of air pollution on respiratory diseases (ICD-10J00-J99) and lung cancer (ICD-10 C33-C34) using a case-crossover design. During the study period 2013–2015, the exposure-response relationship between ambient air pollutants and mortality data was fitted by a quasi-Poisson model. Age-standardized mortality rates for a combined number of respiratory diseases and for lung cancer declined in Shenyang; however, death counts increased with aging. Deaths from respiratory diseases increased by 4.7% (95% CI, 0.00–9.9), and lung cancer mortality increased by 6.5% (95% CI, 1.2–12.0), both associated with a 10 μg/m³ increase in exposure to particulate matter < 2.5 μg in diameter (PM2.5). Moreover, males in Shenyang’s urban areas were more susceptible to the acute effects of PM2.5 and SO₂ exposure; people aged ≥ 65 years had a high susceptibility to ozone, and those aged < 65 years were more susceptible to other air pollutants. These results provided an updated estimate of the short-term effects of air pollution in Shenyang. Since population aging is also associated with increasing mortality from respiratory diseases and lung cancer, reinforcing air quality control measures and health-promoting behaviors is urgent and necessary in Shenyang.

There has been conflicting evidence about possible associations between nonmalignant respiratory conditions (NMRCs) and subsequent risk of lung cancer. Determination of whether or not there is such an association has potential importance for managing NMRCs, for screening of lung cancer, and for understanding mechanisms of carcinogenesis. A hospital-based, case-control study involving interviews with 226 female nonsmoking lung cancer patients and 279 matching population controls was conducted in Shenyang, Northeast China, between January 2004 and December 2007. A standardized interview collected information on a variety of potential risk factors, including a history of physician-diagnosed NMRCs (pulmonary tuberculosis, chronic bronchitis, emphysema, asthma, and bronchiectasis), and age/year in which each condition was first diagnosed. Multivariate logistic regression analyses were applied to assess the associations between NMRCs and subsequent lung cancer risk. Compared with those without, subjects with a history of NMRC experience greater risk of lung cancer (OR=2.0, 95% CI 1.2-3.4), particularly following a diagnosis of pulmonary tuberculosis (OR=4.7, 95% CI 1.6-13.2). The results from subgroup analysis, when limited to small cell lung cancer, showed a 6.2-fold increase in lung cancer risk among asthmatics (95% CI 1.5-25.8). However, there was no evidence of a significant association between chronic bronchitis and lung cancer. This study strengthens the evidence linking NMRCs, especially pulmonary tuberculosis, to lung cancer even in lifelong nonsmoking women.

Alcohol consumption significantly impacts disease burden and has been linked to various diseases in observational studies. However, comprehensive meta-analyses using Mendelian randomization (MR) to examine drinking patterns are limited. We aimed to evaluate the health risks of alcohol use by integrating findings from MR studies. A thorough search was conducted for MR studies focused on alcohol exposure. We utilized two sets of instrumental variables—alcohol consumption and problematic alcohol use—and summary statistics from the FinnGen consortium R9 release to perform de novo MR analyses. Our meta-analysis encompassed 64 published and 151 de novo MR analyses across 76 distinct primary outcomes. Results show that a genetic predisposition to alcohol consumption, independent of smoking, significantly correlates with a decreased risk of Parkinson’s disease, prostate hyperplasia, and rheumatoid arthritis. It was also associated with an increased risk of chronic pancreatitis, colorectal cancer, and head and neck cancers. Additionally, a genetic predisposition to problematic alcohol use is strongly associated with increased risks of alcoholic liver disease, cirrhosis, both acute and chronic pancreatitis, and pneumonia. Evidence from our MR study supports the notion that alcohol consumption and problematic alcohol use are causally associated with a range of diseases, predominantly by increasing the risk.

Background: Nonalcoholic fatty liver disease (NAFLD) increased the risk factor of hepatocellular carcinoma (HCC). NAFLD induces the hepatic-related cancer deaths mostly in middle-aged men. NAFLD enhanced the inflammatory reaction and oxidative stress in the hepatic tissue. Curcumae exhibited the anti-inflammatory and antioxidant effects. In this study, we made an attempt to scrutinize the protective effect of curcumae on obesity-induced HCC via alteration of inflammation, oxidative stress and gut microbiota. Methods: The rats used in this experiment were Wistar rats, 100 mg/kg intraperitoneal injection of diethylnitrosamine (hepatic carcinogen) was used at 2 weeks. After 6 weeks of the experimental study, the rats were randomly divided into high-fat diet (HFD) with or without curcumae-treated group rats and received the treatment for 22 weeks. Hepatic, non-hepatic, cardiac, antioxidant, pro-inflammatory and inflammatory were estimated at the end of the study. The stools of the experimental rats were collected for estimating the gut microbiota. Results: Curcumae-treated group rats exposed reduction of the hepatic nodules in hepatic tissue. Curcumae significantly (P< 0.001) diminished the level of hepatic parameters and antioxidant parameters in the serum. Curcumae significantly (P< 0.001) suppressed the pro-inflammatory cytokines level, viz. interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-2 (IL-2), interleukin-7 (IL-7) and augmented the level of interleukin-10 (IL-10) in the serum and hepatic tissue. Curcumae significantly (P< 0.001) suppressed inflammatory mediators including cyclooxygenase (COX-2), prostaglandin E2 (PGE2) and nuclear factor kappa B (NF-κB) in the serum and hepatic tissue. Furthermore, curcumae increased the gut microbial diversity and richness and decreased the relative abundance of genus Mucispirillum and Clostridium, respectively. Conclusion: Curcumae prevents HFD-induced inflammation during the hepatic carcinoma by modulating the oxidative stress, inflammatory reaction and gut microbiota.