Objectives This study aims to examine whether changes in short-term exposures to particulate matter are associated with changes in lung function, breath rate, and blood pressure among healthy adults and whether smoking status modifies the association. Methods We took advantage of the artificially controlled changes in air pollution levels that occurred during the 2008 Olympic Games in Beijing, China and conducted a panel study of 201 Beijing residents. Data were collected before, during, and after the Olympics, respectively. Linear mixed-effects models and generalized estimating equation models were used to compare measurements of peak expiratory flow, breath rate, blood pressure across the three time points. Results The mean values of peak expiratory flow were 346.0 L/min, 399.3 L/min, and 364.1 L/min over the three study periods. Peak expiratory flow levels increased in 78% of the participants when comparing the during- and pre- Olympics time points, while peak expiratory flow levels decreased in 80% of participants for the post- and during-Olympic periods comparison. In subgroup analyses comparing the during -Olympic to pre-Olympic time points, we found a larger percentage change in peak expiratory flow (+17%) among female, younger and non-smoking participants than among male, elderly and smoking participants (+12%). The percentage of participants with a fast breath rate (>20/min) changed from 9.7%, to 4.9%, to 30.1% among females, and from 7.9%, to 2.6%, to 27.3% among males over the three time points respectively. The changes on blood pressure over the three study periods were not very clear, although there is an increase in diastolic pressure and a decrease in pulse pressure among males during the games. Conclusions The results suggest that exposure to different air pollution levels has significant effects on respiratory function. Smoking, age and gender appear to modify participants’ biological response to changes in air quality.

Non–small cell lung cancer (NSCLC) is the main type of lung malignancy. Early diagnosis and treatments for NSCLC are far from satisfactory due to the limited knowledge of the molecular mechanisms regarding NSCLC progression. Long noncoding RNA (lncRNA) ZNFX1 antisense RNA1 (ZFAS1) has been implicated for its functional role in the progression of malignant tumors. This study aimed to determine the ZFAS1 expression from lung cancer clinical samples and to explore the molecular mechanisms underlying ZFAS1‐modulated NSCLC progression. Experimental assays revealed that clinical samples and cell lines of lung malignant tumors showed an upregulation of ZFSA1. ZFAS1 expression was markedly upregulated in the lung tissues from patients with advanced stage of this malignancy. The loss‐of‐function assays showed that knockdown of ZFAS1‐suppressed NSCLC cell proliferative, as well as invasive potentials, increased NSCLC cell apoptotic rates in vitro and also attenuated tumor growth of NSCLC cells in the nude mice. Further experimental evidence showed that ZFAS1 inversely affected miR‐150‐5p expression and positively affected high‐mobility group AT‐hook 2 (HMGA2) expression in NSCLC cell lines. MiR‐150‐5p inhibition or HMGA2 overexpression counteracted the effects of ZFAS1 knockdown on NSCLC cell proliferative, invasive potentials and apoptotic rates. In light of examining the clinical lung cancer samples, miR‐150‐5p expression was downregulated and the HMGA2 expression was highly expressed in the lung cancer tissues compared with normal ones; the ZFAS1 expression showed a negative correlation with miR‐150‐5p expression but a positive correlation with HMGA2 expression in lung cancer tissues. To summarize, we, for the first time, demonstrated the inhibitory effects of ZFAS1 knockdown on NSCLC cell progression, and the results from mechanistic studies indicated that ZFAS1‐mediated NSCLC progression cells via targeting miR‐150‐5p/HMGA2 signaling.

BackgroundHelicobacter pylori (H. pylori) infection is the main cause of chronic gastritis and duodenal ulcer in children. Little is known about the effect of H. pylori on gastric microbiota in children with duodenal ulcer. This study is aimed at the characteristics of gastric microbiota in children with duodenal ulcer on H. pylori infection.MethodsWe studied 23 children diagnosed with duodenal ulcer by gastric endoscopy because of the gastrointestinal symptoms, 15 children were diagnosed with H. pylori infection, while 8 children were without H. pylori infection. Endoscopic mucosal biopsy samples were obtained for DNA extraction. Microbiomes were analyzed by 16S rRNA profiling and microbial functions were predicted using the software Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt).ResultsBacterial richness and diversity of gastric microbiota in duodenal ulcer with H. pylori-positive were lower than those negative. The gastric microbiota in H. pylori-positive group significantly reduced proportions of six phyla and fifteen genera; only Helicobacter taxa were more abundant in H. pylori-positive group. Co-expression network analysis showed a more complex network of interactions in the H. pylori-positive group than that in the H. pylori-negative group. For the predicted functions, lower abundance in the pathways of carbohydrate metabolism, signal transduction, amino acid metabolism, and lipid metabolism were found in H. pylori-positive group than the H. pylori-negative group. H. pylori colonization reduces a microbial community with genotoxic potential in the gastric mucosa of children with duodenal ulcer.ConclusionsThe presence of H. pylori significantly influences gastric microbiota and results in a lower abundance of multiple taxonomic levels in children with duodenal ulcer. Children with duodenal ulcer exhibit a dysbiotic microbial community with genotoxic potential, which is distinct from that of children with H. pylori infection.Clinical Trial Registration[http://www.chictr.org.cn], identifier [ChiCTR1800015190].

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Objective Bariatric surgery increases the risk of postoperative gallstone formation. Many studies have proposed ursodeoxycholic acid (UDCA) as a preventive agent for postoperative gallstone formation. This study aimed to investigate the effect of UDCA on gallstone formation after bariatric surgery in patients without preoperative gallstones. Methods PubMed, the Web of Science, the Cochrane Library, and EBSCO were searched for articles assessing the effect of UDCA on gallstone formation after bariatric surgery. The outcome was the incidence of postoperative gallstones. Odds ratios were used to assess dichotomous variables, and random‐effects models were used for statistical analyses. Results A total of 18 studies including 4,827 participants met the inclusion criteria. The statistical results showed that the incidence of gallstones in the UDCA group was significantly lower than in the control group. Furthermore, the occurrence of symptomatic gallstones and cholecystectomy was significantly reduced. Conclusions In patients without preoperative gallstones, UDCA can effectively prevent the formation of gallstones after bariatric surgery. In addition, UDCA can significantly reduce the occurrence of symptomatic gallstones and the risk of postoperative cholecystectomy. Doses of 500 to 600 mg/d can be used as a measure to prevent postoperative gallstone formation.