Pyroptosis and inflammation are involved in the development of chronic obstructive pulmonary disease (COPD). However, the cigarette smoke-mediated mechanism of COPD remains unclear. In this study, we aimed to investigate the role of nucleotide-binding domain-like receptor protein-3 (NLRP3) inflammasome-mediated pyroptosis in the death of human bronchial epithelial (HBE) cells after cigarette smoke extract (CSE) exposure. The protein level of NLRP3 in lung tissue was measured after cigarette smoke exposure in vivo. In vitro, HBE cells were treated with CSE. Subsequently, the activity of caspase-1, lactate dehydrogenase (LDH) release, release of interleukin (IL)-1β and NLRP3 expression levels were measured. The involvement of reactive oxygen species (ROS) was also explored. After exposure to CSE, increased release of LDH, the transcriptional and translational upregulation of NLRP3, the caspase-1 activity levels, and enhanced IL-1β and IL-18 release were observed in 16HBE cells. In addition, NLRP3 was required to activate the caspase-1. Our results suggested that pre-stimulated of 16HBE with a caspase-1 inhibitor, or using NLRP3 siRNA to silence NLRP3 expression, also caused the decrease of IL-1β release and pyroptosis. CSE induced inflammation and contributed to pyroptosis through the ROS/NLRP3/caspase-1 pathway in 16HBE cells. The NLRP3 inflammasome participates in CSE-induced HBE cell damage and pyroptosis, which could provide new insights into COPD.

CONTEXT: Attention-deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental disorder in childhood. Exploring the risk factors for ADHD is helpful in preventing ADHD. OBJECTIVE: To explore the association between maternal smoking during pregnancy and the occurrence of ADHD in offspring. DATA SOURCES: PubMed, Embase, and Cochrane Library were searched from inception to May 2017 for studies. STUDY SELECTION: Cohort or case-control studies in which the association between maternal smoking and ADHD in offspring were investigated were eligible if they included odds ratios (ORs), hazard ratios, or risk ratios and 95% confidence intervals (CIs). DATA EXTRACTION: Two investigators independently extracted data on definition of exposure and outcome, number of cases and total sample population, and potential confounders adjusted. Any dose-relationship data for smoking and ADHD risk were also extracted. RESULTS: Fifteen cohort studies and 5 case-control studies with 50 044 cases and 2 998 059 participants were included. Smoking during pregnancy increased the risk of offspring ADHD (OR: 1.60; 95% CI: 1.45–1.76). The risk of ADHD was greater for children whose mothers were heavy smokers (OR: 1.75; 95% CI: 1.51–2.02) than for those mothers were light smokers (OR: 1.54; 95% CI: 1.40–1.70). LIMITATIONS: The limitations of our study included different assessment tools of ADHD and a lack of objective biological measures for maternal smoking. CONCLUSIONS: With our meta-analysis, we provide evidence for an association between maternal smoking and offspring ADHD but do not solve the causality issues concerning potential confounding by other risk factors. More high-quality studies are needed to establish whether the association with smoking is causal.

The etiology of non-genetic intellectual disability (ID) is not fully known, and we aimed to identify the prenatal, perinatal and neonatal risk factors for ID. PubMed and Embase databases were searched for studies that examined the association between pre-, peri- and neonatal factors and ID risk (keywords “intellectual disability” or “mental retardation” or “ID” or “MR” in combination with “prenatal” or “pregnancy” or “obstetric” or “perinatal” or “neonatal”. The last search was updated on September 15, 2015. Summary effect estimates (pooled odds ratios) were calculated for each risk factor using random effects models, with tests for heterogeneity and publication bias. Seventeen studies with 55,344 patients and 5,723,749 control individuals were eligible for inclusion in our analysis, and 16 potential risk factors were analyzed. Ten prenatal factors (advanced maternal age, maternal black race, low maternal education, third or more parity, maternal alcohol use, maternal tobacco use, maternal diabetes, maternal hypertension, maternal epilepsy and maternal asthma), one perinatal factor (preterm birth) and two neonatal factors (male sex and low birth weight) were significantly associated with increased risk of ID. This systemic review and meta-analysis provides a comprehensive evidence-based assessment of the risk factors for ID. Future studies are encouraged to focus on perinatal and neonatal risk factors and the combined effects of multiple factors.

Obesity, overweight and autism spectrum disorder (ASD) remain serious public health problems. Although lots of studies have recently explored the association among obesity, overweight and ASD, the findings are inconsistent. Thus, we conducted a meta-analysis of epidemiological studies to examine the association among obesity, overweight and ASD. PubMed, Embase, and the Cochrane Library were used for literature searches to identify eligible studies published in English before November 15, 2016. Relevant studies estimating the association among obesity, overweight and ASD were included. Fifteen studies encompassing 49,937,078 participants and 1,045,538 individuals with ASD were included in this study. A random effects model was chosen to synthesize the effect sizes of individual studies. The prevalence of obesity was significantly higher in individuals with ASD than in controls (OR = 1.84, 95% confidence interval [CI]: 1.37–2.48, P < 0.001). However, the prevalence of overweight in individuals with ASD was not significantly different from that in controls (OR = 1.07, 95% CI: 0.83–1.38, P = 0.62). Both sensitivity analysis and publication bias testing revealed that the findings were robust. The meta-analysis showed a significant association between obesity and ASD. However, no significant association was identified between overweight and ASD.

Objective To summarise current evidence evaluating the effects of human milk on the risk of bronchopulmonary dysplasia (BPD) in preterm infants. Design We searched for studies on human milk and BPD in English and Chinese databases on 26 July 2017. Furthermore, the references of included studies were also screened. The inclusion criteria in this meta-analysis were the following: (1) preterm infants (<37 weeks); (2) human milk; (3) comparing with formula feeding; (4) the outcome included BPD; and (5) the type of study was randomised controlled trial (RCT) or cohort study. Result A total of 17 cohort studies and 5 RCTs involving 8661 preterm infants met our inclusion criteria. The ORs and 95% CIs of six groups were as follows: 0.78 (0.68 to 0.88) for exclusive human milk versus exclusive formula group, 0.77 (0.68 to 0.87) for exclusive human milk versus mainly formula group, 0.76 (0.68 to 0.87) for exclusive human milk versus any formula group, 0.78 (0.68 to 0.88) for mainly human milk versus exclusive formula group, 0.83 (0.69 to 0.99) for mainly human milk versus mainly formula group and 0.82 (0.73 to 0.93) for any human milk versus exclusive formula group. Notably, subgroup of RCT alone showed a trend towards protective effect of human milk on BPD but no statistical significance. Conclusion Both exclusive human milk feeding and partial human milk feeding appear to be associated with lower risk of BPD in preterm infants. The quality of evidence is low. Therefore, more RCTs of this topic are needed.