Critical COVID-19, Victivallaceae abundance, and celiac disease: A mediation Mendelian randomization study.

Celiac disease exhibits a higher prevalence among patients with coronavirus disease 2019. However, the potential influence of COVID-19 on celiac disease remains uncertain. Considering the significant association between gut microbiota alterations, COVID-19 and celiac disease, the two-step Mendelian randomization method was employed to investigate the genetic causality between COVID-19 and celiac disease, with gut microbiota as the potential mediators. We employed the genome-wide association study to select genetic instrumental variables associated with the exposure. Subsequently, these variables were utilized to evaluate the impact of COVID-19 on the risk of celiac disease and its potential influence on gut microbiota. Employing a two-step Mendelian randomization approach enabled the examination of potential causal relationships, encompassing: 1) the effects of COVID-19 infection, hospitalized COVID-19 and critical COVID-19 on the risk of celiac disease; 2) the influence of gut microbiota on celiac disease; and 3) the mediating impact of the gut microbiota between COVID-19 and the risk of celiac disease. Our findings revealed a significant association between critical COVID-19 and an elevated risk of celiac disease (inverse variance weighted [IVW]: P = 0.035). Furthermore, we observed an inverse correlation between critical COVID-19 and the abundance of Victivallaceae (IVW: P = 0.045). Notably, an increased Victivallaceae abundance exhibits a protective effect against the risk of celiac disease (IVW: P = 0.016). In conclusion, our analysis provides genetic evidence supporting the causal connection between critical COVID-19 and lower Victivallaceae abundance, thereby increasing the risk of celiac disease.

Low-dose polystyrene microplastics exposure impairs fertility in male mice with high-fat diet-induced obesity by affecting prostate function.

The harmful effects of microplastics (MPs) on male fertility are receiving more and more attention. However, the impact of low-dose MPs exposure on the reproductive function of male mice is still unclear. In this study, we exposed male mice to low-dose MPs (25-30 µg/kg body weight/day) or low-dose MPs combined with high-fat diet (HFD) feeding. Our results showed that low-dose MPs exposure or HFD feeding significantly reduced sperm quality and the number of offspring born, while low-dose MPs exposure combined with HFD feeding further enhanced the above effects. The combination of low-dose MPs exposure and HFD feeding resulted in a notable elevation of inflammatory level within the prostate of mice and induced apoptosis of prostate epithelium and a decrease in nutrients (zinc, citrate) in seminal plasma fluid. Our findings in this study could provide valuable clues for better understanding the influence of low-dose MPs exposure on the reproductive system under metabolic disorders and facilitate the development of the prevention of reproductive toxicity caused by MPs exposure.

Exosome-encapsulated lncRNA HOTAIRM1 contributes to PM2.5-aggravated COPD airway remodeling by enhancing myofibroblast differentiation.

Emphysema, myofibroblast accumulation and airway remodeling can occur in the lungs due to exposure to atmospheric pollution, especially fine particulate matter (PM2.5), leading to chronic obstructive pulmonary disease (COPD). Specifically, bronchial epithelium-fibroblast communication participates in airway remodeling, which results in COPD. An increasing number of studies are now being conducted on the role of exosome-mediated cell-cell communication in disease pathogenesis. Here, we investigated whether exosomes generated from bronchial epithelial cells could deliver information to normal stromal fibroblasts and provoke cellular responses, resulting in airway obstruction in COPD. We studied the mechanism of exosome-mediated intercellular communication between human bronchial epithelial (HBE) cells and primary lung fibroblasts (pLFs). We found that PM2.5-induced HBE-derived exosomes promoted myofibroblast differentiation in pLFs. Then, the exosomal lncRNA expression profiles derived from PM2.5-treated HBE cells and nontreated HBE cells were investigated using an Agilent Human LncRNA Array. Combining coculture assays and direct exosome treatment, we found that HBE cell-derived exosomal HOTAIRM1 facilitated the myofibroblast differentiation of pLFs. Surprisingly, we discovered that exosomal HOTAIRM1 enhanced pLF proliferation to secrete excessive collagen secretion, leading to airway obstruction by stimulating the TGF-ß/SMAD3 signaling pathway. Significantly, PM2.5 reduced FEV1/FVC and FEV1 and increased the level of serum exosomal HOTAIRM1 in healthy people; moreover, serum exosomal HOTAIRM1 was associated with PM2.5-related reductions in FEV1/FVC and FVC. These findings show that PM2.5 triggers alterations in exosome components and clarify that one of the paracrine mediators of myofibroblast differentiation is bronchial epithelial cell-derived HOTAIRM1, which has the potential to be an effective prevention and therapeutic target for PM2.5-induced COPD.

Single-cell RNA-seq analysis decodes the kidney microenvironment induced by polystyrene microplastics in mice receiving a high-fat diet.

In recent years, the environmental health issue of microplastics has aroused an increasingly significant concern. Some studies suggested that exposure to polystyrene microplastics (PS-MPs) may lead to renal inflammation and oxidative stress in animals. However, little is known about the essential effects of PS-MPs with high-fat diet (HFD) on renal development and microenvironment. In this study, we provided the single-cell transcriptomic landscape of the kidney microenvironment induced by PS-MPs and HFD in mouse models by unbiased single-cell RNA sequencing (scRNA-seq). The kidney injury cell atlases in mice were evaluated after continued PS-MPs exposure, or HFD treated for 35 days. Results showed that PS-MPs plus HFD treatment aggravated the kidney injury and profibrotic microenvironment, reshaping mouse kidney cellular components. First, we found that PS-MPs plus HFD treatment acted on extracellular matrix organization of renal epithelial cells, specifically the proximal and distal convoluted tubule cells, to inhibit renal development and induce ROS-driven carcinogenesis. Second, PS-MPs plus HFD treatment induced activated PI3K-Akt, MAPK, and IL-17 signaling pathways in endothelial cells. Besides, PS-MPs plus HFD treatment markedly increased the proportions of CD8+ effector T cells and proliferating T cells. Notably, mononuclear phagocytes exhibited substantial remodeling and enriched in oxidative phosphorylation and chemical carcinogenesis pathways after PS-MPs plus HFD treatment, typified by alterations tissue-resident M2-like PF4+ macrophages. Multispectral immunofluorescence and immunohistochemistry identified PF4+ macrophages in clear cell renal cell carcinoma (ccRCC) and adjacent normal tissues, indicating that activate PF4+ macrophages might regulate the profibrotic and pro-tumorigenic microenvironment after renal injury. In conclusion, this study first systematically revealed molecular variation of renal cells and immune cells in mice kidney microenvironment induced by PS-MPs and HFD with the scRNA-seq approach, which provided a molecular basis for decoding the effects of PS-MPs on genitourinary injury and understanding their potential profibrotic and carcinogenesis in mammals.

Single-cell transcriptome analysis of liver immune microenvironment changes induced by microplastics in mice with non-alcoholic fatty liver.

Recent studies have discovered that tiny particles of microplastics (MPs) at the nano-scale level can enter the body of organisms from the environment, potentially causing metabolic ailments. However, further investigation is required to understand the alterations in the immune microenvironment associated with non-alcoholic fatty liver disease (NAFLD) occurrence following exposure to MPs. Experiments were performed using mice, which were given a normal chow or high-fat diet (NCD or HFD, respectively) plus free drinking of sterile water with or without MPs, respectively. Employing an impartial technique known as unbiased single-cell RNA-sequencing (scRNA-seq), the cellular (single-cell) pathology landscape of NAFLD and related changes in the identified immune cell populations induced following MPs plus HFD treatment were assessed. The results showed that mice in the HFD groups had remarkably greater NAFLD activity scores than those from the NCD groups. Moreover, administration of MPs plus HFD further worsened the histopathological changes in the mice's liver, leading to hepatic steatosis, inflammatory cell infiltrations and ballooning degeneration. Following the construction of a sing-cell resolution transcriptomic atlas of 43,480 cells in the mice's livers of the indicated groups, clear cellular heterogeneity and potential cell-to-cell cross-talk could be observed. Specifically, we observed that MPs exacerbated the pro-inflammatory response and influenced the stemness of hepatocytes during HFD feeding. Importantly, treatment with MPs significantly increase the infiltration of the infiltrating liver-protecting Vsig4+ macrophages in the liver of the NAFLD mouse model while remarkably decreasing the angiogenic S100A6+ macrophage subpopulation. Furthermore, mice treated with MPs plus HFD exhibited significantly increased recruitment of CD4+ cells and heightened exhaustion of CD8+ T cells than those from the control group, characteristics typically associated with the dysregulation of immune homeostasis and severe inflammatory damage. Overall, this study offers valuable perspectives into comprehending the potential underlying cellular mechanisms and regulatory aspects of the microenvironment regarding MPs in the development of NAFLD.

Corilagin prevents non-alcoholic fatty liver disease via improving lipid metabolism and glucose homeostasis in high fat diet-fed mice.

Non-alcoholic fatty liver disease (NAFLD) has been considered to be one of the most common chronic liver diseases. However, no validated pharmacological therapies have been officially proved in clinic due to its complex pathogenesis. The purpose of this study was to examine the protective effects of Corilagin (referred to Cori) against NAFLD in mice under a high fat diet (HFD) condition. Mice were fed either a normal control diet (NCD) or HFD with or without Cori (5 or 10 mg/kg body weight) for 15 weeks. In our results, Cori treatment significantly attenuated HFD-induced hepatic steatosis, high NAFLD activity score (NAD) and liver injury. Consistently, Cori treatment remarkably alleviated HFD-induced hepatic lipid accumulation (e.g., triglycerides (TG) and total cholesterol (TC) contents in liver), and improved plasma lipid concentrations (e.g., plasma TG, TC, low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c)). Moreover, Cori treatment ameliorated NAFLD associated metabolic disorders such as glucose intolerance and insulin resistance in HFD-fed mice. Additionally, Cori treatment dramatically changed HFD-induced liver gene expression profiles, and identified overlapped differentially expressed genes (DEGs) between NCD vs. HFD group and HFD vs. HCR (high fat diet plus treatment with Cori) group. With these DEGs, we observed a marked enrichment of Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, which were closely associated with the metabolic balance in liver. Particularly, we found several potential hub proteins against NAFLD development with analyses of protein-protein interaction (PPI) network and qPCR assays. Collectively, our results revealed the important protective effects of Cori against the progress of NAFLD, which was probably mediated through improving dysregulated lipid metabolism and insulin resistance in HFD-fed mice. Additionally, Cori-dependent overlapped DEGs might serve as a featured NAFLD-associated gene expression signature for the diagnosis, treatment, as well as drug discovery and development of NAFLD in the near future.

Maternal Folic Acid Supplementation, Dietary Folate Intake, and Low Birth Weight: A Birth Cohort Study.

Objectives: To investigate the independent and collective effects of maternal folic acid supplementation or dietary folate intake on the risk of low birth weight (LBW), and to further comprehensively examine the joint associations of folic acid supplementation and dietary folate intake with LBW by various clinical subtypes. Design: Participants were recruited from Gansu Provincial Maternity and Child Care Hospital. A standardized and structured questionnaire was distributed to collect demographic factors, reproductive and medical history, occupational and residential history, physical activity, and diet. Data on pregnancy-related complications and birth outcomes were extracted from medical records. Unconditional logistic regression models were used to estimate the odds ratio (OR) and 95% confidence interval (95% CI) for single and joint associations of folic acid supplementation and dietary folate intake with LBW. Setting: A birth cohort data analysis using the 2010-2012 Gansu Provincial Maternity and Child Care Hospital in Lanzhou, China. Participants: In total, 9,231 pregnant women and their children were enrolled in the study. Results: Compared with non-users, folic acid supplementation was associated with a reduced risk of LBW (OR: 0.80, 95% CI: 0.66-0.97), and the reduced risk was mainly seen for term-LBW (OR: 0.59, 95% CI: 0.41-0.85), and multiparous-LBW (OR: 0.72, 95% CI: 0.54-0.94). There were no significant associations between dietary folate intake and LBW, and there was no interaction between folic acid supplement and dietary folate intake on LBW. Conclusions: Our study results indicated that folic acid supplementation was associated with a reduced risk of LBW, and there was no interaction between folic acid supplements and dietary folate intake on LBW.

The role of estrogen receptor ß in fine particulate matter (PM2.5) organic extract-induced pulmonary inflammation in female and male mice.

Fine particulate matter organic extract (Po) was reported to promote inflammation in the lung. Sex differences were reported in many inflammatory diseases. In this study, we investigated the effects of Po exposure on pulmonary inflammatory response and evaluated the role of sex in this process. While mice were exposed to 100 µg/m3 Po for 12 weeks by an inhalation exposure system, the lung histopathological analysis shown obvious inflammation, the cell numbers in bronchoalveolar lavage fluid (BALF) were significantly increased, and most inflammatory cytokines in BALF were upregulated. The results of factorial analysis of variance shown that there was an interaction between sex and Po exposure in the inflammatory cell numbers and the levels of tumor necrosis factor-α (TNF-α), interleukin-5 (IL-5), and growth-related oncogene/keratinocyte chemoattractant (GRO/KC). Notably, these changes and interactions were diminished while Po-exposed mice were administered with the estrogen receptor ß (ERß) antagonist. We speculated that sex might affect the levels of inflammatory indicators in BALF of Po-exposed mice and female mice were more prone to inflammation while exposed to Po. Moreover, ERß was involved in these processes. To our knowledge, this is the first investigation about the role of sex in Po-induced adverse effects.

The modifying effect of trait anxiety on the association of fine particulate matter with heart rate variability variables.

BACKGROUND: Previous studies have shown that exposures to ambient particulate matter with aerodynamic diameter <2.5 µm (PM2.5) and stress are associated with adverse cardiovascular health effects. OBJECTIVES: To investigate the potential modifying effect of trait anxiety on the association between short-term exposures to PM2.5 and HRV variables. METHODS: A panel of 92 middle-aged and elderly adults in Tianjin and Shanghai were recruited for repeated follow-ups with measurements of 24-h personal exposures to air pollutants and Holter ECG monitoring. Heart rate variability (HRV) variables calculated over 5-minute segments during the 24 h, including low frequency power (LF), high frequency power (HF), standard deviation of normal-to-normal intervals (SDNN) and root mean square of successive differences (rMSSD), were included in the analysis. The Trait Anxiety Inventory was used to investigate the long-term general anxiety level of the participants. Generalized linear mixed-effects model was used to analyze the association between exposure factors and HRV variables, and potential effect modification by trait anxiety. RESULTS: Data on 87 participants were included in final analysis after exclusions. Higher exposure to PM2.5 was associated with lower levels of LF, HF, SDNN and rMSSD, and the largest decreases in LF, HF, SDNN and rMSSD were found at 3-h moving average. Trait anxiety significantly modified the associations of PM2.5 with LF, HF, SDNN and rMSSD, with stronger inverse associations found in high trait anxiety group than in low trait anxiety group. For an IQR (27.3 µg/m³) increase in PM2.5 at 3-h moving average, there were decreases of 3.50% (95% CI: -4.46%, -2.54%) and 3.50% (95% CI: -4.49%, -2.50%) in the high trait anxiety group, and decreases of 0.81% (95% CI: -1.22%, -0.40%) and 0.65% (95% CI: -1.07%, -0.23%) in the low trait anxiety group in HF and rMSSD, respectively (both p for interaction<0.01). CONCLUSION: Our study suggests that trait anxiety could modify the association of short-term exposure to PM2.5 with HRV variables, indicating that higher trait anxiety may increase the cardiac susceptibility to air pollution in the study participants.

Ambient particulate air pollution, blood cell parameters, and effect modification by psychosocial stress: Findings from two studies in three major Chinese cities.

The associations between particulate matter (PM) exposure, psychosocial stress and blood cell parameters are bringing novel insights to characterize the early damage of multiple diseases. Based on two studies conducted in three Chinses cities using cross-sectional (Beijing, 425 participants) and panel study (Tianjin and Shanghai, 92 participants with 361 repeated measurements) designs, this study explored the associations between short-term exposure to ambient PM and blood cell parameters, and the effect modification by psychosocial stress. Increasing PM2.5 exposure was significantly associated with decreases in red blood cell (RBC) count and mean corpuscular hemoglobin concentration (MCHC), and increases in mean corpuscular volume (MCV), platelets count (PLT) and platelet hematocrit (PCT) in both studies. For instance, a 10 µg/m3 increment in PM2.5 concentration was associated with a 1.04% (95%CI: 0.16%, 1.92%) increase in PLT (4-d) and a 1.09% (95%CI: 0.31%, 1.87%) increase in PCT (4-d) in the cross-sectional study, and a 0.64% (95%CI: 0.06%, 1.22%) increase in PLT (1-d) and a 0.72% (95%CI: 0.33%, 1.11%) increase in PCT (1-d) in the panel study, respectively. In addition, stronger increases in MCV, PLT, and PCT associated with PM2.5 exposure were found in higher psychosocial stress group compared to lower psychosocial stress group (p for interaction <0.10), indicating that blood cell parameters of individuals with higher psychosocial stress might be more susceptible to the early damages of PM2.5 exposure.

Polystyrene microplastics induce hepatotoxicity and disrupt lipid metabolism in the liver organoids.

Microplastic particles (MP) has been detected in the environment widespread. Human beings are inevitably exposed to MP via multiple routines. However, the hazard identifications, as direct evidence of exposure and health risk, have not been fully characterized in human beings. Many studies suggest the liver is a potential target organ, but currently no study regarding the MP on human liver has been reported. In this study, we used a novel in vitro 3D model, the liver organoids (LOs) generated from human pluripotent stem cells, as an alternative model to the human liver, to explore the adverse biological effect of 1 µm polystyrene-MP (PS-MP) microbeads applying a non-static exposure approach. When the LOs were exposed to 0.25, 2.5 and 25 µg/mL PS-MP (the lowest one was relevant to the environmental concentrations, calculated to be 102 ± 7 items/mL). The potential mechanisms of PS-MP induced hepatotoxicity and lipotoxicity, in aspects of cytotoxicity, levels of key molecular markers, ATP production, alteration in lipid metabolism, ROS generation, oxidative stress and inflammation response, were determined. Specifically, it has been firstly observed that PS-MP could increase the expression of hepatic HNF4A and CYP2E1. Based on these findings, the potential adverse outcome pathways (AOPs) relevant to PS-MP were proposed, and the potential risks of PS-MP on liver steatosis, fibrosis and cancer were implicated. The combined application of novel LOs model and AOPs framework provides a new insight into the risk assessment of MP. Further studies are anticipated to validate the hepatotoxic molecular mechanism of PS-MP based on HNF4A or CYP2E1, and to investigate the MP-induced physical damage and its relationship to hepatic adverse effect for human beings. CAPSULE: Microplastics cause hepatotoxicity and disrupt lipid metabolism in the human pluripotent stem cells-derived liver organoids, providing evidence for human implication.

PM2.5 organic extract mediates inflammation through the ERß pathway to contribute to lung carcinogenesis in vitro and vivo.

An increasing number of researches have shown that fine particulate matter (PM2.5) is closely related to increased respiratory inflammation and can even lead to lung cancer. Estrogen receptor ß (ERß) has been demonstrated to be involved in several cancers. However, the exact role of ERß in PM2.5 organic extract (Po)-promoted inflammation and lung cancer remains unknown. The purpose of this study was to investigate whether ERß is involved in Po induced inflammation and lung cancer. In vitro, our results showed that interleukin-6 (IL-6) and ERß were simultaneously increased in lung bronchial epithelial cells exposed to Po; additionally, inhibition of ERß decreased IL-6 expression and secretion through inactivating ERK and AKT and further promoted cells malignant transformation. Moreover, we performed an animal model of inhalation exposure to Po using female C57BL/6 mice. Although we were unable to find tumor tissue in mice exposed to Po, we detected evidence of lung inflammation, epithelial-to-mesenchymal transition (EMT) phenotype and severe pulmonary injury; in addition, intraperitoneal injection of PHTPP (an ERß inhibitor) showed that the above phenomena have been improved, which demonstrate that Po stimulates IL-6 expression to promote inflammation, EMT phenotype and lung injury through the ERß pathway. In conclusion, our results confirmed the potential toxic effect of PM2.5, and increased our understanding of PM2.5 carcinogenic potential by exploring the mechanism of ERß regulating inflammation.

A novel lncRNA, loc107985872, promotes lung adenocarcinoma progression via the notch1 signaling pathway with exposure to traffic-originated PM2.5 organic extract.

PM2.5 pollution is an important and urgent problem in China that can increase mortality and hospital admissions. Traffic-originated PM2.5 organic component (tPo) mainly contains polycyclic aromatic hydrocarbons (PAHs). Research has shown that PAHs can promote invasion, metastasis, and cancer stem cell properties in lung adenocarcinoma cells, but the exact toxicological mechanism is unknown. In the present study, we investigated the effect of lncRNAs on the progression of lung adenocarcinoma induced by tPo and the underlying mechanisms mediated by lncRNA-signaling pathway interactions. We found that chronic tPo treatment upregulated the expression of loc107985872, which further promoted cell invasion and migration, EMT and cancer stem cell properties via notch1 pathway in lung adenocarcinoma cells. Meanwhile, activation of the notch1 signaling pathway through loc107985872 might be associated with abnormally high expression of its upstream proteins, such as ADAM17, PSEN1 and DLL1. Moreover, tPo exposure induced EMT and the acquisition of cancer stem cell-like properties via the notch1 signaling pathway in vivo. In summary, loc107985872 upregulated by tPo promoted lung adenocarcinoma progression via the notch1 signaling pathway.

Folic acid supplementation, dietary folate intake and risk of small for gestational age in China.

OBJECTIVE: To investigate the hypothesis that folic acid supplementation and dietary folate intake before conception and during pregnancy reduce the risk of small for gestational age (SGA) and to examine the joint effect of folic acid supplementation and dietary folate intake on the risk of SGA. DESIGN: Participants were interviewed by trained study interviewers using a standardized and structured questionnaire. Information on birth outcomes and maternal complications was abstracted from medical records and dietary information was collected via a semi-quantitative FFQ before conception and during pregnancy. SETTING: A birth cohort data analysis using the 2010-2012 Gansu Provincial Maternity and Child Care Hospital. PARTICIPANTS: Women (n 8758) and their children enrolled in the study. RESULTS: Folic acid supplementation was associated with a reduced risk of SGA (OR = 0·72, 95 % CI 0·60, 0·86), with the reduced risk seen mainly for SGA at ≥37 weeks of gestational age (OR = 0·70, 95 % CI 0·58, 0·85) and nulliparous SGA (OR = 0·67, 95 % CI 0·54, 0·84). There was no significant association between dietary folate intake and SGA risk. CONCLUSIONS: Our study suggested that folic acid supplementation was associated with a reduced risk of SGA and the risk varied by preterm status and parity.

LncRNA MALAT1, an lncRNA acting via the miR-204/ZEB1 pathway, mediates the EMT induced by organic extract of PM2.5 in lung bronchial epithelial cells.

Extensive cohort studies have explored the hazards of particulate matter with aerodynamic diameter 2.5 µm or smaller (PM2.5) to human respiratory health; however, the molecular mechanisms for PM2.5 carcinogenesis are poorly understood. Long non-coding RNAs (lncRNAs) are involved in various pathophysiological processes. In the present study, we investigated the effect of PM2.5 on the epithelial-mesenchymal transition (EMT) in lung bronchial epithelial cells and the underlying mechanisms mediated by an lncRNA. Organic extracts of PM2.5 from Shanghai were used to treat human bronchial epithelial cell lines (HBE and BEAS-2B). The PM2.5 organic extracts induced the EMT and cell transformation. High levels of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), mediated by NF-κB, were involved in the EMT process. For both cell lines, there was a similar response. In addition, MALAT1 interacted with miR-204 and reversed the inhibitory effect of its target gene, ZEB1, thereby contributing to the EMT and malignant transformation. In sum, these findings show that NF-κB transcriptionally regulates MALAT1, which, by binding with miR-204 and releasing ZEB1, promotes the EMT. These results offer an understanding of the regulatory network of the PM2.5-induced EMT that relates to the health risks associated with PM2.5.

The risk factors related to bruxism in children: A systematic review and meta-analysis.

OBJECTIVE: This systematic review was performed to determine the risk factors related to bruxism in children. DESIGN: This systematic review was conducted with reporting in agreement to the PRISMA statement and according to guidelines from the Cochrane Handbook for Systematic Reviews of Interventions. We conducted a systematic search of seven online databases, with the last search updated on 1st October 2016. The seven databases were Pubmed, Embase, Cochrane Library database, Web of Science, CNKI, CBM, and WF. The included trial type were RCT, cohort studies, and case-control studies, and bruxism symptoms were assessed by questionnaires and examinations. Eighteen out of the 5637 initially identified studies met the inclusion and exclusion criteria. RESULTS: gender, age, gene, mixed position, anxiety, the nervous, secondhand smoke, high psychological reactions, responsibility, move a lot during sleep, sleeps with mouth open, snores loudly, restless sleep, sleep hours, sleep with light on, noise in room, headache, biting, cheeks tonus, perioral musculature participation, conduct problems, peer problems, emotional symptoms, mental health problems, birth weight, occupation of family head, maternal marital status, hyperactivity, family income seemed to have statistical significance from the present systematic review and meta-analysis. CONCLUSIONS: The risk factors related to bruxism were as follows: Male, gene, mixed position, moves a lot, anxiety, the nervous, psychological reactions, responsibility, secondhand smoke, snore loudly, restless sleep, sleep with light on, noise in room, "sleep hours, ≤8h", headache, objects biting, conduct problems, peer problems, emotional symptoms and mental health problems.

What sleep behaviors are associated with bruxism in children? A systematic review and meta-analysis.

PURPOSE: The aim of this article was to assess the sleep behaviors that serve as risk factors related to bruxism in children ages 0 to 12 years by performing a systematic review and meta-analysis of published studies. METHODS: Seven databases were searched to identify all peer-reviewed articles potentially relevant to the review. Data were pooled for random-effects modeling. Sleep risk factors related to bruxism in this age group are summarized using pooled odds ratios (ORs), 95% confidence intervals (CIs), and P values. RESULTS: Of 5637 initially identified articles, 14 met inclusion criteria. Study qualities of all case-control studies were high. Quality of cross-sectional studies was more variable. The pooled ORs, 95% CIs, and P values were as follows: snoring (2.86, 1.85-4.42, <0.0001), mouth breathing (1.51, 1.04-2.18, 0.029), restless sleep (2.31, 1.89-2.83, <0.0001), drooling (1.79, 1.07-2.97, 0.026), stomach position during sleep (1.70, 1.0-2.39, 0.003), and inadequate sleep time (2.56, 1.48-4.43, 0.001). CONCLUSIONS: Snoring, mouth breathing, restless sleep, drooling, stomach position during sleep, and lack of sleep were the risk factors related to bruxism in children.

Endothelial nitric oxide synthase gene G894T polymorphism and risk assessment for pregnancy-induced hypertension: evidence from 11 700 subjects.

Recent studies have reported the association between endothelial nitric oxide synthase (eNOS) gene G894T polymorphism and pregnancy-induced hypertension (PIH). However, the results have been inconsistent. We conducted a comprehensive meta-analysis to explore this association. A total of 36 case-control studies involving 4028 PIH cases and 7672 controls were ultimately included. In the overall analysis, no association was identified between eNOS gene G894T polymorphism and PIH risk in any of the genetic models. In the subgroup analysis, the results showed that T-allele carriers had a higher risk of PIH than those with the G allele in Asians (G vs. T: odds ratio (OR)=0.76, 95% confidence interval (CI)=0.63-0.91, P=0.002; GT+TT vs. GG: OR=1.32, 95% CI=1.09-1.59, P=0.004; TT vs. GT+GG: OR=1.96, 95% CI=1.26-3.06, P=0.003; TT vs. GG: OR=1.99, 95% CI=1.27-3.11, P=0.003; GT vs. GG: OR=1.23, 95% CI=1.05-1.43, P=0.009). For Latin American and African populations, the association between G894T polymorphism and susceptibility to PIH was only observed in the dominant model. However, no association was observed in Europeans and Americans. Therefore, eNOS gene G894T polymorphism was related to PIH risk, especially for Asians.