Genetic evidence strengthens the bidirectional connection between oral health status and psychiatric disorders: A two-sample Mendelian randomization study.

BACKGROUND: Observational studies cannot accurately infer the causal associations between oral health status and psychiatric disorders. METHODS: We conducted univariate and multivariate Mendelian randomization (MR) analyses using single nucleotide polymorphisms (SNPs) associated with eight oral health statuses (periodontitis, DMFS, Nteeth, toothache, loose teeth, painful gums, bleeding gums, and mouth ulcers) and four psychiatric disorders (Schizophrenia, Major Depressive Disorder (MDD), anxiety and stress-related disorder (ASRD), and Bipolar Disorder (BIP)) as instrumental variables. Genetic data were sourced from the Gene-lifestyle interactions in dental endpoints (GLIDE), UK Biobank, Psychiatric Genomics Consortium (PGC), and Lundbeck Foundation Initiative for Integrative Psychiatric Research (iPSYCH). The inverse variance-weighted (IVW) approach, supported by a comprehensive sensitivity analysis, was employed. RESULTS: Genetically predicted mouth ulcers were significantly linked to higher MDD (OR = 2.17, 95 % CI: 1.33--3.54, P< 0.01) and BIP risks (OR = 2.25, 95 % CI: 1.22-4.15, P = 0.01). BIP heightened bleeding gums risk (OR = 1.01, 95 % CI: 1.00-1.01, P < 0.01). These associations were adjusted for smoking status and alcohol consumption. Painful gums were significantly associated with MDD risk (OR = 96.48, 95 % CI: 2.66-3495.28, P = 0.01), while MDD raised periodontitis risk (OR = 2.15, 95 % CI: 1.24-3.75, P = 0.01), both confounded by smoking and alcohol. Relatively small effects between several variables, while others could not withstand correction for multiple tests. LIMITATIONS: The sample size and limitation to European populations limits the study generalizability. CONCLUSIONS: This study provide evidence of possible causal relationships between several oral health conditions and mental illness. Focusing on oral health and valuing mental health are important for each other and overall health.

Relationship between body composition and pulmonary function in the general population-a cross-sectional study in Ningxia.

Studies considering the relationship between non-obesity-related body composition and lung function are few; therefore, this study aimed to explore these correlations and effects. This cross-sectional study conducted in rural Qingtongxia City and Pingluo County, Ningxia, China, included 776 participants aged 30-75 years. Body composition and lung function were measured using direct segmental multifrequency bioelectrical impedance analysis and a digital spirometer, respectively. Their correlation was assessed using partial correlation analysis, controlling for age and smoking status, and the body composition effect on lung function was analyzed using binomial logistic regression analysis. The body components total body water content, protein content, mineral content, muscle mass, fat-free mass (FFM), skeletal muscle mass, basal metabolic volume, and chest circumference (CC) positively correlated with pulmonary function (forced vital capacity and forced expiratory volume in one second) in both sexes. Neck circumference and hip circumference positively correlated with pulmonary function in women. Additionally, lung function declines more slowly in women (odds ratio [OR] = 0.66, 95% confidence interval [CI] = 0.44-0.98, p = 0.04); CC (OR = 0.92, 95% CI = 0.86-0.98, p = 0.01) increased as a protective factor for decreased lung function. Increased waist circumference (OR = 1.04, 95% CI = 1.00-1.09, p = 0.04) was a risk factor for reduced lung function. FFM contains body composition indicators positively correlating with lung function, excluding fat-related body composition. Abdominal obesity increases the risk of decreased lung function.

Association of Body Composition with Pulmonary Function in Ningxia: The China Northwest Cohort.

Background: In recent decades, obesity has become an epidemic worldwide and is a risk factor for many chronic diseases. Lung function is also a predictor of various chronic diseases. However, research results on the association between obesity and lung function are inconsistent and few studies have evaluated the association between central obesity indicators and lung function. Therefore, this study explored the correlation between central obesity and lung function. Methods: This study is a cross-sectional study. The basic participant characteristics were collected by questionnaire. A tape measure was used to measure waist circumference (WC) and hip circumference (HC). Body fat percentage was measured using an InBody370. Lung function parameters were measured using a digital spirometer connected to a computer (Chestgraph HI-101). R (R4.0.5) software was used for data analysis. A generalized linear model was used to analyze the association between obesity and lung function. Results: This study found that body mass index (BMI) adjusted for WC was negatively correlated with forced vital capacity (FVC) (ß=-0.05 [-0.06, -0.03] in men, ß=-0.05 [-0.07, -0.04] in women) and forced expiratory volume in 1 s (FEV1)(ß=-0.02 [-0.03, -0.00] in men, ß=-0.03 [-0.04, -0.02] in women). Body fat percentage was negatively correlated with FVC (ß=-0.01 [-0.01, -0.01] in men, ß=-0.01 [-0.01, -0.00] in women). Conclusion: Central obesity and combined central and general obesity were more strongly positively correlated with lung function. WC-adjusted BMI was negatively correlated with lung function. Body fat percentage was negatively correlated with lung function.

Long non-coding RNA expression in silicosis and MRAK050699 function in epithelial-mesenchymal transition.

Silicosis is a lung fibrotic disease caused by chronic silica exposure. Aberrations in long non-coding RNA (lncRNA) expression are associated with fibrotic diseases, but the role of lncRNAs in silicosis pathogenesis remains unclear. Here, we investigated the expression of lncRNAs during silicosis and the role of MRAK050699 in epithelial-mesenchymal transition (EMT). Differentially expressed lncRNAs in the lung tissues of normal and silicosis rats were compared, and their biological effects were determined using the Gene Ontology term and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses. There were 1077 differentially expressed lncRNAs (378 upregulated and 699 downregulated). MRAK052509, MRAK139674, AY539881, MRAK050699, XR_6113, and BC167061 were selected to verify expression in silicosis rats using quantitative reverse transcription polymerase chain reaction. MRAK050699 was knocked down in rat alveolar type II epithelial cells, and the molecular mechanism of transforming growth factor-ß (TGF-ß)-induced EMT in these cells was studied. All selected lncRNAs were upregulated in the silicosis rats, consistent with the sequencing results. MRAK050699 knockdown inhibited EMT of RLE-6TN cells by regulating the TGF-ß/Smad3 signaling pathway. Thus, the differential expression of lncRNAs is related to silicosis development, and MRAK050699 plays an important role in EMT, suggesting a potential therapeutic target for silicosis.