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Purpose: To examine the associations between use of statins and risks of various ovarian, uterine, and cervical diseases, including ovarian cancer, endometrial cancer, cervical cancer, ovarian cyst, polycystic ovarian syndrome, endometriosis, endometrial hyperplasia, endometrial polyp, and cervical polyp. Methods: We conducted a cohort study among female participants in the UK Biobank. Information on the use of statins was collected through verbal interview. Outcome information was obtained by linking to national cancer registry data and hospital inpatient data. We used Cox proportional hazards regression to examine the associations. Results: A total of 180,855 female participants (18,403 statin users and 162,452 non-users) were included. Use of statins was significantly associated with increased risks of cervical cancer (adjusted hazard ratio (HR), 1.55; 95% confidence interval (95% CI), 1.05–2.30) and polycystic ovarian syndrome (adjusted HR, 4.39; 95% CI, 1.68–11.49). However, we observed no significant association between use of statins and risk of ovarian cancer, endometrial cancer, ovarian cyst, endometriosis, endometrial hyperplasia, endometrial polyp, or cervical polyp. Conclusion: Our findings suggest that use of statins is associated with increased risks of cervical cancer and polycystic ovarian syndrome, but is not associated with increased or decreased risk of ovarian cancer, endometrial cancer, ovarian cyst, endometriosis, endometrial polyp, or cervical polyp. [ABSTRACT FROM AUTHOR]

Background: Metabolic dysfunction associated with fatty liver disease (MAFLD) is often correlated with obesity and hyperuricemia. The present study aimed to determine the association between serum uric acid (SUA) and central fat distribution in patients with MAFLD. Methods: A total of 485 patients were classified into the following groups: (1) controls without MAFLD and hyperuricemia (HUA), (2) MAFLD with normal SUA, and (3) MAFLD with HUA. DUALSCAN HDS-2000 was used to measure visceral fat (VAT) and subcutaneous fat (SAT). Dual-energy X-ray absorptiometry (DEXA) was used to measure body fat distribution. Results: MAFLD patients with HUA had remarkably higher BMI, fasting insulin, OGIRT AUC, ALT, AST, TG, VAT, SAT, Adipo-IR, trunk fat mass, android fat, and total body fat than MAFLD patients with normal SUA (all p < 0.05). The increase in VAT, SAT, CAP, Adipo-IR, upper limbs fat mass, trunk fat mass, and android fat, as well as the percentage of MAFLD, were significantly correlated with the increase in SUA. The percentage of MAFLD patients with HUA increased significantly with increasing VAT or SAT, as determined by the Cochran–Armitage trend test (all p < 0.05). Furthermore, VAT (OR = 1.01 CI: 1.00, 1.03; p < 0.05) and adipo-IR (OR = 1.09 CI: 1.00, 1.19; p < 0.05) were associated with circling SUA in MAFLD after adjusting for sex, age, TG, TC, HOMA-IR, and BMI. Conclusion: Abdominal fat promotes the co-existence of HUA and MAFLD, while weight loss, especially, decreasing VAT, is of great importance to decrease SUA levels and manage MAFLD. [ABSTRACT FROM AUTHOR]

Background. The associations between hip/knee osteoarthritis (OA) and various psychiatry disorders, as well as the underlying genetic determinants, remain unclear. Methods. Based on the community-based prospective data of UK Biobank, we constructed two matched cohorts to assess the bidirectional associations between OA and five common psychiatry disorders. Then, we further examined the existence of overall genetic association for those disease pairs with demonstrated phenotypic association through polygenic risk score (PRS) prediction using individual-level genotyping data of UK Biobank and LD score regression (LDSC) analysis utilizing publicly available GWAS summary statistics. Last, also based on GWAS summary statistics, we performed enrichment analyses to pinpoint specific genetic determinants that might contribute to the observed overall genetic shares. Results. The phenotypic analyses revealed an elevated risk of hip/knee OA among individuals with any psychiatric disorders, compared to their matched unexposed individuals (hazard ratio HR = 1.62 , 95% confidence interval (CI): 1.57-1.68), and vice versa (HR =1.93, 95% CI: 1.83-2.04). We further observed positive associations of knee OA with depression and stress-related disorder in the PRS analyses, which corroborated with the results of LDSC analyses (r for genetic = 0.20 (95% CI: 0.15-0.25) and r for genetic = 0.29 (95% CI: 0.19-0.40), respectively). Using GWAS summary statistics, we identified several shared genes and pathways, particularly the biological process related to HDAC histones, between knee OA and depression/stress-related disorder. Conclusions. Our study demonstrated a bidirectional association between OA and multiple psychiatric disorders, and the findings of shared genetic architectures between knee OA and depression/stress-related disorder provided possible targets for further mechanistic exploration and intervention development. [ABSTRACT FROM AUTHOR]

Introduction: It is urgent to make a rapid screening of infants at the highest risk for bronchopulmonary dysplasia (BPD) via some succinct postnatal biomarkers, such as Ureaplasma Urealyticum (UU) infection and chest radiograph images. Methods: A retrospective study was performed. Moderate to severe BPD or death was set as the main outcome. The association between putative variables and the main outcome were assessed by bivariate analyses and logistic regression. Results: A total of 134 infants were enrolled. Bivariate analyses showed the gestational age, birth weight, appearances of diffuse opacities or grid shadows/interstitial opacities or mass opacities or cystic lucencies on chest radiographic images, a ductal diameter ≥1.5 mm and whether UU infection was associated with BPD. After adjustment by logistic regression, the risk of BPD with gestational age, sex and specific chest-radiographic manifestations remained significant. Conclusions: Chest radiograph images (appearance of diffuse opacities or grid shadows/interstitial opacities or mass opacities or cystic lucencies) could provide a quick prediction of developing BPD in clinical practice, in addition to gestational age and sex. UU infection was not an independent risk factor for BPD. [ABSTRACT FROM AUTHOR]

Objective. The occurrence of liver fibrosis and fibrosis-related liver cancer is the reason for the increase in morbidity and mortality worldwide. Transforming growth factor-β2 (TGF-β2) is an important mediator of chronic liver fibrosis. This study aims to find the molecular mechanism that mediates HBV infection and induces TGF-β2 and verifies that CREB binding protein acetylation mediates HBV infection and induces TGF-β2 expression. Methods. The acetylated proteins were extracted from HepG2-NTCP cells and HBV-infectedHepG2-NTCP cells. The acetylated proteins were screened by modification enrichment technology and database search. Protein annotation, motif analysis of modification sites, and protein function enrichment analysis of these proteins were performed to roughly clarify the location and function of these acetylated modification proteins in cells. Acylated proteins enriched in the TGF-β pathway were obtained by KEGG pathway enrichment analysis. The effect of the selected acetylated modification protein on the TGF-β pathway was verified by experiments, that is, the target protein gene was knocked out by siRNA, and the expression level of the TGF-β2 was detected by qRT-PCR. Results. Proteins were extracted from HepG2-NTCP cells and HepG2-NTCP cells infected with HBV, and differential acetylation modification proteins were screened. The target protein CREB binding protein was screened by modification enrichment technology and database search. The aggregation analysis of TGF-β pathway showed that CREB binding protein was acetylated at amino acid positions 434 and 439, and enriched in the TGF-β signaling pathway. siRNA targeting CREB binding protein was transfected, and the expression of TGF-β2 in cells was detected by qRT-PCR and western blot, respectively. It was verified that HBV infection-inducedCREB-binding protein acetylation regulated the high expression of TGF-β2. Conclusion. After HBV infection, CREBBP acetylation was up-regulated, which promoted the high expression of TGF-β2. [ABSTRACT FROM AUTHOR]

As traditional methods such as questionnaires for measuring risk propensity are not applicable in some scenarios, a nonintrusive method that could automatically identify individuals' risk propensity could be valuable. This study utilized Defense of the Ancients 2 (DOTA 2) single match data and historical statistics to train predictive models to identify risk propensity by machine learning methods. Self-reported risk propensity scores from 218 DOTA 2 players were paired with their behavioral metrics. The best-performing model occurred with Gaussian process regression. The root mean square error of this model was 1.10, the correlation between predicted scores and self-reported questionnaire scores was 0.44, the R-squared was 0.17, and the test–retest reliability was 0.67. We discussed how selected behavioral features could contribute to predicting risk propensity and how the approach could be of potential value in the application of perceiving individuals' risk propensities. Moreover, the limitations of our study were discussed, and recommendations were made for future studies in this field. [ABSTRACT FROM AUTHOR]

Background: To elucidate the influence of childhood asthma on adult height after consideration of genetic heterogeneity in height.Methods: Based on the UK Biobank, we conducted a matched cohort study, including 13,602 European individuals with asthma diagnosed before 18 years old and 136,008 matched unexposed individuals without such an experience. Ascertainment of asthma was based on self-reported data (97.6%) or clinical diagnosis in healthcare registers (2.4%). We studied three height outcomes, including (1) the attained adult height (in centimeters), (2) the height deviation measured as the difference between a person's rank of genetically determined height (based on generated polygenetic risk score) and their rank of attained adult height in the study population (deviation in % of height order after standardization), and (3) the presence of height deficit comparing genetically determined and attained height (yes or no). We applied linear mixed-effect models to assess the associations of asthma diagnosed at different ages with attained adult height and height deviation, and conditional logistic regression models to estimate the associations of asthma with the risk of height deficit.Results: 40.07% (59,944/149,610) of the study participants were born before 1950, and most of them were men (57.65%). After controlling for multiple covariates, childhood asthma was associated with shorter attained adult height, irrespective of age at asthma diagnosis. However, in the analysis of height deviation (deviation in %), we observed the greatest height deviation among individuals with asthma diagnosed before 4 years of age (- 2.57 [95% CI - 4.14 to - 1.00] and - 2.80 [95% CI - 4.06 to - 1.54] for the age of ≤ 2 and 3-4 years, respectively). The magnitude of height deviation in relation to asthma declined thereafter and became null after age 6. Similarly, there was a statistically significant height deficit in relation to an asthma diagnosis at ages ≤ 2 and 3-4 (odds ratios = 1.21, 95% CI 1.04 to 1.40, and 1.15, 95% CI 1.02 to 1.29) but not thereafter. The result pattern was similar when separately analyzing asthma with or without inhaled glucocorticoid (ICS) use, despite that the estimates were consistently stronger among asthma individuals who used ICS.Conclusions: Our results suggest a notable association of childhood asthma, primarily asthma diagnosed at an early age, with adult height, after consideration of genetic heterogeneity in height and use of ICS. This finding highlights the need for surveillance on the growth problems among children with asthma. [ABSTRACT FROM AUTHOR]

N -nitrosamines are a new class of disinfection byproducts with significant toxicity and carcinogenicity that have attracted extensive attention worldwide in recent years. N -nitrosamines in natural and drinking water would have adverse effects on people. The occurrence of N -nitrosamines in surface water, groundwater, and tap water of the Liujiang River Basin was investigated to disclose the source, fate, and cancer risk of N -nitrosamines in a typical karstic river. The origins of N -nitrosamines contamination were investigated using principal component analysis and multiple linear regression (PCA-MLRA). The results indicated that the concentrations of nine N -nitrosamines species were NDMA (1.7–342 ng/L), NMEA (ND, ND represents not detected), NPYR (2.5–53 ng/L), NDBA (ND-87 ng/L), NDEA (0.2–5.7 ng/L), NDPA (ND-34 ng/L), NPIP (ND-32 ng/L), NMOR (0.1–5.2 ng/L), and NDPhA (ND-0.3 ng/L). 71% of N -nitrosamines in the surface water samples of the Liujiang River's mainstream could be attributed to industrial and aquaculture effluents. Furthermore, 29% of N -nitrosamines could originate from domestic sewage and agricultural operations. In addition, we estimated the cancer risks associated with N -nitrosamines in groundwater and drinking water. For lifetime exposure (from birth to age 70), the average estimated carcinogenic risks of groundwater and tap water from oral intake were 7.4 × 10−5 (7.4 extra cancer cases per 100,000 persons exposed) and 9.7 × 10−5, respectively, which were greater than the US EPA standard (1 × 10−5). N -nitrosamines posed the highest cancer risk to children aged one to six. The experimental results would serve as a data foundation for environmental governance in typical karst regions. • NDMA and NPYR were originated from industrial wastewater. • Jila Subterranean discharged 16% of N -nitrosamines to Liujiang river. • High concentrations of NDMA and NPYR were found in tap water. • Karst groundwater and tap water posed high risk to local residents. [ABSTRACT FROM AUTHOR]

The diagnosis of cancer is a life-changing and stressful experience among most patients. Indeed, previous studies have consistently shown an association between a cancer diagnosis and subsequent risk of common psychiatric disorders, including major depressive disorder, anxiety, stress-related disorders, and substance use. Yet, evidence is limited regarding the role of genetic susceptibility to psychiatric disorders on the association between cancer diagnosis and common psychiatric disorders. Thus, we aimed to assess the role of polygenic risk score (PRS) for psychiatric disorders on the association between cancer diagnosis and subsequent risk of common incident psychiatric disorders adjusting for multiple confounders. We conducted a matched cohort study of UK Biobank including 78,465 cancer patients diagnosed from January 1, 1997 to January 31, 2020 and 392,325 cancer-free individuals individually matched to the cancer patients by birth year, sex and availability of primary care records. The exposure was a first diagnosis of cancer, and the outcome was a first diagnosis of common psychiatric disorders (i.e., major depressive disorder, anxiety and stress-related disorders, or substance use) or prescription of psychotropic medications. We used flexible parametric model and Cox model to estimate the subsequent risk of common psychiatric disorders following a cancer diagnosis and performed further stratified analysis by individual genetic susceptibility (i.e., PRS for major depressive disorder or anxiety and stress-related disorders). The mean age at cancer diagnosis was 62.7. During up to 24 years of follow-up, we observed an increased risk of psychiatric disorders or prescription of psychotropic medications with a peak during the first 6 months after cancer diagnosis (hazard ratio [HR]=4.25; 95% confidence interval [CI] 3.94-4.70), which then decreased rapidly but remained statistically significant throughout the follow-up period (≥13 months: 1.22 [95%CI 1.19-1.26]). The increased risk of psychiatric disorders among cancer patients was largely similar across groups with varying PRSs for major depressive disorder, and anxiety and stress-related disorders. The distinct rise in the risk of common psychiatric disorders after cancer diagnosis seems largely independent of known genetic risk factors for these disorders. These results highlight the need for clinical surveillance of common psychiatric disorders among newly diagnosed cancer patients. [ABSTRACT FROM AUTHOR]

The Guangdong province of China contains the most clearly described high-incidence of hepatocellular carcinoma (HCC) and nasopharyngeal carcinoma (NPC) areas in the world. The geographical heterogeneity of cancer incidence in the region suggests that many carcinogenic risk factors might be present in the regional geochemical environment. This paper presents the concentrations of a wide range of known carcinogens in two high cancer incidence areas in Guangdong and compared them to a low cancer incidence area in the same province. N -Nitrosamines, NO 3 − , NO 2 − , and ammonium were detected in groundwater, surface water, and drinking-water. The concentrations of the 7 trace metal and metalloid elements As, Cd, Ni, Cu, Pb, Zn, and Hg were determined in surface soil samples and all water samples. The results show that, compared with the guidelines or limit values for drinking-water quality in the world, the high cancer incidence areas have hazardous high levels of N -nitrodimethlyamine (NDMA) in all kinds of water. Oppositely, the low cancer incidence area has a safe low level of NDMA in water bodies. The levels of NO 3 − , NO 2 − , and ammonium in water have the same character, although they have different expression between the two high-risk areas. The distribution of the 7 tested trace elements in surface soil has no significant correlation with cancer incidence. On the other hand, high concentrations of carcinogenic N -Nitrosamines in drinking-water and natural water bodies were identified for the first time in the high NPC and HCC incidence area. [ABSTRACT FROM AUTHOR]