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Background: To assess the largely undetermined separate and joint effects of sleep and liver function biomarkers on liver cancer. Methods: Data of 356,894 participants without cancer at baseline in the UK Biobank were analyzed. Sleep score was evaluated using five sleep traits (sleep duration, chronotype, insomnia, snoring, and excessive daytime sleepiness) and dichotomized into healthy or unhealthy sleep. Circulating liver function biomarkers were measured. Cox proportional hazard model was performed to investigate the independent and joint associations of sleep and liver function biomarkers with liver cancer incidence. Results: After a median follow-up time of 13.1 years, 394 cases of incident liver cancer were documented. The multivariable-adjusted hazard ratio (HR) for liver cancer was 1.46 (95% confidence interval: 1.15–1.85) associated with unhealthy sleep (vs. healthy sleep), and was 1.17 (1.15–1.20), 1.20 (1.18–1.22), 1.69 (1.47–1.93), 1.06 (1.06–1.07), 1.08 (1.07–1.09), 1.81 (1.37–2.39), or 0.29 (0.18–0.46) associated with each 10-unit increase in alanine transaminase (ALT), aspartate transaminase (AST), total bilirubin (TBIL), gamma-glutamyl transferase (GGT), alkaline phosphatase (ALP), total protein (TP), or albumin (ALB), respectively. Individuals with unhealthy sleep and high (≥ median) ALT, AST, TBIL, GGT, ALP, or TP or low (< median) ALB level had the highest HR of 3.65 (2.43–5.48), 4.03 (2.69–6.03), 1.97 (1.40–2.77), 4.69 (2.98–7.37), 2.51 (1.75–3.59), 2.09 (1.51–2.89), or 2.22 (1.55–3.17) for liver cancer, respectively. Significant additive interaction of unhealthy sleep with high TP level on liver cancer was observed with relative excess risk due to an interaction of 0.80 (0.19–1.41). Conclusions: Unhealthy sleep was associated with an increased risk of liver cancer, especially in participants with lower ALB levels or higher levels of ALT, AST, TBIL, GGT, ALP, or particularly TP. [ABSTRACT FROM AUTHOR]

Aims: To explore the association of dietary vitamin intake from food and/or supplement with mortality in US adults with diabetes. Materials and Methods: This prospective cohort study was conducted on 5418 US adults with diabetes from the National Health and Nutrition Examination Survey 1999–2018. Vitamin intake from food and supplements was estimated via dietary recall. Sufficient intake from food or food + supplement was defined as ≥ estimated average requirement (EAR) and ≤ tolerable upper intake level (UL), insufficient intake, < EAR; and excess intake, > UL. Medium supplementary intake was classified as > median level and ≤75th percentile; low intake, ≤ median level; and high intake, >75th percentile, as reported by supplement users. Results: A total of 1601 deaths occurred among the participants over a median follow‐up of 11.0 years. Cox regression analysis of the single‐vitamin model demonstrated that sufficient vitamin A and folate intake from food and food + supplement and medium vitamin A and folate intake from supplement; sufficient riboflavin, niacin, and vitamin B6 intake from food and food + supplement; and sufficient thiamin and vitamin E intake from food + supplement were significantly associated with reduced all‐cause mortality (all p < 0.05). In the multivitamin model, sufficient vitamin A and folate intake from food and food + supplement, medium vitamin A and folate intake from the supplement, and sufficient niacin intake from food and food + supplement were inversely associated with mortality (all p < 0.05). Conclusions: Vitamin A and folate intake from food or supplement and niacin intake from food were significantly associated with reduced mortality in US adults with diabetes. [ABSTRACT FROM AUTHOR]

We expected to explore the associations of hearing loss and hearing thresholds at different frequencies with total and cause-specific mortality. In this study, 11,732 individuals derived from the National Health and Nutrition Examination Survey (NHANES) 1999–2012 were included. Data of death was extracted from the NHANES Public-Use Linked Mortality File through December 31, 2015. Cox proportional hazards models were used to explore the associations between hearing loss, hearing thresholds at different frequencies, and total or cause-specific mortality. A total of 1,253 deaths occurred with a median follow-up of 12.15 years. A significant positive dose-response relationship between hearing loss in speech frequency and total mortality was observed, and the HRs and 95% CIs were 1.16 (0.91, 1.47), 1.54 (1.19, 2.00), and 1.85 (1.36, 2.50), respectively, for mild, moderate, and severe speech-frequency hearing loss (SFHL) with a Ptrend of 0.0003. In addition, moderate (HR: 1.90, 95% CI: 1.20–3.00) and greater (3.50, 1.38–8.86) SFHL significantly elevated risk of heart disease mortality. Moreover, hearing thresholds of >25 dB at 500, 1000, or 2000 Hz were significantly associated with elevated mortality from all causes (1.40, 1.17–1.68; 1.44, 1.20–1.73; and 1.33, 1.10–1.62, respectively) and heart disease (1.89, 1.08–3.34; 1.95, 1.21–3.16; and 1.89, 1.16–3.09, respectively). Hearing loss is associated with increased risks of total mortality and heart disease mortality, especially for hearing loss at speech frequency. Preventing or inhibiting the pathogenic factors of hearing loss is important for reducing the risk of death. [ABSTRACT FROM AUTHOR]

Objective: To assess the association of dinitroaniline herbicides as well as their interactions with genetic susceptibility and lifestyle with glucose dysregulation., Methods: A total of 4310 Chinese urban adults from the baseline of the Wuhan-Zhuhai Cohort were included in the cross-sectional study. A follow-up panel from the cohort was included in the longitudinal study, including 158 participants with 432 observations. Glucose dysregulation, including fasting plasma glucose (FPG), homeostasis model assessment of insulin resistance (HOMA-IR), type 2 diabetes mellitus (T2DM), and impaired fasting glucose (IFG) were assessed. Serum dinitroaniline herbicides including benfluralin, trifluralin, and pendimethalin were measured. T2DM-related polygenic risk score (PRS) and healthy life scores were constructed., Results: Cross-sectionally, each 2-fold increase in serum benfluralin was associated with a 1.12%, 2.03%, and 9% increase in FPG, HOMA-IR, and IFG risk, respectively. Each 2-fold increase in serum trifluralin was associated with a 0.70% increase in FPG. Each 2-fold increase in serum pendimethalin was associated with a 2.53% and 24% increase in FPG and IFG risk, respectively (all P < 0.05). Positive associations were found between the dinitroaniline herbicide mixture and glucose dysregulation. Longitudinally, serum benfluralin and pendimethalin were associated with the annual increases in FPG and HOMA-IR (P < 0.05). Joint and interaction effect analysis showed that compared with participants with high benfluralin/trifluralin/pendimethalin, high PRS, and unhealthy lifestyle, those with low benfluralin/trifluralin/pendimethalin, low PRS, and healthy lifestyle showed the greatest declines in FPG, i.e., -15.46%, -13.58%, and -10.51% changes, respectively; and the greatest reductions in IFG risks, i.e., 75%, 61%, and 73% reductions, respectively (all P < 0.05)., Conclusions: This study highlighted the importance of controlling dinitroaniline herbicide exposure and following healthy lifestyles in glucose dysregulation prevention, especially among individuals with high genetic risk of T2DM., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Objective: Numerous circular RNAs (circRNAs) have been verified to execute crucial roles in "asthma-like" progression of the airway smooth muscle cells (ASMCs). The present study aimed to scrutinize the function and mechanism of circ&#95;0000029 in pediatric asthma etiology in vitro ., Methods: A cell model of asthma was developed using ASMCs induced by platelet-derived growth factor BB (PDGF-BB). Western blotting and qRT-PCR were performed to determine the expression levels of circ&#95;0000029, miR-576-5p, and KCNA1 in PDGF-BB-treated ASMCs. Dual-luciferase reporter, RNA-binding protein immunoprecipitation, and RNA pull-down experiments were conducted to validate targeting relationships. CCK-8 and Transwell assays were performed to evaluate the proliferative and migratory potential of ASMCs. The rate of apoptosis was analyzed using flow cytometry., Results: Pronounced circ&#95;0000029 and KCNA1 downregulation and high levels of miR-576-5p were observed in PDGF-BB-treated ASMCs. Circ&#95;0000029 targets miR-576-5p to regulate KCNA1 expression. The loss of KCNA1 and upregulation of miR-576-5p dramatically impeded apoptosis but promoted ASMC migration and proliferation. Ectopic expression of circ&#95;0000029 manifested the opposite outcome among ASMCs. Furthermore, KCNA1 deficiency and miR-576-5p upregulation counteracted the effects of circ&#95;0000029 overexpression on ASMCs., Conclusions: Circ&#95;0000029 represses the abnormal migration and growth of ASMCs by mediating miR-576-5p and KCNA1 expression levels. This suggests that the regulatory axis circ&#95;0000029/miR-576-5p/KCNA1 is a potential target for pediatric asthma treatment., (© 2023 by the Association of Clinical Scientists, Inc.)