Background With population aging, late-onset schizophrenia is attracting increasing attention. The prospective association between frailty and late-onset schizophrenia, along with its underlying mechanisms, remains unclear. This study aimed to investigate the relationship between frailty and late-onset schizophrenia, and assess the potential role of metabolic mechanisms on this association. Methods A total of 489,302 participants without late-onset schizophrenia at baseline were included from UK biobank. Cox proportional hazard regression model was utilized to investigate the association between frailty and late-onset schizophrenia. Elastic net regression was used to determine the metabolic signature associated with frailty. Mediation analysis was employed to assess the mediating role of metabolic signature and specific metabolites on the relationship between frailty and late-onset schizophrenia. Results During a median follow-up of 13.49 years, 705 late-onset schizophrenia cases were identified. Compared to individuals with nonfrailty, the risk of late-onset schizophrenia was increased in those with prefrailty (HR: 1.82, 95% CI: 1.52, 2.19) and frailty (HR: 3.10, 95% CI: 2.44, 3.95). Eighty-three metabolites were identified as being related to frailty (38 positively, 45 negatively). The metabolic signature mediated the association between frailty and late-onset schizophrenia (proportion of mediation effects (PM%): 4.57, 95% CI: 2.22, 7.36). The mediation effect of metabolites from fatty acids, inflammation and lipid metabolism on the relationship between frailty and late-onset schizophrenia was significant, with PM% ranging from 2.41 to 5.93. Conclusions Physical frailty was associated with an increased risk of late-onset schizophrenia, partly by disrupting metabolic signatures (fatty acids, inflammation, and lipid metabolism).

Heavy metal toxicity seriously threatens the health of people, plants, and the food chain in developing countries. A review of the Science Direct, PubMed, Web of Science, Google Scholar, Springer, and Scopus databases was performed to assess the sources, exposure, toxicity mechanism, human health aspects, and detection techniques related to Cd, Cr, Mn, Ni, and Cu between 2019 and 2024. Moreover, AI-powered models particularly Random Forest (RF) for predictive analysis and Convolutional Neural Networks (CNNs) for spatial mapping to highlight significant contamination hotspot, were examined for their efficiency and reliability to identify and detect the distribution of heavy metals. The environment is frequently polluted with heavy metals as a result of improper home waste disposal, industrial and agricultural operations, and overuse of pesticides and fertilizers in developing countries. China contributed the most to heavy metals research, followed by the United States. The accumulation and exposure to heavy metals lead to potential outcomes in humans. Long-term exposure to certain heavy metals is significantly associated with increased risk of developing various cancer types such as prostate, lung, throat, breast, blood, and brain cancers. The current study found in light of the existing identification and detection techniques' pros and cons, X-ray fluorescence spectroscopy (XRF) is a promising technique to quantify and detect heavy metals owing to its rapid, on-site, and non-destructive screening method.Based on gaps found in the literature, the current review suggests that integrating AI algorithms with nanotechnology and new biosensor platforms to accomplish high-precision, real-time environmental monitoring is an important future direction. To protect the community, longitudinal health studies, biomonitoring, and the use of green remediation technologies should be encouraged.

BACKGROUND:Prenatal per- and polyfluoroalkyl substances (PFAS) exposure has been linked to adverse birth outcomes, yet evidence on fetal growth remains limited. METHODS:A total of 2856 pregnant women-fetus dyads were included from Henan Maternal and Child Health Hospital. Sixteen PFAS concentrations were detected. Five fetal ultrasound measurements (biparietal diameter [BPD], head circumference [HC], abdominal circumference [AC], femur length [FL], estimated fetal weight [EFW]) were collected at 18, 24, 32, 35 and 38 weeks, and standardized into gestational age-adjusted standard deviation scores (SDS). Generalized linear models, linear mixed models, and multinomial logistic regression were applied to evaluate associations of PFAS with single-time-point, repeated, and trajectory-based measures. RESULTS:Higher perfluoropentane sulfonate (PFPeS) were associated with reduced BPD-SDS at 24 weeks (β = -13.72%, 95% CI: -22.03%, -5.41%), and lower BPD-SDS and HC-SDS (β range: -6.21% to -6.19%) longitudinally. Elevated perfluorohexane sulfonate (PFHxS) was related to reduced FL-SDS and EFW-SDS (β range: -5.84% to -5.64%) at 32 weeks, and lower FL-SDS longitudinally (β = -3.56%, 95% CI: -5.56%, -1.57%), as well as higher odds of FL‑SDS "lower growth" trajectory (OR = 1.27, 95% CI: 1.06, 1.51). Higher 6:2 chlorinated polyfluorinated ether sulfonate (6:2 Cl‑PFESA) were inversely associated with BPD-SDS, HC-SDS, FL-SDS, and EFW-SDS at 32 weeks (β range: -11.01% to -9.74%), and HC-SDS and EFW-SDS in repeated-measures analyses (β range: -6.94% to -4.84%), while positively associated with EFW-SDS "slow growth" trajectory (OR = 1.36, 95% CI: 1.00, 1.85). These trajectory-based findings were attenuated after multiple testing correction. CONCLUSION:Our findings indicated that prenatal exposure to PFPeS, PFHxS, and 6:2 Cl-PFESA may retard fetal growth.

Climate change has increased the frequency of extreme temperature and humidity events. Although the association between temperature and hand‒foot‒mouth disease (HFMD) is well-established, evidence regarding the synergistic amplification of risk driven by compound temperature‒humidity events remain limited. This study aims to investigate the temperature‒humidity synergistic effects on the HFMD risk and burden across China based on daily HFMD surveillance records and meteorological data from 302 cities during the period 2011–2019. Temperature‒humidity interactions are evaluated using generalized additive models (GAMs). Bivariate compound events are defined based on multiple temperature‒humidity percentile combinations. Exposure‒lag‒response relationships between temperature‒humidity compound events and HFMD risk are quantified using distributed lag nonlinear models (DLNMs) to identify high-risk thresholds with extreme characteristics. The HFMD burden is assessed through attributable case calculations. In over 18 million cases, we identified substantial synergistic effects between high temperature and humidity (S = 1.328, 95% CI: 1.286–1.370). Concurrent exposure above the 70th temperature percentile and 80th humidity percentile constituted high-risk conditions for HFMD (RR: 1.298, 95% CI: 1.222–1.379) at the national level, yet specific thresholds and associated risks exhibited spatial heterogeneity across regions. Subgroup analysis further identified preschool children and regions with economic disadvantages as vulnerable populations. The frequency of high HFMD risk compound events increased by 24% during 2017–2019 compared with 2011–2013. We identified 464,823 HFMD cases attributable to high-risk compound events across China, with the burden increasing most substantially in Northeast and North China. These findings provide a scientific basis for developing climate-adaptive early-warning systems and targeted interventions.

Background: Globally, the increasing frequency of extreme heat events and ozone pollution incidents has significantly intensified public health risks. However, empirical evidence regarding their synergistic impacts remains limited in central China. Methods: A two-stage analysis was conducted using data from 121 counties in Henan (2013-2019). Quasi-Poisson generalized additive models were used to assess county-specific associations, adjusting for PM2.5, RH, and temporal trends. The combined effect of air temperature (non-linear) and ozone (linear) was captured through multiplicative interaction terms. Random-effects meta-analyses were applied to pool the results. Subgroup analyses examined differences by age, sex, marital status, and cause of death. Results: During the study period, 1,280,429 deaths were recorded. Both high temperatures and elevated ozone levels were associated with increased mortality. Their joint effects were stronger than individual exposures. At high ozone levels, mortality risk increased by 2 percentage points (from 9.3 % to 11.3 %) between temperature distribution percentiles 75th and 99th. Under high-temperature conditions (31.4 degrees C, 90th percentile), a 10 mu g/m3 elevation in ozone was associated with a 0.94 % (95 % CI: 0.49 %-1.38 %) increase in mortality. Older adults, females, other marital statuses (including unmarried, divorced, or widowed), and those with cardiovascular or respiratory diseases were more susceptible to its effects. Conclusion: High temperature and ozone synergistically increase mortality risk. Targeted interventions are needed to protect vulnerable groups under climate change.

The association of perinatal exposure to airborne particulate matter (PM) with preterm birth (PTB) remains unclear. This study aimed to investigate possible associations between PM exposure and risk of PTB. There were 61,620 sibling pairs from a retrospective sibling matched cohort study were included. PM exposure was estimated by space-time extremely randomized trees models. Within-group differences in 2.5 and 10 μm particulate (ΔPM2.5 and ΔPM10) maternal exposure levels between corresponding trimesters of two consecutive pregnancies were tested for associations with moderate, very, or all PTB using fixed-effect regression models. Gestational age and difference in gestational age (Δ gestational age) between siblings were treated as secondary outcomes. A total of 1301 (2.1 %) incident PTB cases were confirmed in our study. The exposure-response analyses suggested that each 10 μg/m3 increase in ΔPM2.5 or ΔPM10 were associated with the increased risk of PTB, with significant effect in first trimester (ΔPM2.5 adjusted OR = 1.375, 95 % CI: 1.141, 1.658; ΔPM10 adjusted OR = 1.241, 95 %CI: 1.073, 1.435). Increase in ΔPM2.5 or ΔPM10 in first, second, and third trimester were significantly associated with a shortened gestational age. PTB risk and gestational age shared a near linear exposure-response relationship with increased ΔPM2.5 and ΔPM10 in whole pregnancy. In conclusion, increased ambient PM2.5 exposure is positively associated with reduced gestational age, while increased PM2.5 and PM10 concentration is associated with PTB risk.

BACKGROUND:Ambient ozone pollution is becoming a global health threat under global warming. Evidence on the association between ambient ozone and pregnancy complications and adverse birth outcomes has grown enormously. To provide a comprehensive assessment of the evidence, we performed a systematic review and meta-analysis to outline current epidemiological evidence. METHODS:A systematic literature search up to January 2024 was conducted in PubMed, Web of Science, Cochrane Library and Embase. We included studies that examined the association of ambient ozone exposure with pregnancy complications and birth outcomes. Data extraction was performed independently. All eligible studies were synthesized qualitatively. A random-effects meta-analysis was used to summarize the available effect estimates that calculated with a 10 μg/m3 exposure. We further evaluated whether geographic location, study design, study quality, and exposure assessments explain the heterogeneity. This study protocol was registered with PROSPERO (CRD42024499445). RESULTS:A total of 10,940 records were originally searched, 65 articles were finally included. Our results showed that first trimester ozone exposure significantly increased the risk of preeclampsia (pooled odds ratio (OR) = 1.018, 95%CI: 1.006-1.030). For birth outcomes, short-term ozone exposure was associated with the risk of preterm birth, with the pooled OR of 1.005 (95%CI: 1.002-1.008) and 1.003(95%CI:1.000-1.005). First trimester and whole pregnancy ozone exposure were associated with the risk of small for gestational age, with the pooled OR of 1.007 (95%CI: 1.002-1.012) and 1.030 (95%CI: 1.010-1.050), respectively. CONCLUSION:First trimester ozone exposure was associated with adverse pregnancy complications and adverse birth outcomes. Future investigations that considering local climates and population characteristics are warranted to explore the vulnerability at local and regional levels for tailored preventions.

BACKGROUND AND OBJECTIVES:The association between biological aging and dementia, as well as the underlying mechanism, remains limited. The aim of this study was to investigate the relationships of biological age (BA) with incident dementia and examine the underlying neurobiological mechanisms. METHODS:This study used data from the UK Biobank, a prospective longitudinal study. We included participants free of diagnosed dementia at baseline. BA was evaluated from clinical traits using the Klemera-Doubal method biological age (KDM-BA) and PhenoAge algorithms. Genetic risk of dementia was assessed using the apolipoprotein E (APOE) ε4 genotype and polygenic risk scores (PRSs). Cox proportional hazard regression models were used to estimate the associations of BA and the combined effect of genetic risk and BA with dementia. In addition, the potential roles of brain structures (gray matter volume [GMV], cortical mean thickness, and cortical surface area) in the associations between BA and dementia were evaluated using mediation analysis. RESULTS:A total of 280,918 participants (mean age 56.80 years, 54.59% female) were enrolled in this study. Over a median follow-up of 13.58 years, 4,770 cases of dementia were recorded. Every SD increase in KDM-BA accelerations and PhenoAge accelerations was associated with a 14% (hazard ratio [HR] = 1.14; 95% CI 1.10-1.18) and 15% (HR = 1.15; 95% CI 1.12-1.19) higher incidence of dementia, respectively. Individuals with APOE ε4 and highest PhenoAge accelerations had the highest risk of dementia (HR = 4.20, 95% CI 3.69-4.78) compared with those with non-APOE ε4 and lowest PhenoAge accelerations, with significant interaction effect (Pinteraction < 0.001). We did not find significant modification effects of PRS on the associations between BA accelerations and dementia (Pinteraction = 0.347 for KDM-BA acceleration, Pinteraction = 0.279 for PhenoAge acceleration), as well as APOE ε4 on the association between KDM-BA accelerations and dementia (Pinteraction = 0.212). Mediation analysis showed that the identified GMV, cortical mean thickness, and cortical surface area partly mediated the association between BA accelerations and incident dementia, with proportion-mediated percentage ranging from 6.64% to 17.98%. DISCUSSION:Advanced BA may be a potential risk factor of incident dementia. The risk is possibly mediated through the widespread reduction of brain structures.

Background and aimAs a newly recommended healthy dietary blueprint, the EAT-Lancet diet emphasizes both environmental sustainability and human health. However, its impact on chronic liver diseases remains unclear. This study examined the influence of the EAT-Lancet diet on the risk of metabolic dysfunction-associated steatotic liver disease (MASLD) and other chronic liver diseases.MethodsOur study included 160,394 UK Biobank participants who completed 24-h dietary assessments between April 2009 and June 2012, from which EAT-Lancet diet scores were calculated. The Cox proportional hazards models were used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs) for the primary outcome (MASLD) and secondary endpoints, including cirrhosis, liver cancer, and other liver diseases.ResultsA total of 1,727 cases of MASLD, 602 cases of liver cirrhosis, 103 cases of liver cancer, and 2,053 cases of other liver diseases were identified over a median follow-up period of 13.3 years. Using the lowest tertile as the reference, the highest EAT-Lancet diet index group demonstrated a 33% reduction in MASLD incidence (HR:0.67, multivariate 95%CI: 0.55, 0.80). In several secondary outcome measures, similar associations were also observed. Furthermore, the risk of MASLD was lowest among individuals with both higher EAT-Lancet dietary scores and lower genetic risk (HR = 0.52; 95%CI: 0.36–0.74), although no significant interaction was detected between the two groups.ConclusionAdherence to the EAT-Lancet diet is associated with a reduced risk of chronic liver disease, independent of genetic factors.

Dioxins, a group of environmental pollutants, can cause developmental toxicity through interaction with the aromatic hydrocarbon receptor (AHR). Retinoic acid (RA) functions via binding to retinoic acid receptor (RAR)/retinoid X receptor (RXR). Both AHR and RA pathways can be activated by dioxins. TCDD or atRA exposure similarly alters the expression of the long non-coding RNA (lncRNA) Meg3 in mouse palatal tissue. This study further examined the mechanism of TCDD-induced cleft palate (CP) via the RA pathway in mouse embryonic palatal mesenchymal (MEPM) cells. Results showed that in MEPM cells TCDD treatment increased Meg3 and RARA expression, inhibited cell proliferation, and had a synergistic effect with atRA. RNA pull-down-MS and RIP assays revealed that Meg3 binds to NONO, which belongs to the drosophila behavior human splicing family (DBHS) and have been reported to be associated with cell cycle regulation. NONO interacts with RAR and inhibits RARA expression. TCDD and atRA treatment reduced NONO expression. Silencing Meg3 raised NONO levels and mitigated the impact of TCDD or atRA on RA pathway activation, cell proliferation and survival. These findings suggest that TCDD affects Meg3 and NONO expression and the RA pathway activation, Meg3 interacts with NONO which may regulate RARA in palatal tissue. Thus, we propose that the RA pathway activation in TCDD-induced cleft palate may be mediated by the Meg3-NONO-RAR axis.

BACKGROUND:Maternal vitamin D deficiency (VDD) is a global health concern, with air pollution emerging as a potential risk factor. However, the underlying mechanisms, particularly the mediating role of Ultraviolet Radiation (UVR), remain poorly understood. This study investigated the impact of air pollution exposure, including PM2.5 chemical components, on 25-hydroxyvitamin D [25(OH)D] status in pregnant women, focusing on the mediating role of UVR. METHODS:A prospective cohort of 2258 pregnant women in Henan, China, was established. Average air pollutants and UVR exposure from the last menstrual period to the day before blood sampling were estimated using Kriging interpolation. VDD was defined as 25(OH)D concentrations below 30 nmol/L. Linear and logistic regression models assessed associations among air pollution, UVR, and 25(OH)D status. Dose-response relationships were modeled using restricted cubic spline functions, distributed lag nonlinear models (DLNM) were applied to identify critical exposure windows. Mediation analysis quantified the proportion of the air pollution effect on 25(OH)D levels and VDD risk mediated by UVR. RESULTS:Exposure to most air pollutants demonstrated significant negative correlations with serum 25(OH)D concentrations (PM2.5: β = -0.95, 95 %CI: 1.32, -0.59) and positive associations with VDD risk (PM2.5: OR = 1.13, 95 %CI: 1.09, 1.17). Through DLNM, we identified critical exposure windows at 5-6-week lags where PM2.5, PM10, and sulfate components exerted maximum effects on 25(OH)D reduction, exhibiting identical temporal response patterns. Mediation analysis demonstrated that UVR accounted for 92.51 % of the inverse association between black carbon exposure and 25(OH)D levels. CONCLUSIONS:Air pollution may impair maternal vitamin D status by reducing UVR availability.

A class of persistent organic pollutants, polychlorinated biphenyls (PCBs), are ubiquitous in the environment and human tissues which are continuously and long-term threatened. We aim to investigate the toxic effects and the underlying mechanisms of PCB153 using Caenorhabditis elegans as a model organism. Our findings demonstrated that exposure to an optimized concentration of 2 µmol/L PCB153 had adverse effects on C. elegans, led to reduction of lifespan, body length, frequency of body bending, and head wiggling. Additionally, this exposure led to an increase in the accumulation of reactive oxygen species, superoxide dismutase, lipofuscin and fat content within the organism. Furthermore, gene set enrichment analysis and whole transcriptome sequencing revealed, a significant up-regulation of Cytochrome P450 (CYP) family genes, which are crucial for the xenobiotics metabolism in C. elegans. Knocking down specific genes within the CYPs family, including cyp-35C1, cyp-35A5, cyp-35A3, cyp-34A1, and cyp-34A10, via RNA interference were able to reverse the shortening of lifespan and fat accumulation induced by PCB153 exposure. Moreover, a comprehensive a competing endogenous RNA network was constructed by integrating qPCR-validated differentially expressed mRNA along with lncRNA, circRNA, and miRNA identified by transcriptomic sequencing. This study emphasizes that PCB153 exposure leads to the physiological impairments, particularly fat accumulation and a shorter lifespan, through the modulation of CYP450 family genes. These findings contribute to our understanding of environmental pollutants and their impact on biological systems and provide valuable information on the toxic effects and potential risks associated with PCB153 exposure.

[This corrects the article DOI: 10.1039/C9RA01017C.].

BACKGROUND:The relationship between the triglyceride glucose (TyG) index and depression/anxiety remains unclear. This study prospectively examines whether elevated TyG index increases depression and anxiety risk. METHODS:Our analysis included 383,621 individuals from the UK Biobank who were free of depressive and anxiety disorders at enrollment. TyG index was calculated as ln (fasting triglyceride [mg/dL] × fasting blood glucose [mg/dL]/2). Depression and anxiety symptoms were assessed using primary care data and hospital inpatient records. Multivariable Cox regression analyses evaluated the prospective relationships of TyG index with incident depression and anxiety, with subgroup and sensitivity analyses. RESULTS:Over a median 13.75-year follow-up, 20,548 depression and 18,418 anxiety cases occurred. Participants with TyG index in the upper quartile had 29 % greater hazards for depression (HR = 1.29, 95 %CI: 1.23, 1.35) and 20 % elevated incidence of anxiety disorders (HR = 1.20, 95 %CI: 1.14, 1.25) when benchmarked against the reference group in the lowest quartile. Each standard deviation increase in TyG index was associated with a 21 % higher incidence of depression and an 15 % higher incidence of anxiety, respectively. Furthermore, these associations were stronger in participants aged <60 years, those with upper secondary or higher education, non-smokers (for anxiety), and ever-drinkers and females (for depression). CONCLUSIONS:TyG index is positively associated with incident depression and anxiety disorders, particularly in young adults, individuals with upper secondary or higher education, non-smokers (regarding anxiety), ever-drinkers and females (regarding depression).

Heavy metal exposure contributes to potential public health risk associated with carcinogenesis, particularly in vulnerable populations. This case-control study assessed the susceptibility of cancer patients and healthy individuals to toxic metals such as cadmium (Cd), nickel (Ni), and lead (Pb) in Gilgit-Baltistan, Pakistan, a region with high cancer prevalence. This was a preliminary biomonitoring study in this high risk region integrating demographic and environmental factors to investigate heavy metal exposure in relation to cancer incidence. This study was conducted in a holistic approach, which significantly provides contextual insight into exposure pathways and cancer disparities often overlooked by previously.The blood and urine samples from cohorts (n = 200) were analyzed for Cd, Ni, and Pb using atomic absorption spectrometer. A well-structured questionnaire was developed and administered to cancer patients to assess the association between heavy metals levels in biological samples and demographic, socioeconomic and environmental factors. The current results indicated that cancer patients exhibited higher blood Pb (0.8047 vs. 0.6754 mg/L, P < 0.001) and Ni (0.0694 vs. 0.0293 mg/L, P < 0.001) levels compared to healthy group. Conversely, healthy individuals showed potentially elevated urinary Ni (0.06168 vs. 0.4614 mg/L at P < 0.0001) and Pb levels (0.5455 vs. 0.3315 mg/L at P < 0.0001), suggesting a substantial differences in excretion system or exposure pattern. Subsequently, blood Cd concentrations were also varied with slightly higher levels observed in control than cancer patients (0.0718 vs. 0.0685 mg/L, P < 0.001). Furthermore, it was found that urinary Ni level was positively associated with age, smoking status, fruit/vegetables consumption, socioeconomic status, and physical activity (P < 0.05). Questionnaire findings revealed that cancer patients were predominantly older (> 55 years) with low socioeconomic backgrounds (44 %) and totally reliant on untreated water sources (54 %). Breast cancer was the most prevalent, accounting for 26 % of all reported cases followed by 8 % incidence of prostate cancer and 8 % of lung cancer among the local population. A moderate positive correlation was found between urinary Cd and Pb (r = 0.26) as well as urinary Ni and Pb (r = 0.23). However a strong negative association (r=-0.35) was observed between blood Pb and Cd.These findings underscore the urgent need for targeted public health interventions to reduce heavy metal accumulation in soil, water and foods to mitigate associated cancer risks.

The association between biological aging and dementia, as well as the underlying mechanism, remains limited. The aim of this study was to investigate the relationships of biological age (BA) with incident dementia and examine the underlying neurobiological mechanisms. This study used data from the UK Biobank, a prospective longitudinal study. We included participants free of diagnosed dementia at baseline. BA was evaluated from clinical traits using the Klemera-Doubal method biological age (KDM-BA) and PhenoAge algorithms. Genetic risk of dementia was assessed using the apolipoprotein E (APOE) ε4 genotype and polygenic risk scores (PRSs). Cox proportional hazard regression models were used to estimate the associations of BA and the combined effect of genetic risk and BA with dementia. In addition, the potential roles of brain structures (gray matter volume [GMV], cortical mean thickness, and cortical surface area) in the associations between BA and dementia were evaluated using mediation analysis. A total of 280,918 participants (mean age 56.80 years, 54.59% female) were enrolled in this study. Over a median follow-up of 13.58 years, 4,770 cases of dementia were recorded. Every SD increase in KDM-BA accelerations and PhenoAge accelerations was associated with a 14% (hazard ratio [HR] = 1.14; 95% CI 1.10-1.18) and 15% (HR = 1.15; 95% CI 1.12-1.19) higher incidence of dementia, respectively. Individuals with APOE ε4 and highest PhenoAge accelerations had the highest risk of dementia (HR = 4.20, 95% CI 3.69-4.78) compared with those with non-APOE ε4 and lowest PhenoAge accelerations, with significant interaction effect (Pinteraction < 0.001). We did not find significant modification effects of PRS on the associations between BA accelerations and dementia (Pinteraction = 0.347 for KDM-BA acceleration, Pinteraction = 0.279 for PhenoAge acceleration), as well as APOE ε4 on the association between KDM-BA accelerations and dementia (Pinteraction = 0.212). Mediation analysis showed that the identified GMV, cortical mean thickness, and cortical surface area partly mediated the association between BA accelerations and incident dementia, with proportion-mediated percentage ranging from 6.64% to 17.98%. Advanced BA may be a potential risk factor of incident dementia. The risk is possibly mediated through the widespread reduction of brain structures.

Table S1 shows the application of PRMT inhibitors in gastrointestinal tumors.

Cross-sectional evidence suggested that frailty was an important risk factor for cognitive impairment. However, previous studies only focused on baseline frailty status, not taking into consideration the dynamic changes in frailty status during follow-up. This study aimed to investigate the associations between changes in frailty status and cognitive impairment. This study used data from three prospective cohorts: China Health and Retirement Longitudinal Study (CHARLS), Health and Retirement Study (HRS) and English Longitudinal Study of Ageing (ELSA). Frailty status was evaluated by the frailty index and classified as robust, pre-frailty, or frailty. Cognitive function was assessed by memory, orientation and executive function. Linear mixed regression model was used to evaluate the longitudinal relationship between frailty statuses with cognitive impairment. A total of 49,864 participants with a mean of 2.70 follow-up times were included in the analysis. The median follow-up periods were 2.89 years in the CHARLS, 3.32 years in the ELSA, and 8.40 years in the HRS. Compared with robust participants, both pre-frailty and frailty were significantly associated with declined global cognitive function (beta -0.11, 95% CI: [-0.12, -0.09] for pre-frailty and beta -0.29 [95% CI: -0.30, -0.27] for frailty). Significant associations were also observed for memory (beta -0.27, 95% CI: [-0.29, -0.26] for frailty), orientation (beta -0.15 [95% CI: -0.17, -0.13] for frailty), and executive function (beta -0.21 [95% CI: -0.23, -0.19] for frailty). The subgroup analysis revealed that the CHARLS cohort had the greatest effect, and it was the main source of heterogeneity. Pre-frailty and frailty are associated with an increased risk of cognitive impairment, highlighting the need for early assessment and monitoring of frailty in at-risk populations.

Chronic kidney disease (CKD) is a significant global health issue associated with cardiovascular complications. While coffee, tea, and caffeine consumption have been linked to various health benefits, their relationship with CKD remains unclear. We conducted a cross-sectional analysis of NHANES 1999–2018 data, including 49,827 participants, assessing dietary intake through two 24-hour recalls and determining CKD status via the CKD-EPI equation. Our results showed that after adjusting for covariates, higher coffee consumption (> 352.5 g/day) was associated with lower odds of CKD (OR 0.760, 95% CI 0.701–0.823), as was tea consumption (OR 0.913, 95% CI 0.843–0.89). The highest tertile of caffeine consumption also showed a significantly reduced odds of CKD (OR 0.734, 95% CI 0.674–0.799). These findings suggest that coffee, tea, and caffeine consumption may be associated with better renal function, highlighting potential dietary strategies for CKD prevention.

Effects of ambient fine particulate matter (PM2.5) chemical constituents on preterm birth (PTB) are inconclusive. We performed a sibling-matched cohort study to explore the association between PM2.5 constituents and the risk of PTB. Changes in PM2.5 and the constituents (ΔPM2.5, ΔOC, ΔBC, ΔSO42−, ΔNH4+, ΔNO3−) were calculated as the value at a follow-up pregnancy minus exposures in prior pregnancy. A fixed-effect regression model was used to determine the association of the within-group variation in PM2.5 total mass and constituents with PTB risk. Gestational age differences within matched siblings were also treated as outcomes. A total of 62,334 sibling pairs were analyzed. We observed that each 10 μg/m3 increase in ΔPM2.5 in first, second, and third trimester were not statistically significant associated with the risk of PTB, but shortened gestational age was observed, with -0.009 week (95