Background Bipolar disorder imposes a substantial global health burden. While international clinical guidelines exist, real-world treatment patterns for bipolar disorder in China remains poorly characterized. This study aimed to characterize initial treatment selection, pharmacologic class distribution, and longitudinal prescription adjustments among inpatients with newly diagnosed bipolar disorder in Beijing, China, from 2010 to 2017. Methods A population-based longitudinal study was conducted utilizing data from the Beijing Medical Claim Data for Employees. We included 3034 inpatients newly diagnosed with bipolar disorder using ICD-10 code. We analyzed initial treatment patterns, annual prescription trends, and treatment modifications from the acute phase to maintenance phase. Results Over half (57.3%) of patients started on polypharmacy. Quetiapine was the most prescribed antipsychotic (43.8%), and lithium the most common mood stabilizer (37.7%). Alarmingly, the rate of treatment discontinuation reached 42.7% by the end of the first year after initiating treatment. Prescribing trends showed increasing use of aripiprazole and valproate over time. The high rate of antidepressant use (44.2% during follow-up) and significant treatment discontinuation highlight the complexity of real-world clinical management compared with international guideline recommendations. Conclusions These findings highlight a gap between real-world practices and guideline recommendations, underscoring need for initiatives to promote evidence-based, continuous care for bipolar disorder management in China.

Background/Objectives: This study aims to systematically deconstruct the shared genetic architecture underlying the comorbidity of hypertension (HTN) and type 2 diabetes (T2D) and evaluate how these divergent genetic architectures are associated with differential cardiovascular risk in East Asian population. Methods: This two-stage study first leveraged the largest genetic dataset from >300,000 East Asian individuals to identify pleiotropic loci between hypertension and type 2 diabetes using conjunctional false discovery rates, classifying them into coupling and uncoupling types based on effect directions. Corresponding polygenic risk scores (PRSs) were then constructed and validated in an independent family-based cohort. A logistic regression model was used to examine the associations between different genetic architectures and cardiovascular risk, including comorbidity onset and cardiovascular outcomes. Results: A total of 463 pleiotropic loci were identified, including 439 coupling loci and 24 uncoupling loci. The coupling PRS showed a significant association with single T2D (OR = 1.53; 95% CI: 1.08-2.18; p = 0.017), whereas the other associations were not significant, although the effect estimates were directionally consistent with our hypothesis. Crucially, coupling and uncoupling PRSs showed divergent cardiovascular risk profiles and exhibited distinct gene-environment interactions. Conclusions: Our findings suggest that coupling and uncoupling pleiotropy between hypertension and type 2 diabetes may contribute to the heterogeneity of cardiovascular risk in East Asians. Deconstructing genetic pleiotropy offers a potential framework for precision prevention strategies, although these findings are exploratory and warrant further validation in larger cohorts.

Background/Objectives: Atrial fibrillation (AF) is a complex polygenic disorder; its genetic architecture remains challenging to fully elucidate. Methods: In this study, we leveraged the extensive genetic overlap between AF and a spectrum of cardiometabolic and behavioral factors-collectively defined by Life's Essential 8 (LE8)-to advance our understanding of its etiology. Results: We first estimated significant genetic correlations between AF and all LE8 components (rg: -0.11 to 0.19) using LD score regression. We then applied conditional false discovery rate analysis and detected 970 pleiotropic loci associated with AF and at least one LE8 trait. Subsequent colocalization analysis identified 179 loci harboring shared causal variants between AF and one or more LE8 components, which were further refined into 137 distinct colocalized regions. Through region-based annotation and functional predictors, we finally prioritized 164 candidate genes from these colocalized loci, including 40 novel genes. These candidate genes were enriched in pathways related to heart development and regulation of cardiac contraction, and were also enriched among molecular targets of otological agents. Among all LE8 components, blood pressure demonstrated the most extensive shared genetic architecture with AF, supported by the strongest genetic correlation, highest pleiotropic enrichment, and the greatest number of colocalized loci with AF. Polygenic risk scores constructed from these colocalized loci demonstrated significant associations not only for AF but also for arrhythmia and heart failure. Conclusions: Our findings establish a genetic pleiotropy-informed framework that enhances the discovery of novel risk loci of AF and advances our understanding of the shared genetic architecture and potential biological mechanisms between AF and LE8 components.

OBJECTIVE:To systematically evaluate the association between anticoagulant therapy and long-term outcomes (all-cause mortality, stroke recurrence, and hemorrhage events) in elderly patients with cardiogenic stroke, thereby providing evidence for clinical decision-making. METHODS:A retrospective cohort study design was adopted. A total of 567 elderly patients with cardiogenic stroke from Liang-xiang Hospital in Fangshan District, Beijing, were followed up for 4 years. The primary outcomes included all-cause mortality, stroke recurrence, and hemorrhage events (including intracranial hemorrhage, gastrointestinal bleeding, urinary system bleeding, gingival bleeding, and skin and mucosal hemorrhage). Multivariable Logistic regression was used to analyze the association between anticoagulant therapy and each outcome. All statistical analyses were performed using R software (version 4.2.2). RESULTS:A total of 567 elderly patients were included in this study, with a mean age of (73.92±9.70) years and 49.74% being male. Among them, 142 patients (25.04%) received anticoagulant therapy. During the follow-up period, 266 deaths occurred (crude mortality rate: 46.91%), 107 patients had stroke recurrence (cumulative recurrence incidence: 18.87%), and 28 patients experienced bleeding events (cumulative hemorrhage incidence: 4.94%). Multivariable Logistic regression showed that elderly patients with cardiogenic stroke who received anticoagulant therapy had a significantly lower risk of death (OR=0.22, 95%CI: 0.12, 0.41, P < 0.001). No significant association was found between anticoagulant therapy and the risk of stroke recurrence or hemorrhage (P>0.05). CONCLUSION:Anticoagulant therapy is beneficial in reducing the risk of all-cause mortality in elderly patients with cardiogenic stroke, and no evidence was found that anticoagulant therapy increases the risk of stroke recurrence or hemorrhage. The study supports considering anticoagulant therapy to improve long-term survival in elderly patients with cardiogenic stroke, and larger prospective studies are still needed to further validate the findings.

Growing evidence reveals that indirect genetic effects (IGEs) contribute substantially to human complex traits. However, the genomic architecture and underlying mechanistic pathways of IGEs remain poorly understood. In this study, we employed a two-stage family study design to investigate IGEs and direct genetic effects (DGEs) on blood lipid profiles in the Fangshan Family-based Ischemic Stroke Study in China (FISSIC) cohort. We identified 16 IGE loci resulting in 14 candidate IGE genes, and 20 DGE loci resulting in 22 DGE genes, by an integrative functional mapping approach. The identified IGE genes were predominantly related to behavioral and neuropsychiatric phenotypes, while DGE genes were primarily involved in lipid metabolic pathways. To examine whether IGE genes are associated with lipids through behavioral factors in IGEs, we compared IGE estimates before and after adjusting for behavioral covariates, including healthy food score, drinking status, educational attainment, obesity, physical activity, sleep duration, and smoking status. Adjustment for behavioral factors attenuated the IGE associations, and mediation analysis further indicated that healthy food score partially mediated the association between IGE-GRS and HDL-C (mediation proportion: 17.9%), whereas the proportion mediated by behavioral mediators in the DGE pathway was negligible. Our results suggest that lifestyle behaviors may substantially mediate IGE effects, indicating that they could serve as modifiable factors to mitigate IGE-related genetic susceptibility for lipid or other complex traits.

Objective:To evaluate the genetic nurture effect of parental genotypes on the risk of ische-mic stroke(IS)in offspring and to elucidate the parental origin-specific differences in this effect.Methods:This study utilized data from the"Family Cohort of Common Chronic Non-communicable Diseases in Rural Areas of Northern China".A total of 530 core families and sibling pairs were selected,comprising 1 005 offspring.Single nucleotide polymorphisms(SNPs)within the CTNNA gene family(CTNNA1,CTNNA2 and CTNNA3)were detected.Using offspring as the unit of analysis,parental non-transmitted alleles were inferred based on Mendelian inheritance principles.Rigorous quality control was implemented for genotype imputation,ensuring high reliability of the inferred data.Linear mixed-effects models were constructed to estimate the genetic nurture effect of non-transmitted alleles on offspring IS.These models compared differences between genetic nurture effects and individual genetic effects,distin-guished between paternal and maternal effects,and calculated the statistic η to assess the relative magni-tude of parental effects.Results:A total of 1 005 offspring from 530 families were included,comprising 308 IS patients(30.6％)with a mean age of 56.3 years.Sixteen independent SNPs associated with IS genetic nurture effects were identified(9 in CTNNA2,6 in CTNNA3,and 1 in CTNNA1).The effect sizes ranged from-0.282 to 0.480,with rs117741773(CTNNA2)showing the strongest effect(0.480,95％CI:0.278-0.682).Only four of these SNPs exhibited concurrent individual genetic effects,which acted in the opposite direction to the genetic nurture effects.Parent-of-origin specific analysis revealed that 12 SNPs exhibited genetic nurture effects from a single origin:4 showed exclusively paternal effects(effect size:-0.298 to 0.945;η:1.21 to 63.83),and 8 showed exclusively maternal effects(effect size:-0.489 to 0.602;η:0.03 to 0.44).Conclusion:This study provides evidence that multiple IS susceptibility loci within the CTNNA gene family exhibit significant genetic nurture effects.The findings highlight the complex interplay between inherited genetics and the family environment.The heterogeneity of these effects based on parental origin underscores the significant role of parent-specific genetic nurture in the etiology of IS,offering new insights for understanding the missing heritability in stroke genetics.

Background/Objectives: To evaluate the association between HNF4A rs4812829 and type 2 diabetes (T2D) in a rural Chinese population and to investigate its interaction with blood lipids in the association. Methods: A total of 4496 participants free of diabetes at baseline from a family-based cohort in rural China were included. Demographic, lifestyle, and medical history data were collected via standardized questionnaires. Anthropometric and biochemical measurements were performed using standardized protocols and automated assays on fasting blood samples. Mixed-effects Cox proportional hazards models, accounting for familial clustering, were employed to examine the association between HNF4A rs4812829 and incident T2D risk. Additionally, multiplicative interaction terms were used to assess interactions. Results: After a median follow-up of 10.76 years, 895 incident T2D cases were identified. Under an additive genetic model, each additional G allele of rs4812829 was significantly associated with an increased risk of T2D (HR 1.38, 95% CI 1.19-1.59). A significant multiplicative interaction was observed between rs4812829 and HDL-C (p = 0.004). In genotype-stratified analyses, higher HDL-C levels were strongly associated with lower T2D risk among AA homozygotes (HR 0.04, 95% CI 0.003-0.43) and AG heterozygotes (HR 0.30, 95% CI 0.10-0.84), but not among GG homozygotes (HR 1.32, 95% CI 0.35-4.91). Conclusions: This study finds HNF4A intronic variant rs4812829 is significantly associated with the incident T2D risk in a rural Chinese population, and this association exhibits an interaction with HDL-C levels. These findings support further investigation of HNF4A-related lipid pathways and require replication in independent Chinese and multi-ancestry cohorts before genetic and lipid profiles can be considered for T2D risk stratification.

BACKGROUND:Cardiovascular disease (CVD) is the leading cause of premature mortality in bipolar disorder (BD). While lithium is a first-line mood stabilizer, its long-term cardiovascular safety profile remains debated, with conflicting evidence regarding potential toxicity versus protective effects. This study aimed to evaluate the association between lithium use and incident CVD risk in claims-based cohort of patients with BD. METHODS:We conducted a claims-based longitudinal cohort study using the Beijing Medical Claim Data for Employees (BMCDE) database from 2010 to 2017. Patients newly diagnosed with BD were categorized into lithium and non‑lithium user groups. Inverse probability weighting (IPW) was applied to control for baseline confounding. Weighted Cox proportional hazards models were used to estimate hazard ratios (HRs) for incident CVDs, including ischemic heart disease (IHD) and stroke. RESULTS:The study included 2945 patients (mean age 44.5 years) with a mean follow-up of 3 years. Lithium use was associated with a significantly lower risk of overall CVD (HR = 0.38; 95% CI 0.18-0.78) and specifically IHD (HR = 0.20; 95% CI 0.06-0.67). No significant association was found for stroke (HR = 0.69; 95% CI 0.27-1.75). Subgroup analyses revealed that this lower risk was most pronounced among older individuals, males, and those with pre-existing cardiovascular risk factors. CONCLUSIONS:Lithium use is associated with a reduced risk of incident CVDs, particularly IHD, in patients with BD. These findings suggest that lithium may confer dual psychiatric and somatic benefits, supporting its continued utility in high-risk populations.

Polycyclic aromatic hydrocarbons (PAHs) are a prominent category of ambient air pollutants worldwide, but our understanding of their potential health effects at ambient concentrations is severely limited. Our goal was to investigate the relation between ambient PAHs and daily hospitalizations for cardiovascular disease and explore its potential mechanism. This research included both observational and experimental studies. For population-based study, we collected data on daily hospitalizations for cardiovascular events in 184 major Chinese cities, which cover a population of 280 million individuals, for period of 2014-2017. We utilized a time-series quasi-Poisson regression model to assess the city-specific relations between PAHs and hospitalizations, and then employed a random-effects meta-analysis to aggregate the effect estimates across the cities. We also employed meta-regression models and stratified analyses to explore possible effect modifiers. For animal study, mice were exposed to varying doses of PAHs via tracheal instillation to evaluate the cardiac damage induced by PAHs. Potential mechanisms were elucidated through transcriptomic and proteomic sequencing. On the national scale, each interquartile range (IQR) increase in PAHs concentrations at 0-7 days was related to a 5.18 % (3.27 %-7.12 %) increase in hospital admissions for cardiovascular disease, 5.72 % (3.83 %-7.65 %) for ischemic heart disease, and 6.08 % (3.37 %-8.87 %) for ischemic stroke. The cardiovascular impacts of PAHs remained even after controlling for PM2.5. The associations were more pronounced in cities with lower socioeconomic level, or higher temperatures and relative humidity, as well as in subpopulations with elder age (P < 0.05). We also found consistent associations between each of the seven individual PAHs and cardiovascular outcomes. In animal models, PAHs exposure induces cardiac injury via inflammation and oxidative stress, potentially linked to the PI3K/AKT and MAPK signaling pathways. This nationwide study indicated that ambient PAHs could represent a distinct risk factor for cardiovascular disease. They may contribute to cardiac damage through the regulation of inflammation and oxidative stress.

Background: The hemoglobin glycation index (HGI) has been increasingly recognized for predicting cardiovascular outcomes. However, its association with all-cause and cardiovascular disease (CVD) mortality in the general population remains underexplored. This study aimed to investigate the nonlinear relationship between the HGI and mortality, identify risk thresholds, and evaluate HGI's clinical utility for individualized risk stratification. Methods: 4857 participants from the Fangshan Family-based Ischemic Stroke Study in China (FISSIC) were included. Death dates were obtained by reviewing the death certificates until 2024/7/31. During a median follow-up of 8 years, 652 deaths were identified, including 379 deaths due to CVD. HGI was calculated as HGI = Observed hemoglobin A1c (HbA1c)-Predicted HbA1c. Cox proportional hazard regression models and restricted cubic splines were constructed to assess the relationship of HGI with mortality risk. Results: This study revealed a J-shaped association of HGI with both all-cause and CVD mortality. For all-cause mortality, when HGI was below the threshold point (-0.58), the mortality risk slightly decreased with increasing HGI, with a hazard ratio (HR) of 0.821 (95 %CI: 0.666-1.011, P = 0.064). Conversely, when HGI exceeded-0.58, the mortality risk significantly increased with higher HGI (HR: 1.193, 95 % CI: 1.104-1.289, P < 0.001). CVD mortality exhibited similar threshold effects, with HGI <-0.58 trended toward lower risk (HR: 0.80, 95 % CI: 0.60-1.06, P = 0.114), whereas HGI >-0.58 showed marked risk elevation (HR: 1.23, 95 %CI: 1.11-1.36, P < 0.001). Conclusion: This study demonstrates a nonlinear relationship of HGI with both all-cause and CVD mortality.

OBJECTIVE:To assess the associations between brachial-ankle pulse wave velocity (baPWV), ankle brachial index (ABI) and all-cause and cardiovascular mortality in a rural population in north China. METHODS:The current study utilized the baseline data of Beijing Fangshan family cohort study and the data of the death surveillance system of the Beijing Fangshan District Center for Disease Prevention and Control. The main outcomes were all-cause mortality and cardiovascular mortality. Cardiovascular deaths which included deaths from coronary heart disease (CHD), stroke, heart failure, sudden cardiac death and arrhythmia, were coded according to the International Classification of Diseases, Ninth Revision (ICD-9) and Tenth Revision (ICD-10). The R4.2.2 software was used for statistical analysis, and the adjusted hazard ratios (HR) for all-cause and CVD mortality associated with baPWV and ABI were calculated using Cox proportional hazards regressions with shared frailty models. RESULTS:A total of 7 686 participants were followed up for a median of 6.35 years in Fangshan District, Beijing, China. Totally 576 deaths were identified, with a mortality density of 11.88/1 000 person-years, of which 335 deaths were from cardiovascular diseases. We found that baPWV (HR=1.40, 95%CI: 1.02-1.92) and ABI (HR=3.32, 95%CI: 2.57-4.28) were associated with all-cause mortality after adjusting for confounding factors. ABI was more strongly associated with cardiovascular mortality than baPWV. There was no significant difference in the risk of all-cause mortality among different subgroups. The risk of cardiovascular mortality was significantly increased in the participants with hypertension (HR=1.72, 95%CI: 1.30-2.27). CONCLUSION:baPWV and ABI were associated with all-cause and cardiovascular mortality in a rural population of north China. The association of ABI and cardiovascular mortality was more significant than that of baPWV. And abnormal baPWV or ABI was associated with cardiovascular mortality, especially in people with hypertension.

Background: While parental type 2 diabetes (T2D) is a known risk factor for offspring T2D, the differential impact of maternal versus paternal transmission remains debated. Methods: This prospective family-based cohort study enrolled 4508 diabetes-free adults from Northern China with a median 7.32-year follow-up. Using Cox proportional hazards models, we examined parent-of-origin effects on T2D incidence, adjusting for lifestyle, adiposity, and metabolic covariates. Results: Parental T2D conferred elevated offspring risk (adjusted HR = 1.82, 95% CI:1.44–2.30), and was predominantly driven by maternal transmission. Maternal T2D was robustly associated with offspring risk (HR = 1.89, 95% CI: 1.47–2.43), whereas paternal T2D showed no significant effect (HR = 1.27, 95% CI: 0.88–1.84). Offspring with only maternal T2D history exhibited the highest risk (HR = 2.55, 95% CI: 1.87–3.50; p = 4.70 × 10−9), persisting after full adjustment, while no significant association was observed for paternal diabetes. Lifestyle modified this association: healthy diet (diet score > 2 vs. ≤2: HR = 1.34 vs. 2.76; pinteraction = 9.10 × 10−4) and regular exercise (regular vs. unregular: HR = 1.13 vs. 2.10; pinteraction = 4.20 × 10−2) attenuated maternal transmission. Conclusions: Maternal T2D confers greater intergenerational risk than paternal T2D, with modifiable lifestyle factors mitigating this association. These findings highlight the importance of integrating maternal diabetes history into clinical risk stratification tools and prioritizing lifestyle interventions in the offspring of affected mothers to mitigate inherited risk.

Within-family genome-wide association studies (GWAS) can separate direct genetic effects from non-direct genetic biases introduced by analyses based on unrelated individuals, yet evidence regarding metabolic phenotypes remains sparse. Here, we aim to uncover non-direct genetic effects for metabolic traits and the role of diet in the non-direct genetic mechanism. We conducted family-based GWAS studies on six metabolic traits using data from full siblings (N = 777) and parent–offspring trios (N = 386). We calculated and compared within-family and population-based polygenic score (PGS) associations to identify non-direct genetic effects. Additionally, we assessed the parental indirect genetic effects of diet on offspring's metabolic traits. Within-sibship GWAS analyses were also conducted to evaluate the impact of non-direct genetic effects at the individual variant level. On average, the magnitudes of within-family PGS associations for metabolic traits showed a 35.2 β : 0.44, 95

Background/Objectives: This study aimed to investigate the association between dietary intake and the risk of type 2 diabetes mellitus (T2DM) in a rural northern Chinese population, and to explore potential gene-diet interactions that may influence T2DM susceptibility. Methods: A total of 1747 participants (1138 with T2DM and 609 without) were included, using baseline data from a family-based cohort study in rural northern China. Demographic characteristics, lifestyle factors, and medical history were collected via standardized questionnaires. Dietary intake was assessed using a semi-quantitative food frequency questionnaire, and anthropometric measurements were conducted according to standardized protocols. Based on findings from previous genome-wide association studies, several T2DM-related single-nucleotide polymorphisms were selected for genotyping. Generalized linear models accounting for familial clustering were employed to examine the associations between dietary intake and T2DM risk, and to assess gene-diet interaction. Results: A significant inverse association was observed between fruit intake and T2DM risk. Furthermore, a significant interaction was found between fruit consumption and the CMIP rs2925979 polymorphism: the protective effect of higher fruit intake was evident among individuals carrying the T allele but not among those with the CC genotype. Conclusions: These findings suggest that genetic variation may modify metabolic responses to dietary factors, particularly fruit intake. The results underscore the importance of considering gene-diet interactions in the prevention of T2DM.

ObjectiveTo investigate the parent-of-origin effects (POEs) of genes in the phosphatidyl inositol-bisphosphate (PIP2) hydrolysis pathway on type 2 diabetes (T2D) and preliminarily assess whether environmental factors may modify these effects.MethodsBased on data from an ongoing family-based cohort in Beijing, genetic information of 162 individuals from 53 case-parent triads was used to examine the POE of single nucleotide polymorphisms (SNPs) in the PIP2 pathway on T2D using maximum likelihood estimation based on a log-linear model. Stratified analyses were performed to assess the potential modification of POE by environmental factors, including smoking, drinking, and body mass index (BMI). Further enrichment analysis was conducted based on the POE results.ResultsA total of 214 SNPs from the PIP2 hydrolysis pathway had nominally significant (P < 0.05) POE on T2D, among which rs199684931 (RRm/RRp = 0.28, Pinteraction = 0.03), rs4750491 (RRm/RRp = 4.67, Pinteraction = 0.04), rs1090705 (RRm/RRp = 0.21, Pinteraction = 0.04), rs9663645 (RRm/RRp = 4.75, Pinteraction = 0.04), and rs200488869 (RRm/RRp = 4.75, Pinteraction = 0.04) from PRKCQ exhibited POE–BMI interactions. Specifically, maternal POE was reduced for rs199684931 and rs1090705 in individuals with higher BMI levels, while it increased for rs4750491, rs9663645, and rs200488869 in higher BMI groups. Additionally, 72 of the 214 significant POE SNPs were recognized as methylation quantitative trait loci, hinting at a possible role in regulation. The enrichment analysis validated these findings and the role of the genes in lipid metabolism.ConclusionThe current study provides a preliminary hint that SNPs in the PIP2 pathway genes may exhibit POE on T2D, contributing to its heritability. Notably, five SNPs in the PRKCQ gene demonstrated a potential interaction between POE and BMI on T2D. Further research is necessary to explore the underlying molecular mechanisms and to validate these findings in larger and independent populations.

BACKGROUND AND AIMS:Tobacco control policies enhance cardiovascular health at the population level, but their effects on high-risk individuals, such as those with type 2 diabetes mellitus (T2DM) or hypertension, remain unclear. This study evaluated the association between a tobacco control policy and hospital admissions for stroke and acute myocardial infarction (AMI) in hypertensive and T2DM individuals. DESIGN:Interrupted time series study. SETTING:Beijing, China. PARTICIPANTS:2 144 133 hypertensive and 1 446 750 T2DM patients residing in Beijing from January 2013 to June 2017. INTERVENTION:A comprehensive tobacco control policy package, incorporating all MPOWER components, was implemented in June 2015. MEASUREMENTS:Changes in admission rates and admissions for stroke and AMI. FINDINGS:Patients with T2DM showed immediate decreases in stroke [-9.4% (95% confidence interval = -13.3% to -5.3%)] and AMI [-24.3% (-31.2% to -16.7%)] admission rates after the policy. Similarly, the immediate post-policy change in stroke and AMI admission rates for hypertensive patients was -7.5% (-10.9% to -3.9%) and -23.0% (-29.2% to -16.3%), respectively. However, these reductions did not differ from those without either condition (P-interaction >0.05). For long-term trends, significant decreases were only seen for stroke [T2DM: -32.9% (-39.9% to -25.1%); hypertension: -33.3% (-39.3% to -26.7%)], but not AMI admissions, and again did not differ from those without either disease (P-interaction >0.05). Compared with healthy controls without T2DM or hypertension, patients with both conditions showed greater long-term reductions in stroke admission rates [-29.2% (-37.0% to -20.5%) vs. -14.4% (-26.3% to -0.5%), P-interaction = 0.05), whereas the opposite trend was observed for AMI admissions [7.9% (-15.9% to 38.4%) vs. -29.9% (-46.9% to -7.3%), P-interaction = 0.02]. CONCLUSIONS:Beijing's 2015 comprehensive tobacco control policy appears to be associated with reduced acute myocardial infarction and stroke admissions among high-risk groups (individuals with type 2 diabetes mellitus and hypertension), although admission rates showed no statistically significant difference between high-risk and non-high-risk populations.

Live attenuated and vero-cell-inactivated Japanese Encephalitis vaccines (LJEV, IJEV) have been in common use in young children in China since 1989 and 2004, associated with large reductions in Japanese encephalitis (JE) incidence. In 2013, northern China reported JE outbreaks among adults born before JE vaccine availability, a trend that worsened in 2017-2018. We conducted an open-label, randomized, controlled trial (ChiCTR2500103235) to assess the immunogenicity, immune persistence, and safety of three JE vaccine schedules in 40-69-year-olds to provide evidence for adult targeted JE immunization efforts. Outcomes were seroconversion proportions and seropositive prevalences; adverse events were monitored. The vaccines were immunogenic with no significant difference between vaccination groups. Seropositivity remained above 80% at one year post-vaccination. No serious adverse events occurred. All three schedules had good, persistent immunogenicity and favorable safety profiles in 40-69-year-old adults, providing evidence supporting vaccinating adults in response to the emergence of adult JE in northern China.

Background:Whether specific antihypertensive treatments increase cancer risk in patients with hypertension is still controversial. We aimed to estimate the associations of different antihypertensive treatments with cancer risk in real-world settings. Methods:A longitudinal cohort study was designed in a population of 1.2 million individuals from the CHinese Electronic health Records Research in Yinzhou (CHERRY). Propensity score matching (PSM) and the Cox regression model were used to estimate the associations. Several sensitivity analyses were then performed to reduce potential residual confounding. Results:From 2009 to 2019, a total of 270,320 patients with newly diagnosed hypertension were included in this study. With a median follow-up time of 7.7 years, 14,264 cases of cancer occurred. There were no significant associations of angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, or thiazide diuretics (TDs) with cancer risk (p > 0.05). Compared with other antihypertensive treatments, the use of calcium channel blockers (CCBs) was significantly associated with a marginally mild increase in the risk of all cancers (hazard ratio, HR = 1.05; 95% CI: 1.01, 1.09; p = 0.017). However, this association was no longer observed in sensitivity analyses excluding patients with less than 1, 2, or 3 years of follow-up. Nevertheless, the association between CCBs and the risk of endocrine cancer, especially thyroid cancer, still exists. Conclusion:Despite previous controversy, in this study, we found no clinically meaningful cancer risk associated with antihypertensive medications. However, the association of CCBs with specific cancer still requires further research. These findings should be interpreted with caution due to the potential residual confounding.

We aimed to determine the prevalence and risk factors of epiretinal membrane in a population-based study of residents aged 50 years and older in Fujian Province, Southeast China. The Fujian Eye Study is a population-based cross-sectional eye study in Fujian province, Southeast China. Residents aged 50 years and older were enrolled and did the questionnaire (educational background, income, blood type, disease history, medication history, smoking, drinking and tea consumption, et al.), physical and ophthalmological examinations with height, weight, systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), refraction, intraocular pressure (IOP), slit lamp, nonmydriatic fundus photograph and spectralis optical coherence tomography (OCT) imaging. Nonmydriatic fundus photograph and Spectralis OCT were used to assess ERM according to a standardised protocol. A total of 8173 residents were included in this study. Among them, 8.42% (95% CI 0.0782-0.0902) had ERM in at least one eye. Multiple logistic regression showed the presence of ERM was only associated with urbanization and geographic location, but not with age, sex, refractive error, IOP, SBP, DBP, HR, BMI, hypertension, diabetic mellitus, hyperlipidemia, education, income, smoking, alcohol and tea consumption. ERM is common among Chinese with 8.42% in at least one eye. Urbanization and geographic location are the only associated factors for ERM in Fujian Eye Study.