, Available online , doi: 10.3967/bes2026.119
, Available online , doi: 10.3967/bes2026.126
Objective Evidence on whether lifestyle factors modify associations between short-term exposure to fine particulate matter (PM2.5) and its chemical components and blood pressure (BP) among hypertensive adults remains limited. We investigated these modifications in the Jinchang Cohort. Methods We included 8,748 hypertensive adults with lifestyle data. Daily exposure to PM2.5 and five chemical components was estimated based on residential addresses. Linear mixed-effects models were used to assess interactions between pollutant exposure and lifestyle factors, complemented by stratified and longitudinal lifestyle-pattern analyses. Results Body mass index (BMI), smoking, alcohol consumption, and fruit intake significantly modified several pollutant-BP associations. For diastolic blood pressure (DBP), BMI significantly modified associations with PM2.5 and all five components, with interaction coefficients ranging from 0.11 to 0.16 mmHg. Per interquartile-range increase in exposure, PM2.5 was associated with a 0.77 mmHg increase in mean arterial pressure (MAP; 95% CI: 0.19–1.34) among participants with BMI ≥ 24 kg/m2, while nitrate (NO3-) was associated with a 1.13 mmHg increase in MAP (95% CI: 0.41–1.86) among current smokers. Negative interactions between fruit intake and PM2.5 and all five components were observed for DBP. Longitudinal analyses revealed stronger associations among participants with persistent smoking, alcohol consumption, or low fruit intake. Conclusion Lifestyle factors may modify BP responses to short-term exposure to PM2.5 and its components among hypertensive adults, highlighting potentially susceptible subgroups defined by adiposity, smoking, alcohol consumption, and fruit intake.
Xiuya Xing,
Yiming Gai,
Jingli Zhu,
Wenjun Cheng,
Qinglian Meng,
Qianyao Cheng,
Yinguang Fan,
Hong Su,
Huadong Wang,
Qinghua Xu,
Jian Cheng
, Available online , doi: 10.3967/bes2026.122
, Available online , doi: 10.3967/bes2026.124
Xunrong Cheng,
Jiyan Xu,
Jiayuan Yang,
Xin Yu,
Yanhong Fang,
Chuan Li,
Zhiyuan Tang,
Shaoqi Wang,
Rong Song,
Rubing Pan,
Weizhuo Yi,
Hong Su,
Jian Song
, Available online , doi: 10.3967/bes2026.123
Xiaoshuang Fu,
Sirui Chen,
Jiahao Chen,
Chen Chen,
Yuxin Yang,
Jun Wang,
Xiaoyan Ma,
Jingjing Yang,
Xi Meng,
Huibin Jiang,
Yongqiang Chen,
Zenghang Zhang,
Ziyue Zhu,
Wenhui Shi,
Zhipei Li,
Jiaonan Wang,
Xiaoming Shi,
Yuebin Lv
, Available online , doi: 10.3967/bes2026.116
To delineate the age- and sex-specific distribution patterns of key sex hormones [estradiol (E2), follicle-stimulating hormone (FSH), and testosterone (T)] in Chinese older adult population, with a particular focus on the oldest-old. Based on the “Healthy Aging and Biomarkers Cohort Study” (HABCS), this study included 5,545 participants (2,339 men and 3,206 women), and plasma concentrations of E2, FSH, and T were measured using chemiluminescence. Given the low detection rate of E2 in women (10.7%), it was analyzed as a binary variable (detected vs. undetected). Percentiles for these markers were calculated, and their distributions were analyzed according to sex, age, region, and sociodemographic factors. T levels in men showed a significant decline with age (median: 451.40 ng/dL in the 65–79-year-old group vs. 279.07 ng/dL in the centenarian group), while E2 levels remained stable (approximately 30 pg/mL). The E2 detection rate was highest in female centenarians (13.5%). FSH levels increased significantly with age in both men and women. Testosterone levels were higher in southern China and the detection rate of E2 was higher in educated women. This study provides key population-specific sex hormone reference percentiles for the elderly Chinese population and emphasizes that low E2 levels are a physiological norm in older women.
, Available online , doi: 10.3967/bes2026.104
, Available online , doi: 10.3967/bes2026.103
Ming Yang,
Jingtao Wu,
Lin Tao,
Weitian Tang,
Weitao Su,
Jiaxin Zhao,
Shengmei Zhang,
Yanbing Li,
Yaoyu Hu,
Ang Li,
Yichao Huang
, Available online , doi: 10.3967/bes2026.100
, Available online , doi: 10.3967/bes2026.092
, Available online , doi: 10.3967/bes2026.082
Huihuan Luo,
Yuanting Xie,
Xinyi Fang,
Bin Pan,
Yalan Xiao,
Jingyu Li,
Xiaoqing Hong,
Dongyang Han,
Wenyue Tu,
Haidong Kan,
Yanyi Xu,
Renjie Chen
, Available online , doi: 10.3967/bes2026.059
Objective Prior epidemiological research demonstrated an association between short-term exposure to fine particulate matter (PM2.5) and acute diabetic events, specifically diabetic ketoacidosis (DKA). However, mechanistic investigations remain lacking to substantiate biological link. Methods Twenty 18-week-old male BKS db/db mice were randomly assigned to two groups (n = 10 per group). Ambient PM2.5 suspension (5 mg/kg in 50 μL) or an equal volume of phosphate-buffered saline was intratracheally instilled once daily for three consecutive days. Within 24 hours after the final instillation (Day 3), serum β-hydroxybutyrate was quantified, and liver tissues were collected for transcriptomic profiling (RNA-seq) to explore potential mechanisms linking PM2.5 to ketone body levels (i.e., β-hydroxybutyrate). Results The PM2.5 group exhibited higher 3-hydroxybutyric acid levels than controls. The liver transcriptome differed significantly between groups. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses indicated differentially expressed genes were primarily associated with lipid metabolism. Further, 43 genes exhibited moderate-to-strong correlations with 3-hydroxybutyric acid (16 positive, 27 negative; coefficients 0.56 – 0.76). These genes are involved in fatty acid oxidation, lipogenesis, lipid transport, glucose metabolism, and inflammation. Conclusion PM2.5 exposure may enhance ketogenesis through disruption of hepatic glucolipid metabolism, providing mechanistic insight into its potential role in acute diabetic metabolic decompensation.
, Available online , doi: 10.3967/bes2026.107
Objective Pancreatic ductal adenocarcinoma (PDAC) is characterized by numerous severely hypoxic areas that drives tumor progression. Hypoxia-inducible factor-1 (HIF-1) mediates hypoxic responses mainly through HIF-1α upregulation. However, how HIF-1α influences PDAC aggressiveness remains unclear. Doublecortin-like kinase 1 (DCLK1) is overexpressed in PDAC and facilitates tumor development. This study investigated whether hypoxia regulates DCLK1 to enhance PDAC malignancy. Methods Bioinformatics analyses of Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) datasets were used to assess the prognostic values of HIF-1α and hypoxia score, and the correlation between HIF-1α and DCLK1 expression. mRNA and protein levels of HIF-1α, DCLK1, and epithelial-mesenchymal transition (EMT) markers were detected by reverse transcription polymerase chain reaction and Western blot. Transwell assays detected cell migration and invasion after the inhibition of either HIF-1α or DCLK1. Immunofluorescence staining was performed to analyze the association among HIF-1α, DCLK1, and EMT markers in PDAC tissues. Results Our study demonstrated significant overexpression of HIF-1α and DCLK1 in pancreatic cancer cells under hypoxic conditions. Hypoxia-driven HIF-1α upregulates DCLK1, fostering EMT and enhancing PDAC malignancy. DCLK1 inhibition in PDAC mitigates hypoxia-induced proliferation, invasiveness, and EMT progression. Conclusion HIF-1α boosts DCLK1 in hypoxia, enhancing pancreatic cancer malignancy via EMT. Overall, targeting DCLK1 in the hypoxic tumor microenvironment of PDAC could be a promising therapeutic strategy.
, Available online , doi: 10.3967/bes2026.101
Objective To identify critical exposure windows and thresholds of maternal residential greenness during pregnancy in relation to preterm birth (PTB). Methods Using the sibling-matched birth cohort data from the "China Green City" Nanning, China (2016–2022), conditional logistic regression and restricted cubic splines (RCS) were applied to assess the nonlinear dose-response associations between normalized difference vegetation index (NDVI) and PTB risk across different pregnancy periods and buffer zones. Results The median seasonal NDVI in Nanning was approximately 0.80, with relatively small differences between seasons. Pre-pregnancy residential NDVI (500 m buffer) was associated with higher PTB risk (adjusted odds ratio [OR] per interquartile range [IQR] = 1.16; 95% CI: 1.05–1.27), showing an upward trend with a risk threshold above 0.80. Third-trimester residential NDVI (500 m buffer) was associated with lower PTB risk (adjusted OR per IQR= 0.59; 95% CI: 0.54–0.65), showing an L-shaped dose-response curve with an inflection point at NDVI 0.30. Conclusion The third trimester and pre-pregnancy periods represent critical windows for the association between maternal residential greenness and PTB. Therefore, optimal levels of maternal residential greenness during pregnancy may reduce the risk of PTB.
Jianan Li,
Yiqi Qiu,
Mike Z. He,
Jianlong Fang,
Yu Wang,
Chenfeng Li,
Yueqiao Zhou,
Jiaonan Wang,
Chen Chen,
Chen Mao,
Xiaoming Shi
, Available online , doi: 10.3967/bes2026.091
Objectives While climate warming has driven concurrent heatwave-ozone events, the magnitude of their joint health impacts remains insufficiently quantified. Particularly, the specific ozone (O3) thresholds that trigger changes in heatwave mortality risks have not yet been determined. Methods A time-series study was performed using mortality data (2013–2018) from 59 counties across the Beijing-Tianjin-Hebei region and surrounding areas in China. Applying quasi-Poisson generalized linear models, the study quantified exposure-response relationships, additive interactions, and attributable fractions for the concurrent events. Heatwaves and O3 pollution events were classified by intensity and duration and combined to define different types of concurrent events. Results The study found that when O3 levels exceeded 130 μg/m3 for at least two days during heatwaves, significant additive interactions markedly intensified mortality risks, particularly for circulatory diseases. These concurrent events increased non-accidental mortality by 13.5%, along with circulatory (16.9%), respiratory (13.9%), nervous system (24.1%), and type 2 diabetes (27.0%) mortality. However, nervous system mortality exhibited unique sensitivity to O3 concentrations during concurrent exposure, following a distinct upward trend. Women, older adults (≥ 65 years), and individuals with circulatory diseases were identified as vulnerable populations. From 2013 to 2018, 29,730 deaths were attributable to concurrent events (52.8% circulatory), with the attributable fraction rising by 0.15% annually. Conclusions These findings provide essential empirical evidence for developing an integrated smart early-warning framework, establishing feasible protocols for alert grading, and supporting the design of targeted interventions for vulnerable populations.
, Available online , doi: 10.3967/bes2026.070
Objective Evidence regarding the association between long-term ozone exposure and chronic obstructive pulmonary disease (COPD) has primarily originated from high-income countries, with limited studies in China. Methods This nationwide cross-sectional study included 66,752 Chinese adults. Patients with COPD were identified using post-bronchodilator spirometry. Long-term ozone exposure was estimated using the average ozone concentrations in the grid cells covering the participants’ residential counties. Logistic regression was used to analyze the ozone–COPD association, adjusting for individual-level risk factors and socioeconomic factors. Additive interaction models were employed to assess the modification of the ozone–COPD association by county-level gross domestic product (GDP) per capita and temperature. Results Each 10-µg/m3 increase in annual ozone exposure was significantly associated with a higher risk of COPD (odds ratio [OR]: 1.172, 95% confidence interval [CI]: 1.039−1.322). In comparison with counties in the highest quartile of GDP per capita, the association between ozone exposure and COPD was stronger in counties in the lowest quartile of GDP per capita (P < 0.05). Counties with lower winter temperatures exhibited a stronger ozone–COPD association than those with warmer winters (P < 0.05). The relative excess risks due to the interaction of ozone with GDP per capita and winter temperature were 0.219 (95% CI: 0.095–0.344) and 0.254 (95% CI: 0.103–0.404), respectively. Conclusion Socioeconomically disadvantaged and colder regions exhibited greater susceptibility to ozone-related COPD. Targeted interventions aimed at these vulnerable countries are needed to mitigate inequalities in ozone-related COPD.
, Available online , doi: 10.3967/bes2026.115
, Available online , doi: 10.3967/bes2026.114
Objective Hyperuricemia (HUA) is a growing global health concern linked to gout, kidney damage, and cardiovascular disease, with onset increasingly occurring at younger ages. Recent evidence suggests that circadian rhythm disruption (CRD) contributes to this rising incidence, although the underlying mechanisms remain unclear. Gut microbiota (GM) and their metabolites are known to mediate CRD-related metabolic disorders. Therefore, this study investigated whether circadian disruption induces hyperuricemia and explored the role of GM in this process. Methods Male Sprague-Dawley rats were randomly divided into four groups: a normal 12-h light/12-h dark cycle (LD), constant light (LL), constant dark (DD), and circadian disruption (CD, light-schedule shifting). The CRD model was selected based on plasma uric acid levels. GM composition (16S rRNA sequencing) and plasma metabolomics (LC-MS) were analyzed. Functional effects were validated using indole-3-lactic acid (ILA) gavage, fecal microbiota transplantation (FMT), quantitative polymerase chain reaction (qPCR) for ABCG2, GLUT9, and Ras, and HIEC-6 small interfering RNA (siRNA) experiments. Results Compared with the LD group, the LL group exhibited elevated UA and reduced intestinal ABCG2, without changes in hepatic xanthine oxidase (XOD, the key rate-limiting enzyme in purine synthesis), renal function, or food intake. LL altered GM composition, reduced [Eubacterium]_ruminantium_group, and downregulated ILA. Exogenous ILA alleviated HUA and upregulated ABCG2. FMT from LL rats to antibiotic-treated LD rats increased UA and decreased ABCG2. Ras silencing abolished ILA-mediated ABCG2 upregulation in vitro. Conclusion Light-induced CRD reduces [Eubacterium]_ruminantium_group and ILA, possibly impairing uric acid excretion by downregulating intestinal ABCG2 through Ras, and leading to HUA.
Tianhong Han,
Ruobing Wang,
Jia Liu,
Nanxi Wang,
Hai Chen,
Qian Shen,
Meng Zhu,
Caiwang Yan,
Qiufen Sun,
Guangfu Jin,
Yun Qian,
Lu Wang
, Available online , doi: 10.3967/bes2026.117
Objective Reliable prediction models for identifying populations at high risk for gastric cancer (GC) are lacking. We aimed to identify GC predictive biomarkers in blood and construct a score to evaluate their effectiveness for risk prediction and population stratification in different genetic backgrounds. Methods We performed a nested case-control study using the clinical data of 1,352 individuals with a first diagnosis of GC and 1,502 controls from the Taihu Biobank of Tumor Biomarkers (TBTB) cohort. After dividing the participants into training and testing sets (7:3), we identified GC-associated blood biomarkers and constructed a blood test score (BTS) in the training set, followed by evaluation of its predictive performance and joint effect with polygenic risk score (PRS). Results The BTS comprising 14 biomarkers showed good discrimination, with area under the curve (AUC) of 0.743 (95% confidence interval [CI], 0.722–0.764) in the training set and 0.736 (95% CI, 0.703–0.769) in the testing set. Calibration and decision curve analyses indicated good calibration and clinical applicability. We observed a significant increase (Ptrend < 0.001) in the relative risk of developing GC in the BTS quintiles, with a similar trend for PRS. Compared with individuals with low BTS, those with intermediate and high BTS had higher GC risk, whereas the interaction between BTS and PRS with GC risk was not significant (P = 0.473). Conclusion Our study revealed an association among BTS, genetic factors, and GC risk. The BTS is valuable for predicting the risk of GC and discriminating high-risk individuals.
, Available online , doi: 10.3967/bes2026.097
Objective To develop an evidence-informed, immune-risk-stratified clinical practice guideline for the diagnosis, treatment, and follow-up of adult cryptococcosis in China. Methods A multidisciplinary panel formulated clinical questions; reviewed the available evidence; graded evidence certainty using the Grading of Recommendations Assessment, Development and Evaluation framework, and used a modified Delphi process combining anonymous online voting through Wenjuanxing with face-to-face consultation. Results Forty-four recommendations address immune-risk stratification, targeted screening, pathogen detection, pulmonary and central nervous system cryptococcosis, disseminated and other-site disease, antifungal therapy, intracranial hypertension, immune reconstitution inflammatory syndrome, treatment response, treatment nonresponse, and follow-up. Conclusion This clinical practice guideline complements existing Chinese guidance by providing a unified, disease-specific framework for adult cryptococcosis across immune states and anatomical sites, supporting simultaneous Chinese and English dissemination.
, Available online , doi: 10.3967/bes2026.102
Objective Wildfires have intensified globally; however, evidence of their long-term, multi-disease health impacts across countries at varying development levels remains scarce. Therefore, this study aims to quantify the associations between wildfires and cause-specific mortality while accounting for socioeconomic disparities. Methods Using an ecological panel dataset covering 62 countries from 2000 to 2023, we quantified the global associations between annual wildfire activity, measured using a satellite-derived burn index, and age-standardized mortality from 22 outcomes. Results After adjusting for socioeconomic indicators and temporal trends using mixed-effects models, higher wildfire activity was found to be independently associated with increased all-cause mortality and significantly more deaths from cardiovascular, digestive, and metabolic diseases. Stratified analyses revealed pronounced heterogeneity according to the Human Development Index (HDI): high-HDI countries experienced the largest mortality burden and the broadest range of affected chronic diseases, whereas low-HDI countries showed stronger links to deaths from HIV/AIDS and violence. Conclusion These findings indicate that the health risks of wildfires are neither uniform nor confined to respiratory outcomes but instead reflect the intersection of climate-related hazards, demographic transitions, and disease structure. As wildfires intensify under global warming, our results underscore the need for adaptive health systems and climate policies that consider the differential vulnerabilities across developmental contexts.
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