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.
Hengyu Deng,
Xuefeng Zang,
Enqi Zhao,
Yemei Huang,
Jing Liu,
Yangyu Zhou,
Chen Yang,
Wencong He,
Xiaozhuo Dong,
Hui Chen,
Ziqi Zhao,
Yuhan Zhou,
Xuelei Zang,
Chen Wang,
Liye Zhang,
Xinying Xue
, Available online , doi: 10.3967/bes2026.108
Objective Cryptococcus gattii (C. gattii) is a pathogenic respiratory fungus that rapidly disseminates through the central nervous system. The current clinical treatments for C. gattii infections are limited by prolonged therapeutic courses, high drug dosages, and insufficient antifungal options. This study aimed to explore the molecular mechanisms underlying amphotericin B (AmB) resistance in C. gattii and provide novel insights for developing targeted antifungal strategies. Methods A total of 27 clinical C. gattii isolates were subjected to antifungal susceptibility testing, multilocus sequence typing (MLST) for phylogenetic analysis and resistance-related mutation screening. The CRISPR/Cas9 system was used to construct an SSK2-knockout mutant (ssk2Δ-G4). Capsule and melanin assays, murine pulmonary infection models, and transcriptomic analyses were performed to verify gene function, evaluate therapeutic efficacy, and explore the underlying regulatory mechanisms. Results G4 isolates exhibited prominent AmB resistance with a novel SSK2 c.793A>G missense mutation (p.Thr265Ala; hereafter SSK2T265A). SSK2 knockout significantly enhanced AmB susceptibility, whereas SSK2T265A complementation partially restored the resistant phenotype. AmB treatment markedly reduced pulmonary fungal burden and inflammatory infiltration (P < 0.05) and improved survival (P < 0.001) in ssk2Δ-G4-infected mice. Mechanistically, this mutation upregulated CAT1 expression and enhanced the reactive oxygen species–scavenging capacity and oxidative stress tolerance. Conclusion SSK2 c.793A>G is closely associated with AmB resistance and functionally contributes to the resistance phenotype. SSK2 could serve as a potential therapeutic target for developing AmB synergistic sensitizers and as a research direction for future synergistic treatments of clinically resistant C. gattii strains.
, Available online , doi: 10.3967/bes2026.099
Objective: To investigate the clinical value of peripheral white blood cell (WBC) count and lactate dehydrogenase (LDH) levels in assessing early disease severity in patients with bee sting injuries after admission. Methods: This single-center, retrospective, exploratory cohort study consecutively enrolled adult patients with bee sting injuries who presented to the Emergency Department of the Wu'an First People's Hospital, Hebei Province, between August 2021 and September 2025. Based on their early clinical manifestations after admission and bee sting-adjusted Sequential Organ Failure Assessment (SOFA) scores, patients were classified into a mild group (adjusted SOFA score < 2) and a moderate-to-severe group (adjusted SOFA score ≥ 2). The initial peripheral venous blood test results obtained within 24 h of presentation to the emergency department were collected. A binary logistic regression model was constructed using WBC and LDH levels after natural logarithmic transformation and z-score standardization. Receiver operating characteristic (ROC) curves were generated using model-predicted probabilities, and areas under the curve (AUCs) were compared using the DeLong test. Model performance was further evaluated using calibration curves, decision curve analysis (DCA), and bootstrap internal validation with 1,000 resamples. Results: A total of 56 patients were included in this study. After excluding three patients with missing key data, 53 were included in the final analysis: 33 in the mild group and 20 in the moderate-to-severe group, of whom three died. The WBC count, neutrophil count, blood urea nitrogen (BUN), creatinine (Cr), and lactate dehydrogenase (LDH) levels were significantly higher in the moderate-to-severe group than in the mild group, whereas albumin levels were significantly lower (all P < 0.05). In the exploratory two-variable logistic regression model, both natural log-transformed and z-score-standardized WBC count [Zln(WBC)] and LDH level [Zln(LDH)] were associated with moderate-to-severe bee sting injuries early after admission. The AUCs of the WBC count, LDH level, and the combined model for identifying moderate-to-severe bee sting injuries were 0.780 (95% confidence interval [CI]: 0.638–0.922), 0.774 (95% CI: 0.627–0.922), and 0.827 (95% CI: 0.688–0.966), respectively. Although the AUC of the combined model was numerically higher than that of each individual marker, the DeLong test showed no statistically significant differences (combined model vs. WBC count, P = 0.414; combined model vs. LDH level, P = 0.178). The optimism-corrected AUC for the combined model after bootstrap validation was approximately 0.814. Conclusion: WBC count and LDH levels are readily available biomarkers that may serve as adjunctive indicators for early severity stratification in patients with bee sting injuries.
, 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/bes2026.106
Objective Measles elimination is threatened by the virus’s high infectivity (R0 = 12–18), waning immunity, and persistent immunity gaps. No global study has compared measles seroprevalence before and after elimination. We assessed whether countries that had eliminated measles achieved and maintained the herd immunity threshold and identified key vulnerabilities. Methods For countries with WHO-confirmed measles elimination, we systematically searched PubMed, Web of Science, and Google Scholar for seroprevalence data covering the three years before and the three years after elimination verification. Sample-size-weighted medians and interquartile ranges were calculated to describe seroprevalence, with stratified analyses by age group and country. The overall seroprevalence in the three years before and after elimination verification was also compared. Results Among 31 countries with measles elimination status (351 datasets comprising 562,772 participants), the overall median seroprevalence was 92.8%. Seroprevalence increased significantly with age (P < 0.001), from 56.5% among infants (aged 0–2 years) to 96.8% among older adults (aged > 40 years). Twenty-six percent of the countries had a seroprevalence of ≥ 92%, indicating a low risk of measles transmission, whereas 45% had a seroprevalence of < 85%, indicating a substantial transmission risk. The median seroprevalence decreased significantly from 94.9% during the three years before elimination verification to 83.5% during the three years after verification (P < 0.001). Conclusions Achieving measles elimination does not guarantee that population-level protection will be sustained. Despite high overall seroprevalence, important immunity gaps persist among infants and young children, and some countries do not maintain the required herd immunity threshold following elimination. Targeted interventions are needed to close immunity gaps and strengthen national population immunity to prevent measles resurgence.
Linmei Yao,
Chuanchun Mao,
Yuan Tian,
Yao Lu,
Lu Zhang,
Ge Shen,
Shuling Wu,
Min Chang,
Hongxiao Hao,
Leiping Hu,
Yuanjiao Gao,
Mengjiao Xu,
Yao Xie,
Minghui Li,
Ruyu Liu
, Available online , doi: 10.3967/bes2026.105
Background Serum markers predicting virologic relapse after pegylated interferon-alpha (Peg-IFN-α) discontinuation in patients with chronic hepatitis B (CHB) are lacking. This study aimed to evaluate serum pregenomic RNA (pgRNA), hepatitis B core-related antigen (HBcrAg), and hepatitis B surface antigen (HBsAg) as potential predictors of Peg-IFN-α treatment outcomes and post-treatment virologic relapse in treatment-naïve patients with CHB. Methods A total of 371 treatment-naïve patients with CHB were initially recruited for this study, and 327 patients who completed the entire follow-up period were included in the data analysis. Serum pgRNA and HBcrAg levels were measured by polymerase chain reaction (PCR)-fluorescence probing and enzyme-linked immunosorbent assay (ELISA), respectively. Results Among the 327 followed patients, 112 (34.25%) achieved a virologic response to Peg-IFN-α; 16 (14.29%) experienced virologic relapse over a median follow-up of 12 months. Baseline pgRNA (odds ratio [OR], 0.571), HBcrAg (OR, 0.539), and HBsAg (OR, 0.356) levels correlated with treatment efficacy, demonstrating predictive values with AUCs of 0.821, 0.879, and 0.781, respectively. HBcrAg levels at treatment discontinuation were associated with virologic relapse and showed potential as predictive biomarkers (AUC, 0.790). Conclusions Serum pgRNA, HBcrAg, and HBsAg correlate with Peg-IFN-α response in treatment-naïve CHB. Serum HBcrAg levels at Peg-IFN-α discontinuation show potential as a predictive biomarker for post-treatment virologic relapse and are associated with relapse risk, which may help identify high-risk patients after Peg-IFN-α cessation. Notably, this finding requires further validation in larger cohorts due to the limited number of relapse events.
, 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/bes2026.058
Background Traditional Health Technology Assessments (HTAs) commonly overlook the broader societal and economic externalities of vaccines, leading to systematic undervaluation and suboptimal resource allocation. This study aimed to develop and validate a comprehensive vaccine value framework and prioritize individual elements for future HTA integration. Methods A two-phase mixed-methods approach was employed for framework development. Phase 1 involved a systematic literature review of major databases to construct an initial conceptual framework. Phase 2 utilized a two-round modified Delphi study involving a multidisciplinary expert panel to validate and refine the framework. Six evaluative criteria, categorized under the dimensions of "Relevance" and "Feasibility," were weighted and applied to score each value element. Finally, a comparative analysis of the raw and weighted scores was conducted to identify five priority value elements for future integration into HTAs. Results The final validated framework comprised 5 value categories, 21 value elements, and 75 actionable value items. Although traditional metrics achieved the highest consensus, the following five "broader" elements emerged as top priorities for future inclusion: (1) Enhancement of Health System Security, (2) Macroeconomic Gains, (3) Social Equity and Ethics, (4) Prevention of Institutional Disruptions, and (5) Value to Other Interventions. Conclusion This study established a standardized multitiered roadmap to capture the multifaceted value of vaccines. By introducing actionable Tier-3 indicators, the framework operationalizes the assessment of broader vaccine benefits and offers a practical tool to support equitable and comprehensive evidence-based policymaking. Furthermore, the identification of the five priority value elements provides a feasible pathway for integrating extended vaccine externalities into future HTAs. Ultimately, this standardized framework will facilitate holistic decision-making and support the optimal allocation of resources within national immunization programs.
, Available online , doi: 10.3967/bes2026.057
Objective This study aimed to comprehensively characterize the genomic diversity, evolutionary dynamics, pathogenic potential, antimicrobial resistance, and secondary metabolite capacity of the Nocardia genus using whole-genome analyses. Methods We analyzed 751 publicly available Nocardia genomes using genome-based species delineation, phylogenomics, pangenome analysis, and comparative functional profiling to assess taxonomy, virulence, antibiotic resistance genes (ARGs), and biosynthetic gene clusters (BGCs). Results Phylogenomic analyses resolved five major clades: N. farcinica, N. carnea, N. asteroides, N. transvalensis, and N. otitidiscaviarum groups. The pangenome is open, comprising 467,566 gene clusters and reflecting extensive genomic diversity. Virulence factors and ARGs exhibit clade-specific patterns: the N. farcinica group harbors the most complete virulence repertoire and diverse resistance determinants, whereas the N. carnea and N. asteroides groups carry fewer genes. Analysis of 10,196 BGCs across 46 classes revealed conserved clusters of non-ribosomal peptide synthetases, terpenes, and type I polyketide synthases, with higher biosynthetic potential in the N. farcinica, N. transvalensis, and N. otitidiscaviarum groups. Several genomes encode BGCs associated with antibacterial or anticancer compounds. Conclusion This comprehensive genome analysis of Nocardia, representing the most complete sampling to date, clarifies phylogeny, reclassifies misassigned strains, identifies potential novel species, and reveals clade-specific patterns of virulence, resistance, and secondary metabolism.
, Available online , doi: 10.3967/bes2026.115
, Available online , doi: 10.3967/bes2026.087
, 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.
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/bes2026.110
, Available online , doi: 10.3967/bes2026.111
Coxsackievirus A16 subgenotype B1 is a major cause of hand, foot, and mouth disease in China, but the biological characteristics of the recently emerged dominant B1c clade remain unclear. This study compared the biological traits of clades B1a, B1b, and B1c isolated from Fujian Province. The RD cells most effectively supported viral replication. At 40°C, B1b was temperature-sensitive. Replication titers ranked B1c > B1b > B1a, whereas cytotoxicity ranked B1b > B1c > B1a. B1c exhibited superior replication fitness and thermotolerance without increased cytotoxicity, which explains its codominance with B1a. B1c may enhance transmission, but not clinical severity. Further in vivo and molecular surveillance studies are required to validate these findings.
Shaopeng Guo,
Xiaohui Sun,
Hongxuan Yan,
Kejia Huang,
Chen Chen,
Chi Pan,
Xianyun Wang,
Xiao Liu,
Ao Li,
Weijing Wang,
Jie Xu,
Feng Ning
, Available online , doi: 10.3967/bes2026.112
, 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
, Available online , doi: 10.3967/bes2026.109
To critically examine emerging technologies for assessing foodborne-pathogen viability and to evaluate their relevance for improving food safety monitoring and public-health risk assessment. This review examines the literature on viability-detection using biological indicators such as membrane integrity, infectivity, and virulence. It addresses technologies such as viability dye-based PCR, RNA and CRISPR detection methods, biosensors, bacteriophage assays, Raman spectroscopy, and AI-supported analysis. Compared to conventional culture-based and DNA-only molecular methods, viability-focused techniques support more biologically meaningful detection, particularly for viable but non-culturable (VBNC) cells that may retain pathogenic potential. However, assay performance varies depending on food-matrix complexity, the presence of inhibitors, sensitivity limitations, and the degree of validation. Integrated systems combining multi-modal sensing, microfluidics, and machine learning have shown increasing promise for rapid on-site application, although standardization and regulatory validation remain limited. The emerging viability-focused technologies substantially refine microbial-risk assessment by accurately capturing the infectious potential of foodborne pathogens, including traditionally undetected VBNC populations. Nevertheless, integrating these technologies into routine surveillance remains constrained by matrix interference and the absence of standardized protocols. Future efforts must prioritize developing matrix-resilient methodologies and establishing regulatory validation frameworks to facilitate their practical implementation in food safety management.
, Available online , doi: 10.3967/bes2026.113
, 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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