Background The prevalence of chronic diseases among the Chinese occupational population is rising steadily, with hypertension and diabetes becoming important health concerns. Occupational health examinations (OHE) provide stable population coverage, standardized protocols, and fixed follow-up intervals, offering a robust data foundation for risk assessment. However, most existing hypertension prediction studies rely on cross-sectional data and mainly focus on clinic onset, failing to capture the dynamic progression and cumulation of individual risk. Objective To construct a machine learning-based risk prediction model for blood pressure abnormality in occupational populations, providing a reference for health risk stratification and targeted health interventions. Methods Longitudinal data from 2020 to 2023 were extracted from the occupational health examination database of an institution in Shanghai. After excluding individuals with hypertension in any of the first three years, 3710 workers who participated 4 consecutive years of OHE were included. Six categories of blood pressure-related indicators from 2020 to 2022 were selected, including basic information, lifestyles, occupational exposures, cardiovascular indicators, routine blood tests, and biochemical markers, comprising 30 variables in total. For feature engineering, continuous variables were processed to reflect three-year dynamic characteristics: level (mean), variability (variance), and temporal trend (slope). Categorical variables were incorporated using 2022 values. Least absolute shrinkage and selection operator regression was applied to identify variables for inclusion in the machine learning models. Five models (decision tree, logistic regression, random forest, support vector machine, and XGBoost) were employed to predict blood pressure abnormality risk in 2023. And then sensitive analysis was conducted. The optimal model was selected based on the area under the curve (AUC) of receiver operating characteristic. Feature importance and SHAP analyses were applied to interpret the final model. Results Feature engineering transformed 17 continuous variables into 51 secondary variables, combined with 13 baseline variables, resulted in 24 variables screened out by LASSO regression. The logistic regression model achieved the best performance. Feature importance analysis indicated that the dynamic trajectory of blood pressure played a central role in the model, complemented by other biochemical and lifestyle indicators. SHAP analysis further showed that the model’s ability to not only identify risks of high-normal blood pressure and hypertension but also quantify the specific contribution of individual examination indicators to predicted risk, supporting risk-stratified population management in occupational health management. Conclusion Based on an existing occupational health examination database and routinely collected data, this study has developed a risk prediction model for blood pressure abnormalities in occupational populations. By incorporating dynamic change characteristics from longitudinal examinations, the study demonstrates the feasibility of using routine health data for early risk identification and stratified management. However, its applicability is limited by the availability of repeated examination data and the focus on specific occupational groups, requiring further validation across broader populations and diverse clinic scenarios.

Background Long-term occupational health surveillance facilitates the identification of chronic health risks arising from occupational hazard exposures. However, under low-level exposure conditions in chemical enterprises, traditional workplace-centered risk assessment models are insufficient to fully explain the observed health effects among workers, highlighting the need for individual-focused health management strategies that focus on the worker. Objective To characterize long-term health trends among workers in a chemical enterprise and examine the limitations of workplace hazard monitoring and health surveillance under low-level multiple exposure scenarios, thereby providing a scientific basis for more comprehensive worker health protection measures. Methods We analyzed 972 occupational health examination records collected over a 15-year period (2010–2024) from a chemical enterprise, integrating these with enterprise hazard monitoring reports and workshop air monitoring of volatile organic compounds (VOCs). The annual counts and prevalences of abnormalities in liver function tests, metabolic syndrome-related indicators, and liver imaging were summarized. Temporal trends were evaluated using the Cochran-Armitage trend test. Time-related changes in abnormal health indicators among active workers were evaluated by generalized linear mixed-effects models (GLMMs), adjusting for age and sex. Individual longitudinal profiles were described for nine workers with continuous 15-year records. In addition, paired comparisons of health outcomes were conducted for 81 workers with both pre-employment and periodic examinations. Results Workplace hazard monitoring indicated that airborne concentrations of major occupational contaminants including VOCs, acids and bases, dust, and physical factors were below national occupational exposure limits. However, 62 VOC species—including chlorobenzene, chloromethane, and cyclohexane—were detected in workshop air, suggesting complex mixed organic solvent exposure. From 2010 to 2015, occupational health examination records were primarily based on physicians’ qualitative assessment, yielding generally low abnormality detection rates. During 2016–2024, data collection was complete, and the prevalences of abnormalities in liver function, metabolic syndrome-related indicators, and liver imaging among active workers remained relatively high. Trend analysis indicated that only the abnormality rates of total bilirubin (TBIL) and hypertension showed statistically significant temporal trends; other indicators exhibited no significant linear changes despite high prevalences. After adjusting for age and sex, the GLMMs showed that the abnormality rates of aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), TBIL, and hypertension decreased over time, whereas those of total cholesterol, triglycerides, and fatty liver increased. In a subgroup of 9 workers with continuous 15-year follow-up data, the cumulative number of abnormal health indicators increased in several individuals after 2016. Among the 81 workers with both pre-employment and periodic records, abnormalities in total cholesterol, triglycerides, body mass index, and fatty liver were significantly more prevalent after employment over time, whereas changes in liver function enzymes were not statistically significant. Conclusion With increasing age, workers exhibit a gradual deterioration in liver function and metabolic-related health indicators, reaching abnormality rates comparable to those reported in the general population. These findings suggest that both workplace-related and non-occupational factors jointly contribute to the observed health changes. Consequently, occupational health management should shift towards an "individual-centered" approach. Enhancing workers' health literacy, strengthening workplace health promotion, and extending occupational health services beyond the workplace are essential to comprehensively protect workers' health.

Objective To analyze the coverage of chronic disease-related indicators and the distribution of positive detection rates in occupational medical examinations (OME). Methods A total of 872 862 currently employed workers who underwent OME from 2015 to 2023 were selected as the study participants using a convenience sampling method. According to the year of OME, the study period was divided into three periods: 2015-2017, 2018-2020, and 2021-2023. The examination rates and positive detection rates of five chronic disease-related indicators, including obesity, high blood pressure, hyperglycemia, dyslipidemia, and hyperuricemia, were analyzed. Results Regarding the routine medical examination indicators in OME, the examination rates for systolic and diastolic blood pressure were both 97.4%, while those for body height and weight were both 6.8%. Among the mandatory or optional examination items for specific occupational groups in OMEs, the examination rates of fasting blood glucose, triglycerides, total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol were 35.2%, 18.5%, 18.5%, 7.8%, and 7.9%, respectively. Regarding items not included in OMEs, the examination rates of glycated hemoglobin and uric acid were 0.2% and 19.2%, respectively. The examination rates for systolic and diastolic blood pressure consistently exceeded 95.0%, the examination rates for fasting blood glucose, triglycerides, and uric acid ranged from 32.9% to 37.0%, 16.8% to 21.4%, and 16.9% to 24.1%, respectively, while the rates for body height and weight remained below 10.0% across these three periods. Among workers who completed corresponding OME items, dyslipidemia and hyperuricemia showed relatively higher positive detection rates, with rates of 23.2% and 23.0%, respectively. The positive detection rates of obesity, high blood pressure, and hyperglycemia were relatively lower, at 9.6%, 3.5%, and 1.4%, respectively. Across the three periods, the positive detection rates of dyslipidemia, hyperuricemia, obesity, high blood pressure, and hyperglycemia ranged from 18.0% to 33.7%, 7.0% to 28.5%, 7.8% to 10.9%, 3.3% to 3.9%, and 1.4% to 1.5%, respectively, all showing increasing trends with advancing OME periods (all P<0.01). Conclusion Current OME practices show a mismatch between the coverage of chronic disease-related indicators and the actual health risks among occupational worker populations. Although blood pressure monitoring is well implemented, basic physical indicators (body height and body weight) and key metabolic indicators (blood glucose, blood lipids, and uric acid) are insufficiently covered, limiting comprehensive assessment of occupational health risks. Optimization of monitoring strategies is urgently needed to improve data completeness.

As a primary approach to safeguarding workers' occupational health in China, the work-related injury insurance still has insufficient preventive measures for occupational groups. By reviewing the preventive measures embedded in Germany’s statutory accident insurance (Gesetzliche Unfallversicherung) and Japan’s workers’ accident compensation insurance, this study summarized their best practices and then proposed the following policy directions based on China’s specific context: strengthening the prevention-oriented institutional framework, increasing financial investment in occupational injury prevention, improving the incentive mechanisms of floating premium rate, and promoting data integration and intelligent applications in occupational health management. These measures are expected to shift China’s work-related injury insurance system from a compensation-oriented model to one that emphasizes comprehensive prevention and health promotion, thereby providing useful insights for better safeguarding the health of Chinese workers.

Objective:To explore the molecular mechanism by which interferon regulatory factor 1 (IRF1) affects hepatic ischemia-reperfusion injury (HIRI) by regulating the polarization of Kupffer cells.Methods:Twelve male healthy C57BL/6 wild-type mice weighing 20-25 g and aged 6-8 weeks were divided into a sham operation group ( n=6) and a HIRI group ( n=6); Twelve male healthy C57BL/6 IRF1 gene knockout (IRF1 -/-) mice weighing 20-25 g and aged 6-8 weeks were divided into a sham operation IRF1 -/- group ( n=6) and a HIRI IRF1 -/- group ( n=6). The levels of serum alanine transaminase (ALT) and aspartate transaminase (AST) in mice were measured, and hematoxylin-eosin (HE) staining of liver tissues was performed for Suzuki scoring to evaluate liver injury. Fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to evaluate the mRNA levels of IRF1 and tumor necrosis factor α (TNFα) in liver tissues. Flow cytometry and qRT-PCR were used to detect the proportion and functional changes of M1/M2-type Kupffer cells in liver tissues. IRF1 was overexpressed or knocked down in the mononuclear macrophage cell line ANA1, and a co-culture and hypoxia-reoxygenation system with the hepatocyte cell line AML12 was established. Flow cytometry was used to detect the apoptosis of AML12 cells. Results:At 12 hours after hepatic ischemia-reperfusion in wild-type mice, the liver tissue injury was the most severe. Compared with the sham operation group, the levels of serum ALT [(8 073±83) U/L vs. (81±19) U/L, q=13.59] and AST [(11 170±2 890) U/L vs. (412±210) U/L, q=13.77] in the HIRI group were significantly higher, and the differences were statistically significant (both P<0.001). The Suzuki score reached 5-6 points. At 12 hours after hepatic ischemia-reperfusion in IRF1 gene knockout mice, the liver tissue injury was not obvious. There were no significant differences in the levels of serum ALT [668 (514, 2 344) U/L vs. 254 (147, 285) U/L, q=2.52, P=0.348] and AST [1 936 (1 262, 2 003) U/L vs. 628 (423, 759) U/L, q=1.22, P=0.824] between the HIRI IRF1 -/- group and the sham operation IRF1 -/- group. Compared with the HIRI group, the ratio of M1/M2-type Kupffer cells in the liver of the HIRI IRF1 -/- group decreased [(0.958±0.090) vs. (2.788±0.258), q=2.06, P<0.0001], and the mRNA expression of TNFα decreased [(4.363±0.393) vs. (12.900±5.504), q=5.59, P=0.018], and the differences between the two groups were statistically significant. In the co-culture and hypoxia-reoxygenation experiment using ANA1 cells overexpressing IRF1 and AML12 cells, the proportion of AML12 hepatocytes in late apoptosis was higher than that in the control group [(14.05±4.25) vs. (3.15±1.16), t=2.85, P=0.047], and the difference was statistically significant. In contrast, when the expression of IRF1 was knocked down, the proportion of apoptotic AML12 cells decreased [(9.26±3.04) vs. (13.36±4.64), t=2.15, P=0.098], but the difference was not statistically significant. Conclusion:The IRF1 protein can regulate the polarization of Kupffer cells into M1-type macrophages, promote the inflammatory injury of the liver tissue after ischemia-reperfusion, and increase the apoptosis of hepatocytes.

OBJECTIVE To understand the drug resistance genes,virulence genes and molecular epidemiological characteristics of extensively drug-resistant hypervirulent Klebsiella pneumoniae(XDR-hvKP)strains causing hospital-associated infection.METHODS The clinical isolates of XDR-hvKP were collected from Tongling People's Hospital from Jul.2020 to Dec.2022.The strains were identified by matrix-assisted laser desorption ionization-time-of-flight(MALDI-TOF)mass spectrometry,the common drug resistance genes and virulence genes were an-alyzed by Sanger sequencing,the capsular serotypes were determined by wzi gene sequencing;the drug resistance genes,virulence genes and ST subtypes were observed by means of whole-genome sequencing(WGS)technique.RESULTS Totally 18 strains of XDR-hvKP were collected,55.56％(10/18)of which were isolated from blood specimens,and 61.11％(11/18)were isolated from critical care medicine department.Sanger sequen-cing analysis showed that all of the strains carried blaKPC-2 drug resistance gene;rmpA2(100.00％)and rmpA,i-roN,iutA(94.44％,17/18)were the major virulence genes carried by the strains.WGS analysis indicated that all of the 18 XDR-hvKP isolates carried multiple drug resistance genes such as blaKPC-2 carbapenemase and the viru-lence genes like capsule(rmpA/rmpA2),aerobacterin(iucABCD-iutA),Salmonella(iroN)and yersinin(ybt).All of the ST subtypes were ST 11,and all of the capsular serotypes were KL 64.CONCLUSIONS The ST11-KL64 type XDR-hvKP strains carry blaKPC-2;rmpA,rmpA2,iroN and iutA are the major virulence genes.It is necessary to strengthen the monitoring of key population of the key departments and make joint efforts of multiple departments to contain the transmission of the strains.

OBJECTIVES: Wild-caught Microtus fortis (M. fortis) at the age of 9-15 months can develop epithelial ovarian cancers similar to human epithelial ovarian cancers under natural conditions during experimental animal breeding, but its pathological types and biological characteristics remain unclear. This study aims to analyze the biological characteristics of spontaneous ovarian cancer in M. fortis, intending to develop M. fortis as an animal model for human epithelial ovarian cancer. METHODS: The female M. fortis (9-15 months old) with spontaneous ovarian cancer were selected as the experimental group, and healthy M. fortis from the same litter were selected as the control group. The ovarian pathological changes of the two groups were observed by dissection. Blood routine and biochemical indicators were measured by biochemical analysis. Hematoxylin and eosin (HE) staining was performed to observe the pathological changes in the ovarian cancer tissue of M. fortis. Immunohistochemical staining was used to detect the protein expression of common ovarian cancer markers, and real-time RT-PCR was used to analyze the transcription levels of ovarian cancer-related genes. RESULTS: Spontaneous ovarian cancer in M. fortis mainly affects both ovaries, with tumors appearing solid or cystic. HE staining and histopathological analysis confirmed that the ovarian tumors originated from ovarian surface epithelium. Compared to the control group, the experimental group showed significantly decreased hemoglobin (P<0.01), hematocrit (P<0.05), albumin (P<0.05), and blood glucose levels (P<0.01), while lymphocyte percentage (P<0.05), monocyte percentage (P<0.05), cholesterol (P<0.01), and progesterone (P<0.01) levels were significantly increased. Expression of ovarian cancer-related genes, including ID3, CDC42, RHOA, RB1CC1, NF1, PIN1, MIB1, PDS5A, MCM7, and MLH1, was significantly downregulated (all P<0.05), while PAX8 gene expression was significantly upregulated (P<0.05). Immunohistochemical results showed that Wilms' tumor gene 1 (WT1) protein was mainly distributed throughout the cell, with significantly higher expression in ovarian cancer M. fortis. Tumor protein 53 (TP53) was expressed in both healthy and ovarian cancer M. fortis and was distributed throughout the cell. Hepatocyte nuclear factor 1 beta (HNF1B) and progesterone receptor (PR) protein were highly expressed in the ovarian tissue of healthy M. fortis but were significantly reduced in the ovarian cancer M. fortis, though both were located in the cytoplasm. CONCLUSIONS Spontaneous ovarian cancer in M. fortis is serous ovarian cancer. Compared to healthy M. fortis, significant differences were observed in ovarian tissue morphology, biochemical indicators, ovarian cancer-related gene expression, and protein expression, which show similarity to the biological characteristics of human serous ovarian cancer. This suggests that M. fortis could be an ideal animal model for studying human serous ovarian cancer.
Female ; Ovarian Neoplasms/metabolism* ; Animals ; Carcinoma, Ovarian Epithelial ; Disease Models, Animal ; Humans ; Neoplasms, Glandular and Epithelial/metabolism* ; Ovary/pathology*

OBJECTIVES: Recent evidence suggests that the gut may be a primary site of metformin action. However, studies on the effects of metformin on gut microbiota remain limited, and its impact on gut microbial metabolites such as short-/medium-chain fatty acids is unclear. This study aims to investigate the effects of metformin on gut microbiota, short-/medium-chain fatty acids, and associated metabolic benefits in high-fat diet rats. METHODS: Twenty-four Sprague-Dawley rats were randomly divided into 3 groups: 1) Normal diet group (ND group), fed standard chow; 2) high-fat diet group (HFD group), fed a high-fat diet; 3) high-fat diet + metformin treatment group (HFD+Met group), fed a high-fat diet for 8 weeks, followed by daily intragastric administration of metformin solution (150 mg/kg body weight) starting in week 9. At the end of the experiment, all rats were sacrificed, and serum, liver, and colonic contents were collected for assessment of glucose and lipid metabolism, liver pathology, gut microbiota composition, and the concentrations of short-/medium-chain fatty acids. RESULTS: Metformin significantly improved HFD-induced glucose and lipid metabolic disorders and liver injury. Compared with the HFD group, the HFD+Met group showed reduced abundance of Blautia, Romboutsia, Bilophila, and Bacteroides, while Lactobacillus abundance significantly increased (all P<0.05). Colonic contents of butyric acid, 2-methyl butyric acid, valeric acid, octanoic acid, and lauric acid were significantly elevated (all P<0.05), whereas acetic acid, isoheptanoic acid, and nonanoic acid levels were significantly decreased (all P<0.05). Spearman correlation analysis revealed that Lactobacillus abundance was negatively correlated with body weight gain and insulin resistance, while butyrate and valerate levels were negatively correlated with insulin resistance and liver injury (all P<0.05). CONCLUSIONS Metformin significantly increases the abundance of beneficial bacteria such as Lactobacillus and promotes the production of short-/medium-chain fatty acids including butyric, valeric, and lauric acid in the colonic contents of HFD rats, suggesting that metformin may regulate host metabolism through modulation of the gut microbiota.
Animals ; Metformin/pharmacology* ; Rats, Sprague-Dawley ; Diet, High-Fat/adverse effects* ; Rats ; Gastrointestinal Microbiome/drug effects* ; Male ; Fatty Acids, Volatile/metabolism* ; Fatty Acids/metabolism*

OBJECTIVES: To investigate the impact of high expression of transmembrane and coiled helix structural domain 1 (TMCO1) on prognosis of gastric cancer and the possible mechanisms. METHODS: TMCO1 expression in gastric cancer and its effect on gastric cancer progression and prognosis were analyzed using publicly available databases and clinical data of patients undergoing radical surgery in our hospital, and its possible biological functions were explored using KEGG and GO analyses. In gastric cancer HGC-27 cells, the effects of lentivirus-mediated TMCO1 overexpression and TMCO1 silencing on cell apoptosis, proliferation, invasion and migration were examined. RESULTS: TMCO1 expression was significantly elevated in gastric cancer tissues (P<0.05), and its high expression was positively correlated with cancer progression (P<0.001) and a lowered postoperative 5-year survival rate of the patients (P<0.05). Bioinformatic analyses suggested that TMCO1 may affect gastric cancer cell apoptosis via Wnt signaling. In HGC-27 cells, TMCO1 overexpression significantly promoted tumor cell proliferation, inhibited cell apoptosis, and enhanced cell migration and invasion, whereas TMCO1 silencing produced the opposite effects. Western blotting showed that β-catenin levels were significantly upregulated in TMCO1-overexpressing cells and downregulated in cells with TMCO1 silencing. CONCLUSIONS TMCO1 is overexpressed in gastric cancer tissues, and its high expression promotes gastric cancer progression and affects long-term prognosis of the patients possibly by activating the Wnt/ β-catenin signaling pathway to inhibit apoptosis of gastric cancer cells.
Humans ; Stomach Neoplasms/metabolism* ; Apoptosis ; Prognosis ; Cell Line, Tumor ; Cell Proliferation ; Cell Movement ; Wnt Signaling Pathway ; beta Catenin/metabolism* ; Gene Expression Regulation, Neoplastic

ObjectiveTo explore the role of flurochloridone (FLC) on osteogenic differentiation and the potential mechanism of inhibiting bone formation, and to provide new insights into bone health risks associated with FLC pesticide exposure. MethodsNeonatal rat skull differentiation primary osteoblast model was used to investigate the effects of 1, 10 and 100 μmol·L^-1 FLC exposure on cell viability, osteogenic differentiation alkaline phosphatase (ALP) activity, and bone mineralization nodule formation, respectively. The potential mechanism underlying the inhibition of FLC on osteoblast differentiation was analyzed using osteogenic differentiation gene chip technique, and the expression of key genes and proteins in the pathway was validated using reverse transcription polymerase chain reaction (RT-PCR) and protein immunoblotting (Western blot) methods. ResultsExposure to FLC at a concentration of 100 μmol·L⁻¹ reduced cell proliferation, ALP activity, and the formation of mineralized nodules in primary osteoblasts. Gene chip analyses revealed that exposure to 10 μmol·L⁻¹ FLC induced 15 differentially expressed genes (DEGs). Among these, MMP9 and Tnf were up-regulated, while Nkx3⁃2, Tuft1, Bmp2, Col12a1, Pparg, Enam, Igf1, Bmp5, Bmp3, Calcr, Egf, Igfbp3, and Col14a1 were down-regulated. Results of protein-protein interaction analyses and gene ontology enrichment analyses indicated that FLC inhibited the BMP/SMAD pathway involved in osteogenic differentiation. FLC suppressed the protein expression of BMP2 and Osterix, as well as the expression of key genes critical for osteogenic differentiation and ossification, such as BMP2, Runx2, SMAD1, and SMAD5 in the BMP/SMAD pathway. ConclusionFLC affects osteogenic differentiation and bone formation potential by regulating the BMP/SMAD axis and the expression of osteogenic genes, suggesting its potential risk in bone metabolism.