Objective To investigate the prevalence of Clonorchis sinensis human infections in Congjiang County, Guizhou Province in 2023, so as to provide insights into formulation of the clonorchiasis control strategy. Methods Congjiang County was divided into eastern, western, southern, northern and central areas according to the geographical locations, and one township was randomly sampled from each area. Then, each administrative village was randomly sampled from each township, and 200 permanent residents over 3 years of age were randomly sampled from each village. Participants’ stool samples were collected for detection of C. sinensis eggs with the Kato-Katz technique (two slides for each stool sample), and the prevalence and intensity of C. sinensis infections were calculated. In addition, the risk factors of clonorchiasis were identified among participants using a questionnaire survey. Results A total of 1 001 residents were included, and the prevalence of C. sinensis infections was 16.28% (163/1 001), with mild infections as the predominant category of infection intensity [73.01% (119/163)]. The prevalence rates of C. sinensis human infections were 30.50% (61/200), 1.50% (3/200), 30.35% (61/201), 12.50% (25/200), and 6.50% (13/200) at five survey sites, respectively (χ² = 107.03, P < 0.05), and there was a significant difference in the prevalence of C. sinensis infections between men [22.44% (112/499)] and women [10.16% (51/502)] (χ² = 27.71, P < 0.05). The prevalence of C. sinensis infections was relatively high among participants at ages of 60 to 70 years [26.14% (23/88)], public servants [46.15% (6/13)], and Han ethnic participants [33.33% (5/15)]. The prevalence of C. sinensis infections was higher among participants with a habit of consuming raw or un-dercooked freshwater fish and shrimp [22.06% (90/408)] than among those without the habit [12.31% (73/593)] (χ² = 16.85, P < 0.05), and there was no significant difference in the prevalence of C. sinensis infections between participants with [13.99% (41/293)] and without separation of raw and cooked chopping boards [17.23% (122/708)] (χ² = 1.59, P > 0.05). In addition, the prevalence of C. sinensis infections was 8.70% (2/23) and 16.46% (161/978) among participants with and without fever complicated by discomfort in the right upper abdomen during the past half year (χ² = 0.99, P > 0.05). Conclusions The prevalence of C. sinensis human infections was high in Congjiang County, Guizhou Province in 2023, and infections predominantly occurred among young and middle-aged men. Intensified health education among high-risk residents and alteration of dietary habits of consuming raw or undercooked freshwater fish or shrimp are recommended to reduce the prevalence of C. sinensis human infections.

Metabolic associated fatty liver disease (MAFLD) is fundamentally driven by an imbalance in hepatic fatty-acid flux: the influx of fatty acids exceeds the liver’s capacity for disposal, resulting in excessive hepatic lipid accumulation, predominantly in the form of triglycerides (TGs). The occurrence and progression of MAFLD depend on disordered regulation across multiple metabolic steps, including fatty-acid uptake, de novo lipogenesis (DNL), fatty-acid oxidation (FAO), and very low-density lipoprotein (VLDL) export. Forkhead box protein O1 (FOXO1) is a key transcriptional regulator within the hepatic network coordinating glucose and lipid metabolism. Under metabolic stress and insulin resistance (IR), FOXO1 expression is frequently increased, whereas its inhibitory phosphorylation is reduced. These changes enhance FOXO1 nuclear localization and transcriptional activity, thereby reprogramming the expression of genes related to metabolism in the liver. Because hepatic lipid deposition is the central pathological feature of MAFLD, the functional status of FOXO1 directly influences hepatic lipid homeostasis. Growing evidence suggests that FOXO1 can exert bidirectional, environment-dependent effects on hepatic lipid accumulation; however, the molecular basis for this functional switch remains incompletely understood. This review systematically summarizes the biological functions and regulatory mechanisms of FOXO1 and its roles in hepatic lipid metabolism, with a particular focus on its crosstalk with insulin signaling. FOXO1 expression is shaped by RNA modifications and epigenetic regulation mediated by non-coding RNAs. Its transcriptional output is precisely governed by post-translational modifications—such as phosphorylation and acetylation—as well as by coordinated nucleocytoplasmic shuttling. Notably, these regulatory patterns vary markedly across nutritional states, degrees of insulin resistance, and stages of disease. In the fed state, insulin/IGF-1 signaling activates the PI3K-AKT pathway, promoting the inhibitory phosphorylation of FOXO1 and facilitating additional modifications, including acetylation, methylation, and ubiquitination. Together, these events drive FOXO1 export from the nucleus and dampen its transcriptional activity, suppressing gluconeogenesis and constraining lipogenic programs. Conversely, during fasting or when insulin signaling is weakened, FOXO1 inhibition is relieved. FOXO1 accumulates in the nucleus, binds to DNA, and regulates the transcription of downstream target genes. Mechanistically, FOXO1 can aggravate hepatic lipid accumulation by activating genes involved in TG synthesis while repressing FAO-related pathways, thereby favoring storage over oxidation. However, under specific conditions, FOXO1 may also alleviate the hepatic lipid burden by promoting TG hydrolysis and enhancing VLDL secretion, thereby reducing the net hepatic lipid load. In addition, lipotoxic signals mediated by ceramides and diacylglycerols (Cer/DAG) activate atypical protein kinase C (aPKC), further exacerbating the disruption of the AKT-FOXO1 axis. This vicious cycle ultimately produces a metabolic paradox in which increased hepatic glucose output coexists with persistent, insulin-independent lipogenesis, accelerating MAFLD progression. Importantly, FOXO1 regulation is not uniform: during early metabolic overload, insulin-mediated suppression may remain effective, whereas in advanced insulin resistance, the loss of AKT control permits sustained FOXO1 activity. Such stage-dependent dynamics may help explain why FOXO1 can either promote steatosis or, in certain contexts, support programs that facilitate lipid turnover. Accordingly, interventions should be liver-specific and tuned to the disease stage, aiming to curb maladaptive FOXO1 signaling while preserving its capacity to promote triglyceride hydrolysis and VLDL secretion when advantageous. Overall, this review offers an important perspective on MAFLD pathogenesis, emphasizing FOXO1 as a potential therapeutic target and providing a theoretical basis for developing liver-specific, disease-course-dependent precision interventions.

Neurological disorders such as post-stroke hemiplegia, spinal cord injury, and Parkinson disease represent a major global health burden. Brain-computer interface (BCI), which creates direct communication pathways between the nervous system and external devices, offers a promising strategy for functional restoration. The long-term efficacy of such BCI fundamentally depends on the performance of biomaterials at the neural interface. Ideal materials must concurrently satisfy biocompatibility, electrical conductivity, enduring chemical stability, and mechanical compatibility with brain tissue. This review systematically outlines the application of conductive polymers, inorganic nanomaterials, natural biomaterials, and composites in BCI, with a focus on how advanced designs, such as bionic and encapsulated electrodes, improve signal fidelity and surgical feasibility through structural innovation. It further summarizes key material-modification techniques and analyzes the complex foreign-body response orchestrated by microglia, astrocytes, and peripheral immune cells. Finally, it provides insights into future research directions and clinical translation of BCI-based neurorehabilitation, while highlighting critical challenges including long-term biosafety and the establishment of standardized evaluation frameworks, aiming to bridge the gap between laboratory innovation and effective clinical deployment.

ObjectiveTo investigate the association of physical activity and balance ability with disability, and to further examine the mediating role of balance ability in the relationship between physical activity and disability. MethodsBased on data from 2021 to 2023 National Health and Nutrition Examination Survey (NHANES) cycle, a multivariable Logistic regression model was constructed to evaluate the independent association of physical activity and balance ability with disability, with covariates adjusted in four steps. An interaction model was further developed to assess the multiplicative interaction between physical activity and balance ability. Mediation analysis was performed using the Baron and Kenny three-step approach to examine the mediating role of balance ability, and the proportion of the mediation effect was calculated. The significance of the mediation effect was assessed using the Delta method, and robustness was verified through the Bootstrap method with a fixed random seed. Multiple sensitivity analyses were conducted to ensure the stability of the results. ResultsA total of 3 902 participants were included, with a prevalence of disability of 17.7%. Multivariable regression analysis showed that, after adjusting for all covariates, both light-intensity physical activity (LIPA) (OR = 0.489, 95%CI 0.380 to 0.629, P < 0.001) and high-intensity physical activity (HIPA) (OR = 0.493, 95%CI 0.371 to 0.656, P < 0.001) were significantly associated with a reduced risk of disability, whereas impaired balance ability was significantly associated with an increased risk (OR = 1.579, 95%CI 1.266 to 1.970, P < 0.001). The interaction effect analysis showed that the interaction between physical activity and balance ability were not significant (P > 0.05), however, the main effect of LIPA remained robust (β = -0.597, SE = 0.221, OR = 0.550, P = 0.007), while impaired balance ability was significantly associated with an increased risk of disability (β = 0.577, SE = 0.231, OR = 1.780, P = 0.012). The mediation analysis further indicated that balance ability played a robust mediating role in the association between LIPA and disability, with a mediation proportion of 21.1%. The indirect effect (a × b) was statistically significant (P < 0.001), and the 95% confidence intervals derived from the bootstrap method did not include zero. ConclusionPhysical activity and balance ability are significantly associated with disability, and balance ability may mediate the relationship between physical activity and disability, highlighting its potential value in disability risk assessment and intervention strategies.

OBJECTIVE To investigate the efficacy and safety of omadacycline in the treatment of macrolide-unresponsive Mycoplasma pneumoniae pneumonia （MUMPP） in children. METHODS A retrospective study was conducted on children aged 1-18 years old with MUMPP who were hospitalized in the Department of Pediatrics， the First Affiliated Hospital of Xinjiang Medical University from January 2022 to June 2025. According to the selection of secondary antibiotics after 72 h of initial treatment with macrolides， they were divided into the omadacycline group and the doxycycline group. Based on conventional treatment， children in the omadacycline group were given intravenous infusion of 2.4 mg/kg （once daily） of omadacycline tosylate， while children in the doxycycline group were given oral doxycycline hydrochloride tablets at 2 mg/kg （twice daily）. The efficacy and safety were compared between the two groups of pediatric patients. Univariate analysis and multivariate Logistic regression analysis were performed on clinical efficacy， and subgroup analysis along with multiple sensitivity analyses were conducted to verify the robustness of the conclusions. RESULTS A total of 284 children with MUMPP were included in this study， with 142 in the omadacycline group and 142 in the doxycycline group. In terms of efficacy， although the hospitalization time of children in the omadacycline group was longer than that in the doxycycline group （ P ＜0.05）， the lung lesion absorption rate and clinical efficacy were significantly higher or better than those in the doxycycline group （ P ＜0.05）. The results of multivariate Logistic regression analysis showed that medication （OR＝5.300， 95%CI： 2.526-11.123）， length of hospital stay （OR＝1.348， 95%CI： 1.167-1.556）， and medication duration （OR＝1.422， 95%CI： 1.169-1.729） were influencing factors of clinical efficacy （ P ＜0.05）. The subgroup analysis results showed that the clinical efficacy of omadacycline was significantly better than that of doxycycline in all subgroups （ P ＜0.05）. The results of multiple sensitivity analysis showed that the regression coefficients B of the four models （gradually adjust variables） before and after inverse probability of treatment weighting were significantly greater than 1 （ P ＜0.05）. In terms of safety， there was no statistically significant difference in the inci dence of adverse drug reactions between the two groups of patients （ χ 2 ＝0.447， P ＝0.504）. CONCLUSIONS In the case of hospitalization and prolonged medication， the efficacy of omadacycline in treating childhood MUMPP is superior to that of doxycycline， and its safety is good.

BackgroundThe violent aggressive behaviors of patients with schizophrenia usually have the characteristics of suddenness， unpredictability， high severity， and great difficulty in prevention. Early identification and accurate assessment of their risk of violent aggression have significant clinical significance. ObjectiveTo construct a predictive model for the violence risk in hospitalized patients with schizophrenia， to identify the key factors influencing the occurrence of violent behavior in these patients， so as to provide references for clinical precise quantitative assessment and early intervention. MethodsA total of 200 patients with schizophrenia who were hospitalized at Taiyuan Psychiatric Hospital from March 2022 to September 2024 and met the diagnostic criteria of the International Classification of Diseases， eleventh edition （ICD-11） were collected to form the modeling cohort. They were randomly divided into a training set （n=140） and a test set （n=60） at a ratio of 7∶3. Based on the least absolute shrinkage and selection operator （LASSO） regression algorithm， the feature variables were screened and dimension-reduced. The support vector machine （SVM） from machine learning was selected for model training and prediction. The discrimination efficacy of the model was evaluated by the area under the receiver operating characteristic （ROC） curve （AUC）， accuracy， precision， sensitivity， specificity， F1 value， and Brier value. ResultsLASSO regression screening identified 16 feature variables. Pearson correlation analysis revealed a positive correlation between prior violent behavior frequency and clinical psychiatric symptom scores （r=0.580， P<0.01）， a positive correlation between hospitalization compliance and current disease status （r=0.550， P=0.003）， and a positive correlation between educational level and family per capita monthly income （r=0.367， P<0.01）. The SVM model achieved an AUC of 0.853， accuracy of 0.800， precision of 0.810， sensitivity of 0.895， specificity of 0.636， F1 value of 0.850， and Brier value of 0.168. ConclusionThe SVM model has a relatively high level of applicability and overall predictive performance in the assessment of violent risk in schizophrenia patients， which is helpful for the early identification of violent risks in such patients. ［Funded by Specialized Research Project for Enhancing the Competence of Health Professionals in Taiyuan City （number， Y2023006）］

Background As common public facilities essential to daily life, hair and beauty salons frequently contain various airborne toxic and hazardous pollutants potentially leading to adverse health effects for salon practitioners. Objective To characterize the indoor air pollution profiles of common contaminants in hair and beauty salons in Shanghai and to evaluate the associated health risks for practitioners, in order to provide a scientific basis for strengthening the public health management in Shanghai and protecting the health of practitioners. Methods The air quality monitoring data of hair and beauty salons in Shanghai from 2016 to 2024 were obtained from the “Health Hazard Factors Monitoring Program for Public Places” of the National Institute of Environmental Health, Chinese Center for Disease Control and Prevention. Monitoring indicators included particulate matter ≤10 μm in aerodynamic diameter (PM₁₀), particulate matter ≤2.5 μm in aerodynamic diameter (PM_2.5), formaldehyde, ammonia, benzene, toluene, and xylene. Indicator compliance rates were calculated across various years in accordance with GB 9666-1996 Hygienic standard for barber shop and beauty shop and GB 37488-2019 Hygiene indicators and limit for public places; specifically, PM_2.5 was assessed against the limits stipulated in GB/T 18883-2022 Standards for indoor air quality. A questionnaire survey was conducted among salon practitioners to collect weekly working days and daily working hours. The non-carcinogenic risks associated with inhalation exposure to formaldehyde, ammonia, benzene, toluene, and xylene as well as the carcinogenic risks posed by formaldehyde and benzene were evaluated following WS/T 777-2021 Technical guide for environmental health risk assessment of chemical exposure and the U.S. Environmental Protection Agency inhalation risk model. Results The overall compliance rates of PM₁₀, formaldehyde, ammonia, benzene, and toluene in the air of hair and beauty salons in Shanghai from 2016 to 2024 were 92.13%, 96.59%, 96.15%, 94.93%, and 94.97%, respectively; the overall compliance rate of xylene was a little lower (85.92%), and the overall compliance rate of PM_2.5 was 57.18%. The P₅₀ concentrations of PM₁₀, PM_2.5, formaldehyde, ammonia, benzene, toluene, and xylene did not exceed the corresponding limits. The P₅₀ of non-carcinogenic risk indicator (hazard quotient, HQ) for formaldehyde, ammonia, benzene, toluene, and xylene were <1. The probabilities of non-carcinogenic risk HQ >1 for formaldehyde and xylene were 41.4% and 10.9%, respectively, which were higher than that of other pollutants. The P₅₀ of carcinogenic risk (CR) for formaldehyde and benzene were between 1.0×10⁻⁶ and 1.0×10⁻⁴, while the probabilities of CR >1.0×10⁻⁴ were 16.9% and 14.0%, respectively. Conclusion The overall compliance rate of common pollutant concentrations in the air of hair and beauty salons in Shanghai is high, and the hygienic condition meets the requirements of national standards. The non-carcinogenic health risks posed by formaldehyde and xylene to employees (with formaldehyde being more prominent), as well as the carcinogenic risks associated with formaldehyde and benzene, deserve heightened attention in future health supervision.

BACKGROUND:Studies have shown that rheumatoid arthritis and osteoporosis are positively correlated,but the causal relationship and related mechanisms have not yet been confirmed.With the cross-fertilization of computer science and life sciences,Mendelian randomization and bioinformatics analyses based on genome-wide association study(GWAS)and transcriptome sequencing data can assess the causal relationship between two diseases,explore the related mechanisms,and mine the therapeutic targets,which will be beneficial to the precision treatment of rheumatoid arthritis combined with osteoporosis.OBJECTIVE:To explore the causal relationship between rheumatoid arthritis and osteoporosis using two-sample Mendelian randomization and to mine potential co-morbid targets and potential targeted drugs through summary-data-based Mendelian randomization and bioinformatics analyses,aiming to provide theoretical basis for mechanism exploration and precision treatment in the field of rheumatoid arthritis combined with osteoporosis.METHODS:(1)Firstly,GWAS data of rheumatoid arthritis,osteoporosis,and cis-expression quantitative trait locus(cis-eQTL)in Asian and European populations were downloaded from the GWAS Catalog,IEU Open GWAS,FinnGen,and eQTLGen databases,and were used for two-sample Mendelian randomization analysis and summary-data-based Mendelian randomization analysis.(2)Transcriptome sequencing data of rheumatoid arthritis(GSE93272 and GSE15573)were downloaded from the GEO database for bioinformatics analysis.(3)Subsequently,forward and inverse Mendelian randomization analyses between rheumatoid arthritis and osteoporosis were performed,and inverse variance weighted was used as the main metric for the analyses,and the results were corroborated with MR Egger,simple mode,weighted median and weighted mode.(4)Then,the genes closely related to rheumatoid arthritis and osteoporosis were identified based on the summary-data-based Mendelian randomization analysis,and the co-disease targets of rheumatoid arthritis and osteoporosis were mined based on cross-analysis.Meanwhile,the biological functions of the co-morbid targets were verified based on bioinformatics analysis and cellular experiments.(5)In addition,a rheumatoid arthritis risk prediction nomogram was constructed based on DYRK2,and its prediction performance was verified by receiver operating characteristic curve,correction curve and decision curve.Finally,the target potential drugs were mined based on Enrichr database and molecular docking was performed.RESULTS AND CONCLUSION:(1)Forward Mendelian randomization analysis of rheumatoid arthritis and osteoporosis showed statistically significant results except for GCST90044540 and GCST90086118,and all other results indicated a significant causal relationship and positive correlation between rheumatoid arthritis and osteoporosis.(2)Inverse Mendelian randomization analysis suggested that no significant causal relationship was seen between osteoporosis and rheumatoid arthritis.(3)Summary-data-based Mendelian randomization analysis identified a total of 412 and 344 genes positively associated with rheumatoid arthritis and osteoporosis,and 421 and 347 genes negatively associated.Based on the cross-analysis,26 co-morbid genes were subsequently obtained.Among them,DYRK2 was a potential therapeutic target,and subsequent bioinformatics analysis and cellular experiments confirmed its important role in the progression of rheumatoid arthritis and osteoporosis.(4)Furthermore,the constructed nomogram has excellent predictive performance.Finally,four potential DYRK2-targeting drugs(undecanoic acid,metyrapone,JNJ-38877605,and ACA)were discovered and molecular docking also demonstrated reliable targeting ability.(5)In conclusion,based on GWAS data from Asian and European populations,we successfully demonstrated that rheumatoid arthritis and osteoporosis are causally related at the genetic level,DYRK2 is a potential therapeutic target,and four small molecules are potential target drugs.

BACKGROUND:Studies have shown that rheumatoid arthritis and osteoporosis are positively correlated,but the causal relationship and related mechanisms have not yet been confirmed.With the cross-fertilization of computer science and life sciences,Mendelian randomization and bioinformatics analyses based on genome-wide association study(GWAS)and transcriptome sequencing data can assess the causal relationship between two diseases,explore the related mechanisms,and mine the therapeutic targets,which will be beneficial to the precision treatment of rheumatoid arthritis combined with osteoporosis.OBJECTIVE:To explore the causal relationship between rheumatoid arthritis and osteoporosis using two-sample Mendelian randomization and to mine potential co-morbid targets and potential targeted drugs through summary-data-based Mendelian randomization and bioinformatics analyses,aiming to provide theoretical basis for mechanism exploration and precision treatment in the field of rheumatoid arthritis combined with osteoporosis.METHODS:(1)Firstly,GWAS data of rheumatoid arthritis,osteoporosis,and cis-expression quantitative trait locus(cis-eQTL)in Asian and European populations were downloaded from the GWAS Catalog,IEU Open GWAS,FinnGen,and eQTLGen databases,and were used for two-sample Mendelian randomization analysis and summary-data-based Mendelian randomization analysis.(2)Transcriptome sequencing data of rheumatoid arthritis(GSE93272 and GSE15573)were downloaded from the GEO database for bioinformatics analysis.(3)Subsequently,forward and inverse Mendelian randomization analyses between rheumatoid arthritis and osteoporosis were performed,and inverse variance weighted was used as the main metric for the analyses,and the results were corroborated with MR Egger,simple mode,weighted median and weighted mode.(4)Then,the genes closely related to rheumatoid arthritis and osteoporosis were identified based on the summary-data-based Mendelian randomization analysis,and the co-disease targets of rheumatoid arthritis and osteoporosis were mined based on cross-analysis.Meanwhile,the biological functions of the co-morbid targets were verified based on bioinformatics analysis and cellular experiments.(5)In addition,a rheumatoid arthritis risk prediction nomogram was constructed based on DYRK2,and its prediction performance was verified by receiver operating characteristic curve,correction curve and decision curve.Finally,the target potential drugs were mined based on Enrichr database and molecular docking was performed.RESULTS AND CONCLUSION:(1)Forward Mendelian randomization analysis of rheumatoid arthritis and osteoporosis showed statistically significant results except for GCST90044540 and GCST90086118,and all other results indicated a significant causal relationship and positive correlation between rheumatoid arthritis and osteoporosis.(2)Inverse Mendelian randomization analysis suggested that no significant causal relationship was seen between osteoporosis and rheumatoid arthritis.(3)Summary-data-based Mendelian randomization analysis identified a total of 412 and 344 genes positively associated with rheumatoid arthritis and osteoporosis,and 421 and 347 genes negatively associated.Based on the cross-analysis,26 co-morbid genes were subsequently obtained.Among them,DYRK2 was a potential therapeutic target,and subsequent bioinformatics analysis and cellular experiments confirmed its important role in the progression of rheumatoid arthritis and osteoporosis.(4)Furthermore,the constructed nomogram has excellent predictive performance.Finally,four potential DYRK2-targeting drugs(undecanoic acid,metyrapone,JNJ-38877605,and ACA)were discovered and molecular docking also demonstrated reliable targeting ability.(5)In conclusion,based on GWAS data from Asian and European populations,we successfully demonstrated that rheumatoid arthritis and osteoporosis are causally related at the genetic level,DYRK2 is a potential therapeutic target,and four small molecules are potential target drugs.

Abnormal synaptic plasticity is an early pathological feature of Alzheimer disease (AD). Synaptic damage and dysfunction initiate neuronal degeneration and death, ultimately leading to cognitive impairment. Traditional Chinese medicine (TCM) can effectively ameliorate cognitive dysfunction through multitarget regulation of synaptic plasticity. This review summarizes the mechanisms by which TCM, including active components, single herbs, and classical formulas, modulates synaptic plasticity, offering new insights for future research and clinical applications. Relevant experimental studies published between 2020 and 2024 were retrieved from major databases, including China National Knowledge Infrastructure, the National Science and Technology Library, Wanfang Data, Elsevier, ScienceDirect, PubMed, SpringerLink, and Web of Science. Network pharmacology and bioinformatics approaches were used to predict the therapeutic effects and mechanisms of TCM on AD-related synaptic plasticity. In total, 15 TCM single herbs and 11 TCM formulas were identified as enhancing AD-related synaptic plasticity. Additionally, 15 active ingredients targeting synaptic plasticity in AD were retrieved from TCM databases over the past decade. This review provides novel perspectives and strategic directions for future AD research and therapeutic development.