Background Per- and poly-fluoroalkyl substances (PFAS) can influence gestational diabetes mellitus (GDM); however, current studies on their association are limited and have yielded inconsistent findings. Objective To investigate the association between maternal exposure to PFAS, as measured by urinary concentrations in early pregnancy, and the risk of developing GDM. Methods Based on the Wuhu Birth Cohort in Anhui Province conducted between 2020 and 2023, this study included 1910 pregnant women. Urine samples were collected during the first trimester, and a 75 g oral glucose tolerance test (OGTT) was completed at 24–28 gestational weeks. The concentrations of six PFAS in urine were measured using ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). Participants were categorized into low, medium, and high exposure groups according to tertiles of individual PFAS concentrations. Logistic regression analysis was employed to assess the potential impact of early-pregnancy PFAS exposure levels on the risk of GDM, with stratified analyses by maternal age and fetal sex. A generalized weighted quantile sum regression (gWQS) model was applied to evaluate the relative weight distribution of the six PFAS in their mixture effect. Results The logistic regression results revealed that both medium exposure to perfluorohexane sulfonate (PFHxS) (OR=1.475, 95%CI: 1.040, 2.093) and high exposure to perfluorononanoic acid (PFNA) (OR=1.430, 95%CI: 1.013, 2.018) were positively associated with diagnosed GDM. This association was more pronounced among women older than 28 years. Among pregnant women carrying male fetuses, high-level exposures to per fluorohexanoic acid (PFHxA) (OR=1.708, 95%CI: 1.006, 2.899) and PFHxS (OR=2.116, 95%CI: 1.247, 3.584) showed positive associations with diagnosed GDM. In contrast, among those carrying female fetuses, moderate perfluorooctanesulfonic acid (PFOS) exposure was associated with a lower risk of GDM (OR=0.542, 95%CI: 0.311, 0.946). The gWQS results demonstrated that PFOS (0.48) and perfluorobutane sulfonate (PFBS) (0.34) contributed the most to the mixture effect. Conclusion Early-pregnancy exposure to PFAS (particularly PFHxS and PFNA) may be an etiological factor for GDM, with maternal age and fetal sex potentially acting as effect modifiers in this association.

With the integration of 5G communication technology and robotic surgical systems, remote robot-assisted thoracic surgery is overcoming geographical barriers, offering an innovative approach to addressing the uneven distribution of medical resources. This study conducted a systematic literature review—using databases such as PubMed and CNKI, with the search period extending up to 2025—incorporating clinical studies, case reports, and review articles to comprehensively evaluate the clinical efficacy and safety of 5G-enabled remote robot-assisted thoracic surgery (5G-RRATS). The analysis also examined current technological limitations and potential future development trajectories. Existing evidence indicates that, given adequate technical support, 5G-RRATS can achieve perioperative outcomes comparable to those of conventional local robotic surgeries across procedures including pulmonary wedge resection, lobectomy, and esophagectomy. Furthermore, it demonstrates potential advantages in minimizing surgical incisions and reducing intraoperative blood loss. Nevertheless, challenges related to network stability, latency control, interdisciplinary collaboration between medical and engineering teams, and legal, regulatory, and ethical considerations continue to hinder widespread clinical adoption. Looking ahead, the emergence of a "one-to-many" remote surgical model, combined with the integration of artificial intelligence and augmented reality technologies, as well as advancements in low-orbit satellite communications, may enable 5G-RRATS to further advance precision and efficiency in thoracic surgery, thereby facilitating equitable access to high-quality care for a broader patient population.

ObjectiveTo construct an actor-network for integrating physical activity into rehabilitation services based on the World Health Organization Rehabilitation in Health Service System framework and actor-network theory (ANT). MethodsContent analysis was employed using the six building blocks of health service systems as the theoretical framework. Actors related to rehabilitation services were extracted and categorized into a rehabilitation actor pool, while a physical activity actor pool was formed based on four major physical activity scenarios. Actors from both pools were integrated, deduplicated and classified to form a final list of integrated actors. Using ANT, the construction process of the actor network integrating physical activity into rehabilitation was analyzed through the four stages of translation: problematization, interessment, enrollment and mobilization. ResultsA dynamic integration network was constructed, comprising human actors (patients, rehabilitation professionals, researchers, sports coaches, government departments, medical institutions, community organizations and industry media, etc.) and non-human actors (assistive devices, sports infrastructure, smart equipment, information systems, online exercise guidance systems, laws and regulations, strategic documents, and exercise prescriptions, etc.). The study identified maximizing rehabilitation outcomes as the mandatory passage point and elaborated on the critical role of government departments as focal actors in coordinating various stakeholders. ConclusionThe integration of physical activity into rehabilitation services is a dynamic network constructed by diverse actors through a process of translation. ANT provides an operational theoretical framework for cross-departmental governance of rehabilitation policies in China, promotes the spatial expansion of the rehabilitation field, and drives its transformation toward a networked and ecological system. The government needs to play a leading role in facilitating role reconstruction and synergy among heterogeneous actors in both the sports and rehabilitation sectors through mechanism design, to create a bidirectional empowerment mechanism that fosters mutual progress and ensures the sustainable development of integrated services.

Objective:To explore the relationship between post-traumatic growth and stress perception as well as the chain-mediated roles of psychological resilience and navigating social support in patients with primary liver cancer(PLC), in order to provide theoretical ideas for the nursing and intervention of PLC patients.Methods:Convenience sampling was used to select PLC patients admitted to the First Affiliated Hospital, Third Affiliated Hospital, and Fourth Affiliated Hospital of Xinjiang Medical University from October 2023 to May 2024 as the research subjects. A cross-sectional survey was conducted using Posttraumatic Growth Inventory, the Chinese Perceived Stress Scale, Perceived Social Support Scale, and the Connor-Davidson Resilience Scale.Results:A total of 236 PLC patients were ultimately included, including 189 males and 47 females. Age distribution was as follows: 18-40 years years (7 cases), 41-60 years (128 cases), and ≥61 years (101 cases). Posttraumatic growth showed a significant negative correlation with perceived stress ( r=-0.512, P<0.01), while demonstrating positive correlations with psychological resilience and perceived social support ( r=0.605, 0.515, both P<0.01). Psychological resilience and perceived social support had mediating and chain mediating effects between perceived stress and posttraumatic growth, with mediating effects of -0.176 and -0.069, accounting for 29.24% and 11.46% of the total effect, respectively. The chain mediating effect value was 0.073, accounting for 12.13% of the total effect. Conclusions:The pathway of stress perception on post-traumatic growth in patients with PLC is indirect, and stress perception can contribute to the growth of post-traumatic growth in patients through psychological resilience, and navigating social support.

Objective To investigate the roles of glucose-regulated protein 75(GRP75)and voltage-dependent anion channel 1(VDAC1)in heroin-induced arrhythmia.Methods Based on transcriptomic data from primary myocardial cells treated with heroin and the GSE31821 dataset from the Gene Expression Omnibus(GEO),differentially expressed genes(DEGs)were identified using R software.Enrichment analysis of DEGs was performed.The protein-protein interaction(PPI)network was constructed using STRING database,and key genes were selected using Cytoscape.Molecular docking of key genes was performed using HDOCK,followed by in vivo valida-tion.A total of 60 SD rats were randomly divided into control,model,model+7 d,model+14 d,and model+21 d groups.A rat model of heroin addiction was established,and the expression levels of DEGs in myocardial tissue were assessed using immunohistochemical staining and quantitative real-time PCR.Results A total of 51 DEGs primarily enriched in muscle cell development,myofibrils,actin binding,arrhythmic right ventricular cardiomyopathy,calcium signaling,and apoptosis pathways were identified.Based on the PPI and Cytoscape analyses,GRP75 and VDAC1 were identified as key genes.Molecular docking indicated a strong interaction between GRP75 and VDAC1,which form a stable complex.The results of immunohistochemical staining and qRT-PCR showed that the expression levels of GRP75 and VDAC1 were significantly increased in the model group compared to those in the control group(P＜0.05),and their expres-sion increased(P＜0.05)with the intervention period of heroin in a time-dependent manner.Conclusion GRP75 and VDAC1 may con-tribute to heroin-induced arrhythmogenesis.

Evidence-based treatment strategies for patients with cardiovascular disease and diabetes have been updated in recent years. However, substantial gaps remain between guideline recommendations and clinical practice, which justify the urgent need to improve the quality of care for patients with these conditions. The Chinese Society of Cardiology and the Chinese Society of Diabetes, in collaboration with the American Heart Association and the American Diabetes Association, designed the China Diabetes Cardiovascular project. The China Diabetes Cardiovascular project is a nationwide registry study aimed at improving the quality of care for patients with acute coronary syndrome and diabetes in China. Launched in 2021, this project has enrolled 36 hospitals across mainland China. Patients with a primary discharge diagnosis of comorbid acute coronary syndrome and diabetes will be eligible to participate. Pre-defined performance measures will be adopted to evaluate the quality of care for these patients. Multiple quality improvement strategies will be adopted, including providing monthly quality reports based on these measures, conducting a series of training courses, and distributing educational materials. A comprehensive dataset, encompassing patients' characteristics, medical history, treatment before and during the current hospitalization, and discharge medications for secondary prevention, will be collected through a web-based data collection platform. This project has the potential to improve the quality of care and reduce the care disparities in the management of patients with these diseases. Moreover, with its comprehensive data collection, this project will provide a strong foundation for exploring key clinical questions.

Objective This study sought to accelerate the establishment of a Parkinson's disease mouse model by intracerebral injection of α-synuclein preformed fibrils(α-Syn PFF)into B6-hSNCA-A53T transgenic mice to induce rapid development of Parkinson's-like pathological features.Methods C57BL/6J background α-Syn A53T transgenic mice were selected as the model group,with isogenic C57BL/6J mice as the control group.α-Syn PFF was delivered into the bilateral striatum using stereotactic brain injection.After modeling,the open-field test was used to assess spontaneous activity and anxiety-like behaviors,while the rotarod,grip strength,and pole tests evaluated motor coordination and limb muscle tone.The buried food test was conducted to assess olfactory function.Immunohistochemical staining was performed to investigate neuroinflammation and pathological α-synuclein in the mouse brain.Results Compared with the control group,1 month after the α-Syn PFF injection,model mice showed increased locomotion in the open-field test,with no significant differences in the rotarod,grip strength,or pole tests,but prolonged food-seeking time.Two months after model establishment,the model group showed significantly reduced locomotor activity in open field testing,impaired motor coordination in rotarod,grip strength and pole tests,and olfactory dysfunction in buried food tests.Phosphorylated α-synuclein accumulation was observed in the substantia nigra,cortex,and hippocampus,accompanied by pronounced microglial activation,Lewy body deposition,and substantial dopaminergic neuron loss in the substantia nigra.Conclusions A53T mice developed olfactory dysfunction and motor impairments more rapidly after α-Syn PFF injection.Significant pathological changes were observed,including the aggregation of α-synuclein/Lewy body in the substantia nigra,cortex,and hippocampus,and the loss of dopaminergic neurons in the substantia nigra.This model can serve as a rapidly established animal model for α-synucleinopathy-related Parkinson's disease.

Fundus neovascularization is a significant cause of ocular diseases, mainly including retinal neovascularization and choroidal neovascularization. Anti-vascular endothelial growth factor therapy, though effective, has limitations such as a short half-life, non-responsiveness, and drug resistance. 6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3), a key regulator of glycolysis, affects the generation of pathological blood vessels by modulating the metabolism of vascular endothelial cells. Small molecule inhibitors targeting PFKFB3 protein have been confirmed in animal and cell models to significantly inhibit pathological angiogenesis, showing good therapeutic potential. However, most of them are still in the preclinical research stage. In the future, it is necessary to further investigate the mechanism of PFKFB3 gene, optimize the specificity and safety of the inhibitors, and explore the effects of combining them with existing therapies, so as to provide new strategies for the treatment of fundus neovascular diseases.

Aim To analyze the correlation between N6-methyladenosine(m6 A)and ferroptosis in acute myo-cardial infarction(AMI).Methods Two microarray datasets GSE34198 and GSE59867 was explored from GEO data-base.Both AMI and control samples were analyzed for differentially expressed genes.GO,KEGG,and GSVA analysis of the screened differential genes was performed using R.Machine learning was used to screen ferroptosis associated genes for DRA,GBM,LASSO and randomForest characteristic genes.The expression data of the core ferroptosis gene and m6A-related genes were analyzed by Pearson correlation analysis,and the m6A modified genes and ferroptosis associated genes with strong correlation were screened.Finally,10 cases of AMI and 10 control whole blood samples from the Fifth Affiliated Hospital of Xinjiang Medical University were collected,and the expression of related genes was verified by RT-qPCR and Western blot.Results 431 common differentially expressed genes were extracted from two datasets,GO and KEGG analysis showed that these genes were mainly enriched in TNF signaling pathway,FoxO signaling pathway and B cell receptor signaling pathway.The enrichment pathways of differentially expressed genes by GSVA were cuproptosis,netotic cell death,entotic cell death,alkaliptosis and ferroptosis.The characteristic genes of ferroptosis associated genes were screened by machine learning,and 19 core ferroptosis associated genes were screened from them.The expression data of ferroptosis associated genes and m6A-related genes were analyzed by Pearson correlation analysis.LRPPRC-IREB2,LRPPRC-ATG5,YTHDC2-IREB2,HNRNPA2B1-IREB2 and YTHDC2-ATG5 were the most correlated top five genes.The results of RT-qPCR and Western blot showed that the gene expression levels of LRPPRC,YTHDC2,HNRN-PA2B1,IREB2 and ATG5 were significantly lower than those of the control group(P＜0.001),which was consistent with the gene expression in the database.Conclusion m6A methylation is associated with ferroptosis in AMI.By regula-ting m6A methylation-related genes,ferroptosis in AMI can be regulated.It provides a new idea for the further study of the pathogenesis of the disease.

Aim To analyze the correlation between N6-methyladenosine(m6 A)and ferroptosis in acute myo-cardial infarction(AMI).Methods Two microarray datasets GSE34198 and GSE59867 was explored from GEO data-base.Both AMI and control samples were analyzed for differentially expressed genes.GO,KEGG,and GSVA analysis of the screened differential genes was performed using R.Machine learning was used to screen ferroptosis associated genes for DRA,GBM,LASSO and randomForest characteristic genes.The expression data of the core ferroptosis gene and m6A-related genes were analyzed by Pearson correlation analysis,and the m6A modified genes and ferroptosis associated genes with strong correlation were screened.Finally,10 cases of AMI and 10 control whole blood samples from the Fifth Affiliated Hospital of Xinjiang Medical University were collected,and the expression of related genes was verified by RT-qPCR and Western blot.Results 431 common differentially expressed genes were extracted from two datasets,GO and KEGG analysis showed that these genes were mainly enriched in TNF signaling pathway,FoxO signaling pathway and B cell receptor signaling pathway.The enrichment pathways of differentially expressed genes by GSVA were cuproptosis,netotic cell death,entotic cell death,alkaliptosis and ferroptosis.The characteristic genes of ferroptosis associated genes were screened by machine learning,and 19 core ferroptosis associated genes were screened from them.The expression data of ferroptosis associated genes and m6A-related genes were analyzed by Pearson correlation analysis.LRPPRC-IREB2,LRPPRC-ATG5,YTHDC2-IREB2,HNRNPA2B1-IREB2 and YTHDC2-ATG5 were the most correlated top five genes.The results of RT-qPCR and Western blot showed that the gene expression levels of LRPPRC,YTHDC2,HNRN-PA2B1,IREB2 and ATG5 were significantly lower than those of the control group(P＜0.001),which was consistent with the gene expression in the database.Conclusion m6A methylation is associated with ferroptosis in AMI.By regula-ting m6A methylation-related genes,ferroptosis in AMI can be regulated.It provides a new idea for the further study of the pathogenesis of the disease.