BackgroundThe middle school stage represents a crucial period for the development of borderline personality features. Negative parenting styles and emotional regulation strategies are associated with the formation of borderline personality features. However， the moderating role of emotional regulation strategies between negative parenting styles and borderline personality features among middle school students remains unclear. ObjectiveTo explore the moderating influence of emotional regulation strategies in the relationship between negative parenting styles and borderline personality features among middle school students， and to provide references for the intervention of borderline personality features. MethodsIn October 2023， a total of 5 965 middle school students from three middle schools in Nanning， Guangxi Zhuang Autonomous Region were selected by cluster sampling， and assessed by the Borderline Personality Features Scale for Children （BPFS-C）， the Egna Minnen Barndoms Uppfostran （EMBU）， and the Emotion Regulation Questionnaire-Chinese Revised Version （ERQ-CRV）. Pearson correlation analysis was used to test the correlation between the scores of each scale， and the model 1 of the Process macro program was used to conduct the moderating effect test. ResultsA total of 5 572 middle school students （93.41%） completed this study， and 1 388 of them （24.91%） were identified as having high borderline personality features. The BPFS-C score of middle school students was positively correlated with the score of the negative parenting style dimension of EMBU （r=0.367， P<0.01）， negatively correlated with the score of the cognitive reappraisal dimension of ERQ-CRV （r=-0.168， P<0.01）， and positively correlated with the score of the expression inhibition dimension of ERQ-CRV （r=0.344， P<0.01）. Cognitive reappraisal played a negative moderating effect between negative parenting styles and borderline personality features （β=-0.072， 95% CI： -0.104–-0.041， P<0.01）， while expressive suppression played a positive moderating effect （β=0.076， 95% CI： 0.055–0.097， P<0.01）. ConclusionCognitive reappraisal strategy may help mitigate the negative influence of negative parenting styles on middle school students' borderline personality features， while expressive suppression may exacerbate the harm of negative parenting styles to the borderline personality features of middle school students.

Randomized controlled trial(RCT) represents the "gold standard" for estimating the causal effects of interventions; however, their implementation in the field of health policy evaluation is frequently hindered by logistical feasibility and ethical constraints. Target Trial Emulation (TTE), a framework originating in clinical epidemiology, facilitates rigorous causal inference from observational data by explicitly emulating the design of an idealized "target trial". Recently, the application of TTE has transitioned from individual-level clinical interventions—such as pharmacological or surgical treatments—to population-level health policy evaluations. This interdisciplinary translation is not a localized conceptual shift but necessitates a series of comprehen-sive methodological adaptations. This paper systematically delineates the core logic of extending the TTEframework into the realm of health policy, providing a profound analysis of the transformation and reconstruction of critical elements, including study units, intervention definitions, time zero, causal estimands, and analytical strategies. Furthermore, it examines the unique challenges inherent in policy contexts, such as policy heterogeneity, staggered adoption, concurrent policy interference, and data granularity limitations. The paper also evaluates the integration of analytical methods, such as instrumental variables (IV) and difference-in-differences (DID), within the TTE framework. This synthesis aims to provide methodological guidance and prospective insights for conducting high-quality policy evaluations using real-world data (RWD).

Objective To investigate the protective effect and underlying mechanism of human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Exo) on renal ischemia-reperfusion injury (IRI). Methods hucMSC-Exos were isolated and characterized. A mouse renal IRI model was established and the animals were divided into Sham, IRI, IRI+hucMSC-Exo, IRI+hucMSC-Exo+JY-2 and Sham+JY-2 groups. Serum creatinine (Scr) and blood urea nitrogen (BUN) were measured. Hematoxylin-eosin (HE) staining was used to evaluate renal histopathology. Enzyme-linked immune absorbent assay was performed to determine serum interleukin (IL)-1β and IL-18 levels. Western blotting was used to detect the expression of activating transcription factor 3 (ATF3), Toll-like receptor 4 (TLR4), nuclear factor (NF)-κB, NOD-like receptor protein 3 (NLRP3), cysteineyl aspartate specific proteinase (Caspase)-1 p20 and Gasdermin D(GSDMD). Real-time fluorescent quantitative polymerase chain reaction was employed to measure ATF3, TLR4 and NF-κB messenger RNA (mRNA). Immunohistochemistry was conducted to examine NLRP3, Caspase-1 p20 and GSDMD. An in vitro hypoxia/reoxygenation (H/R) model was established in HK-2 cells and divided into Control, H/R, H/R+hucMSC-Exo, H/R+hucMSC-Exo+JY-2 and Control+JY-2 groups. Western blotting was used to detect the expression of ATF3, TLR4 and NF-κB. Real-time fluorescent quantitative polymerase chain reaction was used to measure NLRP3, GSDMD and Caspase-1 mRNA. Results HucMSC-Exos were successfully isolated and identified. Compared with the Sham group, the IRI group exhibited elevated Scr and BUN, higher tubular injury scores, increased protein expression levels of ATF3, TLR4, NF-κB p65, NLRP3, Caspase-1 p20 and GSDMD, and raised mRNA expression levels of ATF3, TLR4, NF-κB. Compared with the IRI group, the IRI+hucMSC-Exo group showed decreased Scr and BUN, lower tubular injury scores, up-regulated ATF3 protein and mRNA, down-regulated TLR4, NF-κB p65, NLRP3, Caspase-1 p20 and GSDMD protein, and declined TLR4 and NF-κB mRNA. Compared with the IRI+hucMSC-Exo group, the IRI+hucMSC-Exo+JY-2 group exhibited increased Scr and BUN levels, elevated renal tubular injury scores, decreased ATF3 protein expression levels, elevated protein expression levels of TLR4, NF-κB p65, NLRP3, Caspase-1 p20, and GSDMD, decreased ATF3 mRNA expression levels, and elevated mRNA expression levels of TLR4 and NF-κB. (all P < 0.05). Compared with the Control group, the expression levels of ATF3, TLR4 and NF-κB p65 proteins were increased in the H/R group, and the expression levels of NLRP3, Caspase-1 and GSDMD mRNA were increased. Compared with the H/R group, the expression level of ATF3 protein was increased, the expression levels of TLR4 and NF-κB p65 proteins were decreased, and the expression levels of NLRP3, Caspase-1 and GSDMD mRNA were decreased in the H/R+hucMSC-Exo group. Compared with the H/R+hucMSC-Exo group, the expression level of ATF3 protein was decreased, the expression levels of TLR4 and NF-κB p65 proteins were increased, and the expression levels of NLRP3, Caspase-1 and GSDMD mRNA were increased in the H/R+hucMSC-Exo+JY-2 group (all P < 0.05). Conclusions HucMSC-Exos alleviate renal IRI by up-regulating ATF3, thereby negatively regulating the TLR4/NF-κB signaling pathway and subsequently inhibiting pyroptosis.

[Objective]To explore the prevention and treatment of type-2 diabetes(T2DM)secondary to depression by using classical formulas,based on the theory of"thirst induced by depression"as described in the Huangdi Neijing,and systematically review relevant texts in traditional Chinese medicine literature.[Methods]Utilizing the"thirst induced by depression"theory from the Huangdi Neijing,this study employs literature research to analyze ancient texts such as Jingui Yaolue,Zhubing Yuanhou Lun and Shennong Bencao Jing for theoretical support regarding the causes,pathogenesis and transmission of depressive syndromes and consumption disorders.This foundation allows for an exploration of the mechanisms through which depressive syndromes lead to consumption and the therapeutic strategies for managing T2DM secondary to depression in clinical practice.Finally,a test case was attached to support it.[Results]The concept of"Yin syndrome"characterized by"weakened organ Qi"shares a common pathological basis with"consumption",particularly during the"weakened five organs"stage.The pathological progression is similar to that seen in the development of T2DM secondary to depression.Specifically,the"Yin syndrome"associated with"weakened organ Qi"may evolve into a consumption syndrome due to prolonged Qi stagnation and increasing heat.Therefore,based on the pathological sequence of"fluid deficiency—Qi stagnation—heat transformation",the entire pathological process of depression leading to T2DM can be categorized into three stages for diagnosis and treatment:"early stage—progressive stage—end stage".The attached test case was of hot Qi stagnation and fluid injury type depression,treated to relieve heat for notifying fluid,clearing Qi and relieving depression,administered with revised Lily Powder and achieved good curative effect.[Conclusion]In the early stage of depression leading to T2DM,the primary condition is fluid and blood deficiency,treated by nourishing fluids,with reference to the Baihe Dihuang Decoction.During the progressive stage,Qi stagnation predominates alongside fluid deficiency,treated by regulating Qi and resolving stagnation,with references to the Chaihu Baihe Decoction.In the end stage,characterized by internal heat,the treatment focuses on clearing heat and nourishing fluids,with representative formulas including Guolou Muli San and Baihe San,depending on the presence or absence of Qi stagnation.

Objective:Investigate key genes influencing vascular calcification through bioinformatics analysis and experimental validation.Methods:Three vascular calcification datasets (GSE159832, GSE229679 and GSE37558) were obtained from the Gene Expression Omnibus database. Subsequently, gene ontology (GO), Kyoto encyclopedia of genes and genomes (KEGG), and conventional gene set enrichment analysis (GSEA) were performed on the common differential expressed genes(DEGs). For in vitro validation, a vascular smooth muscle cell calcification model was established by stimulating mouse primary vascular smooth muscle cells with high phosphate and calcium chloride (Pi+CaCl 2). Cells were divided into a control group and a Pi+CaCl 2 group. To investigate the role of TK1, cells were transfected with TK1-targeting siRNA (siTK1) or control siRNA (siControl) prior to Pi+CaCl 2 stimulation, creating siControl+Pi+CaCl 2 and siTK1+Pi+CaCl 2 groups. The association between key DEGs and vascular calcification was assessed at the protein and mRNA levels using Western blot and quantitative real-time PCR, respectively. Changes in the phosphorylation of the downstream effector, AKT (p-AKT/AKT), were also measured. Results:A total of 2275, 449, and 381 DEGs were identified from the three vascular calcification datasets (GSE159832, GSE229679, and GSE37558), respectively. Two common DEGs-phosphoserine aminotransferase 1 and thymidine kinase 1 (TK1)-were identified across all datasets. GO enrichment analysis revealed that TK1 was significantly enriched in pathways related to ribosome biogenesis, assembly, and rRNA processing and maturation. GSEA-KEGG analysis indicated significant enrichment in the PI3K-AKT signaling pathway, pathways in cancer, neurodegenerative diseases, cytoskeleton, and smooth muscle contraction. Conventional GSEA of TK1 further confirmed significant enrichment in pathways including dynein, epithelial tight junctions, axon guidance, and vascular smooth muscle contraction pathways. At the experimental level, both protein and mRNA expression of TK1, along with the p-AKT/AKT ratio, were significantly lower in the Pi+CaCl 2 group compared to the control group (all P<0.05). Furthermore, compared to the siControl+Pi+CaCl 2 group, the siTK1+Pi+CaCl 2 group exhibited decreased expression of differentiation markers, increased expression of calcification markers, and a further reduced p-AKT/AKT ratio (all P<0.05). Conclusion:Integrated bioinformatics and cellular validation demonstrate a correlation between TK1 expression and vascular calcification, suggesting a potential protective role for TK1 in this pathological process.

Objective:To explore highly efficient ventilation protection technology for large-space workplaces adapted to the production process in composite material impregnation.Methods:A composite material impregnation room was selected as the research subject from August to December 2023. Occupational health investigation, on-site detection, and physical simulation of air distribution were used to analyze the distribution of the xylene concentrations in the impregnation room. In addition, the causes for excessive concentrations were analyzed, and the combination ventilation design of enclosed negative pressure cabinets and jet directional supply of fresh air was proposed. The concentration of xylene, the capture velocity and the differential pressure of ventilation facilities before and after the transformation were tested on the spot. The rationality of the airflow organization was determined through smoke testing, and the ventilation protection effects before and after the transformation were analyzed.Results:The time-weighted average allowable concentration ( CTWA) of xylene was reduced from 41.73 mg/m 3 to 7.78 mg/m 3, and the CTWA of xylene were reduced by 81.4%. The values of capture velocity at all areas were higer than 0.5 m/s, and the values of velocity unevenness in all regions were lower than or equal to 0.25. The differential pressure between the enclosed cabinet and the impregnation room corridor was -2 to -1 Pa. The overall velocity distribution at all areas was relatively uniform, the airflow organization was reasonable, and negative pressure was formed inside the enclosed cabinet. Conclusion:The combination ventilation design of xylene, the capture velocity and the differential pressure of ventilation facilities effectively reducing the xylene concentration in the workplace, and provide a reference for ventilation protection of xylene workplace.

Acral melanoma(AM)is a distinct and aggressive subtype of melanoma characterized by high metastatic potential and poor prognosis.The pathogenesis and therapeutic strategies for advanced AM differ significantly from those of other melanoma subtypes,yet AM has received relatively less attention.AM exhibits high heterogeneity and a low tumor mutation burden.Mutations in braf,nras,and the tert promoter occur at much lower frequencies in AM than in cutaneous melanoma,limiting the effectiveness of treatments such as recombinant B-Raf proto oncogene serine/threonine protein kinase(BRAF)inhibitors.Additionally,reduced tumor immunogenicity due to low tumor-infiltrating lymphocyte levels contributes to the limited efficacy of immune checkpoint inhibitors,including anti-programmed death-1 and anti-cytotoxic T-lymphocyte-associated protein 4 therapies.Recent discoveries of novel therapeutic targets,such as receptor tyrosine kinases and cyclin-dependent kinases,along with emerging immune checkpoints,including V-domain immunoglobulin suppressor of T cell activation,adenosine A2A receptor,T cell immunoglobulin and ITIM domain,and T cell immunoglobulin and mucin-domain containing-3,offer new prospects for improving AM patient outcomes.Many AM treatments remain in the experimental stage,with research focusing on small-molecule targeted therapies,immune checkpoint inhibitors,and tumor microenvironment modulation.Combination strategies incorporating next-genera-tion cell therapies,oncolytic virus therapies,and therapeutic vaccines are also gaining prominence.Notably,clinical trials of personalized mRNA cancer vaccines have been promising,while antibody-drug conjugate and radionuclide-conjugated therapies present additional opportunities for enhancing AM prognosis.This article summarizes the cellular immune characteristics,mutation profiles,and tumor microenvironment of AM,as well as the current therapeutic strategies and advancements in the hope of expanding clinical benefits for AM patients.

Objective:To explore the causal association between insulin-like growth factor-1(IGF-1)and colorectal cancer(CRC)based on two sample Mendelian randomization(MR)analysis.Methods:A bidirectional two sample MR analysis was conducted based on publicly aggregated data from the IEU OpenGWAS project.The inverse variance weighted(IVW)method was used as the main analysis model to assess the causal relationship between IGF-1 and CRC.Additional analyses were performed using weighted median(WM),MR-Egger regression,weighted mode estimator(WME),and simple mode(SM)methods.Sensitivity analysis was performed to assess the robustness of the results.Results:A total of 386 single nucleotide polymorphisms(SNPs)were selected as instrumental variables(IVs)with IGF-1 as the exposure factor.The MR analysis results revealed a positive causal association between IGF-1 and the risk of CRC[odds ratio(OR)=1.178,95％confidence interval(CI):1.092-1.272)](P＜0.001),and the association remained significant after adjusting for height[OR(95％CI)=1.214(1.111,1.327)](P＜0.001).Cochran's Q-test showed heterogeneity among the IVs(P＜0.05),while the horizontal pleiotropy of IV was not detected by the MR-Egger regression(P＞0.05).The leave-one-out analysis showed that the MR results were robust.Reverse MR analysis indicated no reverse causal relationship between IGF-1 and CRC[OR(95％CI):1.017(0.997,1.037)](P=0.103).Conclusion:There is a causal relationship between IGF-1 level and CRC,and elevated IGF-1 level could be a risk factor for CRC.

Skin diseases significantly affect the quality of life of approximately 190 million individuals worldwide.The complexity and diversity of their clinical manifestations are the major challenges for traditional diagnostic approaches,and exploring novel diagnostic strategies has become an urgent priority.In recent years,deep learning(DL)technology has been increasingly applied in the intelligent recognition of skin diseases,demonstrating substantial potential.This study provides a systematic review of the research progress of DL in dermatological diagnosis from three major dimensions.First,at the data input level,it focuses on the characterization and preprocessing of multimodal data,including dermoscopic images,ultrasound images,and histopathological slides.Second,at the algorithmic model level,it explores ensemble learning frameworks,multimodal data fusion strategies,multicenter collaborative training approaches,and interpretable model construction.Finally,at the task recognition level,it evaluates the performance of DL models in benign skin disease screening,malignant skin lesion differentiation,and binary as well as multiclass classification tasks.By comprehensively reviewing advancements in DL-based skin disease diagnostic models from multiple perspectives,this paper aims to provide valuable insights for the further optimization and clinical translation of intelligent diagnostic systems.

Objective:To explore the correlation between serum nidogen-2 (NID-2) and thoracic aortic calcification in patients with chronic kidney disease (CKD), and construct a risk prediction model based on NID-2 to evaluate its value in predicting the risk of the severe thoracic aortic calcification and cardiovascular and cerebrovascular events in CKD patients.Methods:It was a prospective cohort study. Patients with CKD at stage 3 to 5D in the Zhongda Hospital Affiliated to Southeast University from January 2022 to January 2023 were enrolled. Syngo.via software was used to evaluate the volume of thoracic aortic calcification, and enzyme-linked immunosorbent assay was employed to determine the level of serum NID-2. According to the volume of thoracic aortic calcification, the patients were divided into three groups: no calcification group, mild calcification group and severe calcification group. The top 25% of the patients were defined as no or mild calcification group, and the latter 75% were defined as severe calcification group. The follow-up period was one year. During the follow-up period, cardiovascular and cerebrovascular events, as well as all-cause death among the enrolled patients were recorded. Logistic regression analysis was used to screen the influencing factors of thoracic aortic calcification. Based on the results of logistic regression analysis, a nomogram prediction model was constructed. The receiver operating characteristic curve (ROC curve), calibration curve, and decision curve were employed to evaluate the discrimination, calibration and clinical practicality of the nomogram model.Results:A total of 132 patients were included, with 91 males (68.94%) and age of (56.51±16.37) years. There were 60 CKD 3-5 stage patients (non-dialysis, 45.45%) and 72 CKD 5D patients (dialysis, 54.55%). Serum ND-2 levels differed significantly among healthy individuals, dialysis patients and non-dialysis patients ( H=70.651, P<0.001). There was no statistically significant difference in serum NID-2 level between the no or mild calcification group and the severe calcification group in dialysis patients ( Z=350.00, P=0.426). The serum NID-2 level in the severe calcification group was significantly higher than that in the no or mild calcification group in non-dialysis patients ( Z=242.00, P=0.019). In non-dialysis patients, there was a statistically significant correlation between serum NID-2 level and volume of thoracic aortic calcification ( r=0.40, P<0.001). In dialysis patients, there was no statistically significant correlation between serum NID-2 level and volume of each segment of thoracic aortic calcification (all P>0.05). The univariate logistic regression analysis showed that, age, hemoglobin, serum albumin, estimated glomerular filtration rate, NID-2, hypertension, type 2 diabetes mellitus and cerebral infarction were correlated factors of thoracic aortic calcification in non-dialysis patients (all P<0.05). Multivariate logistic regression analysis showed that age ( OR=1.22, 95% CI 1.08-1.50, P=0.010) was an independent correlated factor of thoracic aortic calcification in non-dialysis patients. The above related variables of univariate logistic regression analysis were incorporated into a nomogram to construct a predictive model for severe vascular calcification in non-dialysis patients, yielding an AUC of 0.94 (95% CI 0.89-0.99) in ROC curve, with a sensitivity of 83% and a specificity of 95%. A nomogram model based on above variables for predicting cardiovascular and cerebrovascular events in non-dialysis patients demonstrated an AUC of 0.95 (95% CI 0.90-1.00) in ROC curve, with a sensitivity of 95% and a specificity of 87%. Conclusions:In non-dialysis patients, serum NID-2 level in the severe calcification group is significantly higher than that in the no or mild calcification group. The serum NID-2 is a related factor of thoracic aortic calcification and cardiovascular and cerebrovascular events in non-dialysis patients. The nomogram prediction model constructed by combining NID-2 with age, hemoglobin, serum albumin, estimated glomerular filtration rate, hypertension, type 2 diabetes mellitus and cerebral infarction has a high predictive value for the risk of thoracic aortic calcification as well as cardiovascular and cerebrovascular events in non-dialysis patients.