The inflammatory microenvironment is closely associated with the initiation and progression of osteoarthritis （OA）， specifically manifesting as macrophage activation， dysregulation of inflammatory cytokines， and redox imbalance. Following an overview of the pathological characteristics of the OA inflammatory microenvironment， this paper reviews the research progress on the mechanism of traditional Chinese medicine （TCM） intervening in OA by modulating the inflammatory microenvironment. It has been found that TCM monomers/active ingredients （such as total alkaloids from Strychnos nux-vomica ， quercetin， triptolide， etc.）， herb pairs （e.g. Angelica pubescens - Gentiana macrophylla ， Carthami Flos-Lycopodii Herba）， and TCM formulas （such as Zhuanggu jianxi formula， Duhuo jisheng decoction and Rongjin niantong formula， etc.） can inhibit macrophage activation， reduce the release of proinflammatory cytokines and the generation of reactive oxygen species by inhibiting multiple signaling pathways， including nuclear factor-κB， Wnt/ β -catenin， and mitogen-activated protein kinase， thereby alleviating the articular inflammatory microenvironment， restoring local joint homeostasis， and slowing the progression of OA.

Objective To systematically evaluate the predictive models for re-admission in patients with heart failure (HF) in China. Methods Studies related to the risk prediction model for HF patient re-admission published in The Cochrane Library, PubMed, EMbase, CNKI, and other databases were searched from their inception to April 30, 2024. The prediction model risk of bias assessment tool was used to assess the risk of bias and applicability of the included literature, relevant data were extracted to evaluate the model quality. Results Nineteen studies were included, involving a total of 38 predictive models for HF patient re-admission. Comorbidities such as diabetes, N-terminal pro B-type natriuretic peptide/brain natriuretic peptide, chronic renal insufficiency, left ventricular ejection fraction, New York Heart Association cardiac function classification, and medication adherence were identified as primary predictors. The area under the receiver operating characteristic curve ranged from 0.547 to 0.962. Thirteen studies conducted internal validation, one study conducted external validation, and five studies performed both internal and external validation. Seventeen studies evaluated model calibration, while five studies assessed clinical feasibility. The presentation of the models was primarily in the form of nomograms. All studies had a high overall risk of bias. Conclusion Most predictive models for HF patient re-admission in China demonstrate good discrimination and calibration. However, the overall research quality is suboptimal. There is a need to externally validate and calibrate existing models and develop more stable and clinically applicable predictive models to assess the risk of HF patient re-admission and identify relevant patients for early intervention.

The development and validation of clinical prediction models based on artificial intelligence (AI) and machine learning methods have become increasingly widespread. However, the prediction model bias risk and applicability evaluation tool developed in 2019 (i.e., PROBAST-2019) has shown significant limitations. Therefore, an expanded and updated version of the PROBAST-2019 tool was released in 2025, known as the PROBAST+AI tool. The tool is divided into two parts including model development and model evaluation. It aims to comprehensively and systematically evaluate potential methodological quality issues in model development, bias risks in model evaluation, and the applicability of models, regardless of the modeling method used. This paper provides a systematic interpretation of the PROBAST+AI tool's items and case analyses, with the aim of guiding and assisting researchers engaged in related studies and promoting the high-quality development of clinical predictive model research.

Objective To analyze the role and mechanism of PD-L1 in oral cancer metastasis based on TCGA and GEO databases.Methods The expression characteristics and clinical significance of the PD-L1 in oral cancer were analyzed using the TCGA database.PD-L1 mRNA levels were detected by quantitative reverse transcription-polymerase chain reaction(RT-qPCR)in various oral cancer cell lines.CCK-8,scrath test,Transwell-migration,and matrigel-invasion assays were employed to assess the effects of PD-L1 on proliferation,migration,and invasion of oral cancer cells.The interaction network between PD-L1 and functional genes in patients with oral cancer was constructed using STRING software and the GEO database,and key pathways were screened by Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analysis.The regulatory relationship between PD-L1 and key genes was validated by RT-qPCR.Results TCGA data revealed that PD-L1 was highly expressed in patients with oral cancer and was correlated with lymph node metastasis(P＜0.01).PD-L1 was also highly expressed in oral cancer cell lines and its inhibition significantly inhibited the proliferation,migration,and invasion of Cal27 and SCC25 cells(P＜0.05).KEGG analysis indicated that PD-L1 activated the Janus kinase(JAK)/signal transducer and activator of transcription(STAT)pathway by upregulating C-X-C motif chemokine ligand(CXCL)9 and CXCL10,thereby promoting STAT1 expression to regulate oral cancer metastasis.Inhibition of the JAK/STAT pathway further suppressed the proliferation,migration,invasion,and expression of STAT1,CXCL9,and CXCL10 in Cal27 and SCC25 cells(P＜0.05).Conclusions PD-L1 may promote oral cancer cell proliferation,migration,and invasion by upregulating CXCL9 and CXCL10 to regulate the JAK/STAT pathway and enhance STAT1 expression,ultimately driving oral cancer growth and metastasis.

Urolithiasis represents a prevalent clinical challenge marked by high recurrence rates and morbidity，with existing preventive strategies struggling to effectively curb its epidemic trajectory，thereby posing a significant threat to public health. The etiology of this condition is intricate，involving a complex network of interactions spanning classical supersaturation-crystallization theory，Randall’s plaque theory，and multifactorial elements such as cellular injury，inflammatory responses，metabolic derangements，the gut-kidney axis，immune dysregulation，and genetic predisposition. However，the critical mechanisms initiating stone formation and the early pathophysiological processes remain incompletely elucidated，constituting the core impasse in current preventive strategies. This review systematically synthesizes classical theories and cutting-edge advancements in urolithiasis etiology research，emphasizing the urgent need to integrate emerging technologies，including high-dimensional omics，advanced imaging modalities，and artificial intelligence，to dissect pivotal pathological nodes in early stone formation. Such interdisciplinary efforts are essential to overcome cognitive bottlenecks and ultimately achieve personalized，precision-based prevention strategies.

Objective:This meta-analysis compares the postoperative outcomes of the double-flap technique (DFT) versus esophagogastrostomy (EG), jejunal interposition (JI), double-tract reconstruction (DTR), and gastric tube anastomosis (GTA) following proximal gastrectomy for gastric cancer.Methods:Prospective and retrospective studies published from database inception until June 2025 were retrieved from PubMed, Embase, Web of Science, Scopus, CNKI, and Wanfang databases. Studies reporting at least one predefined outcome with extractable data were included. Outcomes of interest consisted of incidence of gastroesophageal reflux, overall postoperative complications, anastomotic leakage, anastomotic stenosis, and digestive reconstruction time. Two investigators independently performed literature screening, data extraction, and quality assessment. Randomized controlled trials (RCTs) were evaluated with the Cochrane ROB 2.0 tool, retrospective cohort studies with the Newcastle-Ottawa Scale (NOS), and single-arm studies with the JBI critical appraisal tool. Dichotomous outcomes were pooled using risk ratios (RRs), and continuous variables were summarized with standardized mean differences (SMDs), using fixed- or random-effects models based on I2 statistics. Publication bias was assessed via funnel plots and Egger's test.Results:A total of 55 studies published between 2007 and 2025 were included, comprising 5 RCTs and 50 retrospective studies. Among 4,380 patients, 732 underwent EG, 454 GTA, 1,480 DTR, 468 JI, and 1,246 DFT. Quality assessment indicated that all except six retrospective cohort studies (rated as moderate quality) were of high quality or had low risk of bias. Among the five reconstruction methods, DFT showed the lowest incidence of gastroesophageal reflux (6.6%, 82/1,246) and overall postoperative complications (11.6%, 144/1,246). JI had the lowest rate of anastomotic leakage (1.3%, 6/468), followed by DFT (1.4%, 18/1,246), and DTR had the lowest rate of anastomotic stenosis (2.4%, 36/1,480), followed by DFT (7.5%, 94/1,246). DFT required the longest operative time for reconstruction ([141.2 ± 597.6] minutes), and DTR required the shortest ([50.1 ± 39.0] minutes). Compared to EG, DFT was associated with a significantly lower risk of gastroesophageal reflux (RR=0.13 ,95%CI: 0.03-0.55, P = 0.01), and no significant differences were observed in overall complications (RR=0.98, 95%CI: 0.55-1.74, P = 0.93), anastomotic leakage (RR = 0.81, 95%CI: 0.04-18.43, P = 0.90), or anastomotic stenosis (RR = 0.75, 95%CI: 0.09-6.39, P = 0.79). Compared to JI, DFT showed no significant differences in gastroesophageal reflux (RR = 0.36, 95%CI: 0.10-1.25, P=0.11), overall complications (RR=2.06, 95%CI: 0.30-14.11, P=0.46), anastomotic leakage (RR=2.05, 95%CI: 0.26-16.18, P=0.49), or anastomotic stenosis (RR=0.83, 95%CI: 0.10-7.17, P=0.87). Similarly, compared to DTR, DFT had a lower risk of overall complications (RR=0.70, 95%CI: 0.50-0.98, P=0.04) but a longer reconstruction time (SMD: 2.55, 95%CI: 0.31-4.79, P=0.03). No significant differences were found in gastroesophageal reflux (RR = 0.68, 95%CI: 0.35-1.30, P=0.24), anastomotic leakage (RR=0.59, 95%CI: 0.16-2.17, P=0.43), or anastomotic stenosis (RR=2.44 , 95%CI: 0.44-13.64, P=0.31). Compared to GTA, DFT was associated with a significantly lower risk of gastroesophageal reflux (RR = 0.53, 95%CI: 0.33-0.88, P=0.01), but again there were no significant differences in overall complications (RR = 0.69, 95%CI: 0.41-1.16, P=0.16), anastomotic leakage (RR = 0.25, 95%CI: 0.03-2.14, P=0.21), or anastomotic stenosis (RR=0.65, 95%CI: 0.24-1.76, P=0.40). No significant publication bias was detected in the analysis (Egger's test P>0.05). Conclusions:Among the five common anastomotic methods after proximal gastrectomy, DFT demonstrates superior anti-reflux efficacy, outperforming EG and GTA in particular in preventing gastroesophageal reflux. DFT also exhibits a lower overall complication risk compared with DTR but maintains anastomotic safety comparable with that of the other techniques.

Urolithiasis represents a prevalent clinical challenge marked by high recurrence rates and morbidity，with existing preventive strategies struggling to effectively curb its epidemic trajectory，thereby posing a significant threat to public health. The etiology of this condition is intricate，involving a complex network of interactions spanning classical supersaturation-crystallization theory，Randall’s plaque theory，and multifactorial elements such as cellular injury，inflammatory responses，metabolic derangements，the gut-kidney axis，immune dysregulation，and genetic predisposition. However，the critical mechanisms initiating stone formation and the early pathophysiological processes remain incompletely elucidated，constituting the core impasse in current preventive strategies. This review systematically synthesizes classical theories and cutting-edge advancements in urolithiasis etiology research，emphasizing the urgent need to integrate emerging technologies，including high-dimensional omics，advanced imaging modalities，and artificial intelligence，to dissect pivotal pathological nodes in early stone formation. Such interdisciplinary efforts are essential to overcome cognitive bottlenecks and ultimately achieve personalized，precision-based prevention strategies.

Objective To analyze the role and mechanism of PD-L1 in oral cancer metastasis based on TCGA and GEO databases.Methods The expression characteristics and clinical significance of the PD-L1 in oral cancer were analyzed using the TCGA database.PD-L1 mRNA levels were detected by quantitative reverse transcription-polymerase chain reaction(RT-qPCR)in various oral cancer cell lines.CCK-8,scrath test,Transwell-migration,and matrigel-invasion assays were employed to assess the effects of PD-L1 on proliferation,migration,and invasion of oral cancer cells.The interaction network between PD-L1 and functional genes in patients with oral cancer was constructed using STRING software and the GEO database,and key pathways were screened by Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analysis.The regulatory relationship between PD-L1 and key genes was validated by RT-qPCR.Results TCGA data revealed that PD-L1 was highly expressed in patients with oral cancer and was correlated with lymph node metastasis(P＜0.01).PD-L1 was also highly expressed in oral cancer cell lines and its inhibition significantly inhibited the proliferation,migration,and invasion of Cal27 and SCC25 cells(P＜0.05).KEGG analysis indicated that PD-L1 activated the Janus kinase(JAK)/signal transducer and activator of transcription(STAT)pathway by upregulating C-X-C motif chemokine ligand(CXCL)9 and CXCL10,thereby promoting STAT1 expression to regulate oral cancer metastasis.Inhibition of the JAK/STAT pathway further suppressed the proliferation,migration,invasion,and expression of STAT1,CXCL9,and CXCL10 in Cal27 and SCC25 cells(P＜0.05).Conclusions PD-L1 may promote oral cancer cell proliferation,migration,and invasion by upregulating CXCL9 and CXCL10 to regulate the JAK/STAT pathway and enhance STAT1 expression,ultimately driving oral cancer growth and metastasis.

Objective:This meta-analysis compares the postoperative outcomes of the double-flap technique (DFT) versus esophagogastrostomy (EG), jejunal interposition (JI), double-tract reconstruction (DTR), and gastric tube anastomosis (GTA) following proximal gastrectomy for gastric cancer.Methods:Prospective and retrospective studies published from database inception until June 2025 were retrieved from PubMed, Embase, Web of Science, Scopus, CNKI, and Wanfang databases. Studies reporting at least one predefined outcome with extractable data were included. Outcomes of interest consisted of incidence of gastroesophageal reflux, overall postoperative complications, anastomotic leakage, anastomotic stenosis, and digestive reconstruction time. Two investigators independently performed literature screening, data extraction, and quality assessment. Randomized controlled trials (RCTs) were evaluated with the Cochrane ROB 2.0 tool, retrospective cohort studies with the Newcastle-Ottawa Scale (NOS), and single-arm studies with the JBI critical appraisal tool. Dichotomous outcomes were pooled using risk ratios (RRs), and continuous variables were summarized with standardized mean differences (SMDs), using fixed- or random-effects models based on I2 statistics. Publication bias was assessed via funnel plots and Egger's test.Results:A total of 55 studies published between 2007 and 2025 were included, comprising 5 RCTs and 50 retrospective studies. Among 4,380 patients, 732 underwent EG, 454 GTA, 1,480 DTR, 468 JI, and 1,246 DFT. Quality assessment indicated that all except six retrospective cohort studies (rated as moderate quality) were of high quality or had low risk of bias. Among the five reconstruction methods, DFT showed the lowest incidence of gastroesophageal reflux (6.6%, 82/1,246) and overall postoperative complications (11.6%, 144/1,246). JI had the lowest rate of anastomotic leakage (1.3%, 6/468), followed by DFT (1.4%, 18/1,246), and DTR had the lowest rate of anastomotic stenosis (2.4%, 36/1,480), followed by DFT (7.5%, 94/1,246). DFT required the longest operative time for reconstruction ([141.2 ± 597.6] minutes), and DTR required the shortest ([50.1 ± 39.0] minutes). Compared to EG, DFT was associated with a significantly lower risk of gastroesophageal reflux (RR=0.13 ,95%CI: 0.03-0.55, P = 0.01), and no significant differences were observed in overall complications (RR=0.98, 95%CI: 0.55-1.74, P = 0.93), anastomotic leakage (RR = 0.81, 95%CI: 0.04-18.43, P = 0.90), or anastomotic stenosis (RR = 0.75, 95%CI: 0.09-6.39, P = 0.79). Compared to JI, DFT showed no significant differences in gastroesophageal reflux (RR = 0.36, 95%CI: 0.10-1.25, P=0.11), overall complications (RR=2.06, 95%CI: 0.30-14.11, P=0.46), anastomotic leakage (RR=2.05, 95%CI: 0.26-16.18, P=0.49), or anastomotic stenosis (RR=0.83, 95%CI: 0.10-7.17, P=0.87). Similarly, compared to DTR, DFT had a lower risk of overall complications (RR=0.70, 95%CI: 0.50-0.98, P=0.04) but a longer reconstruction time (SMD: 2.55, 95%CI: 0.31-4.79, P=0.03). No significant differences were found in gastroesophageal reflux (RR = 0.68, 95%CI: 0.35-1.30, P=0.24), anastomotic leakage (RR=0.59, 95%CI: 0.16-2.17, P=0.43), or anastomotic stenosis (RR=2.44 , 95%CI: 0.44-13.64, P=0.31). Compared to GTA, DFT was associated with a significantly lower risk of gastroesophageal reflux (RR = 0.53, 95%CI: 0.33-0.88, P=0.01), but again there were no significant differences in overall complications (RR = 0.69, 95%CI: 0.41-1.16, P=0.16), anastomotic leakage (RR = 0.25, 95%CI: 0.03-2.14, P=0.21), or anastomotic stenosis (RR=0.65, 95%CI: 0.24-1.76, P=0.40). No significant publication bias was detected in the analysis (Egger's test P>0.05). Conclusions:Among the five common anastomotic methods after proximal gastrectomy, DFT demonstrates superior anti-reflux efficacy, outperforming EG and GTA in particular in preventing gastroesophageal reflux. DFT also exhibits a lower overall complication risk compared with DTR but maintains anastomotic safety comparable with that of the other techniques.

Objective:To explore the metabolic basis and related molecular mechanism of oral squamous cell carcinoma(OSCC)path-ogenesis.Methods:20 Chinese hamsters were divided into 2 groups(n=10).OSCC models were induced by dimethylbenzanthracene(DMBA)in 10 of the animals and the other 10 were used as the controls.LC-MS chromatography-mass spectrometry was used to iden-tify the metabolites in the buccal pouch,and multidimensional statistical analysis of the metabolites was performed with the orthogonal partial least squares discriminant analysis model.Variable Importance for the Projection(VIP)＞1 and P＜0.05 were used as the criteria to screen the differential metabolites between the 2 groups.KEGG pathway annotation and enrichment analysis for the metabolites were performed to screen the significantly differential pathways.Results:The hamster cheek pouches painted with 0.5％DMBA for 18 weeks were diffused with leukoplakia and loaded obvious papillary protrusions,which were diagnosed as OSCC by pathological examination.Lipids and lipid-like molecules were the main differential metabolites.Reprogramming of unsaturated fatty acid biosynthesis,cholesterol accumulation,enhanced catabolism of tryptophan,up-regulation of aspartate,increased synthesis of pyrimidine and purine,etc.were important metabolic features in the occurrence and development of OSCC.Conclusion:Molecular intervention targeting the related met-abolic pathways is expected to inhibit OSCC pathogenesis and progression.