ObjectiveThis study aimed to investigate the action mechanism by which Banxia Xiexintang （BXT） inhibits epithelial-mesenchymal transition （EMT） in chronic atrophic gastritis （CAG） rats by regulating the interleukin-17（IL-17）/extracellular regulated protein kinases（ERK）/CCAAT enhancer binding protein β（C/EBPβ）signaling pathway， thereby providing new theoretical evidence for the treatment of CAG with classic traditional Chinese medicine formulas. MethodsA CAG rat model was established by using the combined factor method. After successful modeling， the rats were randomly divided into the model group， low-， medium-， and high-dose groups （0.549， 1.098， 2.196 g·kg^-1， respectively） of BXT， and the positive drug group （vitacoenzyme， 0.3 g·kg^-1）. A normal control group was also set up. After 8 weeks of intervention， the pathological changes of gastric tissue were evaluated. The enzyme-linked immunosorbent assay （ELISA） was used to detect the contents of IL-17， tumor necrosis factor-α （TNF-α）， cyclooxygenase-2 （COX-2）， and C/EBPβ in serum， as well as the contents of EMT markers in gastric mucosal tissue including E-cadherin， N-cadherin， and vimentin. The immunohistochemistry method was employed to determine the localization and protein expression levels of IL-17， p-ERK， and C/EBPβ in gastric mucosal tissue. Western blot was used to detect the protein expressions of C/EBPβ， ERK， and its phosphorylated form （p）-ERK in gastric mucosa. Real-time polymerase chain reaction （Real-time PCR） was applied to measure the mRNA expression levels of ERK， COX-2， and C/EBPβ in gastric mucosa. ResultsCompared with those in the normal control group， the rats in the model group showed gastric mucosal glandular atrophy and inflammatory cell infiltration. The protein and their related mRNA expressions of C/EBPβ， ERK， and p-ERK in gastric mucosa were significantly increased （P<0.05，P<0.01）. The levels of IL-17， TNF-α， COX-2， and C/EBPβ in serum were significantly increased （P<0.01）. The contents of N-cadherin and vimentin in gastric mucosal tissue were significantly increased， while the content of E-cadherin was significantly decreased （P<0.01）. Compared with the model group， after intervention with different doses of BXT， the pathological damage of the gastric mucosa was improved to varying degrees. The protein and mRNA expressions of C/EBPβ， ERK， and p-ERK in gastric mucosa were significantly reduced （P<0.05，P<0.01）. The levels of IL-17， TNF-α， COX-2， and C/EBP β in serum were significantly decreased （P<0.01）. The contents of N-cadherin and vimentin in gastric mucosa tissue were decreased， while the content of E-cadherin was increased （P<0.05，P<0.01）. ConclusionBXT can effectively improve the pathological damage of gastric mucosal tissue in CAG rats. Its action mechanism may be related to reducing the levels of IL-17 and TNF-α in serum， regulating the IL-17/ERK/C/EBPβ signaling pathway and inhibiting the EMT process.

Objective To systematically evaluate the differences in outcomes between functional mitral regurgitation (FMR) and degenerative mitral regurgitation (DMR) in patients treated with transcatheter edge-to-edge repair (TEER) using the MitraClip device. Methods A systematic literature search was conducted in PubMed, Embase, the Cochrane Library, Web of Science, the CNKI, Wanfang Database, VIP Database, and the CBM from their inception to January 2024. Two researchers independently performed study selection, data extraction, and risk of bias assessment. The quality of cohort studies was evaluated using the Newcastle-Ottawa Scale (NOS). A meta-analysis was performed using Stata 18.0 software. Results A total of 13 cohort studies involving 6 402 patients were included, comprising 4 161 patients in the FMR group and 2 241 in the DMR group. All included studies had NOS scores of ≥6 points. The meta-analysis revealed that compared to the DMR group, the FMR group had a higher 1-year all-cause mortality rate [OR=1.53, 95%CI (1.30, 1.81), P＜0.01] and a higher 1-year rehospitalization rate for heart failure [OR=1.90, 95%CI (1.60, 2.26), P＜0.01]. Conversely, the FMR group had a lower post-procedural mean transmitral gradient [SMD=–0.47, 95%CI (–0.65, –0.30), P＜0.01] and a lower rate of subsequent mitral valve surgery [OR=0.41, 95%CI (0.20, 0.83), P=0.01]. Conclusion Following MitraClip therapy, patients with FMR exhibit favorable short-term outcomes, but their mid- to long-term outcomes are inferior to those of patients with DMR. When determining the treatment strategy with MitraClip, the specific etiology of mitral regurgitation should be considered for a more accurate prediction of therapeutic efficacy and prognosis.

Background: and Purpose Vertebrobasilar fusiform aneurysms (VBFAs) carry substantial morbidity and mortality, but optimal management for unruptured VBFAs remains unclear. We compared the safety and efficacy of conservative management (CM), stent-assisted coiling (SAC), and flow diverters (FDs) in patients with unruptured VBFAs, focusing on long-term prognosis. Methods: This study included data from a nationwide Chinese cohort of patients with vertebrobasilar dissecting aneurysms. Inverse probability of treatment weighting (IPTW) balanced confounders across groups. The primary outcome was poor prognosis (modified Rankin Scale score >2). Secondary outcomes included aneurysm rupture, ischemic stroke, compression symptoms, and VBFA-related deaths. Logistic regression estimated odds ratios (ORs) and 95% confidence intervals (CIs). Subgroup and sensitivity analyses were performed. Results: Among 1,115 patients with unruptured VBFAs, 838 (median age, 54 years; 655 men) were included. After IPTW, baseline characteristics were balanced. Median follow-up was 54 months. FD was associated with a lower risk of poor prognosis than CM (OR, 0.48 [95% CI, 0.30 to 0.77]; p=0.002), with no difference between CM and SAC. FD also reduced aneurysm rupture (OR, 0.20 [95% CI, 0.07 to 0.60]; p=0.004) and compression symptoms (OR, 0.30 [95% CI, 0.13 to 0.68]; p=0.004) versus CM. Time-to-event analyses further revealed significant differences in vertebral artery lesions and Type I–II VBFAs, whereas no significant differences were observed in basilar or vertebrobasilar junction lesions or in Type III–IV VBFAs. Conclusions Compared with CM, FD was associated with improved long-term outcomes in unruptured VBFAs, particularly in vertebral artery lesions and Type I–II VBFAs, although residual confounding cannot be excluded.

ObjectiveType I interferon (IFN-I) signaling is essential for antiviral innate immunity, yet its sustained or excessive activation contributes to the pathogenesis of several autoimmune diseases and interferonopathies, such as systemic lupus erythematosus and Aicardi-Goutières syndrome. Current strategies targeting this pathway, exemplified by JAK inhibitors, act mainly on downstream signal transduction and provide limited direct control over upstream IFN-I production, while also carrying the risk of broad immunosuppression. Phyllanthus emblica L. has long been used in traditional medicine for inflammatory disorders, but the bioactive constituent responsible for its regulation of IFN-I signaling and the underlying molecular mechanism have not been clearly defined. This study aimed to identify the active anti-inflammatory component of P. emblica and to characterize its mechanism of action on the IFN-I pathway in macrophages. MethodsActive components ofP. emblica and their candidate targets were screened by network pharmacology using the TCMSP and DrugBank databases (oral bioavailability≥30%, drug-likeness≥0.18) and intersected with inflammation-related genes retrieved from public databases. The predicted interaction between EGCG and IFN-I pathway proteins (TBK1, IRF3, STAT1) was evaluated by molecular docking, with BX795 and GSK8612 used as reference TBK1 inhibitors. Mechanistic experiments were performed in THP-1-derived macrophages and primary bone marrow-derived macrophages (BMDM). Upstream signaling was activated by transfection of the nucleic acid analogs poly(I∶C) and poly(dA∶dT) or by lipopolysaccharide (LPS) stimulation, whereas downstream signaling was activated by exogenous IFN-β. An siRNA-mediated TREX1 knockdown model was used to mimic endogenous nucleic acid-driven interferonopathy. Expression of IFN-β1 and interferon-stimulated genes (ISGs) was measured by RT-qPCR, protein phosphorylation by Western blot, and IFN-β secretion by ELISA. Cellular thermal shift assay (CETSA) and drug affinity responsive target stability (DARTS) were used to probe the interactionbetween EGCG and IRF3. ResultsNetwork pharmacology identified (-)-epigallocatechin-3-gallate (EGCG) as a candidate IFN-I-suppressive constituent of P. emblica, with predicted binding to TBK1, IRF3, and STAT1. Molecular docking yielded binding energies of -9.2, -7.2, and -8.2 kcal/mol for TBK1, IRF3, and STAT1, respectively, indicating an affinity for TBK1 comparable to that of the reference inhibitors BX795 (-5.7 kcal/mol) and GSK8612 (-6.4 kcal/mol). EGCG suppressed IFN-β1 and ISG mRNA expression under poly (I∶C), poly (dA∶dT), and LPS stimulation in both THP-1 macrophages and BMDM. At the protein level, EGCG reduced the phosphorylation of TBK1 and IRF3 without affecting the levels of the upstream sensors cGAS and RIG-I, and lowered IFN-β secretion in a concentration-dependent manner. CETSA and DARTS showed that EGCG did not enhance the thermal stability or protease resistance of IRF3, indicating that its effect on IRF3 is indirect. Following IFN-β stimulation, prolonged EGCG treatment reduced STAT1 phosphorylation in a time-dependent manner without an apparent change in IRF9, and partially attenuated ISG transcription; this effect was not monotonicly concentration-dependent, and CXCL10 showed the most consistent suppression. In TREX1-knockdown cells, the elevated mRNA levels of ISG15, ISG56, and CXCL10 were reduced by EGCG. ConclusionEGCG suppresses IFN-I responses by concurrently inhibiting TBK1-IRF3-dependent IFN‑β production and JAK-STAT1-mediated downstream transcription. These in vitro findings provide a mechanistic basis for the anti-inflammatory use of P. emblica in traditional medicine and identify EGCG as a candidate for further evaluation in interferon-driven autoimmune disease models.

China's mental health service system is transitioning from an expansion-oriented stage focused primarily on addressing resource shortages and improving access to care toward a more mature stage that places greater emphasis on service quality， operational efficiency， patients' rights， and long-term outcomes. The principal challenge is no longer merely an insufficient overall supply of mental health resources， but rather inadequate alignment among service goals， the structure of service provision， payment incentives， allocation of responsibilities， and professional capacity. Recent incidents involving inappropriate psychiatric admissions and misuse of medical insurance funds in a small number of institutions， although not representative of the mental health sector as a whole， have exposed several structural risks within an inpatient-dominated service model. These include misalignment between inpatient services and medical insurance payment incentives， expansion of institutions and beds outpacing the development of professional capacity and quality governance， excessive concentration of social-risk management responsibilities in medical institutions， and inadequate continuity of care across hospitals， communities， and families. In practice， psychiatric hospitalization may simultaneously serve the multiple functions of clinical treatment， institutional financing， and the management of social risks. When the boundaries among these functions are unclear， and outpatient care， day services， community-based rehabilitation， and social support lack stable institutional and financial support， hospitalization may become systematically overused. The next stage of reform should shift mental health services from a hospital- and inpatient-dominated model toward a stratified and continuous system centered on patients' needs； establish medical insurance payment and evaluation mechanisms that balance costs， quality， functional outcomes， and long-term value； clarify the responsibilities of medical institutions， communities， families， and relevant government sectors； and make professional competence， ethical standards， patients' rights， and institutional governance the foundations of quality improvement. The key to the high-quality development of mental health services in China lies neither in simply increasing or reducing the number of psychiatric beds nor solely in strengthening post hoc regulation， but in aligning institutional incentives with patients' interests and promoting symptom improvement， functional recovery， and social participation.

By analyzing the current application of multi-modal data in the diagnosis of gastric "inflammation-cancer" transformation， this study explored the feasibility and strategies for constructing a disease-syndrome integrated diagnosis and treatment system. Based on traditional Chinese medicine （TCM） phenomics， we proposed utilizing multi-modal data from literature research， cross-sectional studies， and cohort follow-ups， combined with artificial intelligence technology， to establish a multi-dimensional diagnostic and treatment index system. This approach aims to uncover the complex pathogenesis and transformation patterns of gastric "inflammation-cancer" progression. Additionally， by dynamically collecting TCM four-diagnostic information and modern medical diagnostic information through a long-term follow-up system， we developed three major modules including information extraction， multi-modal phenotypic modeling， and information output， to make it enable real-world clinical data-driven long-term follow-up and treatment of chronic atrophic gastritis. This system can provide technical support for clinical diagnosis， treatment evaluation， and research， while also offering insights and methods for intelligent TCM diagnosis.

With the widespread adoption of low-dose CT screening and the extensive application of high-resolution CT, the detection rate of sub-centimeter lung nodules has significantly increased. How to scientifically manage these nodules while avoiding overtreatment and diagnostic delays has become an important clinical issue. Among them, lung nodules with a consolidation tumor ratio less than 0.25, dominated by ground-glass shadows, are particularly worthy of attention. The therapeutic challenge for this group is how to achieve precise and complete resection of nodules during surgery while maximizing the preservation of the patient's lung function. The "watershed topography map" is a new technology based on big data and artificial intelligence algorithms. This method uses Dicom data from conventional dose CT scans, combined with microscopic (22-24 levels) capillary network anatomical watershed features, to generate high-precision simulated natural segmentation planes of lung sub-segments through specific textures and forms. This technology forms fluorescent watershed boundaries on the lung surface, which highly fit the actual lung anatomical structure. By analyzing the adjacent relationship between the nodule and the watershed boundary, real-time, visually accurate positioning of the nodule can be achieved. This innovative technology provides a new solution for the intraoperative positioning and resection of lung nodules. This consensus was led by four major domestic societies, jointly with expert teams in related fields, oriented to clinical practical needs, referring to domestic and foreign guidelines and consensus, and finally formed after multiple rounds of consultation, discussion, and voting. The main content covers the theoretical basis of the "watershed topography map" technology, indications, operation procedures, surgical planning details, and postoperative evaluation standards, aiming to provide scientific guidance and exploration directions for clinical peers who are currently or plan to carry out lung nodule resection using the fluorescent microscope watershed analysis method.

Chronic pancreatitis is a chronic inflammatory disease characterized by progre-ssive fibrosis of pancreatic tissue. Its pathological features primarily include parenchymal fibrosis, intraductal stone formation or calcification deposits, as well as segmental stenosis and dilation of the pancreatic duct. Prolonged chronic inflammatory stimulation not only leads to progressive pancreatic dysfunction but may also trigger the formation of pancreatic pseudocysts and even malignant transformation. In the comprehensive treatment of chronic pancreatitis, the core clinical goals are the removal of pancreatic duct stones, restoration of unobstructed pancreatic duct drainage, and preservation of residual pancreatic function. Traditional treatment strategies have been based on the principle of progressive intervention and early surgical management. In recent years, with advancements in extracorporeal shock wave lithotripsy, the application of new techniques such as endoscopic retrograde cholangiopancreatography combined with laser lithotripsy under direct cholan-gioscopic visualization, and improvements in pancreas-preserving surgical approaches, the debate over the superiority of progressive intervention versus early surgical treatment has intensified. Against this backdrop, the treatment mode of Xi′an Jiaotong University Pancreatic Disease Center (hereinafter referred to as "Western Pancreas") has emerged, emphasizing a personalized, multimodal treatment strategy based on different types of pancreatic duct stones. The treatment mode of "Western Pancreas" integrates lithotripsy, endoscopic treatment, and surgical interventions to optimize patient outcomes. By conducting a comprehensive analysis of domestic and international pancreatic duct stone classi-fication systems and drawing from our team′s clinical experience in managing over a thousand cases of chronic pancreatitis, the authors have further refined and proposed a classification system for pancreatic duct stones under the treatment mode of "Western Pancreas". This refinement aims to enhance the overall diagnostic and therapeutic standards for chronic pancreatitis.

Objective To evaluate the efficacy and safety of the antibody-drug conjugate(ADC)vedotinumab combined with programmed cell death protein 1(PD-1)inhibitors as neoadjuvant therapy in patients with bladder cancer.Methods This retrospective study included 54 patients with bladder cancer who underwent neoadjuvant therapy at the Department of Urology,Peking University First Hospital,between Jun.2023 and Jun.2025.Among them,26 patients received vedotinumab combined with a PD-1 inhibitors,and 28 patients received gemcitabine plus cisplatin(GC).Clinical data,pathological complete response(pCR)rates,and pathological downstaging rates were collected.Treatment-related adverse events(TRAEs)were also assessed in both groups.Results There were no statistically significant differences between the two groups in terms of age,sex,smoking history,tumor grade and stage,depth of invasion,or human epidermal growth factor receptor 2(HER2)expression,indicating good baseline comparability(P＞0.05).The pCR rate in the vedotinumab plus PD-1 inhibitor group was 57.69％(15/26),significantly higher than that of the GC group at 25.00％(7/28)(P＜0.05).Pathological downstaging occurred in 5 patients in either group,with no statistically significant difference(P＞0.05).The main TRAEs in the vedotinumab plus PD-1 inhibitor group were peripheral sensory neuropathy and rash,and no grade 3-4 severe adverse events were observed.In contrast,the GC group predominantly experienced bone marrow suppression,with 4 cases of grade 3-4 adverse events.Conclusion Vedotinumab combined with PD-1 inhibitors demonstrated significantly superior efficacy and favorable safety compared with the conventional GC regimen as neoadjuvant therapy for bladder cancer.

Objective:To evaluate the levels and source of cadmium exposure by dietary pathway among middle-aged and elderly people ≥40 in cadmium-contaminated areas of China.Methods:A total of 7 193 people aged 40-89 years from four typical cadmium-contaminated areas in China were selected as the study subjects. Food Frequency Questionnaire (FFQ), Total Diet Study (TDS) and a 3-day-24-hour dietary recall survey were conducted. Dietary cadmium intake and food sources through dietary pathways were assessed based on cadmium content in foods, consumption amounts and intake frequencies.Results:The mean age of the participants was 63.39±12.21 years, with 50.05% being males. The average monthly dietary cadmium intake was 7.39 μg/(kg·BW). Staple foods and vegetables were the primary sources of dietary cadmium intake, accounting for 57.51% and 32.48%, respectively. The monthly dietary cadmium intake in all surveyed regions did not exceed the Provisional Tolerable Monthly Intake (PTMI) recommended by the Joint FAO/WHO Expert Committee on Food Additives (JECFA).Conclusion:The monthly dietary cadmium intake among middle-aged and elderly people in cadmium-contaminated areas of China is relatively low, with the risk remaining at an acceptable level. Staple foods and vegetables are the most significant contributors to dietary cadmium intake.