Background and Aims:Critical limb ischemia(CLI)represents the end stage of lower extremity arterial disease.Infrapopliteal artery lesions,due to their complex anatomical and pathological characteristics,pose significant therapeutic challenges,with patients facing high rates of amputation and mortality.In recent years,endovascular treatment techniques have evolved rapidly;however,controversy remains regarding the optimal treatment strategy.To systematically compare the efficacy of different treatment modalities,this study conducted a network Meta-analysis to comprehensively evaluate balloon angioplasty(BA),bare-metal stents(BMS),drug-coated balloons(DCB),drug-eluting stents(DES),and orbital atherectomy(OA)in the treatment of CLI involving infrapopliteal artery lesions,providing evidence to guide clinical decision-making on optimal endovascular therapy.Methods:A comprehensive search of multiple medical databases was performed,and 17 randomized controlled trials with a total of 2 379 patients were included.A network Meta-analysis was conducted.The primary outcomes were 1-year primary patency rate,target lesion revascularization(TLR)rate,and major amputation rate.Results:DCB showed the highest efficacy in 1-year primary patency,significantly outperforming DES(OR=4.55,95%CI=1.14-20.00),BMS(OR=15.77,95%CI=3.50-71.00),and BA(OR=9.02,95%CI=2.43-33.47).DCB also demonstrated the lowest 1-year TLR rate,significantly lower than BA(OR=0.40,95%CI=0.22-0.72).There were no statistically significant differences among treatment methods in terms of the 1-year major amputation rate;however,the cumulative ranking analysis suggested that DES may be the most effective in reducing major amputation risk.Conclusion:DCB offers clear advantages in improving primary patency and reducing TLR rates,while DES may be the most effective strategy for reducing the risk of major amputation.DCB and DES should be prioritized in the endovascular treatment of CLI involving infrapopliteal artery lesions.

Background and Aims:Studies have shown that the long non-coding RNA(lncRNA)FGD5-AS1 functions as an oncogene in gastric cancer(GC).Our previous bioinformatics analysis revealed potential binding sites between FGD5-AS1 and microRNA-142-3p(miR-142-3p),as well as between miR-142-3p and pyruvate dehydrogenase kinase 1(PDK1).Therefore,this study aimed to investigate the expression and functional role of the FGD5-AS1/miR-142-3p/PDK1 axis in GC cells.Methods:Dual-luciferase reporter assays were used to verify the targeting relationships between FGD5-AS1 and miR-142-3p,and between miR-142-3p and PDK1.qRT-PCR was conducted to measure the expression levels of FGD5-AS1,miR-142-3p,and PDK1 in GC tissues.A knockdown model of FGD5-AS1(sh-FGD5-AS1)and an miR-142-3p inhibitor were constructed and transfected,alone or in combination,into BGC823 GC cells.Cellular behaviors,including proliferation(CCK8,EdU),apoptosis(flow cytometry),migration,and invasion(Transwell assays),were assessed,along with related protein expression(Western blot).A subcutaneous xenograft model in nude mice was used to evaluate the effect of FGD5-AS1 on tumor growth in vivo.Results:The dual-luciferase assays demonstrated that miR-142-3p mimics significantly reduced the luciferase activity of wild-type(WT)FGD5-AS1 and PDK1 reporters(both P<0.05),but had no effect on mutant(MUT)reporters,confirming a direct binding relationship.Knockdown of FGD5-AS1 led to upregulation of miR-142-3p and downregulation of PDK1 in GC cells,with reduced proliferation,migration,and invasion,and enhanced apoptosis(all P<0.05);these effects were reversed by the miR-142-3p inhibitor.In vivo,FGD5-AS1 knockdown significantly inhibited tumor growth in nude mice and decreased Ki-67 and PDK1 expression in tumor tissues(all P<0.05).Conclusion:FGD5-AS1 may act as a ceRNA that sponges miR-142-3p,thereby relieving its suppression on PDK1,and promoting GC cell proliferation and invasion as well as tumor progression.The FGD5-AS1/miR-142-3p/PDK1 axis plays a critical role in the development of GC and may serve as a potential therapeutic target.

Background and Aims:Gamma-aminobutyric acid(GABA),the principal inhibitory neurotransmitter in the central nervous system,has been increasingly recognized in recent years as being closely associated with various liver-related diseases,such as hepatic encephalopathy,liver cirrhosis,and hepatocellular carcinoma.Abnormal GABA expression is strongly linked to pathological processes including cognitive impairment and neuroinflammation.Although numerous studies have investigated the mechanistic roles of GABA in neurological complications of liver disease,a systematic overview of the field's research trends,collaborative networks,and emerging hotspots remains lacking.This study employs bibliometric methods to comprehensively map the evolution and frontier topics in GABA and liver-related disease research from 2005 to 2024,aiming to inform future research planning and resource allocation in this area.Methods:English-language publications from 2005 to 2024 related to GABA and liver-related diseases were retrieved from the Web of Science Core Collection.Eligible articles were analyzed using VOSviewer,CiteSpace,and the R package"bibliometrix"to visualize and evaluate contributions by countries/regions,institutions,authors,and journals.Additional analyses included keyword clustering,co-citation analysis,and thematic evolution of research topics.Results:A total of 237 articles were included,contributed by 1 340 authors across 456 institutions in 47 countries,and published in 168 journals.The United States and China are leading contributors in this field.Although countries such as the United Kingdom and Italy had fewer publications,they demonstrated higher average citation counts,indicating strong research quality.Notably,Spain's Centro Investigación Principe Felipe and the research team led by Felipo Vicente exhibited high academic influence.Neurochemistry International and Hepatology were identified as core journals,with Hepatology having the highest impact factor(12.9).Keyword clustering revealed major research focuses including the regulatory role of GABA in the neural mechanisms of hepatic encephalopathy,the impact of liver-related metabolic disorders on neurotransmitter balance,the development and evaluation of GABA receptor-targeted therapeutics,and the function of the GABAergic system in the pathogenesis of hepatocellular carcinoma.As research deepens,the frequency of emerging keywords has diversified,with recent emphasis on terms such as"quality of life,""gene expression,"and"fatty liver disease,"reflecting a shift from fundamental mechanisms to clinical translation and interdisciplinary integration.Conclusion:The relationship between GABA and liver diseases has become a focal point of interdisciplinary research.Investigations have expanded from pathological mechanisms to therapeutic applications,with growing interest in GABA's roles in hepatic encephalopathy,metabolic dysregulation,and tumor progression.Future studies should explore the specific functions of GABA receptor subtypes,promote the development of precision-targeted therapies,and investigate novel mechanisms such as the gut microbiota-GABA metabolism-brain-liver axis to broaden the clinical and translational potential of GABA in neurological,metabolic,and oncological contexts.

Background and Aims:Carotid plaque instability is a critical pathological basis for ischemic stroke.Identifying key molecular markers to evaluate plaque stability has important clinical implications.Recent studies have emphasized the regulatory roles and predictive value of long non-coding RNAs(lncRNAs)in plaque stability.In our previous transcriptome sequencing analysis of human stable and unstable carotid plaques,we identified lncRNA C-C motif chemokine ligand 3 antisense RNA 1(CCL3-AS1)as significantly upregulated in unstable plaques,suggesting a potential association with plaque instability.Therefore,this study aimed to validate CCL3-AS1 expression in an expanded plaque sample cohort and to explore its role and underlying molecular mechanism in carotid plaque destabilization.Methods:Carotid plaque specimens were obtained from patients undergoing carotid endarterectomy and classified into stable and unstable groups(n=15 per group)based on HE and Sirius red staining.qRT-PCR was used to validate the expression of candidate lncRNA CCL3-AS1.The localization and co-expression of CCL3-AS1 with macrophages in plaques were determined by RNA fluorescence in situ hybridization(FISH)combined with immunofluorescence staining.In vitro,THP1-derived macrophages were transduced with lentivirus or treated with antisense oligonucleotides(ASO)to overexpress or knock down CCL3-AS1,respectively,and the expression levels of inflammatory cytokines and matrix metalloproteinases(MMPs)were assessed.In vivo,an unstable carotid plaque model was established by tandem ligation of the right carotid artery in apolipoprotein E-deficient(ApoE-/-)mice,followed by local overexpression of CCL3-AS1.The effects on plaque morphology,macrophage infiltration,and MMP-9 expression were evaluated.Additionally,bioinformatic prediction using the catRAPID v2.1 omics platform was performed to identify potential RNA-binding proteins interacting with CCL3-AS1.RNA stability assays and RNA-binding protein immunoprecipitation(RIP)were conducted to verify the regulatory mechanism of MMP-9 expression.Results:CCL3-AS1 was significantly upregulated in unstable carotid plaques and was predominantly localized to the cytoplasm of plaque-infiltrating macrophages.In vitro,overexpression of CCL3-AS1 markedly increased the expression of MCP-1,TNF-α,IL-1β,iNOS,and MMP-9 in macrophages,whereas knockdown had the opposite effect.In the ApoE-/-mouse model of unstable carotid plaques,CCL3-AS1 overexpression led to fibrous cap rupture,increased infiltration of pro-inflammatory macrophages,enhanced MMP-9 secretion,and promoted plaque instability.Co-expression analysis revealed a strong correlation between CCL3-AS1 and MMP-9 expression(r=0.89,P=0.001).RNA stability assays demonstrated that CCL3-AS1 delayed the degradation of MMP-9 mRNA.Bioinformatic prediction identified heterogeneous nuclear ribonucleoprotein K(hnRNP-K)as a potential binding partner of CCL3-AS1.RIP and FISH co-localization confirmed the interaction,suggesting that CCL3-AS1 enhances MMP-9 mRNA stability through binding to hnRNP-K,thereby promoting its expression.Conclusion:As a macrophage-enriched inflammatory lncRNA,CCL3-AS1 may promote carotid plaque instability by enhancing MMP-9 expression via hnRNP-K-mediated mRNA stabilization.This lncRNA represents a potential molecular target for early intervention and stratification of ischemic stroke.

Lower extremity atherosclerotic occlusive disease(ASO)is a common peripheral arterial disease with a steadily increasing global incidence.As a key pathological change in ASO,arterial calcification plays a crucial role in its pathogenesis,diagnostic evaluation,treatment strategies,and prognosis.In recent years,with the continuous advancement of imaging and biomarker detection technologies,quantitative assessment and clinical research on arterial calcification have deepened,providing new perspectives for individualized diagnosis and treatment.This review begins with the pathophysiological mechanisms of arterial calcification and systematically summarizes current detection methods,its impact on endovascular therapy,and recent progress in prognostic evaluation,aiming to provide theoretical support and practical reference for precision treatment of ASO patients.

Low anterior resection syndrome(LARS)is a common bowel dysfunction syndrome following sphincter-preserving surgery for rectal cancer,characterized by stool storage dysfunction and evacuatory dysfunction.It has become a critical factor adversely affecting patients' quality of life and long-term clinical outcomes.Currently,the pathogenic mechanisms of LARS remain incompletely elucidated,and high-quality evidence to guide clinical practice is still lacking.However,emerging evidence suggests that strategic optimization across the clinical management pathway—including precision oncology planning,surgical technique selection,multidimensional symptom profiling,proactive prevention protocols,and comprehensive symptom management—may effectively reduce LARS severity and improve survivorship outcomes.Given the absence of consensus guidelines for LARS management among clinicians across China,the Chinese Society of Coloproctology of Chinese Medical Doctor Association organized domestic experts in relevant fields.Through systematic review of global research findings,integration of international expertise and guidelines,and adaptation to domestic clinical realities,we developed the Chinese expert consensus on the diagnosis and treatment of low anterior resection syndrome(2025 edition).This consensus elaborates on key aspects including the definition,clinical manifestations,risk factors,pathophysiological mechanisms,symptom assessment,treatment modalities,and prevention strategies for LARS,aiming to standardize the diagnosis and management of LARS in China.

To further standardize and improve the management of colorectal liver metastases(CRLM)in China,the Chinese guidelines for the diagnosis and comprehensive treatment of colorectal cancer liver metastases(2025 edition)have been systematically updated based on previous versions and the latest international and domestic evidence.The updated guideline refines diagnostic pathways,strengthens multidisciplinary team collaboration,and comprehensively upgrades therapeutic strategies-including surgical resection,neoadjuvant and adjuvant treatments for patients eligible for no evidence of disease(NED)status,and systemic therapy for those who are not.It also expands the scope of genetic testing,incorporates innovative local ablative therapies,and emphasizes standardized follow-up and long-term management.The guideline aims to promote individualized and precision-based treatment,ultimately improving clinical outcomes and patient survival.It serves as a practical,evidence-based reference for healthcare providers managing CRLM across China.

Most patients with biliary tract cancer are diagnosed at advanced stage and lose the opportunity for radical surgery resulting in dismal prognosis.In recent years,with advances in therapeutic approaches,conversion therapy has gradually been implemented in some cases of initially unresectable biliary tract cancer,enabling a subset of patients to achieve opportunities for radical surgery.To further standardize conversion therapy of biliary tract cancer and improve the overall efficacy,the Branch of Biliary Surgery,Chinese Society of Surgery,Chinese Medical Association and Working Group of Biliary Surgeons,Chinese College of Surgeons,Chinese Medical Doctor Association,based on the latest evidence-based medical evidence and specific practices in the treatment of biliary tract cancer in China,organized discussion among experts in the field.Following the discussion,the"Expert consensus on conversion therapy of biliary tract cancer(2025)"was developed.This consensus aims to address key issues in the field of biliary tract cancer conversion therapy,standardize diagnostic and therapeutic procedures and protocols,and lay the foundation for further advancing research and practice in this area.

Primary liver cancer(PLC)is a prevalent malignancy with high incidence and mortality rates globally.Hepatocellular carcinoma(HCC),primarily resulting from hepatitis B virus infections in Asia,constitutes most PLC cases.Despite advancements in targeted therapies and localized treatments,the 5-year survival rate remains low,indicating limited efficacy of current approaches.The advent of immunotherapy,particularly immune checkpoint inhibitors(ICIs),has brought new hope for patients with PLC.However,the liver's unique immune microenvironment presents significant challenges to the effectiveness of immunotherapy in HCC.This article reviews recent research developments in liver cancer immunotherapy,focusing on ICIs,combination therapies,emerging treatments,and prospective future directions.

Magnetism possesses both"force"and"field"properties,enabling non-contact interactions.Hepatopancreatobiliary(HPB)surgery is a field characterized by continuous innovation.In 2015,our team first proposed the concept of"magnetic surgery,"and subsequently advanced it from technical exploration to a disciplinary framework through organizing international conferences,founding a dedicated journal,and compiling textbooks.Many innovations originated in HPB practice:magnetic biliary and pancreatic anastomosis and magnetic recanalization for biliary strictures have significantly improved traditional approaches;magnetic vascular anastomosis has enabled rapid implantation of donor livers,supporting laparoscopic liver transplantation;and magnetic anchoring has provided multidimensional traction and exposure while reducing Trocar use and associated damage,thereby optimizing laparoscopic procedures.Looking ahead,multidisciplinary integration will drive the continued evolution of magnetic surgery,such as combining magnetic navigation with micro-nano surgical robots to achieve real-time tracking and guidance inside the body.These advances may overcome the limitations of conventional image guidance in applications like tumor ablation and catheter puncture.Ultimately,magnetic surgery is expected to evolve toward greater precision,minimal invasiveness,and intelligence,offering transformative solutions for HPB surgery and beyond.