Background and Aims:Postoperative pancreatic fistula(POPF)is one of the most severe and common complications following pancreaticoduodenectomy(PD)and is a major cause of mortality after PD.Given the multiple risk factors associated with PD-POPF,developing an effective predictive model is of significant clinical importance.This study was conducted to explore the predictive performance of the triglyceride-glucose(TyG)index combined with serological indicators for POPF following PD.Methods:The preoperative general data,laboratory indicators within one week before surgery,and postoperative complication data of 291 patients who underwent PD at the Department of General Surgery,Second Hospital of Lanzhou University,from January 2019 to June 2024,were retrospectively collected.Patients were randomly divided into a modeling group(203 cases)and a validation group(88 cases)using a computer-generated random number method at a 7∶3 ratio.Univariate Logistic regression and multivariate binary Logistic regression(Back-Wald method)were performed on the modeling group data.Based on regression analysis results,a predictive model was constructed and visualized using a nomogram.The discriminative ability of the nomogram model was evaluated by the area under the receiver operating characteristic(ROC)curve(AUC).A calibration curve was used to assess the agreement between predicted and actual probabilities,and a decision curve analysis was conducted to evaluate the clinical application value of the model.Subgroup analysis was performed on potential factors influencing the outcome variables.Results:Among the 291 patients,70 developed POPF,with 49 cases in the modeling group and 21 in the validation group.There was no statistically significant difference between the two groups(all P>0.05).Univariate analysis in the modeling group identified body mass index(BMI),triglycerides,TyG index,albumin(ALB),platelet count(PLT),absolute lymphocyte count(LYM),and absolute neutrophil count(NEUT)as significant factors associated with POPF(all P<0.05).Multivariate analysis revealed that BMI,TyG index,ALB,PLT,LYM,and NEUT were independent influencing factors for POPF(all P<0.05).A PD-POPF risk prediction model and nomogram were constructed based on these results.The model achieved an AUC of 0.80(0.73-0.86),and when applied to the validation group,the ROC analysis yielded an AUC of 0.80(0.70-0.90).The calibration curves of both the modeling and validation groups closely aligned with the standard curve.Subgroup analysis indicated that tumor nature and tumor stage had minimal impact on PD-POPF risk factors,demonstrating good model stability.Conclusion:The TyG index,along with BMI,PLT,NEUT,ALB,and LYM,is closely associated with PD-POPF occurrence.The risk prediction model based on the TyG index and these influencing factors exhibits good predictive performance and holds significant clinical value for guiding early intervention.

Indocyanine green(ICG)is one of the near-infrared fluorescent contrast agents approved for clinical use in fluorescence-guided surgery.Although widely applied,it still has some limitations.In recent years,various targeted fluorescent agents have been explored in pancreatic cancer patients;however,there is still no standardized consensus among surgeons regarding fluorescence-guided surgery for pancreatic cancer.In 2023,the first the international consensus report on fluorescent surgery navigation for pancreatic tumors was published,gathering perspectives from 38 pancreatic surgeons worldwide on current practices and future directions.A total of 76 statements were anonymously voted on using the Delphi method,resulting in 61 recommended statements.This consensus offers valuable guidance for the implementation of fluorescence-guided surgery in pancreatic tumor operations in China,yet its clinical application should be adapted in consideration of local expert opinions and patient-specific factors.This article interprets key aspects of the consensus,including the use of ICG,intraoperative fluorescence imaging techniques,and the fluorescence heterogeneity of pancreatic tumors,in combination with the authors'clinical experience,with the aim of providing reference and insight for the application of fluorescence-guided surgery in pancreatic tumors.

Background and Aims:N6-methyladenosine(m6A)epigenetic modification plays a crucial role in post-transcriptional gene expression regulation and various physiological and pathological processes,including tumorigenesis.The m6A reader IGF2BP2 significantly enhances mRNA stability and translation efficiency and is abnormally expressed in multiple cancers.However,the specific biological function of IGF2BP2 in pancreatic cancer remains unclear.Therefore,this study investigated the expression of the m6A reader IGF2BP2 in pancreatic cancer and its effects on pancreatic cancer cell functions.Methods:The expression levels of m6A-related writers,erasers,and readers were analyzed using The Cancer Genome Atlas(TCGA),the Genotype-Tissue Expression(GTEX)database,and the Gene Expression Omnibus(GEO).Kaplan-Meier survival analysis was conducted to assess the relationship between IGF2BP2 expression and the prognosis of pancreatic cancer patients.Immunohistochemistry was used to validate IGF2BP2 expression in clinical specimens of pancreatic cancer tissues and adjacent normal tissues.Functional experiments,including CCK-8 assay,flow cytometry for cell cycle analysis,colony formation assay,and Transwell migration assay,were performed to evaluate changes in cell proliferation,cell cycle distribution,colony formation ability,and migration capacity after IGF2BP2 knockdown in pancreatic cancer cells.Results:TCGA-GTEX and GEO database analyses showed that IGF2BP2 was highly expressed in pancreatic cancer tissues(both P<0.05)and that its high expression was associated with poor overall survival(both P<0.05).Immunohistochemical staining of clinical specimens confirmed that IGF2BP2 protein expression was higher in pancreatic cancer than in adjacent normal tissue.Functional experiments demonstrated that IGF2BP2 knockdown significantly reduced the proliferation ability of pancreatic cancer cells,arrested more cells in the G0-G1 phase,decreased colony formation,and impaired cell migration(all P<0.05).Conclusion:The m6A reader IGF2BP2 is highly expressed in pancreatic cancer tissues and is closely associated with poor prognosis in patients with this disease.Its mechanism of action may be related to the promotion of cancer cell growth and migration.

Pancreatic cancer(PC)is a highly malignant digestive system tumor with extremely high mortality and recurrence rates.While traditional surgical resection and chemotherapy remain the main treatment options,challenges such as high postoperative recurrence and poor prognosis persist.Therefore,exploring more effective comprehensive treatment strategies is crucial for improving patient survival and prognosis.This review systematically summarizes recent advances in systemic therapy for PC,with a focus on the application and efficacy of chemotherapy,targeted therapy,and immunotherapy.Additionally,it discusses the potential of neoadjuvant therapy,integrated traditional Chinese and Western medicine approaches,and conversion therapy in enhancing the effects of conventional chemotherapy.Studies have shown that targeted therapy can enhance antigen presentation and reduce side effects,while immune checkpoint inhibitors,cancer vaccines,and adoptive cell immunotherapy help mitigate tumor immune evasion and improve the tumor microenvironment.Despite continuous innovation in treatment approaches,clinical management of PC,particularly for advanced-stage patients,still faces significant challenges.Future research should focus on early diagnosis,precision medicine,and personalized treatment strategies to further improve cure rates and patient survival quality,providing more effective therapeutic options for clinical practice.

In recent years,the diagnosis and treatment of inguinal hernia have become increasingly refined,with individualized treatment plans gaining greater standardization.Building on the"Guidelines for the Diagnosis and Treatment of Adult Inguinal Hernias(2018 Edition),"over 70 experts from related fields conducted extensive discussions and revised the guidelines based on evidence-based medical evaluation standards.This updated edition focuses on advancements in the diagnosis and treatment of adolescent inguinal hernias,scrotal hernias,management of hernia-related complications,and postoperative education and follow-up.It aims to provide a scientific and standardized reference for domestic medical institutions and healthcare professionals,further enhancing the quality and consistency of inguinal hernia management.

Background and Aims:Acute pancreatitis(AP)accompanied by intestinal injury and intestinal barrier dysfunction can significantly worsen AP prognosis.Currently,there is no effective clinical treatment for AP-related intestinal dysfunction.Ulinastatin(UTI)is a conventional drug used for AP treatment due to its ability to inhibit trypsin activity and exert anti-inflammatory effects.However,whether UTI directly improves AP-related intestinal injury remains unclear.Therefore,this study was conducted to investigate the therapeutic effects and potential mechanisms of UTI in AP-related intestinal dysfunction.Methods:Thirty rats were equally randomized into three groups and received intraperitoneal injections of PBS(control group),20%L-arginine(AP group),or 20%L-arginine+UTI(UTI group).Tail vein blood samples were collected at 0,24,and 48 h after the initial injection of L-arginine(or PBS),and the rats were euthanized after the final blood collection to obtain pancreatic and terminal ileum tissues.Serum levels of amylase,lipase,intestinal fatty acid-binding protein(I-FABP),and diamine oxidase(DAO)were measured using ELISA.Histopathological examinations of the pancreas and terminal ileum were conducted.Western blot was used to detect the protein expression levels of tumor necrosis factor α(TNF-α),interleukin 6(IL-6),interleukin 1β(IL-1β),and interleukin 10(IL-10)in terminal ileum tissue.Western blot and qRT-PCR were used to assess the protein and mRNA expression levels of Toll-like receptor 4(TLR4)and nuclear factor κB(NF-κB)p-p65 in the terminal ileum.Results:Compared with the control group,both the AP and UTI groups exhibited significant AP changes(elevated serum amylase and lipase levels,pancreatic histopathological damage)and AP-related intestinal injury(decreased I-FABP and DAO levels,ileal histopathological damage).However,these alterations were significantly less severe in the UTI group compared to the AP group(all P<0.01).Compared with the control group,both the AP and UTI groups showed significantly increased protein expression of pro-inflammatory factors(TNF-α,IL-1β,IL-6)and the anti-inflammatory factor IL-10 in the ileal tissue;however,the UTI group exhibited significantly lower levels of pro-inflammatory factors and higher levels of IL-10 compared to the AP group(all P<0.01).Additionally,compared with the control group,both the AP and UTI groups displayed significant upregulation of TLR4 and NF-κB p-p65 protein and mRNA expressions in ileal tissue,but the upregulations were significantly lower in the UTI group compared to the AP group(all P<0.01).Conclusion:UTI can inhibit the activation of the TLR4/NF-κB signaling pathway in the ileal tissue of AP rats,thereby reducing pro-inflammatory cytokine levels and increasing anti-inflammatory cytokine levels.Therefore,in addition to its anti-pancreatitis effects,UTI may have a direct therapeutic effect on AP-related intestinal dysfunction.

Background and Aims:Coactivator-associated arginine methyltransferase 1(CARM1)is involved in the regulation of RNA and protein processing.Recent studies have revealed its crucial role in tumorigenesis and cancer progression.However,the correlation between CARM1 expression,pan-cancer prognosis,and the immune microenvironment remains unclear.This study was conducted to investigate the relationship between CARM1 expression and pan-cancer prognosis,immune microenvironment,and its potential biological mechanisms using bioinformatics approaches.Methods:Using the TCGA,GTEx,and HPA databases,the expression pattern of CARM1 in various cancers and its prognostic relevance were analyzed.The correlation between CARM1 expression and the tumor microenvironment,as well as immune checkpoint genes,were analyzed using TCGA data.The PPI network of CARM1-interacting genes was constructed using the STRING database.GSEA was performed to investigate the potential biological mechanisms of CARM1 in pan-cancer.Results:Compared to normal tissues,CARM1 was upregulated in most tumor tissues,and its expression was associated with prognosis in multiple cancers.CARM1 expression was correlated with immune cell infiltration and immune checkpoint gene expression.Enrichment analysis suggested that CARM1 might alter the biological function of urinary system tumors by affecting ribosome biogenesis.Additionally,it may influence the biological functions of digestive system tumors by modulating arginine biosynthesis,DNA replication,and the cell cycle.Conclusion:CARM1 is aberrantly expressed in tumor tissues and may serve as a prognostic biomarker for multiple cancers.It is associated with the tumor microenvironment and immune checkpoint gene expression in pan-cancer and may contribute to tumorigenesis through multiple biological pathways,making it a potential therapeutic target for pan-cancer treatment.

Acute pancreatitis(AP)is a severe digestive system emergency characterized by high morbidity and mortality,with a complex pathogenesis involving multiple signaling pathways.Among them,the RhoA/ROCK signaling pathway plays a crucial role in the onset and progression of AP,influencing pancreatic inflammation,fibrosis,microcirculatory regulation,and interactions with other signaling pathways.Studies have shown that inhibiting the RhoA/ROCK signaling pathway can effectively alleviate AP severity,reduce inflammatory cytokine levels,and improve pancreatic microcirculation,offering new therapeutic insights and potential strategies for AP treatment.Therefore,this review systematically summarizes the structure and function of the RhoA/ROCK signaling pathway,explores its mechanistic role in AP progression,and further discusses its potential clinical applications.By integrating existing research findings,this paper aims to provide new perspectives on the role of this signaling pathway in AP and offer a theoretical foundation for future basic research and clinical applications.

Pancreatic cancer is a highly aggressive malignancy with a poor prognosis,and surgical resection remains the only potentially curative treatment.However,since most patients are diagnosed at a locally advanced or metastatic stage,the feasibility of upfront surgery is limited.In recent years,neoadjuvant and conversion therapy have emerged as crucial strategies for borderline resectable and locally advanced pancreatic cancer,aiming to increase the R0 resection rate and improve survival outcomes.Studies have shown that FOLFIRINOX and gemcitabine plus nab-paclitaxel are commonly used neoadjuvant chemotherapy regimens,with the former being more suitable for patients with good performance status,while the latter is better tolerated across a broader patient population due to its lower toxicity.Additionally,radiotherapy,such as stereotactic body radiotherapy(SBRT),can enhance local tumor control,increase tumor cell eradication,and minimize damage to normal tissues,thereby optimizing overall treatment efficacy.Despite the significant advantages of this approach,challenges remain,including the management of toxic side effects and the optimization of treatment protocols.Future research will focus on personalized precision medicine,integrating genomic sequencing and radiomics to refine neoadjuvant/conversion therapy strategies and exploring the combination of chemotherapy,radiotherapy,immunotherapy,and targeted therapy to improve long-term survival in pancreatic cancer patients.This paper summarizes recent advancements in neoadjuvant/conversion therapy combined with radiotherapy for pancreatic cancer and discusses its potential role in modulating tumor biology and optimizing treatment strategies.

Objective:To investigate the causal effects of plasma lipidomics on pancreatitis using Mendelian ran-domization(MR)and evaluate the roles of intra-pancreatic fat deposition(IPFD)and gallstone disease in this relation-ship.Methods:A bidirectional MR analysis was conducted,with 179 plasma lipids as exposures and acute pancreati-tis(AP)and chronic pancreatitis(CP)as outcomes.Data were sourced from genome-wide association studies(GWAS),the UK Biobank,and the FinnGen project.Two-step Mendelian randomization(TSMR)and multivariable Mendelian ran-domization(MVMR)analyses were applied to assess the mediating roles of IPFD and gallstone disease in the associa-tion between plasma lipids and pancreatitis.Results:MR analysis identified two sterols negatively associated with AP(P＜0.05)and seven sterols negatively associated with CP(P＜0.05).One phospholipid showed a positive association with CP(P＜0.05).IPFD was positively associated with both AP and CP.Gallstone disease was confirmed as a risk fac-tor for AP.However,TSMR analysis indicated that neither IPFD nor gallstone disease mediated the relationship be-tween plasma lipids and pancreatitis.Conclusion:The causal relationship exists among plasma lipomics and AP/CP,also between IPFD,cholelithiasis and pancreatitis.These findings highlight novel risk factors and potential biomarkers to support early diagnosis and intervention for pancreatitis.