ObjectiveTo investigate the value of intestinal fatty acid-binding protein （I-FABP） in predicting 6-week mortality in patients with liver cirrhosis after successful endoscopic hemostasis for esophagogastric variceal bleeding （EVB）. MethodsA retrospective analysis was performed for the clinical data of 207 patients with liver cirrhosis who underwent successful endoscopic treatment for EVB （including ligation and sclerotherapy） in The Affiliated Hospital of Yanbian University from September 2020 to June 2025， with the endpoint of 6-week bleeding-related mortality. ELISA was used to measure the serum level of I-FABP on admission， and a stratified analysis was performed based on the quartiles of I-FABP measurements. The Mann-Whitney U test was used for comparison of non-normally distributed continuous data between two groups； the chi-square test was used for comparison of categorical data between two groups. The Kaplan-Meier survival analysis， Cox regression analysis， and restricted cubic spline （RCS） curve were used to investigate the association between I-FABP and mortality. Machine learning models were used to further quantify the impact of I-FABP on mortality. The integrated Brier score and an integrated cumulative/dynamic area under the curve were used to assess the importance of time-dependent variables， and the receiver operating characteristic （ROC） curve was used to assess the performance of the predictive model. ResultsDuring the study， 29 patients （14.0%） died within 6 weeks after successful endoscopic hemostasis， with a median time to death of 16 （8—26） days. The mortality group had a significantly higher serum level of I-FABP than the survival group （Z=-3.731， P<0.001）. The Kaplan-Meier survival analysis showed that there was a significant difference in 6-week mortality between the groups of patients based on I-FABP quartiles （χ²=12.78， P=0.005）. The multivariable Cox regression analysis showed that an increase in I-FABP （hazard ratio=1.87， P=0.003） was an independent influencing factor for 6-week mortality. The RCS analysis showed a linear relationship between I-FABP and 6-week mortality （P_non-linear=0.280， P_overall=0.029）. Machine learning models showed that there was a dynamic change in the importance of I-FABP over time， and Brier score loss and the loss of cumulative/dynamic area under the curve after permutation showed that I-FABP was an important variable affecting 6-week mortality rate. ConclusionI-FABP level is independently associated with the risk of 6-week mortality endoscopic hemostasis for EVB in patients with liver cirrhosis， and therefore， it can be used as a potential biomarker for poor short-term prognosis.

Objective:To assess the efficacy and safety profile of antaitasvir phosphate combined with yiqibuvir in the treatment of chronic hepatitis C (CHC) of various genotypes, without cirrhosis or with compensated cirrhosis.Methods:394 cases with CHC from 22 centers were collected from October 2021 to April 2023. They were randomly assigned to receive either the experimental drugs (antaitasvir phosphate 100 mg+yiqibuvir 600 mg) or placebo treatment in a 3∶1 ratio. The patients were administered drugs once a day for 12 consecutive weeks, and then followed up for 24 weeks after treatment cessation. All subjects were unblinded at the four-week follow-up following drug discontinuation, with the experimental drug group continuing to complete subsequent post-discontinuation follow-up. The placebo group was switched to receive the experimental drugs for a repeated 12-week treatment period and followed up for another 24 weeks after discontinuation of the drug (placebo delayed treatment phase).The sustained virologic response rate (SVR12) was observed for subjects in the double-blind phase and the placebo delayed-treatment phase at 12 weeks after treatment cessation.Virological resistance analysis was performed on subjects who failed treatment. The primary efficacy endpoint was SVR12. The number and percentage of subjects who achieved "HCV RNA

Body weight abnormalities, including overweight, obesity, and underweight, have become a dual public health challenge in Chinese adults: overweight and obesity lead to a variety of chronic complications, while underweight increases the risks of malnutrition, sarcopenia, and organ dysfunction. To systematically address these issues, multidisciplinary experts in endocrinology, sports science, nutrition, and psychiatry from various regions have held multiple weight management seminars. Based on the latest epidemiological data and clinical evidence, they expanded the guideline to include assessment and intervention strategies for underweight, in addition to the core content of obesity management. This guideline outlines the etiological mechanisms, evaluation methods, and multidimensional management strategies for overweight and obesity, covering key areas such as diagnosis and assessment, medical nutrition therapy, exercise prescription, pharmacological intervention, and psychological support. It is intended to provide a scientific and standardized approach to weight management across the adult population, aiming to curb the rising prevalence of obesity, mitigate complications associated with abnormal body weight, and improve nutritional status and overall quality of life.

Porcine deltacoronavirus(PDCoV)is the main pathogen of porcine deltacoronavirus dis-ease.After infection,pigsmanifest a series of main symptoms,such as persistent vomiting,watery diarrhea and severe dehydration.Pigs at almost all growth stages are likely to be infected with the virus,especially suckling piglets are much sensitive to the virus.Once PDCoV infects the host,it u-sually causes significant immunosuppression.In recent years,studies on the immunosuppressive mechanism of PDCoV have gradually attracted widespread attention.The results showed that mul-tiple proteins of PDCoV were involved in the regulation of host innate immunity,revealing the mechanism of these proteins in regulating host innate immunity.In this paper,the interaction mechanism between PDCoV protein and host innate immunity were rsummarized,which will pro-vide a theoretical basis for further understanding the pathogenesis of PDCoV and effective preven-tion and control of porcine delta coronavirus disease.

To establish a TaqMan-based multiplex RT-qPCR method for the identification of Japa-nese encephalitis virus(JEV),Porcine reproductive and respiratory syndrome virus(PRRSV),and Classical swine fever virus(CSFV),this study designed and synthesized three pairs of specific primers and probes based on the conserved sequences of JEV E,PRRSV ORF6,and CSFV E2 a-vailable in the NCBI GenBank.By optimizing the reaction system and protocol,a multiplex RT-qPCR method for detecting these three viruses was developed and applied to the detection of clini-cal samples.The results showed that the established TaqMan multiplex RT-qPCR specifically am-plified the gene fragments of JEV,PRRSV,and CSFV,and did not amplify other non-target genes,indicating good specificity of the method.Intra-assay and inter-assay repeatability tests showed that the coefficient of variation(Cv)values were all below 3％,demonstrating that the method has ex-cellent repeatability.Sensitivity tests revealed that the minimum detectable amount for the recom-binant plasmids of the three viruses was 100 copies/pL.Using the established method,a total of 969 samples,including blood,aborted fetuses,semen,and deceased pigs,from 26 pig farms in Guizhou Province were tested.The detection rates were 34.3％(332/969)for JEV,28.3％(274/969)for PRRSV,and 19.8％(192/969)for CSFV.The co-infection rates were 10.1％(98/969)for JEV and PRRSV,12.1％(117/969)for JEV and CSFV,and 14.6％(141/969)for CSFV and PRRSV.Additionally,the triple co-infection rate of JEV,PRRSV,and CSFV was 7.9％(77/969).These results indicate that the TaqMan multiplex RT-qPCR method developed in this study is ef-fective for detecting these three viruses in pig farms,providing technical support for identifying vi-ral causes of reproductive disorders.

Japanese encephalitis virus(JEV)belongs to the genus Flavivirus and the family Flavi-viridae,and is classified as a single-stranded,positive-sense RNA virus.The disease known as Japa-nese encephalitis(JE),which results from JEV infection,is a viral zoonosis that is prevalent worldwide and poses a significant public health concern.JEV infection activates a variety of signa-ling pathways,leading to a series of changes that are crucial to the virus's pathogenesis.Among these pathways,Toll-like receptors(TLRs)are particularly significant,and their diverse range and complex signal transduction mechanisms present substantial challenges for the prevention and con-trol of JEV.Currently,there is no specific treatment for JEV.Although some vaccines have been developed to prevent JE,eradicating JEV remains difficult due to its zoonotic transmission cycle and the limited efficacy of the available vaccines.This article reviews the alterations in various TLR signaling pathways induced by JEV infection in the host,aiming to provide insights into the patho-genic mechanisms of JEV and to identify potential new antiviral targets.

Porcine reproductive and respiratory syndrome virus(PRRSV)is the pathogen of porcine reproductive and respiratory syndrome(PRRS),and its infection mainly causes abortion,stillbirth in sows and piglet respiratory infections,which are widely prevalent in the world and seriously jeopardize the development of the world's animal husbandry industry.PRRSV infection of the host is capable of inducing significant immunosuppression,and in recent years,the study of the mecha-nism of PRRSV immunosuppression has become a hot topic,with studies showing that numerous PRRSV proteins are involved in the regulation of host innate immunity and elucidating the mecha-nism by which PRRSV proteins modulate host innate immunity.In this paper,we reviewed the progress of research on the interaction mechanism between PRRSV proteins and host innate im-munity to provide a theoretical basis for a comprehensive understanding of the pathogenesis of PRRSV and the prevention and control of PRRS.

To identify clinical viral diseases characterized by reproductive disorders and abortion,a quadruple qPCR method was established for simultaneous detection of PRV,PPV,PCV2 and AS-FV.Four pairs of specific primers and probes were designed according to the conserved genes of four viruses in the NCBI gene bank.The annealing temperature,primer concentration and probe concentration of the reaction were optimized,and the specificity,sensitivity and repeatability of the method were tested.The results showed that the method could not detect other pathogens except the target ones.The minimum detection limit of PRV,PPV,PCV2 and ASFV was 10 copies.Intra-group and inter-group repeatability tests showed that the coefficient of variation of C,values be-tween different batches was less than 3％,indicating that the method was highly specific,sensitive and stable.Establishment of an efficient and sensitive quadruple qPCR method provides technical reference for the clinical prevention and control of porcine pseudorabies virus disease,porcine circo-virus disease,porcine parvovirus disease and African swine fever.

This study investigates the effects of pseudorabies virus(PRV)infection on the antiviral immune signaling pathways and type Ⅰ interferon factors in mouse trigeminal ganglion(TG)cells.In this experiment,primary TG cells were infected with PRV at a multiplicity of infection(MOI)of 1,while mice were infected via a drop-nose method using 106,29 TCID50 of PRV.Real-time fluorescence quantitative PCR(qPCR),Western blot and ELISA were used to assess gene tran-scription,protein expression,and the secretion of IFN-α and IFN-β.The results indicated that PRV infection of mouse TG primary cells led to alterations in the gene and protein expression of RIG-Ⅰ,MAVS,and IRF3,as well as the phosphorylation of IRF3 and IKBα both in vivo and ex vivo.ELISA results showed that PRV infection could regulate the secretion of IFN-α and IFN-β in mouse primary TG cells and mouse TGs.The results of RIG-Ⅰ signaling pathway-related proteins and the secretion of IFN-a and IFN-β were analyzed using Western blot after using siRNA to interfere with RIG-Ⅰ expression in TG cells.The results showed that siRIG-Ⅰ successfully inter-fered with RIG-Ⅰ protein expression in TG cells and caused changes in the expression of down-stream proteins such as MAVS and IRF3,and also regulated the secretion of IFN-α and IFN-β in TG cells.Furthermore,the results indicated that PRV infection induced the expression of RIG-Ⅰ in mouse TG progenitor cells,regulating the antiviral immune response of type Ⅰ interferon factors in TG cells through the RIG-Ⅰ-MAVS-IRF3 signaling axis.Notably,PRV inhibited the expression of IRF3 in TG cells while significantly upregulating the expression of IFN-β during the later stages of infection,which may be an important factor in the important reason for the rapid mortality ob-served in mice during the late stages of PRV infection.This experiment elucidates part of the anti-viral immune mechanism mediated by the RIG-Ⅰ-MAVS-IRF3 signaling pathway in regulating type Ⅰ interferon factor after PRV infection of mouse TG cells,as well as the discovery of differ-ent trends of IRF3 protein changes in vivo and ex vivo,laying the groundwork for future in-depth studies.

Lysine-specific demethylase 1(LSD1),a member of the flavin-dependent amine oxidase fam-ily,is a crucial"eraser"of lysine methylation.It reversibly removes methyl groups from histone H3K4me1/2 and H3K9me1/2,thereby regulating gene expression and chromatin function.Located with-in the nucleus,LSD 1 influences various biological processes in tumors,including proliferation,invasion,and metastasis.Previous studies have demonstrated that LSD1 is significantly overexpressed in gynecolog-ical cancers such as ovarian cancer,cervical cancer,and endometrial cancer,and its overexpression is closely associated with poor patient survival and unfavorable prognosis.Research indicates that LSD1 may promote tumor cell proliferation,invasion,and metastasis through the PI3K/AKT and mTOR signaling pathways,while also suppressing tumor cell autophagy and immune surveillance,contributing to immune evasion.In cervical cancer,LSD1 interacts with HPV16 E7,facilitating the epithelial-mesenchymal tran-sition(EMT)process.Furthermore,LSD1 inhibitors have shown promising therapeutic potential in ani-mal studies,particularly in restoring the sensitivity of ovarian cancer cells to platinum-based chemothera-py.This review summarizes the molecular mechanisms,functional targets,and associated signaling path-ways of LSD1 in gynecological cancers,as well as the mechanisms of action of various LSD1 inhibitors,aiming to provide new insights for targeted therapies in gynecological malignancies.