Malignant gastric outlet obstruction (MGOO) occurs in 2% to 25% of patients with pancreatic ductal adenocarcinoma (PDAC) who do not undergo surgical intervention. Over the past decade, duodenal self-expandable metal stent (D-SEMS) has been widely used for MGOO and has demonstrated high technical (89.1% to 100%) and clinical (85.7% to 94.3%) success rates.Endoscopic ultrasonography-guided gastroenterostomy (EUS-GE) has emerged as a promising alternative with comparable technical (89.3% to 98.9%) and clinical (89.0% to 100%) success rates. Notably, EUS-GE reduces the 6-month reintervention rate by approximately 25% relative to D-SEMS in patients with MGOO, thus making it an increasingly popular treatment option. Despite its advantages, EUS-GE may not be suitable for patients with massive ascites, extensive peritoneal carcinomatosis, gastric linitis plastica, or an inaccessible small bowel. Moreover, EUSGE requires a longer procedure time and incurs higher overall costs, even when considering the increased reintervention rate associated with D-SEMS. While the risk of adverse events is similar between EUS-GE and D-SEMS, EUS-GE requires a higher level of operator expertise to ensure safety and may also require deeper levels of anesthesia than D-SEMS. Advancements in cancer therapy have prolonged survival in PDAC patients, but most do not require reintervention for MGOO, unlike those with other malignancies. Thus, EUS-GE may be suitable for patients with a longer life span who are willing to undergo deep anesthesia at a high-volume center with an experienced specialist. Given these considerations, more comprehensive studies are needed before EUS-GE can be recommended as a standard replacement for D-SEMS in the treatment of MGOO.

Objectives:To investigate the mechanism underlying the protective effects of polydatin(PD)a-gainst oxygen-glucose deprivation(OGD)-induced neuronal injury and acute spinal cord injury(SCI).Methods:The mouse hippocampal neuronal cell line HT22 was used in in vitro experiments.The cytotoxicity of PD was assessed using the CCK-8 assay:cells were treated with 0,1,3,10,30 and 100μM PD for 24h to de-termine the safe concentration range.After OGD modeling(24h),cells were treated with different concentrations of PD(0,3,10,and 30μM),and cell viability was measured via CCK-8 to identify the optimal protective concentration.Autophagy markers(LC3 and P62)were detected by immunofluorescence and Western blot(WB);Autophagosome formation was observed using transmission electron microscopy;And the apoptosis rate was e valuated by TUNEL staining.For in vivo studies,an acute SCI model was established in C57BL/6 mice using Allen's impact method.Animals were divided into sham,SCI model,and PD treatment(20mg/kg)groups,with n=10 per group.Tissues were collected on 7d and 14d post-injury.Spinal cord pathology was examined by HE staining on 7d and 14d.Immunofluorescence was performed on 14d to evaluate glial scar formation(GFAP+),neuronal survival(MAP2+),cell proliferation(BrdU+),and autophagy level(LC3 Ⅱ).Results:In vitro results showed that 1-100μM PD did not exhibit significant cytotoxicity toward HT22 cells.The optimal concentration of PD was determined to be 10μ M after OGD induction.Compared with the OGD group,10μM PD significantly enhanced cell viability after OGD[OGD group:(54.63±3.90)％vs OGD+PD(1 0μ M)group:(84.35±1.38)％,P＜0.05]and effectively attenuated autophagy activation,as evidenced by a decreased LC3Ⅱ/Ⅰratio(OGD group:11.0±0.57 vs OGD+PD group:3.50±0.28,P＜0.05),increased P62 accumulation(OGD group:0.55±0.04 vs OGD+PD group:0.93±0.06,P＜0.05),reduced number of autolysosomes,and significantly lower apoptosis rate[OGD group:(35.33±2.6)％vs OGD+PD group:(19.67±1.76)％,P＜0.05].In vivo,HE staining confirmed that pathological damage in spinal cord tissue was markedly alleviated in the PD-treated group compared with the SCI model group.Immunofluorescence results indicated that PD treatment inhibited fibrous scar formation(SCI group:2.32±0.19mm2 vs PD group:1.07±0.24mm2,P＜0.05),reduced neuronal damage(SCI group:1.72±0.28mm vs PD group:0.93±0.12mm,P＜0.05)and promoted cell proliferation[SCI group:(16.14±2.24)％vs PD group:(39.09±3.16)％,P＜0.05],and downregulated LC3 Ⅱ expression(SCI group:62.81±5.25 vs PD group:34.09±3.98,P＜0.05).Conclusions:PD ameliorates neural damage by concurrently suppressing autophagy and apoptosis,providing a dual-pathway therapeutic strategy for SCI.

Modern education emphasizes the improvement of the comprehensive quality of the educated,and medical ed-ucation has particularly high requirements for students'practical abilities.Therefore,it is necessary to continuously analyze and optimize the education work when conditions permit.This paper first introduces the"Trinity Teaching"model and the college student medical technology skills competition.Based on this,it analyzes the advantages and disadvantages of the current training for college student medical technology skills competition,the value of applying the"Trinity Teaching"model,and explores its specific application methods,including the use of group work mode and building a large-scale teaching service system to serve medical teaching work.

OBJECTIVE To establish a risk prediction model for antibiotic-associated diarrhea(AAD)in intensive care unit(ICU)patients receiving mechanical ventilation so as to provide bases for early identification of high-risk population and formulation of corresponding individualized prevention strategies.METHODS A total of 1016 pa-tients who received mechanical ventilation and were treated with antibiotics in the ICU of The First Medical Center of Chinese PLA General Hospital from Jan.1,2020 to Jun.30,2022 were retrospectively enrolled in the study and were divided into the AAD group with 200 cases and the non-AA group according to the diagnostic criteria for AAD.Multivariate logistic regression analysis was performed for risk factors for AAD in the ICU patients receiv-ing mechanical ventilation,and the nomogram prediction model was established with R software.The performance of the model was evaluated by means of receiver operating characteristic(ROC)curves and calibration curves.RESULTS Among the 1016 patients who underwent mechanical ventilation,200 had AAD,and the incidence rate of AAD was 19.69％.Multivariate logistic regression analysis showed that hemoglobulin[OR=0.990,95％CI(0.983 to 0.997)],C-reactive protein[OR=1.046,95％CI(1.009 to 1.085)],serum phosphorus[OR=0.498,95％CI(0.328 to 0.755)],serum lipase[OR=1.001,95％CI(1.000 to 1.002)],ceftriaxo ne sodium[OR=2.331,95％CI(1.253 to 4.334)],linezolid[OR=2.387,95％CI(1.329 to 4.289)],fluconazole[OR=2.083,95％CI(1.238 to 3.505)]and sedatives[OR=0.307,95％CI(0.160 to 0.590)]were the risk factors for the AAD in the ICU patients receiving mechanical ventilation.The area under ROC curve(AUC)of the predic-tion model established based on the risk factors was 0.705 for the training set,0.751 for the validation set.Hos-mer-Lemeshow test indicated that the predicated probability of the model was consistent with the actual risk for the occurrence(x2=6.057,5.304,P=0.641,0.725).CONCLUSION The nomogram model that is established based on the above influencing factors can quantitatively predict the risk for AAD in the ICU patients undergo-ing mechanical ventilation,and it has certain clinical predictive efficiency.

This study aims to establish BHK-21 stable cell lines expressing APN from four species(human,pig,dog,and cat),the APN fragments were amplified from pEGFP-C1-APN plasmids of the four species stored in the laboratory to generate the recombinant plasmids pcDNA4.0-APN.Af-ter the recombinant plasmids were transfected into BHK-21 cells,the stable BHK-21 cell lines ex-pressing the APNs were selected by two rounds of limited dilution.The constructed BHK-21 cell lines were identified by indirect immunofluorescence assay(IFA),and their susceptibility to PD-CoV and TGEV was tested for these four cell lines.Virus infection experiments revealed that PD-CoV infected cells expressing human,pig,and dog APNs,while it did not infect cells expressing cat APN.Simultaneously,TGEV infected cells expressing pig,dog,and cat APNs,but did not infect cells expressing human APN.The results suggest that the risk of cross-species infection for different coronaviruses and the established cell line can be used effectively to evaluate the virus in-fection.The findings also revealed that PDCoV has the potential risk of cross-species infection of human and dog,and TGEV has the potential risk of cross-species infection of dog and cat.These results provide a basis for the prevention and control strategy of coronaviruses.

Chronic pain causes physical suffering and can have major psychological impacts in patients.Chronic pain can induce depressive disorder,and clinical studies have consistently shown that chronic pain and depression frequently co-occur,suggesting the possibility of shared pathogenic mechanisms underlying these conditions.Acupuncture,as an alternative therapy,has been widely used for analgesia and to treat depression,with demonstrated clinical efficacy.The therapeutic mechanism of acupuncture is related to neural and endocrine regulation.This review considers the mechanism of chronic pain accompanied by depression,in relation to the brain regions and neural circuits affected by acupuncture treatment.This review provides a new approach for the treatment of depression caused by chronic pain.

Chronic diseases in the elderly are characterised by high incidence rates and prolonged duration.Regular participation in multi-component exercise programs promotes both the physical and mental health of the elderly with chronic diseases and reduces the risk of morbidity,making it the key to prevent chronic diseases in the elderly.This review introduces the concepts of multi-component exercise,elucidates the mechanism in improvement of physical and cognitive functions and evaluates the applications as well as the advantages and disadvantages in the management of chronic diseases in the elderly.This review intends to provide references for clinicians who undertake management role of the chronic diseases in elderly populations.

Objectives:To investigate the mechanism underlying the protective effects of polydatin(PD)a-gainst oxygen-glucose deprivation(OGD)-induced neuronal injury and acute spinal cord injury(SCI).Methods:The mouse hippocampal neuronal cell line HT22 was used in in vitro experiments.The cytotoxicity of PD was assessed using the CCK-8 assay:cells were treated with 0,1,3,10,30 and 100μM PD for 24h to de-termine the safe concentration range.After OGD modeling(24h),cells were treated with different concentrations of PD(0,3,10,and 30μM),and cell viability was measured via CCK-8 to identify the optimal protective concentration.Autophagy markers(LC3 and P62)were detected by immunofluorescence and Western blot(WB);Autophagosome formation was observed using transmission electron microscopy;And the apoptosis rate was e valuated by TUNEL staining.For in vivo studies,an acute SCI model was established in C57BL/6 mice using Allen's impact method.Animals were divided into sham,SCI model,and PD treatment(20mg/kg)groups,with n=10 per group.Tissues were collected on 7d and 14d post-injury.Spinal cord pathology was examined by HE staining on 7d and 14d.Immunofluorescence was performed on 14d to evaluate glial scar formation(GFAP+),neuronal survival(MAP2+),cell proliferation(BrdU+),and autophagy level(LC3 Ⅱ).Results:In vitro results showed that 1-100μM PD did not exhibit significant cytotoxicity toward HT22 cells.The optimal concentration of PD was determined to be 10μ M after OGD induction.Compared with the OGD group,10μM PD significantly enhanced cell viability after OGD[OGD group:(54.63±3.90)％vs OGD+PD(1 0μ M)group:(84.35±1.38)％,P＜0.05]and effectively attenuated autophagy activation,as evidenced by a decreased LC3Ⅱ/Ⅰratio(OGD group:11.0±0.57 vs OGD+PD group:3.50±0.28,P＜0.05),increased P62 accumulation(OGD group:0.55±0.04 vs OGD+PD group:0.93±0.06,P＜0.05),reduced number of autolysosomes,and significantly lower apoptosis rate[OGD group:(35.33±2.6)％vs OGD+PD group:(19.67±1.76)％,P＜0.05].In vivo,HE staining confirmed that pathological damage in spinal cord tissue was markedly alleviated in the PD-treated group compared with the SCI model group.Immunofluorescence results indicated that PD treatment inhibited fibrous scar formation(SCI group:2.32±0.19mm2 vs PD group:1.07±0.24mm2,P＜0.05),reduced neuronal damage(SCI group:1.72±0.28mm vs PD group:0.93±0.12mm,P＜0.05)and promoted cell proliferation[SCI group:(16.14±2.24)％vs PD group:(39.09±3.16)％,P＜0.05],and downregulated LC3 Ⅱ expression(SCI group:62.81±5.25 vs PD group:34.09±3.98,P＜0.05).Conclusions:PD ameliorates neural damage by concurrently suppressing autophagy and apoptosis,providing a dual-pathway therapeutic strategy for SCI.

Objectives:Using data from the heart transplant patient dataset of our center,we aimed to develop a preoperative risk scoring model specifically suitable for the Chinese population undergoing heart transplantation.This model was established to predict the likelihood of graft failure within the first year post-surgery and classify recipients according to their risk level.Methods:A retrospective study was conducted at a single center on 1 210 consecutive heart transplant recipients between June 2004 and December 2022.Risk factor screening was performed using univariate and multivariate logistic regression analyses.Variable selection was carried out through a stepwise backward procedure based on the Akaike Information Criterion(AIC).The regression coefficients obtained from the final model were employed as weighting factors in the multifactor analysis.The study utilized the area under the receiver operating characteristic(ROC)area under curve(AUC)as a metric to evaluate the performance of the model.Patients were stratified into low,medium,and high-risk groups based on the distribution of the calculated scores.Survival analysis was conducted on the various risk groups using the Kaplan-Meier method,with statistical comparisons performed using the log-rank test.A significance level of P<0.05 was deemed statistically significant.Results:A risk scoring model,denoted as the heart transplant(HTx)score,was developed,comprising 11 variables and yielding a total score of 20.6 points.In comparison to the low-risk group,the OR for 1-year graft failure in the medium-risk group was 2.0(95%CI:1.1-3.6,P=0.02),while the high-risk group had an OR of 9.8(95%CI:5.4-17.7,P<0.01).The risk scoring model exhibited strong discriminative ability with an AUC of 0.712(95%CI:0.646-0.778)and an internally validated bias-corrected AUC of 0.713.The results of the Hosmer-Lemeshow goodness-of-fit test indicated that the predictive model demonstrated a strong calibration ability(Hosmer-Lemeshow χ2=2.92,P=0.71).Within the cohort,the AUC values for the IMPACT score,UNOS score,RSS score,Mayo score,BO score,and TRS score models were 0.645,0.651,0.632,0.589,0.610,and 0.604,respectively.These findings suggest that the HTx scoring model exhibited superior predictive performance compared to the aforementioned models in forecasting outcomes within our cohort.The Kaplan-Meier survival analysis revealed statistically significant differences in long-term survival rates between the three risk groups,a noticeable decrease in long-term survival rates were observed with increasing levels of HTx risk stratification(P<0.05).Conclusions:Present results indicate a significant association between the developed HTx risk scores and graft failure within the initial year post-surgery,present model effectively categorizes the heart transplant recipients into low,medium,and high-risk groups and is valuable for risk stratification.

Objective To investigate the effect and mechanism of curculigoside(CUR)on hippocampal neuron injury in epileptic rats.Methods Forty-eight rats were selected,and the epileptic rat models were established by induction with 35 mg/kg pentylenetetrazol.The epileptic rats were randomly divided into the epilepsy group,the epilepsy+low-dose CUR group(the epilepsy+CUR-L group),the epilepsy+high-dose CUR group(the epilepsy+CUR-H group),and the epilepsy+CUR-H+PI3K activator 740Y-P group(the epilepsy+CUR-H+740Y-P group),with 12 rats in each group.Another 12 rats that were intraperitoneally injected with the same amount of normal saline were taken as the control group.Four weeks after administration,the behavioral changes of rats in each group were observed.Nissl staining was applied to determine the neuronal changes in hippocampal tissue.Immunohistochemistry was applied to detect the number of microglia in hippocampal tissue.ELISA was applied to detect the levels of interleukin-6(IL-6),IL-1β,and gamma-aminobutyric acid(GABA)in hippocampal tissue.TUNEL staining was applied to analyze the level of neuronal apoptosis in hippocampal tissue.Western blot was applied to detect the phosphorylation levels of PI3K,Akt and mTOR in hippocampal tissue.Results Compared with the control group,the Racine score and the frequency of epileptic seizures in rats,and the number of microglia,level of IL-6,level of IL-1β,the apoptosis rate of neurons,and levels of p-PI3K/PI3K,p-Akt/Akt,p-mTOR/mTOR in hippocampal tissue in the epilepsy group were obviously increased(P<0.05),while the level of GABA in hippocampal tissue was obviously reduced(P<0.05),and the arrangement of neurons in hippocampal tissue was disordered,with neuronal loss.Compared with the epilepsy group,the Racine score,and the frequency of epileptic seizures in rats,and the number of microglia,levels of IL-6,levels of IL-1β,the apoptosis rates of neurons,and levels of p-PI3K/PI3K,p-Akt/Akt,p-mTOR/mTOR in hippocampal tissue in the epilepsy+CUR-L group and the epilepsy+CUR-H group were significantly decreased(P<0.05),while the levels of GABA in hippocampus tissue were significantly increased(P<0.05),the loss and necrosis of neurons in hippocampus tissue were decreased,and the disorder of cell arrangement was improved.Compared with the epilepsy+CUR-H group,the Racine score and the frequency of epileptic seizures in rats,and the number of microglia,level of IL-6,level of IL-1β,the apoptosis rate of neurons,and levels of p-PI3K/PI3K,p-Akt/Akt,p-mTOR/mTOR in hippocampal tissue in the epilepsy+CUR-H+740Y-P group were significantly increased(P<0.05),while the level of GABA in hippocampus tissue was significantly decreased(P<0.05),the loss and necrosis of hippocampal neurons increased,and the cell arrangement was disordered.Conclusion CUR may reduce hippocampal neuron damage in epileptic rats by downregulating the PI3K/Akt/mTOR signaling pathway.