Objective:To investigate the main causes of failed endoscopic retrograde cholangiopancreatography (ERCP) in children and the remedial treatment strategies.Methods:This retrospective cohort study analyzed the clinical data of 21 children who experienced failed ERCP at Beijing Children′s Hospital, Capital Medical University between January 2021 and December 2024. Data was collected included demographic information, clinical diagnoses, and ERCP outcomes. The annually trend in the ERCP failure rate was analyzed. Patients were categorized by etiology into the following groups: chronic pancreatitis, post-surgical status, pancreatic trauma, pancreas divisum, non-neoplastic pancreatic lesions, and ulcerative colitis. The relationship between etiologies and ERCP failure was analyzed by Fisher exact test.Results:A total of 175 ERCP procedures were included, of which 21 procedures failed (12.0%). The failure rate decreased annually from 2021 to 2024: 18.2% (4/22), 13.2% (5/38), 11.4% (5/44), and 9.9% (7/71), respectively. The etiological distribution among the 21 failed cases was as follows: chronic pancreatitis 28.6% (6/21), pancreatic duct stenosis following pancreatic trauma 23.8% (5/21), post-surgical status 14.3% (3/21), pancreas divisum 9.5% (2/21), acute pancreatitis 9.5% (2/21), non-neoplastic pancreatic lesions 9.5% (2/21), and pancreatic duct stenosis associated with ulcerative colitis 4.8% (1/21). Remedial treatments included surgical intervention (2 cases), ultrasound-guided percutaneous drainage (3 cases), and repeat ERCP (2 cases). For post-surgical and pancreatic trauma patients, failure was primarily due to bile duct stenosis, pancreatic duct stenosis, or pancreaticobiliary duct disruption. Active surgical interventions such as cholangiojejunostomy and pancreaticojejunostomy, and ultrasound-guided drainage following ERCP failure led to significant clinical improvement.Conclusions:A stratified management approach guided by etiology is essential following failed ERCP in children. Early and active remedial treatment, particularly surgical interventions, is recommended for post-surgical and pancreatic trauma cases.

Objective:To investigate the main causes of failed endoscopic retrograde cholangiopancreatography (ERCP) in children and the remedial treatment strategies.Methods:This retrospective cohort study analyzed the clinical data of 21 children who experienced failed ERCP at Beijing Children′s Hospital, Capital Medical University between January 2021 and December 2024. Data was collected included demographic information, clinical diagnoses, and ERCP outcomes. The annually trend in the ERCP failure rate was analyzed. Patients were categorized by etiology into the following groups: chronic pancreatitis, post-surgical status, pancreatic trauma, pancreas divisum, non-neoplastic pancreatic lesions, and ulcerative colitis. The relationship between etiologies and ERCP failure was analyzed by Fisher exact test.Results:A total of 175 ERCP procedures were included, of which 21 procedures failed (12.0%). The failure rate decreased annually from 2021 to 2024: 18.2% (4/22), 13.2% (5/38), 11.4% (5/44), and 9.9% (7/71), respectively. The etiological distribution among the 21 failed cases was as follows: chronic pancreatitis 28.6% (6/21), pancreatic duct stenosis following pancreatic trauma 23.8% (5/21), post-surgical status 14.3% (3/21), pancreas divisum 9.5% (2/21), acute pancreatitis 9.5% (2/21), non-neoplastic pancreatic lesions 9.5% (2/21), and pancreatic duct stenosis associated with ulcerative colitis 4.8% (1/21). Remedial treatments included surgical intervention (2 cases), ultrasound-guided percutaneous drainage (3 cases), and repeat ERCP (2 cases). For post-surgical and pancreatic trauma patients, failure was primarily due to bile duct stenosis, pancreatic duct stenosis, or pancreaticobiliary duct disruption. Active surgical interventions such as cholangiojejunostomy and pancreaticojejunostomy, and ultrasound-guided drainage following ERCP failure led to significant clinical improvement.Conclusions:A stratified management approach guided by etiology is essential following failed ERCP in children. Early and active remedial treatment, particularly surgical interventions, is recommended for post-surgical and pancreatic trauma cases.

Objective:To investigate the therapeutic effectiveness of endoscopic retrograde cholangiopancreatography (ERCP) and stent implantation in the treatment of pancreaticobiliary injuries in children.Methods:A retrospective analysis was conducted on the clinical data of children diagnosed with pancreaticobiliary injury and undergoing ERCP and stent implantation at Beijing Children′s Hospital, Capital Medical University from January 2021 to December 2022. Demographic information, clinical data, endoscopic treatment methods, postoperative complications and clinical prognosis of the children were collected. The etiology, location of pancreaticobiliary injury, occurrence of complications after endoscopic treatment, and the time for improvement and recovery after endoscopic treatment were analyzed. The patients were divided into five groups according to the etiologies of pancreaticobiliary duct injuries: post-surgical, pancreatic trauma, acute pancreatitis, chronic pancreatitis, and systemic lupus erythematosus groups. They were also classified into four groups according to the sites of pancreaticobiliary duct injuries: common bile duct, pancreatic head, pancreatic body, and pancreatic tail groups. Multi-factor analysis of variance was used for comparing the time of improvement and recovery among different groups.Results:Among 22 patients, there were 8 males and 14 females, and the age was 7.5 (3.3,10.8) years. There were 19 cases of pancreatic or bile duct fistula, and 3 cases of pancreatic or bile duct stenosis. A total of 33 endoscopic procedures were performed on the 22 patients, out of which, 3 duct stenosis were failed to insert the stent because the catheter failed to pass through the stenosis site. The success rate was 91% (30/33). The pancreatic duct or bile duct stent was inserted, with the stent located at pancreatic or bile duct fistula. Postoperative complications included pancreatitis in 3 cases (9%, 3/33), hyperamylasemia in 5 cases (15%, 5/33), and postoperative infection in 4 cases (12%, 4/33). All patients were followed up for more than 1 year. Significant improvement was observed in external drainage and imaging monitoring among patients with successfully placed stents. There was no significant difference in the improvement time of ERCP in the treatment of pancreaticobile duct injury caused by different etiology ( F=0.65, P=0.637). However, there were significant differences in healing time ( F=6.46, P=0.004), among which the healing time of injuries caused by systemic lupus erythematosus was significantly different from that after surgery, trauma, acute pancreatitis and chronic pancreatitis (all P<0.05). There was no significant difference in the improvement and healing time among different injury sites (all P>0.05). Conclusions:ERCP and stent implantation can safely and effectively improve the clinical symptoms of children with pancreaticobiliary injury. Early intervention can improve long-term prognosis.

Objective To explore the relationship between PANoptosis and hepatic ischemia-reperfusion injury (HIRI), and to screen the key genes of PANoptosis in HIRI. Methods PANoptosis-related differentially expressed genes (PDG) were obtained through the Gene Expression Omnibus database and GeneCards database. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) were used to explore the biological pathways related to PDG. A protein-protein interaction network was constructed. Key genes were selected, and their diagnostic value was assessed and validated in the HIRI mice. Immune cell infiltration analysis was performed based on the cell-type identification by estimating relative subsets of RNA transcripts. Results A total of 16 PDG were identified. GO analysis showed that PDG were closely related to cellular metabolism. KEGG analysis indicated that PDG were mainly enriched in cellular death pathways such as apoptosis and immune-related signaling pathways such as the tumor necrosis factor signaling pathway. GSEA results showed that key genes were mainly enriched in immune-related signaling pathways such as the mitogen-activated protein kinase (MAPK) signaling pathway. Two key genes, DFFB and TNFSF10, were identified with high accuracy in diagnosing HIRI, with areas under the curve of 0.964 and 1.000, respectively. Immune infiltration analysis showed that the control group had more infiltration of resting natural killer cells, M2 macrophages, etc., while the HIRI group had more infiltration of M0 macrophages, neutrophils, and naive B cells. Real-time quantitative polymerase chain reaction results showed that compared with the Sham group, the relative expression of DFFB messenger RNA in liver tissue of HIRI group mice increased, and the relative expression of TNFSF10 messenger RNA decreased. Cibersort analysis showed that the infiltration abundance of naive B cells was positively correlated with DFFB expression (r=0.70, P=0.035), and the infiltration abundance of M2 macrophages was positively correlated with TNFSF10 expression (r=0.68, P=0.045). Conclusions PANoptosis-related genes DFFB and TNFSF10 may be potential biomarkers and therapeutic targets for HIRI.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Objective To develop a machine learning-based risk prediction model for postoperative acute kidney injury(AKI)and a model for mortality in obese patients admitted to intensive care unit(ICU)in order to improve early warning and prognostic evaluation to support clinical decision-making.Methods Data of obese postoperative ICU patients were retrospectively retrieved from the MIMIC-Ⅳ and eICU databases for statistical analysis.Ultimately,2 520 patients(670 from MIMIC-Ⅳ and 1 850 from eICU databases)were included to build the risk prediction models for AKI and mortality.The data included demographic information,vital signs,laboratory findings,surgical types,comorbidities,and medication use.After data cleaning and preprocessing,Boruta feature selection was applied,followed by the construction of prediction models using 7 machine learning algorithms,that is,Gradient Boosting Machine(GBM),Generalized Linear Model(GLM),k-Nearest Neighbors(KNN),Na?ve Bayes(NB),Neural Network(NNET),Support Vector Machine(SVM),and XGBoost.Model performance was evaluated through cross-validation and external validation.Results In the risk prediction models of AKI,the SVM model achieved the highest AUC value of 0.80 in the testing set and 0.71 in the external validation test.For the risk prediction models of mortality,the GBM model outperformed others in the prediction,attaining an AUC value of 0.91 in the testing set.Conclusion Risk predictive models for postoperative AKI and mortality in obese ICU patients are successfully constructed,and are valuable tools for clinicians to optimize early intervention and improve clinical outcomes for the patients.

Objective To investigate the status of population dynamics and distribution changes of Aedes aegypti in Guangdong Province.Methods Continuous monitoring was conducted from May 2018 to July 2024 in Wushi Town and Qishui Town,Leizhou City,Zhanjiang City,Guangdong Province.Additionally,a survey of the distribution of Ae.aegypti along the Leizhou Peninsula coast was carried out.Results The density of Ae.aegypti in Zhanjiang showed a gradual decline from 2018 to 2024.The last detection of adult Ae.aegypti in Wushi Town was in September 2021,and the last larva was found in October 2023.No Ae.aegypti was detected in Qishui Town during surveys from 2021 to 2024.A survey of 18 coastal villages in the Leizhou Peninsula revealed no detections of Ae.aegypti.Conclusions This study provides a basis for understanding the distribution and population density fluctuations of Ae.aegypti,assessing its invasion risk,and scientifically conducting relevant prevention and control efforts.