ObjectiveTo explore the mechanism by which Sini San （SNS） inhibits ferroptosis， alleviates inflammation and myocardial injury， and improves myocardial infarction （MI）. MethodsThe active ingredients of SNS were obtained by searching the Traditional Chinese Medicine System Pharmacology Platform （TCMSP） database， its target sites were predicted using the SwissTargetPrediction Database， and the core components were screened out using the CytoNCA plug-in. The targets of MI and ferroptosis were obtained by using GeneCards， Online Mendelian Inheritance in Man （OMIM） database， DrugBank， Therapeutic Target Database （TTD）， FerrDb database and literature review， respectively. The intersection of these targets of SNS-MI-ferroptosis was plotted as a Venn diagram. The protein-protein interaction （PPI） network was constructed using the STRING database， and the visualization graph was prepared using Cytoscape. The core targets were screened out using the CytoNCA plug-in， and the biological functions were clustered by the MCODE plug-in. Gene Ontology （GO） functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis were performed using the David database. Molecular docking was performed using AutoDock and visualized with PyMOL2.5.2. The Kunming mice were randomly divided into the control group， the model group， the SNS group， and the trimetazidine （TMZ） group. The mice were subcutaneously injected with isoprenaline （ISO， 5 mg·kg^-1·d^-1） to establish an MI model. The drug was continuously intervened for 7 days. The ST-segment changes were recorded by electrocardiogram （ECG）， and the tissue morphology changes were observed by hematoxylin-eosin （HE） staining. Cardiomyocyte ferroptosis was investigated by transmission electron microscopy. Serum creatine kinase （CK）， creatine kinase isoenzyme （CK-MB）， lactate dehydrogenase （LDH）， reduced glutathione （GSH）， and malondialdehyde （MDA） levels were detected by biochemical assay. Enzyme-linked immunosorbent assay （ELISA） was used to detect serum levels of interleukin （IL）-6 and 4-hydroxynonenal （4-HNE）. Immunohistochemical staining was employed to detect IL-6 and phosphorylated signal transducer and transcription activator 3 （p-STAT3） in cardiac tissues. Western blot was used to detect STAT3 and p-STAT3 in cardiac tissues. Real-time PCR was used to detect the levels of IL-6， IL-18， solute carrier family 7 member 11 （SLC7A11）， arachidonic acid 15-lipoxygenase （ALOX15）， and glutathione peroxidase 4 （GPx4） in cardiac tissues. ResultsA total of 121 active ingredients of SNS were obtained， and 58 potential targets of SNS in the treatment of MI by regulating ferroptosis were screened. The three protein modules with a score5 were mainly related to the inflammatory response. The GO function was mainly related to inflammation， and KEGG enrichment analysis showed that SNS mainly regulated ferroptosis- and inflammation- related signaling pathways. Molecular docking indicated that the core component had a higher binding force to the target site. Animal experiments confirmed that SNS reduced the level of p-STAT3 （P0.01）， down-regulated the expression of ALOX15 mRNA （P0.01）， up-regulated the level of serum GSH， and the expressions of SLC7A11 and GPx4 mRNA， reduced MDA and 4-HNE levels （P0.05， P0.01）. Additionally， SNS improved the mitochondrial injury induced by cardiomyocyte ferroptosis， reduced the area of MI， alleviated inflammation and myocardial injury， lowered the levels of serum CK， CK-MB， LDH， IL-6， and the mRNA expression levels of IL-16 and IL-18 （P0.05）， and improved ST segment elevation. ConclusionSNS can reduce ISO-induced STAT3 phosphorylation levels， inhibit ferroptosis in cardiomyocytes， alleviate inflammation and myocardial injury， thereby improving MI.

ObjectiveTo explore the mechanism by which Sini San （SNS） inhibits ferroptosis， alleviates inflammation and myocardial injury， and improves myocardial infarction （MI）. MethodsThe active ingredients of SNS were obtained by searching the Traditional Chinese Medicine System Pharmacology Platform （TCMSP） database， its target sites were predicted using the SwissTargetPrediction Database， and the core components were screened out using the CytoNCA plug-in. The targets of MI and ferroptosis were obtained by using GeneCards， Online Mendelian Inheritance in Man （OMIM） database， DrugBank， Therapeutic Target Database （TTD）， FerrDb database and literature review， respectively. The intersection of these targets of SNS-MI-ferroptosis was plotted as a Venn diagram. The protein-protein interaction （PPI） network was constructed using the STRING database， and the visualization graph was prepared using Cytoscape. The core targets were screened out using the CytoNCA plug-in， and the biological functions were clustered by the MCODE plug-in. Gene Ontology （GO） functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis were performed using the David database. Molecular docking was performed using AutoDock and visualized with PyMOL2.5.2. The Kunming mice were randomly divided into the control group， the model group， the SNS group， and the trimetazidine （TMZ） group. The mice were subcutaneously injected with isoprenaline （ISO， 5 mg·kg^-1·d^-1） to establish an MI model. The drug was continuously intervened for 7 days. The ST-segment changes were recorded by electrocardiogram （ECG）， and the tissue morphology changes were observed by hematoxylin-eosin （HE） staining. Cardiomyocyte ferroptosis was investigated by transmission electron microscopy. Serum creatine kinase （CK）， creatine kinase isoenzyme （CK-MB）， lactate dehydrogenase （LDH）， reduced glutathione （GSH）， and malondialdehyde （MDA） levels were detected by biochemical assay. Enzyme-linked immunosorbent assay （ELISA） was used to detect serum levels of interleukin （IL）-6 and 4-hydroxynonenal （4-HNE）. Immunohistochemical staining was employed to detect IL-6 and phosphorylated signal transducer and transcription activator 3 （p-STAT3） in cardiac tissues. Western blot was used to detect STAT3 and p-STAT3 in cardiac tissues. Real-time PCR was used to detect the levels of IL-6， IL-18， solute carrier family 7 member 11 （SLC7A11）， arachidonic acid 15-lipoxygenase （ALOX15）， and glutathione peroxidase 4 （GPx4） in cardiac tissues. ResultsA total of 121 active ingredients of SNS were obtained， and 58 potential targets of SNS in the treatment of MI by regulating ferroptosis were screened. The three protein modules with a score5 were mainly related to the inflammatory response. The GO function was mainly related to inflammation， and KEGG enrichment analysis showed that SNS mainly regulated ferroptosis- and inflammation- related signaling pathways. Molecular docking indicated that the core component had a higher binding force to the target site. Animal experiments confirmed that SNS reduced the level of p-STAT3 （P0.01）， down-regulated the expression of ALOX15 mRNA （P0.01）， up-regulated the level of serum GSH， and the expressions of SLC7A11 and GPx4 mRNA， reduced MDA and 4-HNE levels （P0.05， P0.01）. Additionally， SNS improved the mitochondrial injury induced by cardiomyocyte ferroptosis， reduced the area of MI， alleviated inflammation and myocardial injury， lowered the levels of serum CK， CK-MB， LDH， IL-6， and the mRNA expression levels of IL-16 and IL-18 （P0.05）， and improved ST segment elevation. ConclusionSNS can reduce ISO-induced STAT3 phosphorylation levels， inhibit ferroptosis in cardiomyocytes， alleviate inflammation and myocardial injury， thereby improving MI.

AIM: To analyze changes in the anterior chamber angle structure in patients with implantable collamer lens with central-port(ICL V4c)implantation, and to investigate their associations with preoperative anterior segment anatomical parameters.METHODS: Retrospective case study. Patients with myopia or myopia combined with astigmatism who underwent ICL V4c implantation in the Refractive Surgery Center of the Department of Ophthalmology, the 2nd Affiliated Hospital of Harbin Medical University between July 2024 and November 2024 were recruited. Preoperative and postoperative uncorrected visual acuity, best-corrected visual acuity, intraocular pressure, anterior chamber angle(ACA), white-to-white distance(WTW), anterior chamber depth(ACD), angle to angle distance(ATA), horizontal sulcus-to-sulcus distance(HSTS), vertical sulcus-to-sulcus distance(VSTS),crystalline lens rise(CLR), pupil diameter(PD), iris thickness at 750 μm from the scleral spur(IT750),maximal iris thickness(ITM), iris curvature(I-Curv), and iris cross-sectional area(I-Area), angle opening distance(AOD750), thetrabecular-iris angle(TIA750)and the trabecular-iris space area(TISA750)in the temporal, nasal, superior, and inferior directions,as well as the vault at various postoperative time points were measured.RESULTS: The study involved 40 patients(79 eyes)with myopia or myopia combined with astigmatism who underwent ICL V4c implantation(10 males and 30 females)with the mean age of 24.73±3.79 y. Compared with preoperative measurements, at 1 mo postoperatively, the AOD750, TIA750, and TISA750 parameters at the four angles(temporal, nasal, superior, and inferior)all showed a significant reduction(P<0.01). Statistically significant differences in vault were observed at postoperative 1d(0.49±0.1), postoperative 1 wk(0.43±0.14), and postoperative 1 mo(0.41±0.14)(all P<0.001). Correlation analysis indicated that the postoperative state of the anterior chamber angle was jointly influenced by anterior chamber parameters(ACD, ATA, HSTS、VSTS), iris morphology(I-Area, IT750), pupil size(PD), and surgical factors(ICL size, early vault), and that the combination of influencing factors varied across different orientations. Regression analysis showed that ACD was positively correlated with all postoperative anterior chamber angle parameters(P<0.05). IT750 exhibited negative correlations with the temporal and inferior angles(P<0.05). I-Area was positively correlated with temporal AOD750 and TISA750(P<0.05), and PD had negative correlations with temporal TIA750 and nasal AOD750(P<0.05).CONCLUSION: Postoperative anterior chamber angle narrowing is a common phenomenon after ICL V4c implantation. The degree of change exhibits a significant correlation with multiple preoperative anterior segment anatomical parameters. Preoperative comprehensive assessment of ACD, PD, and IT750 may facilitate the evaluation of the risk of postoperative angle changes and the enhancement of surgical safety.

AIM: To investigate the effect of luteolin on tissue fibrosis in the filtering area following glaucoma trabeculectomy, and its relationship with the Wnt3a/β-catenin signaling pathway.METHODS: Rabbits were selected to establish a fibrosis model after glaucoma trabeculectomy, and randomly divided into the sham operation group, model group, luteolin-L group and luteolin-H group. Dynamic monitoring of postoperative intraocular pressure was performed in all groups. Slit-lamp biomicroscopy was used to observe postoperative conjunctival morphological changes, conjunctival healing degree, corneal integrity, and anterior chamber inflammatory responses in the filtering bleb area. HE staining was performed to evaluate conjunctival epithelial integrity, subepithelial fibrous proliferation, and inflammatory cell infiltration in the filtering tissues. Masson's trichrome staining was applied to assess collagen deposition and the degree of tissue fibrosis. The expression of α-SMA was observed by immunohistochemical staining. The mRNA and protein expression levels of Wnt3a, Wnt7a, Wnt2b, β-catenin, LC3-I, LC3-II and p62-SQSTM1 in conjunctival tissues of the operative area were quantitatively detected by RT-qPCR and Western blot, respectively.RESULTS:Postoperative dynamic monitoring showed that the luteolin-H group achieved significantly better intraocular pressure control than the luteolin-L group compared with the model group(all P<0.05). Slit lamp observations confirmed that luteolin effectively ameliorated postoperative conjunctival injury, alleviated anterior chamber inflammatory response, and maintained the structural stability of the filtering area. HE and Masson staining revealed that luteolin intervention reduced conjunctival epithelial damage and inflammatory cell infiltration, markedly inhibited fibroblast proliferation, neovascularization and excessive collagen deposition, and significantly delayed the progression of filtering bleb scarring, with stronger effects in the luteolin-H group than luteolin-L group compared with the model group. Immunohistochemical staining demonstrated that luteolin intervention decreased the positive expression rate of α-SMA. Molecular assays indicated that the luteolin-H group had lower expression levels of Wnt3a, β-catenin and LC3-II/LC3-I, and the highest p62-SQSTM1 level in the operative site relative to the model group and luteolin-L group(all PSymbol|@@0.05). No significant intergroup differences were observed in Wnt2b and Wnt7a expression. These findings suggested that luteolin could specifically regulated the Wnt3a pathway and dose-dependently suppressed the activation of the Wnt3a/β-catenin pathway after glaucoma trabeculectomy, downregulated LC3-II/LC3-I expression, upregulated p62-SQSTM1 levels, and inhibited excessive autophagy activation.CONCLUSION: Luteolin can significantly inhibit filtering bleb fibrosis after trabeculectomy, which may reduce the degree of fibrosis via the Wnt3a/β-catenin pathway.

Abdominal obesity represents the predominant obesity phenotype in China.Compared to peripheral obesity,individuals with abdominal obesity are more prone to metabolic disorders,cardiovascular diseases,and higher mortality rates.Catgut embedding therapy at acupoints has demonstrated significant clinical efficacy in preventing and treating abdominal obesity.However,standardized clinical guidelines for its application in abdominal obesity management have not yet been established.This review comprehensively summarizes the clinical applications of catgut embedding therapy for simple abdominal obesity and abdominal obesity with various complications,aiming to provide clinical evidence and theoretical guidance for its use in preventing and treating abdominal obesity.

Objective To investigate the expression of GJB4 gene in pancreatic cancer tissue and its correlation with clinicopathology.Methods The expression levels of GJB4 mRNA in pancreatic cancer and adjacent cancer tissues were analyzed using bioinformatics to analyze the Cancer Genome Atlas(TCGA)and Genotype-Tissue Expression(GTEx)RNA sequencing datasets.A total of 120 pancreatic cancer samples and 40 adjacent cancer samples from the Pathology Department of The Second Affiliated Hospital of Kunming Medical University from January 2019 to December 2023 were collected and sorted.Immunohistochemistry staining method was used to detect the expression difference of GJB4 protein between the two groups.RT-qPCR method was used to detect the expression levels of GJB4 in four pancreatic cancer cell lines.Univariate and multivariate Cox regression and Kaplan-Meier curves were used to analyze the clinical pathological data of GJB4 and pancreatic cancer patients.DAVID functional annotation bioinformatics and GSEA enrichment analysis were used to explore the relevant pathways of GJB4 in pancreatic cancer.Results The expression level of GJB4 mRNA in pancreatic cancer was higher than that in adjacent tissues,and the high expression of GJB4 was significantly associated with poor prognosis of patients(P<0.05).Immunohistochemical analysis showed that GJB4 protein was brown-yellow granular in pancreatic cancer tissues,mainly expressed in cytoplasm and cell membrane,and GJB4 protein expression was up-regulated in pancreatic cancer(P<0.05).The RT-qPCR test results showed that out of 4 pancreatic cancer cell lines,3 of them had upregulated expression(P<0.05).COX regression analysis showed that GJB4 gene was an independent risk factor in the prognosis of pancreatic cancer patients.The results of GO enrichment analysis showed that GJB4 was related to the transmembrane transport,ion channel,signal release and membrane potential regulation of pancreatic cancer.GSEA analysis showed that GJB4 was enriched in the Wnt/β-catenin signaling pathway.Conclusion In pancreatic cancer,the high expression level of GJB4 is closely related to the clinicopathological features of the patients,which may predict the poor prognosis of the patients.GJB4 may be involved in regulating the Wnt/β-catenin signaling pathway of pancreatic cancer,and is expected to be one of the potential biomarkers of pancreatic cancer prognosis.

Objective To develop an active monitoring model for adverse drug events(ADEs)related to antimicrobial use in children based on the China hospital pharmacovigilance system(CHPS).Methods Trigger items for the active monitoring model were initially drafted through a review of relevant literature,adverse reaction databases,and drug label warnings,and subsequently refined using the Delphi method.A retrospective analysis was performed on pediatric inpatients who received antibiotics at Anning First People's Hospital between January 1 and December 31,2024.The detection rate and positive predictive value(PPV)of the active monitoring model were calculated and compared with spontaneous ADE reports from the same period.Risk factors for ADEs were further analyzed using logistic regression.Results 25 trigger items were established for the active monitoring model.Among 1,784 cases,233 ADEs were identified,yielding a detection rate of 13.06%(233/1,784).The spontaneous reporting rate of adverse events during the same period was 1.85%(33/1,784).The difference between the two was statistically significant(P<0.001).There were 727 positive trigger events,with 299 cases of ADE detected,resulting in an overall PPV of 41.13%(299/727).Logistic regression revealed that antibiotic use exceeding 3 days(OR=1.454,95%CI:1.012-2.088)was significantly associated with ADE occurrence.Conclusion Compared with conventional spontaneous reporting,the active monitoring model can significantly improve the detection rate of ADEs of pediatric antimicrobial drugs and achieve active and real-time monitoring of drug adverse events.

Objective To analyze the current status and influencing factors of occupational stress, job burnout and sleep quality among workers in the secondary industry in Jinshan District, Shanghai City. Methods A total of 1 418 workers from six key industries in Jinshan District, Shanghai City were selected as the study subjects by the stratified cluster sampling method. The Occupational Stress Core Scale, Maslash Burnout Inventory General Survey and Pittsburgh Sleep Quality Index were used to investigate occupational stress, job burnout and sleep quality of the workers. Results The detection rates of occupational stress, job burnout and sleep disturbance among the study subjects were 33.6%, 65.4% and 23.3%, respectively. Multivariate logistic regression analysis showed that the workers with a monthly income <5 000 yuan had a higher risk of occupational stress than those with a monthly income ≥5 000 yuan (P<0.01). The workers with ≥5.0 years of service had a higher risk than those with <1.0 year (P<0.05). Lack of physical exercise, employment in medium- and large-sized enterprises, and shift work were risk factors of occupational stress in the workers (all P<0.01). The workers aged 18-<30 years had a higher risk of job burnout than those aged 45-<60 years (P<0.05). The workers monthly income <5 000 yuan was associated with a higher risk of job burnout than those with ≥9 000 yuan (P<0.05). The workers with 1.0-<10.0 years or ≥15.0 years of service had higher job burnout risks than those with <1.0 year (all P<0.05). Being unmarried, lack of physical exercise, and employment in medium- and large-sized enterprises were risk factor of job burnout in the workers (all P<0.05). The workers with an educational level of high school or above had a higher risk of sleep disturbance than those with junior school or below (P<0.05). The workers who work >56 hours per week had a higher risk than those working ≤40 hours per week (P<0.01). Conclusion There is a high detection rate of occupational stress, job burnout, and sleep disturbance in the secondary industry workers in Jinshan District, Shanghai City. Special attention should be given to workers with low income, lack of physical exercise, employment in medium- and large-sized enterprises, shift work, long service duration, and long weekly working hours to protect their physical and mental health.

Objective:To observe the effect of moxibustion on angiogenesis-related indicators in knee joint synovial tissue of adjuvant arthritis model rats,and to explore the mechanism of moxibustion in inhibiting vascular endothelial growth factor(VEGF)expression in synovial tissue and further limiting the activation of Rho family proteins Rac1 and Cdc42,thereby inhibiting angiogenesis during rheumatoid arthritis(RA)treatment.Methods:Forty-eight male Sprague-Dawley rats were equally divided into a normal group,a model group,a moxibustion group,and a moxibustion+VEGF agonist group according to the random principle.The complete Freund's adjuvant method was used for modeling.On the 12th day after modeling,the moxibustion group and the moxibustion+VEGF agonist group were subjected to suspended moxibustion at bilateral Zusanli(ST36),Guanyuan(CV4),and Ashi points for 20 min each time,once a day,for a total of 15 times.The moxibustion+VEGF agonist group received VEGF agonist(tirofiban hydrochloride hydrate)injection in the knee joint cavity at the same time.Hematoxylin-eosin staining was used to evaluate the pathological changes of rat synovial tissue in each group.Immunohistochemistry was used to observe the CD31 expression level in rat synovial tissue.Western blotting was used to detect the levels of VEGF,Rac1,and Cdc42 protein in rat synovial tissue,and polymerase chain reaction(PCR)was used to detect the VEGF mRNA expression.Results:Compared to the normal group,the expression levels of CD31 protein and VEGF mRNA and protein in rat synovial tissue in the model group increased significantly(P<0.01),and the expression levels of phospho-Rac1 and phospho-Cdc42 proteins also increased significantly(P<0.01).After moxibustion intervention,the expression levels of CD31 protein and VEGF mRNA and protein in the moxibustion group were significantly lower than those in the model group(P<0.01),while the differences in each indicator between the moxibustion+VEGF agonist group and the model group were not statistically significant(P>0.05).Compared to the moxibustion group,the expression levels of CD31 protein,VEGF mRNA and protein,phospho-Cdc42,and phospho-Rac1 in the moxibustion+VEGF agonist group increased significantly(P<0.01).Conclusion:Moxibustion improved synovial inflammation in RA by inhibiting angiogenesis.The mechanism may be to regulate angiogenesis-related VEGF,restrict the activation of Rac1 and Cdc42,and inhibit pseudopodia formation in vascular endothelial cells,thereby reducing angiogenesis.

Objective To analyze the misdiagnosis issues and its contributing factors in 2 cases of failed rescue from severe acute methanol poisoning.Methods Clinical data of the 2 patients who died despite emergency treatment were retrospectively reviewed.Misdiagnosis-related problems were summarized and their root causes were investigated.Results Major misdiagnoses included:① Incomplete and insufficient inquiry of medical history;②Insufficient knowledge of methanol-toxic manifestations;③Failure to scientifically properly interpret arterial blood gas analysis in auxiliary examinations;④Unfamiliarity with methanol poisoning because of its rarity at primary hospitals.The primary causes of misdiagnosis were:①Patients and their families failed to promptly provide a history of methanol poisoning ingestion in a timely manner;② Although the 2 patients were poisoned at the same time,they visited the hospital separately with a time interval of up to 24 hours;③Physicians lacked vigilance and in-depth understanding of the systemic disease mainly characterized by central nervous system damage,visual impairment and metabolic acidosis;④ Physicians made subjective assumptions,had narrow thinking,and lacked the ability to comprehensively analyze the condition.Conclusions Correct diagnosis is the key to reducing the misdiagnosis in the emergency management of severe acute methanol poisoning.Emergency physicians must master the diagnostic criteria of acute methanol poisoning proficiently,and strive for early diagnosis and treatment to improve the prognosis of patients.In addition,public education on poisoning prevention should be strengthened to raise public awareness and reduce the incidence of methanol poisoning.