Objective To understand the current situation of healthcare-associated infection(HAI)in China,pro-vide data support and decision-making basis for formulating scientific and effective strategies for HAI prevention and control.Methods A nationwide cross-sectional survey on HAI was conducted among various types and levels of medical institutions in China according to a unified protocol of bedside surveys and case investigations.Results In 2024,a total of 5 736 medical institutions and 2 751 765 patients were surveyed.Among them,34 889 HAI cases were identified,with a prevalence rate of 1.27％.The number of HAI episodes was 38 032,and case prevalence rate was 1.38％.The prevalence rate of HAI in medical institutions in different regions of China ranged from 0.66％to 2.35％.Among medical institutions of different scales,those with a bed capacity of ≥900 had the high-est incidence of HAI,reaching 1.65％.The most common infection site was the lower respiratory tract(44.66％),followed by the urinary tract(12.94％),surgical site(9.32％),upper respiratory tract(7.02％),and bloodstream infection(5.78％).The top 3 departments with the highest HAI rates were the general intensive care unit(10.02％),department of neurosurgery(5.51％),and department(group)of hematology(5.34％).A total of 23 238 strains of HAI pathogens were detected,with 10 714 strains(46.10％)from lower respiratory tract speci-mens.The top 5 detected strains were Klebsiella pneumoniae(14.76％),Pseudomonas aeruginosa(13.33％),Escherichia coli(12.79％),Acinetobacter baumannii(9.23％),and Staphylococcus aureus(7.88％).231 944 pa-tients underwent class Ⅰ incision surgery were monitored,with 1 647 cases experienced surgical site infection,and the prevalence rate of surgical site infection was 0.71％.The number of patients who should undergo pathogen de-tection(patients receiving therapeutic and therapeutic combined prophylactic antimicrobial agents)was 715 179,while the actual number was 480 492,with a pathogen detection rate of 67.18％.425 225 patients received patho-genic detection before treatment,with a detection rate of 59.46％.Conclusion The overall HAI prevalence in Chi-na is lower,showing disparities among medical institutions of different regions and scales.Therefore,precise imple-mentation of measures is necessary for HAI prevention and control,with a focus on high-risk institutions and high-risk departments,key areas,and critical procedures.All levels of medical institutions should continuously reduce the incidence of HAI by strengthening monitoring,standardizing the use of antimicrobial agents,and reinforcing basic HAI prevention and control measures.

Aim To explore the mechanism of hispidu-lin in the treatment of cervical cancer by using network pharmacology and molecular docking methods and veri-fy it by in vitro experiments.Methods Cervical canc-er HeLa and SiHa cells were cultivated in vitro,and CCK-8 assay,cloning assay,scratch assay,transwell as-say,and flow cytometry were used to detect the effects of hispidulin on cell proliferation,migration,invasion,and apoptosis.SwissTarget Prediction was used to ob-tain predicted targets for hispidulin.Potential targets for cervical cancer were screened in GeneCards disease database.R software Venn package was used to obtain the intersection target genes of hispidulin and cervical cancer,STRING website and Cytoscape software were used to obtain protein-protein interaction(PPI)net-work,and the core targets were screened.The GEIPA data analysis platform was employed to analyze the dif-ferential gene expression levels of core targets in cervi-cal cancer.Gene Ontology(GO)and Kyoto Encyclo-pedia of Genes and Genomes(KEGG)enrichment a-nalysis were performed,and molecular docking was car-ried out on key targets.Western blot was used to detect the regulatory effects of hispidulin on the expression of key proteins PI3K,p-Akt,as well as core target pro-teins MMP9 and RARP1 in the PI3K/Akt signaling pathway.Results Cell experiments showed that after treatment with hispidulin,the proliferation and colony formation abilities of HeLa and SiHa cells significantly decreased in a concentration-and time-dependent man-ner.At the same time,the lateral and longitudinal mi-gration and invasion abilities of HeLa cells decreased,and the level of apoptosis significantly increased.A to-tal of 87 intersection targets between hispidulin and cervical cancer were obtained,and eight core targets,namely,Akt1,EGFR,SRC,ESR1,PTGS2,GSK3β,MMP9,and PARP1,were selected based on the degree values in network topology analysis.KEGG enrichment screening identified PI3K/Akt signaling pathway,canc-er pathway,and other signaling pathways.The molecu-lar docking results showed that hispidulin had strong affinity activity with AktⅠ,P13K,MMP9,and RARP1.Western blot results showed downregulation of PI3K,p-Akt expression,as well as MMP9 and RARP1 expres-sion.Conclusions Hispidulin can inhibit the prolif-eration,migration,invasion,and promote apoptosis of cervical cancer cells by downregulating the PI3K/Akt signaling pathway and the expression of MMP9 and RARP1.

Aim To investigate the pharmacological mechanism of Ebselenin(Ebselen,EbSe)in the treat-ment of Escherichia coli(E.coli)infection,which had no significant inhibitory effect on Gram-negative bacte-ria,based on previous studies.Methods After EbSe intervention in E.coli infected Raw264.7 cells,the via-bility of Raw264.7 cells was determined by CCK-8 method,the morphology and structure of Raw264.7 cells were observed by electron microscope,and the in-tracellular bacterial load of Raw264.7 cells was calcu-lated by coated plate method.Polarization status of peritoneal macrophages,Raw264.7 intracellular NO and ROS content and intracellular HO-1 expression in Raw264.7 and E.coli acutely infected mice after E.co-li infection by flow cytometry.qPCR was used to detect the expression of related mRNAs in Raw264.7 cells.qPCR was used to detect the intracellular GSH content in Raw264.7 cells by spectrophotometric assay,and the state of cytoskeletal proteins was observed by immuno-fluorescence.Western blot assay was performed to de-tect the intracellular Txnrd1 expression level.Results Microtiter method,CCK-8,and electron microscopy observations showed that EbSe had no effect on the growth of E.coli and Raw264.7 cells in vitro.The re-sults of smear plate counting showed that EbSe reduced the intracellular bacterial load of Raw264.7 in the in-fected group.Flow cytometry results showed that EbSe upregulated the number of M2-type macrophages.The EbSe-treated infected group had reduced intracellular NO and ROS levels and increased GSH levels.The qPCR results showed that the expression of IL-6,IL-1β,and iNOS was decreased,and the expression of HO-1,Txnrd1,and Glut1 was increased in DHB4-in-fected Raw264.7 cells after EbSe treatment.Cytoskel-etal staining showed that the morphology of the EbSe-treated infected cells was similar to that of oxPAPC-in-duced cells.Western blot results showed the expres-sion of Txnrd1 protein in EbSe-treated infected cells in-creased.Conclusion EbSe exerts anti-E.coli acute infection effect by regulating macrophage polarization and inhibiting macrophage excessive inflammatory state.

Objective To investigate the effect of G9a histone methyltransferase inhibitor BIX01294 on the proliferation of vascular smooth muscle cell(VSMC)and its underlying mechanism.Methods Twelve SD rats were divided into the control group and the treatment group,with 6 rats in each group.The rats were anesthetized by intraperitoneal injection with sodium pentobarbital,then exposed the common carotid artery and the internal and external carotid artery after disinfection and skin preparation,ligated the distal end of the internal and external jugular veins,clamped the proximal end of the common carotid artery,cut the external carotid artery,inserted the balloon catheter,blocked the blood flow by compression,and ligated the proximal end of the external carotid artery after withdrawing the balloon.The common carotid artery clamping state of rats in the treatment group was maintained after withdrawing the balloon,then restored the blood flow after perfusion with 100 μmol/L BIX01294 solution for 30 seconds;rats in the control group were restored the blood flow after perfusion with PBS for 30 seconds.VSMC were divided into the normal group and the BIX01294 groups.Cells in the normal group were cultured in low glucose medium containing 2%fetal bovine serum,and cells in the BIX01294 groups were co-treated with 2.5,5.0,7.5 and 10.0 μmol/L BIX01294 on the basis of the normal group,respectively.CCK-8 assay and EDU assay were used to detect the cell activity and proliferative ability respectively,to screen appropriate concentration of BIX01294.The cell apoptosis was detected by TUNEL assay between the normal group and the BIX01294 group,and the control group and the treatment group.Western blot was used to detect the expression levels of autophagy-and apoptosis-related proteins in the normal group and BIX01294 group.Results Compared with 0 μmol/L,the activity and proliferative ability of VSMC decreased in a concentration-dependent manner after treatment with BIX01294 at different concentrations(P<0.05).Compared with the normal group,the apoptosis level of VSMC in the BIX01294 group was increased(P<0.05),the expression of VSMC autophagy-and apoptosis-related proteins of LC3Ⅰ/Ⅱ and Bax were up-regulated(P<0.05),and the expression of Bcl-2 and p62 proteins were down-regulated(P<0.05).In vivo test results showed that BIX01294 local perfusion aggravated the apoptosis of carotid VSMC.Conclusion BIX01294 activates VSMC autophagy and apoptosis and inhibits its proliferation.

Aim To explore the mechanism of hispidu-lin in the treatment of cervical cancer by using network pharmacology and molecular docking methods and veri-fy it by in vitro experiments.Methods Cervical canc-er HeLa and SiHa cells were cultivated in vitro,and CCK-8 assay,cloning assay,scratch assay,transwell as-say,and flow cytometry were used to detect the effects of hispidulin on cell proliferation,migration,invasion,and apoptosis.SwissTarget Prediction was used to ob-tain predicted targets for hispidulin.Potential targets for cervical cancer were screened in GeneCards disease database.R software Venn package was used to obtain the intersection target genes of hispidulin and cervical cancer,STRING website and Cytoscape software were used to obtain protein-protein interaction(PPI)net-work,and the core targets were screened.The GEIPA data analysis platform was employed to analyze the dif-ferential gene expression levels of core targets in cervi-cal cancer.Gene Ontology(GO)and Kyoto Encyclo-pedia of Genes and Genomes(KEGG)enrichment a-nalysis were performed,and molecular docking was car-ried out on key targets.Western blot was used to detect the regulatory effects of hispidulin on the expression of key proteins PI3K,p-Akt,as well as core target pro-teins MMP9 and RARP1 in the PI3K/Akt signaling pathway.Results Cell experiments showed that after treatment with hispidulin,the proliferation and colony formation abilities of HeLa and SiHa cells significantly decreased in a concentration-and time-dependent man-ner.At the same time,the lateral and longitudinal mi-gration and invasion abilities of HeLa cells decreased,and the level of apoptosis significantly increased.A to-tal of 87 intersection targets between hispidulin and cervical cancer were obtained,and eight core targets,namely,Akt1,EGFR,SRC,ESR1,PTGS2,GSK3β,MMP9,and PARP1,were selected based on the degree values in network topology analysis.KEGG enrichment screening identified PI3K/Akt signaling pathway,canc-er pathway,and other signaling pathways.The molecu-lar docking results showed that hispidulin had strong affinity activity with AktⅠ,P13K,MMP9,and RARP1.Western blot results showed downregulation of PI3K,p-Akt expression,as well as MMP9 and RARP1 expres-sion.Conclusions Hispidulin can inhibit the prolif-eration,migration,invasion,and promote apoptosis of cervical cancer cells by downregulating the PI3K/Akt signaling pathway and the expression of MMP9 and RARP1.

Aim To investigate the pharmacological mechanism of Ebselenin(Ebselen,EbSe)in the treat-ment of Escherichia coli(E.coli)infection,which had no significant inhibitory effect on Gram-negative bacte-ria,based on previous studies.Methods After EbSe intervention in E.coli infected Raw264.7 cells,the via-bility of Raw264.7 cells was determined by CCK-8 method,the morphology and structure of Raw264.7 cells were observed by electron microscope,and the in-tracellular bacterial load of Raw264.7 cells was calcu-lated by coated plate method.Polarization status of peritoneal macrophages,Raw264.7 intracellular NO and ROS content and intracellular HO-1 expression in Raw264.7 and E.coli acutely infected mice after E.co-li infection by flow cytometry.qPCR was used to detect the expression of related mRNAs in Raw264.7 cells.qPCR was used to detect the intracellular GSH content in Raw264.7 cells by spectrophotometric assay,and the state of cytoskeletal proteins was observed by immuno-fluorescence.Western blot assay was performed to de-tect the intracellular Txnrd1 expression level.Results Microtiter method,CCK-8,and electron microscopy observations showed that EbSe had no effect on the growth of E.coli and Raw264.7 cells in vitro.The re-sults of smear plate counting showed that EbSe reduced the intracellular bacterial load of Raw264.7 in the in-fected group.Flow cytometry results showed that EbSe upregulated the number of M2-type macrophages.The EbSe-treated infected group had reduced intracellular NO and ROS levels and increased GSH levels.The qPCR results showed that the expression of IL-6,IL-1β,and iNOS was decreased,and the expression of HO-1,Txnrd1,and Glut1 was increased in DHB4-in-fected Raw264.7 cells after EbSe treatment.Cytoskel-etal staining showed that the morphology of the EbSe-treated infected cells was similar to that of oxPAPC-in-duced cells.Western blot results showed the expres-sion of Txnrd1 protein in EbSe-treated infected cells in-creased.Conclusion EbSe exerts anti-E.coli acute infection effect by regulating macrophage polarization and inhibiting macrophage excessive inflammatory state.

Aim To investigate the effect of cordycepin(COR)on gentamicin(GEN)-induced nephrotoxicity and the molecular mechanism of inhibiting oxidative stress and ferroptosis induced by GEN.Methods The oral SD rats were divided into a control group,GEN group,and GEN+COR group.Following the success-ful setting up of the animal model,the serum creatinine(CR)and urea nitrogen(BUN)levels of rats were measured,and renal tissue injury was assessed using HE staining.In addition,the contents of malondialde-hyde and glutathione in kidney tissues of SD rats in each group were detected,and the expressions of fer-roptosis markers GPX4 and SLC7A11 were analyzed by Western blot.Results Compared with the control group,CR and BUN in GEN-stimulated group signifi-cantly increased(P＜0.01),and the level of CR and BUN was effectively reduced after 50 mg·kg-1 COR oral administration.HE results also showed that COR could alleviate the kidney tissue damage caused by GEN.COR could reverse the increase of malondialde-hyde level and the decrease of glutathione level caused by GEN in rat kidney tissue,and COR could restore the decrease of GPX4 and SLC7A11 protein levels induced by GEN.Conclusion COR can reduce GEN-induced kidney injury by inhibiting oxidative stress and ferrop-tosis.

Objective To investigate the clinical efficacy and safety of facilitated percutaneous coronary intervention(PCI)with half-dose recombinant staphylokinase(r-SAK)in patients with ST-segment elevation myocardial infarction(STEMI)who are expected to undergo PCI within 120 minutes.Methods From October 2021 to August 2022,a total of 200 STEMI patients in eight centers were included and randomly assigned in a 1﹕1 ratio to either r-SAK group or control group.Patients received loading doses of aspirin and ticagrelor and intravenous heparin and were randomized to receive an intravenous bolus of either 5 mg r-SAK or normal saline prior to PCI.The outcomes were set as ST-segment resolution(STR)at 60-90 minutes after PCI,the proportion and transition of pathological Q waves on the 5th day after PCI,and the proportion of high-sensitivity cardiac troponin T(hs-cTnT)peaking within 12 hours of onset.The safety outcome was major bleeding events defined as Bleeding Academic Research Consortium(BARC)≥type 3 bleeding during hospitalization.Results Compared with the control group,the r-SAK group had a higher proportion of STR≥70%within 60-90 minutes after PCI(58.3%vs.40.3%,P=0.009);a lower proportion of pathological Q waves(59.1%vs.74.1%,P=0.040);a lower rate of Q wave progression(14.8%vs.43.2%,P＜0.001);a higher rate of Q wave disappearance(12.5%vs.3.7%,P=0.027);and a higher proportion of hs-cTnT peaking within 12 hours of symptom onset[31/40(77.5%)vs.17/33(51.5%),P=0.027].Regarding the safety outcome,no significant difference in BARC≥type 3 bleeding was found between the two groups during hospitalization(P＞0.05).Conclusions For STEMI patients who were expected to undergo primary PCI within 120 minutes of symptom onset,the facilitated PCI with half-dose r-SAK significantly increased the proportion of STR≥70%at 60-90 minutes after PCI,reduced the formation of pathological Q waves,and shortened the time to peak hs-cTnT,without increasing the risk of bleeding,which should be an alternative reperfusion strategy worthy of further study.

Objective To investigate the clinical efficacy and safety of facilitated percutaneous coronary intervention(PCI)with half-dose recombinant staphylokinase(r-SAK)in patients with ST-segment elevation myocardial infarction(STEMI)who are expected to undergo PCI within 120 minutes.Methods From October 2021 to August 2022,a total of 200 STEMI patients in eight centers were included and randomly assigned in a 1﹕1 ratio to either r-SAK group or control group.Patients received loading doses of aspirin and ticagrelor and intravenous heparin and were randomized to receive an intravenous bolus of either 5 mg r-SAK or normal saline prior to PCI.The outcomes were set as ST-segment resolution(STR)at 60-90 minutes after PCI,the proportion and transition of pathological Q waves on the 5th day after PCI,and the proportion of high-sensitivity cardiac troponin T(hs-cTnT)peaking within 12 hours of onset.The safety outcome was major bleeding events defined as Bleeding Academic Research Consortium(BARC)≥type 3 bleeding during hospitalization.Results Compared with the control group,the r-SAK group had a higher proportion of STR≥70%within 60-90 minutes after PCI(58.3%vs.40.3%,P=0.009);a lower proportion of pathological Q waves(59.1%vs.74.1%,P=0.040);a lower rate of Q wave progression(14.8%vs.43.2%,P＜0.001);a higher rate of Q wave disappearance(12.5%vs.3.7%,P=0.027);and a higher proportion of hs-cTnT peaking within 12 hours of symptom onset[31/40(77.5%)vs.17/33(51.5%),P=0.027].Regarding the safety outcome,no significant difference in BARC≥type 3 bleeding was found between the two groups during hospitalization(P＞0.05).Conclusions For STEMI patients who were expected to undergo primary PCI within 120 minutes of symptom onset,the facilitated PCI with half-dose r-SAK significantly increased the proportion of STR≥70%at 60-90 minutes after PCI,reduced the formation of pathological Q waves,and shortened the time to peak hs-cTnT,without increasing the risk of bleeding,which should be an alternative reperfusion strategy worthy of further study.

Objective:To investigate the clinical management,complications,and prognostic prediction model of bronchopulmonary dysplasia(BPD)in preterm infants.Methods:A total of 854 very preterm infants(gestational age ≤ 32 weeks)admitted to the Neonatal Intensive Care Unit(NICU)of Shanghai Children's Hospital from January 2018 to December 2022 were retrospectively enrolled.After applying inclusion and exclusion criteria,713 infants were included.Based on the 2018 National Institute of Child Health and Human Development(NICHD)diagnostic criteria for BPD,the cohort was divided into a BPD group(n=164)and a non-BPD group(n=549).Clinical data of infants and maternal characteristics were compared between groups.Univariate and stepwise multivariate logistic regression analyses were performed to identify independent risk factors for BPD and evaluate clinical management.A nomogram model was subsequently developed to predict BPD prognosis.Results:Gestational age,duration of non-invasive ventilation,total oxygen therapy time,total hospital stay,hemodynamically significant patent ductus arteriosus(hsPDA),maximum diameter of patent ductus arteriosus(PDA),fetal growth restriction(FGR),use of vasoactive agents,and proportion of pulmonary surfactant administration were identified as independent risk factors for BPD(all P＜0.05,OR＞0).The nomogram model demonstrated excellent predictive performance,with an area under the receiver operating characteristic curve(AUC)of 0.93 and a calibration curve slope approaching 1.The Hosmer-Lemeshow goodness-of-fit test indicated satisfactory model calibration(x2=8.2865,P=0.406).Conclusion:Gestational age,non-invasive ventilation duration,total oxygen therapy time,total hospital stay,hsPDA,PDA maximum diameter,FGR,vasoactive agents,and pulmonary surfactant use are critical predictors of BPD in preterm infants.The prognostic models for BPD incidence and severity,constructed based on these factors,exhibit strong predictive accuracy and may serve as a valuable clinical tool for risk stratification and early intervention.