Objective To identify the key factors affecting the risk of medical surges and their coupling relation5 ships,providing strategic support for medical institutions to optimize risk management and emergency governance.Methods 17 influencing factors were determined based on WSR theory,and an expert scoring method was employed to assess the impact strength among the factors.The DEMATEL method was applied to calculate the centrality,cau5 sality,influence,and being influenced degrees of the influencing factors.The ISM method was used to construct a hierarchical structure of the influencing factors related to medical surge risks,thereby revealing the connections and interaction mechanisms among these factors.Results Seven critical influencing factors were identified,including the crisis decision-making capacity and leadership effectiveness of emergency managers,the completeness of the emer5 gency system and dynamic execution capabilities,and the cross-departmental coordination mechanism and com5 mand collaboration efficiency.Deep driving factors and coupling pathways were also revealed.Conclusion The risk of medical surges exhibits multi-factorial coupling cascade effects;attention should be directed towards the construc5 tion of mid-to-deep level mechanisms such as information systems,institutional frameworks,and organizational management,to enhance targeted capabilities and systemic resilience in risk governance.

Objective To explore the coupling mechanism between medical surge response resources and the spread of secondary risks during public health emergencies,as well as the effectiveness of relevant interventions.Methods Based on complex network theory,a dual-layer network model of medical resources and secondary events was constructed.The interactive feedback between medical resource status and secondary event risk,as well as the effects of network structure,were analyzed through MATLAB simulations,REPAST agent-based modeling,and mean-field analysis.Results Simulation and prediction results show that an increase in first-layer resource-deficient nodes significantly raises the activation rate and transmission speed of secondary events,while the clustering and spread of secondary events in the second layer,in turn,intensify resource depletion,creating a negative feedback loop.Mean-field analysis indicates a nonlinear positive correlation between the adequacy of medical resources and the likelihood of secondary events.Network structure analysis reveals that when the average node degree exceeds 8,resource allocation efficiency improves markedly.Conclusion There exists a dynamic coupling and bidirectional feedback relationship between medical resource status and secondary event risks.Enhancing the flexible allocation and responsiveness of medical resources,improving multi-sectoral collaborative monitoring and coordinated regulation,optimizing network connectivity and coordination mechanisms for resource distribution,and establishing dynamic monitoring and tiered early warning systems are key strategies for strengthening the resilience of healthcare systems and effectively containing the spread of secondary events.

Objective To explore the significance of the toxicity mechanism of butyl benzyl phthalate(BBP)in prevention and treatment of pulmonary fibrosis.Methods In this study,we used network toxicology combined with molecular docking technology to screen the targets of BBP and those related to pulmonary fibrosis through PubChem,GeneCards and other databases,and analyzed the intersecting genes by using a Wayne diagram.Protein-protein interaction networks were constructed to screen the core targets,and the pathway mechanisms were revealed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes.Finally,molecular docking using AutoDock was performed to verify the binding patterns of core targets and BBP.Results A total of 91 potential targets of BBP-induced lung fibrosis were screened,among which PTGS2 and CYP3A4 were the core targets(binding energies of-1.84 kcal/mol and-1.68 kcal/mol,respectively).Enrichment analysis showed that BBP regulated the fibrosis process through G protein-coupled receptor signaling pathway,calcium signaling pathway and cyclic adenosine monophosphate signaling pathway.Molecular docking confirmed that BBP was stably bound to the core target through hydrogen bonding and hydrophobic interaction.Conclusion This study provides preliminary insights into the molecular mechanism of BBP-induced pulmonary fibrosis through network toxicology,and PTGS2 and CYP3A4 may play key roles in BBP-induced pulmonary fibrosis,which provides a novel reference for the exploration of the mechanism of toxicant-disease association.

AIM To explore the clinical effects of Modified Shashen Maidong Decoction combined with western medicines on patients with pediatric Mycoplasma pneumoniae pneumonia due to Yin Deficiency and Lung Heat Pattern.METHODS Ninety-eight patients were randomly assigned into control group(49 cases)for 7-day administration of Cefuroxime and Minocycline Hydrochloride,and observation group(49 cases)for 7-day administration of Modified Shashen Maidong Decoction,Cefuroxime and Minocycline Hydrochloride.The changes in symptom relief time,inflammatory factors(CRP,IL-6,TNF-α),blood gas indices(SaO2,PaO2,PaCO2),T lymphocyte subsets(CD3+,CD4+,CD8+),TCM syndrome scores,pulmonary function indices(PEF,FVC,FEV1)and incidence of adverse reactions were detected.RESULTS The observation group demonstrated shorter symptom relief time(P＜0.05).After the treatment,the two groups displayed decreased inflammatory factors,PaCO2,CD8+,TCM syndrome scores(P＜0.05),and increased SaO2,PaO2,CD3+,CD4+(P＜0.05),especially for the observation group(P＜0.05).No significant difference in incidence of adverse reactions was found between the two groups(P＞0.05).CONCLUSION For the patients with pediatric Mycoplasma pneumoniae pneumonia due to Yin Deficiency and Lung Heat Pattern,Modified Shashen Maidong Decoction combined with western medicines can safely and effectively improve clinical symptoms and lung functions.

BACKGROUND:Pathological cardiac hypertrophy is a risk factor for various heart diseases,but its pathogenesis remains unclear.Circular RNAs are strongly associated with cardiac hypertrophy.However,the role of circular RNA CHACR in cardiac hypertrophy and its regulatory mechanisms have not been clarified.OBJECTIVE:To investigate the role of circular RNA CHACR in pressure overload-induced cardiac hypertrophy and the underlying mechanisms.METHODS:(1)Transverse aortic constriction was used to induce cardiac hypertrophy in vivo after in situ injection of cyclic RNA CHACR overexpressing lentivirus into the heart for 1 week.Heart mass/tibia length ratio and lung mass/tibia length ratio were calculated;cardiomyocyte surface area was measured;hypertrophic marker gene expression levels were detected;myocardial fibrosis degree was detected,and cardiac function was assessed.(2)H9c2 cardiomyocytes were treated with circular RNA CHACR overexpressing lentivirus for 72 hours,and then treated with 1 μmol/L angiotensin Ⅱ for 24 hours to induce hypertrophy of cardiomyocytes.The hypertrophy was assessed by measuring the surface area of cardiomyocytes,the expression level of hypertrophic marker genes,and the protein/DNA ratio.Oxidative stress damage was assessed by detecting reactive oxygen species levels and mitochondrial membrane potential.RESULTS AND CONCLUSION:(1)The expression level of circular RNA CHACR was significantly decreased in both in vivo and in vitro myocardial hypertrophy models(P＜0.01).(2)The overexpression of circular RNA CHACR significantly inhibited the cardiac hypertrophy induced by transverse aortic constriction,including reducing the enlarged heart volume,significantly decreasing the increased heart mass/tibia length ratio(P＜0.05),lung mass/tibia length ratio(P＜0.05),and cardiomyocyte surface area(P＜0.05),and decreasing the upregulated expression levels of hypertrophic markers atrial natriuretic peptide(P＜0.05)and brain natriuretic peptide(P＜0.05).(3)Cardiac fibrosis induced by transverse aortic constriction in mice was significantly inhibited by enforcing expression of circular RNA CHACR,as evidenced by reduced fibrotic area(P＜0.01)and decreased expression levels of the fibrosis marker gene Acta1(P＜0.05).(4)Overexpression of circular RNA CHACR significantly improved cardiac function in mice,including significantly increased ejection fraction(P＜0.05)and fractional shortening(P＜0.01).(5)Enforced expression of circular RNA CHACR significantly inhibited angiotensin Ⅱ-induced cardiomyocyte hypertrophy,including a significant reduction in cardiomyocyte surface area(P＜0.05),downregulation of atrial natriuretic peptide(P＜0.05),and brain natriuretic peptide(P＜0.05)expression levels,and a significant decrease in protein/DNA ratio(P＜0.05).(6)Overexpression of circular RNA CHACR significantly inhibited the elevation of reactive oxygen species levels(P＜0.001)and the decrease in mitochondrial membrane potential(P＜0.05)induced by angiotensin Ⅱ.These results confirm that the expression level of circular RNA CHACR is significantly decreased in cardiac hypertrophy at both in vivo and in vitro myocardial hypertrophy models,and overexpression of circular RNA CHACR significantly inhibits cardiac hypertrophy,alleviates cardiac fibrosis,improves cardiac function,and significantly attenuates angiotensin Ⅱ-induced oxidative stress damage.

Objective:The differentially expressed genes(DEGs)and activated signaling pathways in systemic sclerosis(SSc)were screened by bioinformatics methods,and Chinese medicines for potential treatment of SSc were explored,providing a new theoretical basis for the study of SSc and the screening of potential markers.Methods:The data sets GSE58095,GSE130953,GSE33463 and GSE58613 were selected from GEO database and divided into skin group and peripheral blood group according to the sample source.The DEGs of SSc patients was analyzed by R language,and the Wayne diagram was drawn to take the intersection of the two groups.Metascape was used for GO enrichment analysis and KEGG pathway enrichment analysis,and STRING and Cytoscape were used for protein interaction network analysis to find key pathways and hub genes.The core genes were mapped to the medical on-tology information retrieval platform,and related Chinese medicines for SSc treatment were screened.The effective components of Chi-nese medicines were obtained through TCMSP and HERB databases,and the target letters of active ingredients were obtained through swiss database.The"drug-active ingredient-target"network was constructed by Cytoscape.Results:Total 218 DEGs were identified from the skin group of patients with SSc,and 283 DEGs were screened from peripheral blood of patients with SSc.Among them,there were 7 DEGs co-upregulated in skin and peripheral blood,namely ISG15,LGALS3BP,BST2,C1QB,IFI27,CEACAM1 and FBP1.CAMK2N1 was up-regulated in skin but down-regulated in peripheral blood,ARG1 was down-regulated in skin but up-regulated in pe-ripheral blood.GO and KEGG analysis of SSc DEGs showed that these genes were significantly enriched in inflammatory response,he-moglobin complex,immune receptor activity and extracellular matrix.The results of protein interaction network suggest that more than 10 genes such as COL1A1,CTGF12,IL1B,IFNG and JUN may be potential markers of SSc and core genes of therapeutic targets.The potential Chinese medicines screened for SSc treatment include ginseng,sanguisorba,convolvula,wolfberry,safflower,etc.The main components of these herbs were β-sitosterol,quercetin,kaempferol,stigmasterol,luteolin,sitosterol,Spinasterol,and the target were AKR1B1,AR,CYP1B1,XDH,etc.Conclusion:This study uses bioinformatics to screen out core genes that may be potential markers and therapeutic targets for SSc,which is expected to be a new target for the early diagnosis and mechanism research of SSc.Meanwhile,the mapped Chinese medicine and its effective components can provide ideas for the research and development of Chinese medicine compounds for the treatment of SSc.

Objective To construct the K64 capsule depolymerase recombinant protein,Dep44,and investigate its potential application against carbapenem-resistant Klebsiella pneumoniae(CRKP)infections.Methods The de-polymerase-encoding phage vB_Kpn_HF1013(GenBank:PP803128)was isolated and genomically analyzed to screen for candidate depolymerases.The recombinant protein Dep44 was constructed and functionally verified for depolymerase activity.Dep44 sensitive range was validated and Dep44 antimicrobial activity was assessed by bio-film disruption and serum sterilization assays.Results The tail spike protein of phage vB_Kpn_HF1013 exhibited depolymerase activity and recombinant protein Dep44 specifically degraded K64 CRKP capsule.Biofilm eradication assays demonstrated that recombinant Dep44 at both 2 μg/mL and 10 μg/mL significantly disrupted bacterial bio-films relative to the control.Serum bactericidal assays showed that Dep44 exhibited synergistic activity with serum,dependent on the complement system,as Dep44 alone lacked bactericidal properties.Conclusion Dep44 effec-tively targets and degrades K64 CRKP capsule,disrupts biofilms,and enhances serum bactericidal activity,high-lighting its potential for managing K64 CRKP infections and clearing biofilms from medical devices.

Objective:To investigate the prevalence and influencing factors of depression,anxiety and comorbid depression-anxiety symptoms among college freshmen,providing a theoretical basis for promoting their mental health.Methods:From Jan to Feb 2022,an online questionnaire survey was conducted,involving 483 online questionnaires from college freshmen(184 males,299 females).The depression-anxiety-stress self-rating scale,smartphone dependence self-rating scale for adolescents,and Pittsburgh sleep quality index(PSQI)were used for online surveys.The influencing factors of depression,anxiety,and their comorbidity among college freshmen were analyzed by multivariable logistic regression analysis.Results:The detection rates of smartphone dependence,sleep disorders,depression,anxiety and comorbid depression-anxiety symptoms among college freshmen were 26.1%,12.8%,26.3%,32.1%,and 23.6%,respectively.The detection rates of depression,anxiety and comorbid depression-anxiety symptoms in male students were significantly higher than those in female students(P＜0.05).Multivariable logistic regression analysis showed that self-perceived poor mental health,smartphone dependence and sleep disorders were risk factors for depression,anxiety and comorbid depression-anxiety symptoms.Low satisfaction with college life was a risk factor for depression.Medical specialty was a risk factor for anxiety and comorbid depression-anxiety symptoms(P＜0.05).Conclusions:Male college freshmen show higher rates of depression,anxiety,and their comorbidity.Low satisfaction with college life,self-perceived poor mental health,high academic pressure,smartphone dependence,medical specialty,and sleep disorders may be risk factors for depression,anxiety and comorbid depression-anxiety symptoms among college freshmen.

OBJECTIVE: CRISPR-Cas protects bacteria from exogenous DNA invasion and is associated with bacterial biofilm formation and pathogenicity. METHODS: We analyzed the type I-F CRISPR-Cas system of Legionella pneumophila WX48, including Cas1, Cas2-Cas3, Csy1, Csy2, Csy3, and Cas6f, along with downstream CRISPR arrays. We explored the effects of the CRISPR-Cas system on the in vitro growth, biofilm-forming ability, and pathogenicity of L. pneumophila through constructing gene deletion mutants. RESULTS: The type I-F CRISPR-Cas system did not affect the in vitro growth of wild-type or mutant strains. The biofilm formation and intracellular proliferation of the mutant strains were weaker than those of the wild type owing to the regulation of type IV pili and Dot/Icm type IV secretion systems. In particular, Cas6f deletion strongly inhibited these processes. CONCLUSION The type I-F CRISPR-Cas system may reduce biofilm formation and intracellular proliferation in L. pneumophila.
Legionella pneumophila/pathogenicity* ; CRISPR-Cas Systems ; Biofilms/growth & development* ; Phenotype ; Bacterial Proteins/metabolism* ; Gene Deletion

Objective To identify the key factors affecting the risk of medical surges and their coupling relation5 ships,providing strategic support for medical institutions to optimize risk management and emergency governance.Methods 17 influencing factors were determined based on WSR theory,and an expert scoring method was employed to assess the impact strength among the factors.The DEMATEL method was applied to calculate the centrality,cau5 sality,influence,and being influenced degrees of the influencing factors.The ISM method was used to construct a hierarchical structure of the influencing factors related to medical surge risks,thereby revealing the connections and interaction mechanisms among these factors.Results Seven critical influencing factors were identified,including the crisis decision-making capacity and leadership effectiveness of emergency managers,the completeness of the emer5 gency system and dynamic execution capabilities,and the cross-departmental coordination mechanism and com5 mand collaboration efficiency.Deep driving factors and coupling pathways were also revealed.Conclusion The risk of medical surges exhibits multi-factorial coupling cascade effects;attention should be directed towards the construc5 tion of mid-to-deep level mechanisms such as information systems,institutional frameworks,and organizational management,to enhance targeted capabilities and systemic resilience in risk governance.