Background: and Purpose Symptomatic intracranial hemorrhage (sICH) following endovascular thrombectomy (EVT) is a severe complication associated with adverse functional outcomes and increased mortality rates. Currently, a reliable predictive model for sICH risk after EVT is lacking. Methods: This study used data from patients aged ≥20 years who underwent EVT for anterior circulation stroke from the nationwide Taiwan Registry of Endovascular Thrombectomy for Acute Ischemic Stroke (TREAT-AIS). A predictive model including factors associated with an increased risk of sICH after EVT was developed to differentiate between patients with and without sICH. This model was compared existing predictive models using nationwide registry data to evaluate its relative performance. Results: Of the 2,507 identified patients, 158 developed sICH after EVT. Factors such as diastolic blood pressure, Alberta Stroke Program Early CT Score, platelet count, glucose level, collateral score, and successful reperfusion were associated with the risk of sICH after EVT. The TREAT-AIS score demonstrated acceptable predictive accuracy (area under the curve [AUC]=0.694), with higher scores being associated with an increased risk of sICH (odds ratio=2.01 per score increase, 95% confidence interval=1.64–2.45, P<0.001). The discriminatory capacity of the score was similar in patients with symptom onset beyond 6 hours (AUC=0.705). Compared to existing models, the TREAT-AIS score consistently exhibited superior predictive accuracy, although this difference was marginal. Conclusions The TREAT-AIS score outperformed existing models, and demonstrated an acceptable discriminatory capacity for distinguishing patients according to sICH risk levels. However, the differences between models were only marginal. Further research incorporating periprocedural and postprocedural factors is required to improve the predictive accuracy.

Objectives: . Head and neck squamous cell carcinoma (HNSCC) exhibits high recurrence rates, particularly in cases of radioresistant HNSCC (RR-HNSCC). Non-thermal plasma (NTP) therapy effectively suppresses the progression of HNSCC. However, the therapeutic mechanisms of NTP therapy in treating RR-HNSCC are not well understood. In this study, we explored the regulatory role of NTP in the RR-HNSCC signaling pathway and identified its signature genes. Methods: . After constructing two RR-HNSCC cell lines, we prepared cell lysates from cells treated or not treated with NTP-activated media (NTPAM) and performed RNA sequencing to determine their mRNA expression profiles. Based on the RNA sequencing results, we identified differentially expressed genes (DEGs), followed by a bioinformatics analysis to identify candidate molecules potentially associated with NTPAM therapy for RR-HNSCC. Results: . NTPAM reduced RR-HNSCC cell viability in vitro. RNA sequencing results indicated that NTPAM treatment activated the reactive oxygen species (ROS) pathway and induced ferroptosis in RR-HNSCC cell lines. Among the 1,924 genes correlated with radiation treatment, eight showed statistical significance in both the cell lines and The Cancer Genome Atlas (TCGA) cohort. Only five genes—ABCC3, DUSP16, PDGFB, RAF1, and THBS1—showed consistent results between the NTPAM data sequencing and TCGA data. LASSO regression analysis revealed that five genes were associated with cancer prognosis, with a hazard ratio of 2.26. In RR-HNSCC cells, NTPAM affected DUSP16, PDGFB, and THBS1 as activated markers within 6 hours, and this effect persisted for 12 hours. Furthermore, enrichment analysis indicated that these three DEGs were associated with the extracellular matrix, transforming growth factor-beta, phosphoinositide 3-kinase/protein kinase B, and mesenchymal-epithelial transition factor pathways. Conclusion . NTPAM therapy exerts cytotoxic effects in RR-HNSCC cell lines by inducing specific ROS-mediated ferroptosis. DUSP16, PDGFB, and THBS1 were identified as crucial targets for reversing the radiation resistance induced by NTPAM therapy, providing insights into the mechanisms and clinical applications of NTPAM treatment in RR-HNSCC.

Background: and Purpose Symptomatic intracranial hemorrhage (sICH) following endovascular thrombectomy (EVT) is a severe complication associated with adverse functional outcomes and increased mortality rates. Currently, a reliable predictive model for sICH risk after EVT is lacking. Methods: This study used data from patients aged ≥20 years who underwent EVT for anterior circulation stroke from the nationwide Taiwan Registry of Endovascular Thrombectomy for Acute Ischemic Stroke (TREAT-AIS). A predictive model including factors associated with an increased risk of sICH after EVT was developed to differentiate between patients with and without sICH. This model was compared existing predictive models using nationwide registry data to evaluate its relative performance. Results: Of the 2,507 identified patients, 158 developed sICH after EVT. Factors such as diastolic blood pressure, Alberta Stroke Program Early CT Score, platelet count, glucose level, collateral score, and successful reperfusion were associated with the risk of sICH after EVT. The TREAT-AIS score demonstrated acceptable predictive accuracy (area under the curve [AUC]=0.694), with higher scores being associated with an increased risk of sICH (odds ratio=2.01 per score increase, 95% confidence interval=1.64–2.45, P<0.001). The discriminatory capacity of the score was similar in patients with symptom onset beyond 6 hours (AUC=0.705). Compared to existing models, the TREAT-AIS score consistently exhibited superior predictive accuracy, although this difference was marginal. Conclusions The TREAT-AIS score outperformed existing models, and demonstrated an acceptable discriminatory capacity for distinguishing patients according to sICH risk levels. However, the differences between models were only marginal. Further research incorporating periprocedural and postprocedural factors is required to improve the predictive accuracy.

Aim To explore the effect of astragalosideⅣ(AS-Ⅳ)on lipopolysaccharide(LPS)-induced po-larization and migration of RAW 264.7 macrophages and the underlying mechanism.Methods 1 mg·L-1 LPS was used to construct cell migration model.Scratch assay was utilized to determine cell migration rate.Immunofluorescence staining was utilized to de-tect the expression and location of F4/80,iNOS and Arg-1.CCK-8 assay was used to determine the viabili-ty of RAW 264.7 cells.Griess assay was used to measure NO content.Molecular docking was used to analyze the interaction between AS-Ⅳ and the core tar-gets such as cGAS and STING protein.Western blot was employed to detect the expression of iNOS,Arg-1,cGAS,STING,NF-κB p65 and p-NF-κB p65 protein.Results AS-Ⅳ significantly inhibited the migration and M1 polarization of RAW 264.7 cells induced by LPS.Moreover,AS-Ⅳ could interact with cGAS and STING protein,especially cGAS.Further Western blot assay showed that AS-Ⅳ significantly downregulated the expression of iNOS,cGAS,STING and p-NF-κB p65 protein.Conclusions AS-Ⅳ could promote mac-rophage M1 to M2 polarization,thereby inhibited mac-rophage migration through restraining the cGAS/STING/NF-κB signaling pathway,which provides a new therapeutic target for AS-Ⅳ to improve the early inflammatory response of AS.

Objective To discuss the potential mechanisms by which programmed cell death(PCD)might contribute to the pathogenesis of diabetic kidney disease(DKD).Methods Retrieve the datasets GSE30529 and GSE30122 from the Gene Expression Omnibus database and analyze them to obtain differentially expressed genes(DEGs)associated with DKD.Utilize the Gene Set Enrichment Analysis website,the ferroptosis database,and the autophagy database,along with relevant literature,to identify genes associated with apoptosis,necroptosis,pyroptosis,autophagy,and ferroptosis.Cross-reference these genes with the DKD DEGs to identify PCD-related genes that are differentially expressed in DKD.Perform Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analyses to explore the biological functions and potential pathways of the core genes.Conduct a protein-protein interaction network analysis to examine the interaction relationships of the target genes,and use the CytoHubba plugin in Cytoscape to screen for Hub genes.Results In the GSE30529 dataset,a total of 460 DEGs were identified,while the GSE30122 dataset yielded 992 DEGs.After merging and removing duplicates,932 DEGs were obtained.By intersecting these DEGs with PCD-related genes,61 apoptosis-related genes,7 necroptosis-related genes,39 pyroptosis-related genes,18 autophagy-related genes,and 16 ferroptosis-related genes associated with DKD were identified.The KEGG analysis results indicated that the DEGs related to apoptosis,necroptosis,pyroptosis,and autophagy in PCD were primarily enriched in pathways associated with diabetic complications,including the AGE-RAGE,IL-17,NF-κB,and TNF signaling pathways.In contrast,DEGs related to ferroptosis were mainly enriched in the fatty acid degradation pathway.GO enrichment analysis revealed that the biological processes of the differentially expressed PCD related genes in DKD were primarily involved in the regulation of signals such as NF-κB-inducing kinase/NF-κB,IL-1,and IL-17.Conclusions Differentially expressed PCD-related genes in DKD are mainly enriched in related signal pathways such as AGE-RAGE,IL-17,NF-κB and TNF,suggesting a critical role of PCD in the pathogenesis of DKD.

Objective To study the epidemiological characteristics of special pathogenic infection in Wenchang area following the super typhoon"Yagi"disaster,and provide basis for the diagnosis,treatment,prevention and control of infectious diseases in disaster-affected areas.Methods Clinical characteristics and pathogenic data of 7 groups of patients infected with 9 species of zoonotic pathogens and opportunistic pathogens were analyzed retrospectively.The 7 groups included:pre-typhoon landfall group(August 6 to September 5,2024),post-typhoon landfall group(September 6 to October 5,2024),and groups in the past years of the same period(A2023,B2022,C2021,D2020,E2019,September 6 to October 5 of each year in 2019-2023).Epidemiological characteristics of patients as well as distribution and resistance of pathogens were compared and analyzed.Results In post-typhoon landfall group,26 patients were infected.The overall infection rate of the post-typhoon landfall group was higher than all groups except B2022 group(all P＜0.05).The infected cases mainly distributed in coastal areas.The main route of infection was outside the hospital(88.5％).Male accounted for 80.8％,agricultural workers accounted for 53.9％,and 69.2％of the cases occurred within 10 days after the typhoon.The major infection sites were multiple site co-infection,bloodstream infection,and soft tissue infection.The main pathogens maintained high sensitivity to commonly used antimicrobial agents.The accuracy of clinical initial empirical antimicrobial use was relatively low(45.5％in post-typhoon landfall group vs 62.8％in the groups of the same period in the past).The clinical cure rate decreased to 76.9％,and mortality increased to 7.7％.The mortality of patients infected with Burkholderia pseudomallei and kidney infected with Leptospira were 25.0％and 50.0％,respectively.Conclusion After ty-phoon disaster,special pathogen infection significantly increases and the prognosis is poor.It is recommended to emphasize blood culture and molecular biology testing to facilitate early diagnosis and precise treatment,optimize prevention and control measures,and enhance the accuracy of clinical empirical medication.

Objective To understand the current situation of reprocessing reusable sterilized items in the central sterile supply departments(CSSD)of hospitals and provide a scientific basis for further standardized management.Methods Using the convenience sampling method,a self-designed questionnaire on the current situation of reprocessing of reusable disinfection items in CSSDs was used to conduct a survey in 31 provinces(autonomous regions and municipalities)from June 11th to 23rd,2024.The questionnaire covered 2 aspects,including the basic situation of the hospital and the reprocessing of disinfection items.Results A total of 1 835 questionnaires were distributed,and 1 603 valid questionnaires were retrieved.Regarding the use of reusable disinfection items,with the most frequently used items being humidification bottles,tourniquets,breathing bags and their accessories,and ventilator tubing systems etc.Among them,1 558 hospitals(97.19％)established standardized disposal procedures,and 996 hospitals(62.13％)assigned dedica-ted personnel to be responsible.In terms of the reprocessing procedures of reusable disinfection items,all 1 603 hospitals carried out drying process for the items;the main packaging method was plastic self-sealing bags(59.95％),and 541 hospitals(33.75％)sterilized the packaging materials.Additionally,935 hospitals(58.33％)used oil-free air compressors;among them,51 hospitals(58.62％)installed activated carbon filters at the end of the compressors.Conclusion The current situation of reprocessing reusable sterilized items in CSSDs of nationwide hospitals needs improvement.It is recommended to strengthen the training of professional disinfection knowledge,unify the sterilization standards for plastic self-sealing bags,develop a storage management system,and adopt a medical air compressor system without oil and water to reduce the risk of hospital infections.

With the rapid development of generative artificial intelligence(GAI)technologies,their widespread application in academic research and writing is continuously expanding the boundaries of sci-entific inquiry.However,this trend has also raised a series of ethical and regulatory challenges,inclu-ding issues related to authorship,content authenticity,citation accuracy,and accountability.In light of the growing involvement of AI in generating academic content,establishing an open,controllable,and trustworthy ethical governance framework has become a key task for safeguarding research integrity and maintaining trust within the academic community.This expert consensus outlines ethical requirements across key stages of AI-assisted academic writing-including topic selection,data management,citation practices,and authorship attribution.It aims to clarify the boundaries and ethical obligations surrounding AI use in academic writing,ensuring that technological tools enhance efficiency without compromising in-tegrity.The goal is to provide guidance and institutional support for building a responsible and sustainable research ecosystem.

Chronic kidney disease(CKD)is a chronic disease characterized by renal structural damage and dysfunction.At present,there is still a lack of effective therapeutic drugs and prevention and treatment methods for CKD in clinical practice.More and more studies have shown that necroptosis,as a new type of programmed cell death,plays a vital role in the onset and progression of CKD.Targeting key molecules in the necroptosis pathway,such as RIPK1,RIPK3 and MLKL,the development of small molecule inhibitors has become an emerging strategy for the treatment of CKD,and has shown significant potential to pro-tect the kidneys and alleviate renal fibrosis in a variety of in vitro and in vivo models.Therefore,this article summarizes the re-search progress of the mechanism of necroptosis in recent years,and focuses on the potential role of necroptosis in the pathogene-sis of CKD and the therapeutic potential of targeting this path-way,providing a new perspective and research direction for the prevention and treatment of CKD in the future.

AIM:To investigate the role of SET and MYND domain-containing protein 3(SMYD3)-mediated histone H3 lysine 4 trimethylation(H3K4me3)dysregulation in pulmonary vascular remodeling in a rat model of pulmo-nary arterial hypertension associated with atrial septal defect(PAH-ASD).METHODS:The PAH-ASD rat model was created using transseptal puncture and radiofrequency ablation techniques.The rats were randomly assigned to 5 groups:normal,sham,PAH-ASD,PAH-ASD+vehicle(Veh),and PAH-ASD+BCI-121(SMYD3 inhibitor).Four weeks after modeling,lung tissues and pulmonary vessels were harvested for subsequent analysis.Western blot analysis was conducted to evaluate the protein levels of SMYD3,H3K4me3,transforming growth faction-β1(TGF-β1),and collagen type Ⅲ(Col Ⅲ).The mRNA expression of TGF-β1 was quantified using RT-qPCR.Histological assessment of pulmonary vascu-lar fibrosis,vascular wall thickness and smooth muscle proliferation was executed through Masson's trichrome and HE staining.Co-immunoprecipitation(Co-IP)assay was performed to investigate the interactions among SMYD3,H3K4me3,and TGF-β1.Hemodynamic parameters,including mean pulmonary artery pressure(mPAP),were quantified using a computerized physiological signal acquisition system.RESULTS:The Western blot analysis indicated a significant in-crease in the protein levels of SMYD3,TGF-β1,Col Ⅲ,and H3K4me3 in the PAH-ASD group compared with the sham group(P<0.05).RT-qPCR corroborated the elevation of TGF-β1 mRNA expression in the PAH-ASD group(P<0.05).Furthermore,Masson's trichrome and HE staining techniques revealed more pronounced pulmonary vascular fibrosis,an augmented vascular wall area,and an elevated vascular area index within the PAH-ASD group(P<0.05).Additionally,the right ventricular hypertrophy index(RVHI)and mPAP were significantly elevated in the PAH-ASD group(P<0.05).The administration of BCI-121 resulted in a significant reduction of SMYD3,TGF-β1,Col Ⅲ,and H3K4me3 levels(P<0.05),while also mitigating pulmonary vascular fibrosis,RVHI,mPAP,pulmonary vascular area,and area index(P<0.05).Co-IP confirmed direct interactions among SMYD3,H3K4me3,and TGF-β1.CONCLUSION:Histone methyl-transferase SMYD3-mediated histone H3K4me3 modification plays a role in the pulmonary vascular remodeling of PAH-ASD model rats.The underlying mechanism may involve the regulation of pulmonary vascular proliferation and fibrosis me-diated by the overexpression of TGF-β1 and Col Ⅲ.