ObjectiveTo investigate the possible mechanism of Jishe Qushi Capsule （脊蛇祛湿胶囊， JQC） in treating rheumatoid arthritis （RA） from the perspective of macrophage polarization mediated by neutrophil extracellular traps （NETs）. MethodsTwenty-four female SD rats were randomly divided into four groups， blank control group， model group， JQC group， and peptidylarginine deiminase 4 （PAD4） inhibitor group with 6 rats in each group. All groups but the blank control group were subjected to the induction of collagen-induced arthritis （CIA）. After successful model establishment， rats in the JQC group received intragastric administration of JQC 1.47 g/kg daily； rats in the PAD4 inhibitor group received intraperitoneal injections of the PAD4 inhibitor 4 mg/kg weekly. Rats in the blank， model， and PAD4 inhibitor groups received 2 ml of pure water daily by gavage. All treatments lasted 4 weeks. Joint lesions of each group were assessed on day 7， 14， 21， 28， and 35 after model establishment， and arthritis index （AI） scores were recorded. At 24 h after the final administration， histopathology of knee joints， including HE staining， safranin O-fast green staining， and TRAP staining， was performed. Flow cytometry was used to detect the counts of M1 and M2 macrophages in peripheral blood. ELISA was used to determine serum levels of TRACP， NETs， TNF-α， IL-1β， and iNOS. Western Blotting and qRT-PCR were used to measure MPO， NE， RANKL， OPG， and p65 protein and mRNA expression in knee cartilage tissue. ResultsCompared with the blank control group， the model group showed increased AI scores （P＜0.05）， marked synovial inflammatory infiltration， angiogenesis， and bone-cartilage destruction， increased TRAP-positive osteoclasts， increased M1 macrophages and decreased M2 macrophages， elevated serum TRACP， NETs， TNF-α， IL-1β， and iNOS （P＜0.05）， elevated MPO， NE， RANKL， and p65 protein/mRNA expression and decreased OPG protein/mRNA expression in knee cartilage tissue （P＜0.05）. Compared with the model group， the JQC group exhibited improved synovial inflammation， angiogenesis， and bone-cartilage damage， reduced AI scores on day 21， 28， and 35， decreased osteoclast counts， decreased M1 macrophages and increased M2 macrophages， reduced serum TRACP， NETs， TNF-α， IL-1β， and iNOS （P＜0.05）， decreased MPO， NE， RANKL， and p65 protein/mRNA expression and increased OPG expression （P＜0.05）. Compared with the PAD4 inhibitor group， the JQC group showed significantly lower AI scores， reduced M1 macrophages， increased M2 macrophages （P＜0.05）， reduced serum TRACP， TNF-α， IL-1β， and iNOS， decreased MPO， RANKL， and p65 expression， and increased OPG levels （P＜0.05）. ConclusionThe therapeutic mechanism of JQC for RA may involve inhibition of NETs formation， downregulation of the RANKL/NF-κB signaling pathway， and regulation of macrophage M1/M2 polarization imbalance， thereby suppressing osteoclastogenesis and inflammatory bone destruction.

Objectives: . The prognostic value of the pretreatment albumin-to-alkaline phosphatase ratio (AAPR) in head and neck cancer (HNC) remains uncertain. This meta-analysis aimed to evaluate the predictive role of AAPR for survival outcomes in patients with HNC. Methods: . A comprehensive search of the Cochrane Library, PubMed, and Embase databases was conducted to identify relevant studies published up to July 30, 2024. We included studies on AAPR and survival outcomes in HNC patients. Results: . Eight studies comprising 1,737 HNC patients were analyzed using random-effects models. Lower AAPR values were significantly correlated with worse overall survival (hazard ratio [HR], 2.08), progression-free survival (HR, 2.00), and disease-free survival (HR, 2.18). Sensitivity analyses confirmed the robustness of these results, with no significant publication bias detected. Conclusion . Our findings suggest that pretreatment AAPR could serve as a valuable and cost-effective prognostic indicator in HNC, potentially aiding clinicians in risk stratification and treatment decision-making. However, additional validation studies are warranted to confirm its clinical applicability.

Objective: To analyze the status of wasting among primary and secondary school students in Guangxi from 2021 to 2025, to explore the factors associated with wasting, so as to provide scientific evidence for improving student s nutrition. Methods: Based on the National Surveillance and Intervention Program on Common Diseases and Health Risk Factors among Students, a stratified cluster random sampling was adopted from 2021 to 2025 to recruit 71 077, 236 511, 243 466, 249 619 and 246 259 primary and secondary school students in Guangxi for physical examination and questionnaire survey. The χ 2 test was used for intergroup comparisons. Chi-square trend test was used to conduct trend analysis. Multilevel Logistic regression model was employed to identify factors associated with wasting. Results: The overall wasting detection rate was 11.65% during 2021-2025. Over the five year period, the rate exhibited a S shaped fluctuation pattern characterized by "decline-rise-decline" and the difference across years was statistically significant ( χ 2=230.53, P <0.05). Multilevel Logistic regression analysis showed that male students ( OR = 1.63 ), primary school students ( OR =1.53) and junior high school students ( OR =1.12), boarding students ( OR =1.08), and students with adequate sleep duration ( OR =1.12) were positively correlated with the risk of wasting (all P <0.05). Students who consumed sugar sweetened beverages ≥1 time/day ( OR =0.93), ate fresh fruit ≥1 time/day ( OR =0.95), had moderate to vigorous physical activity for more than 60 minutes per day ( OR =0.88), and had moderate to vigorous physical activity for more than 60 minutes per day on more than half of weekend days ( OR =0.88) were negatively correlated with the risk of wasting (all P <0.05). Conclusions Wasting status among primary and secondary school students in Guangxi improved between 2021 and 2025, though fluctuations persisted. Greater attention should be paid to the nutritional status of male students and boarding students. While cultivating balanced dietary habits and appropriate exercise behaviors, the complex relationship between sleep and malnutrition should also be given due consideration.

Objective To investigate the effects and underlying mechanisms of down-regulating m6A demethylase fat mass and obesity-associated protein(FTO)on proplatelet formation in the MEG-01 megakaryocytic cells.Methods ①MEG-01 cells were treated with 1 nmol/L phorbol myristate acetate(PMA)(treatment group)or DMSO(control group)for 72 h.FTO expression was measured by Western blotting and RT-qPCR.② MEG-01 cells were infected with targeted FTO shRNA(knockdown group,sh-FTO)or negative control shRNA(negative control group,sh-NC)viruses.FTO knockdown group and negative control group MEG-1 cells were treated with 1 nmol/L PMA for 72 h,and the protein and mRNA expression levels of FTO were detected by Western blotting and RT-qPCR.Cell cycle,viability and apoptosis were assessed by propidium iodide(PI)DNA staining,CCK-8 assay and Annexin V-FITC/PI double staining and TUNEL staining.The expression of cleaved Caspase-3 protein was determine by Western blotting.Megakaryocyte maturation was assessed by CD41/CD61 staining.Proplatelet formation was observed under bright field and detected by CD61 immunofluorescence assay.The expression of apoptosis-related molecules(Caspase3,BAD,BAK1,BCL2 and MCL1)was detected by RT-qPCR,and the protein change of BCL2 was further verified by Western blotting.The dataset was screened out from the gene expression omnibus(GEO)database,and then analyzed with University of California,Santa Cruz(UCSC)genome browser to compare the methylation sequencing peaks on BCL2 mRNA,and m6A methylated RNA immunoprecipitation(m6A-RIP)was used to assess the m6A methylation levels of BCL2 target gene mRNAs in MEG-01 megakaryocytes.Then,the changes in the m6A methylation enrichment level of BCL2 mRNA were observed between the sh-NC group and the sh-FTO group.mRNA stability and ribosome profiling assays were performed to assess translational efficiency of target genes.Results ①PMA treatment upregulated the expression of FTO at protein(P＜0.05)and mRNA(P＜0.01)levels.② FTO shRNA resulted in reduced FTO expression at both mRNA and protein levels(P＜0.01).Compared to the negative control group,the FTO knockdown group showed more cells arrested at the G1/S phase[(60.80±1.29)%vs(72.13±1.18)%,P＜0.01],significantly reduced cell viability[(1.17±0.03)%vs(0.69±0.05)%,P＜0.01],increased Annexin V-FITC/PI positive cells[(12.87±0.83)%vs(17.45±1.58)%,P＜0.01],more TUNEL positive cells[(1.03±0.27)%vs(17.49±9.91)%,P＜0.01],enhanced protein level of cleaved Caspase-3(P＜0.01),decreased proportion of CD41/CD61 positive cells[(51.63±1.13)%vs(34.08±0.53)%,P＜0.01],and less proplatelet formation in MEG-01 megakaryocytes[(26.49±6.73)%vs(13.31±5.97)%,P＜0.01].③Compared to sh-NC group,the FTO knockdown group had significantly decreased protein and mRNA expression of anti-apoptotic molecule BCL2(P＜0.01).UCSC GEO sequencing data revealed there were m6A methylation modification sites on BCL2 mRNA,which was verified through m6A-RIP experiment in MEG-01 megakaryocytes.Compared with GAPDH mRNA,BCL2 mRNA exhibited a significantly enriched m6A signal(P＜0.01).Compared to sh-NC group,a significant increase in m6A methylation modification was observed on BCL2 mRNA.BCL2 mRNA stability was significantly decreased,and its translation efficiency significantly was decreased(P＜0.01).Conclusion m6 A demethylase FTO rgulates BCL2 mRNA stability and translation efficiency,thereby promoting proplatelet formation in MEG-01 megakaryocytes.

Objective To explore the repair effect and mechanism of human amniotic mesenchymal stem cells(hAMSCs)on endometrial injury.Methods hAMSCs were isolated using a two-enzyme digestion and then cultured.The third-passage(P3)cells were harvested to detect the surface markers by flow cytometry and to identify their trilineage differentiation potentials.Eighteen nulliparous female SD rats(8～9 weeks old,weighing 250～280 g)were randomly divided into 3 groups(n=6):normal control group,model group,and hAMSCs group.A rat model of intrauterine adhesions(IUA)was established in SD rats by using curettage combined with lipopolysaccharide(LPS)infection.In 2 weeks after modeling,the hAMSCs group received a bilateral uterine horn transplantation of 0.2 mL hAMSCs(1.0×10? cells/mL),while the model group received a same volume of PBS into both uterine horns.All rats were sacrificed in 2 weeks after transplantation.HE and Masson staining was used to observe endometrial thickness and gland number as well as endometrial fibrosis area.RT-qPCR and Western blotting were performed to detect the mRNA and protein levels of TGF-β1,Smad3,Smad7,epithelial-mesenchymal transition(EMT)markers(E-cadherin,Vimentin),fibrosis factor α-SMA,and endometrial estrogen receptor(ER)and progesterone receptor(PR)in endometrial tissues.Results The obtained cells were identified as hAMSCs due to the characteristics of surface markers and differentiation potentials.Compared with the normal control group,the model group showed decreased endometrial thickness,reduced gland number,increased fibrosis area,and enhanced mRNA and protein levels of fibrosis-related factors TGF-β1,Smad3,Vimentin,and α-SMA(P<0.01),while down-regulation of fibrosis-inhibiting molecule Smad7,the EMT marker E-cadherin,and endometrial receptors ER and PR at both mRNA and protein levels(P<0.01).hAMSCs transplantation increased endometrial thickness and gland number,decreased fibrosis area,and down-regulated mRNA expression of the aforementioned fibrosis-related factors(P<0.01),and up-regulated the mRNA expression levels of Smad7,E-cadherin,ER,and PR(P<0.01).The hAMSCs group also exhibited obviously down-regulated protein levels of TGF-β1,Smad3,and α-SMA(P<0.05),while enhanced protein levels of Smad7 and PR(P<0.05).Conclusion Intrauterine transplantation of hAMSCs can promote the repair of endometrial injury,and inhibits endometrial EMT and fibrosis through the TGF-β1/Smad7 signaling pathway.

Objective:To investigate the safety and efficacy of flow diverter (FD) in the treatment of middle cerebral artery (MCA) dissection aneurysms.Methods:Patients with MCA dissection aneurysm received FD treatment at the Department of Neurosurgery, Jinjiang Hospital and the Cerebrovascular Disease Center of the First Affiliated Hospital of Naval Medical University from January 2021 to December 2023 were included retrospectively. The success rate of procedure, incidence of complications, occlusion rate of aneurysms, and clinical outcome were evaluated.Results:A total of 23 patients were included, with a success rate of 100% for FD implantation and a periprocedural complication rate of 8.7%. Nineteen patients (82.6%) completed angiography follow-up within an average of 7.2 months, of which the aneurysms of 16 patients (84.2%) were completely occluded, 3 (15.8%) were partial occluded, and 2 (10.5%) experienced in-stent restenosis; 14 (73.7%) showed stenosis of covered branch openings, of which 2 (10.5%) had branch occlusions, with no relevant clinical symptoms. The median clinical follow-up time was 23.2 months, with 95.7% of patients achieving good outcome (modified Rankin scale score ≤2).Conclusion:FD is safe and effective in the treatment of MCA dissection aneurysms, and precise device selection and release is the key to improving procedural safety.

OBJECTIVE To evaluate the application effect of implementation strategies in the prevention and control of sur-gical site infection(SSI),and to review its research progress.METHODS A scoping review method was employed,invol-ving systematic searches across databases such as Web of Science,PubMed,Cochrane,CNKI and Wanfang.After screening based on the inclusion and exclusion criteria,the included literature was analyzed and reported in a standard-ized manner.RESULTS A total of 47 articles were included.Most studies adopted comprehensive evidence-based practices(EBP)(≥2 types)and employed multimodal implementation strategies(≥3 items)to facilitate the implementation of SSI prevention and control EBP.Within the framework of the WHO multimodal strategy,42,39,39 and 24 studies re-spectively applied the four implementation strategies of system change,education and training,monitoring and feedback and reminder and communication,while only 9 studies applied the strategy of creating a safety culture.The highest pro-portion of studies(31.91％,15/47)employed a combination of four implementation strategies,with the common combi-nation being"system change+education and training+monitoring and feedback+reminder and communication"(29.79％,14/47),and this combination of four implementation strategies demonstrated outstanding performance in en-hancing EBP compliance.Totally 26(55.32％)showed decrease in the incidence of SSI after intervention(P＜0.05).CONCLUSIONS Implementation strategies are crucial for the successful implementation of SSI prevention and con-trol EBP.Multimodal implementation strategies are common approaches to facilitate the implementation of EBP.In the future,it is necessary to further standardize the application of scientific methods and improve the effect evaluation of im-plementation strategies,providing a reference for the sustained and widespread application of EBP in clinical practice.

Creutzfeldt-Jakob disease(CJD)is a rapidly progressive and fatal neurodegenerative disorder caused by prions,with certain infectivity and iatrogenic transmission risks.With the rapid progress and application of new dia-gnostic biomarkers and detection methods,as well as the construction and improvement of surveillance and reporting systems,the detection of CJD in patients domestically and internationally has shown an increasing trend year by year.Due to its long incubation period and heterogeneity of early symptoms,early identification and diagnosis of the disease is difficult,increasing the risk of transmission within medical institutions.Currently,there is a lack of con-sensus on the infection prevention and control of CJD.In order to timely identify and diagnose CJD as well as effec-tively block its transmission in medical institutions,this consensus summarizes 15 clinical concerns and formulates 24 specific recommendations based on the latest domestic and international research findings and clinical evidence,as well as combines with clinical practice,aiming to standardize healthcare-associated infection prevention and control measures for CJD and reduce its transmission risk in medical institutions.

Acute kidney injury (AKI) has high morbidity and mortality, but effective clinical drugs and management are lacking. Previous studies have suggested that macrophages play a crucial role in the inflammatory response to AKI and may serve as potential therapeutic targets. Emerging evidence has highlighted the importance of forkhead box protein O1 (FoxO1) in mediating macrophage activation and polarization in various diseases, but the specific mechanisms by which FoxO1 regulates macrophages during AKI remain unclear. The present study aimed to investigate the role of FoxO1 in macrophages in the pathogenesis of AKI. We observed a significant upregulation of FoxO1 in kidney macrophages following ischemia-reperfusion (I/R) injury. Additionally, our findings demonstrated that the administration of FoxO1 inhibitor AS1842856-encapsulated liposome (AS-Lipo), mainly acting on macrophages, effectively mitigated renal injury induced by I/R injury in mice. By generating myeloid-specific FoxO1-knockout mice, we further observed that the deficiency of FoxO1 in myeloid cells protected against I/R injury-induced AKI. Furthermore, our study provided evidence of FoxO1's pivotal role in macrophage chemotaxis, inflammation, and migration. Moreover, the impact of FoxO1 on the regulation of macrophage migration was mediated through RhoA guanine nucleotide exchange factor 1 (ARHGEF1), indicating that ARHGEF1 may serve as a potential intermediary between FoxO1 and the activity of the RhoA pathway. Consequently, our findings propose that FoxO1 plays a crucial role as a mediator and biomarker in the context of AKI. Targeting macrophage FoxO1 pharmacologically could potentially offer a promising therapeutic approach for AKI.

Creutzfeldt-Jakob disease(CJD)is a rapidly progressive and fatal neurodegenerative disorder caused by prions,with certain infectivity and iatrogenic transmission risks.With the rapid progress and application of new dia-gnostic biomarkers and detection methods,as well as the construction and improvement of surveillance and reporting systems,the detection of CJD in patients domestically and internationally has shown an increasing trend year by year.Due to its long incubation period and heterogeneity of early symptoms,early identification and diagnosis of the disease is difficult,increasing the risk of transmission within medical institutions.Currently,there is a lack of con-sensus on the infection prevention and control of CJD.In order to timely identify and diagnose CJD as well as effec-tively block its transmission in medical institutions,this consensus summarizes 15 clinical concerns and formulates 24 specific recommendations based on the latest domestic and international research findings and clinical evidence,as well as combines with clinical practice,aiming to standardize healthcare-associated infection prevention and control measures for CJD and reduce its transmission risk in medical institutions.