Objective: To identify the spatio-temporal clustering analysis of mumps in Wenzhou City, Zhejiang Province from 2010 to 2023, so as to provide the basis for improving mumps prevention and control strategies. Methods: Data of mumps cases in Wenzhou City from 2010 to 2023 were collected from the Monitoring and Reporting Management System of Chinese Disease Prevention and Control Information System. The spatio-temporal clustering characteristics of mumps incidence were identified using spatial autocorrelation analysis and spatio-temporal scan analysis. Results: A total of 20 455 mumps cases were reported in Wenzhou City from 2010 to 2023, with an average annual incidence of 17.54/105. There were 12 919 male and 7 536 female cases, with a male-to-female ratio of 1.71∶1. The children aged 5-<10 years had the highest incidence of mumps at 135.29/105. The incidence of mumps showed a downward trend from 46.82/105 in 2010 to 3.59/105 in 2023 (P<0.05). The incidence of mumps peaked from May to July and from November to January during 2010 and 2012, the winter peak became less evident after 2013, and no seasonal trends were observed after 2020. Spatial autocorrelation analysis showed there was a positive spatial correlation of mumps of other years, with the exception of 2018 (all Moran's I >0, all P<0.05). Lucheng District, Longwan District, Ouhai District, Cangnan County and Rui'an City were high-high clustering sites. Spatio-temporal scan analysis showed that the primary clustering area was centered in Nanbaixiang Street, Ouhai District, covering 50 towns (streets), with the clustering time from April 2010 to August 2013; the secondary clustering area was centered in Zaoxi Town, Cangnan County, covering 24 towns (streets), with the clustering time from January 2010 to June 2013. Conclusions The incidence of mumps in Wenzhou City from 2010 to 2023 showed a downward trend. The urban areas, Cangnan County and Rui'an City were the clustering areas.

Long non-coding RNAs(lncRNAs)regulate gene expression at the transcriptional,post-transcription-al,or epigenetic levels,and play crucial roles in tumor cell proliferation,invasion,apoptosis,and metabolism.With ongoing research,an increasing number of human microproteins encoded by lncRNAs have been discovered,although their complete functional characterization remains to be explored.This article reviews the research progress on the func-tions and partial mechanisms of the small integral membrane protein(SMIM)family encoded by lncRNAs in tumor ini-tiation and progression.

In recent years,artificial intelligence(AI)technologies,particularly those represented by deep learn-ing,have demonstrated tremendous potential in the advancement of medical applications.This article reviews recent re-search progress in AI applications for the diagnosis and treatment of triple-negative breast cancer,aiming to inform the development of clinically relevant AI algorithms that align with real-world practice scenarios.The ultimate objectives in-clude enhancing diagnostic accuracy through efficient computational approaches,reducing manual labor burdens,im-proving patient prognosis,and facilitating the identification of therapeutic targets in oncology through AI-driven predic-tive modeling.

Long non-coding RNAs(lncRNAs)regulate gene expression at the transcriptional,post-transcription-al,or epigenetic levels,and play crucial roles in tumor cell proliferation,invasion,apoptosis,and metabolism.With ongoing research,an increasing number of human microproteins encoded by lncRNAs have been discovered,although their complete functional characterization remains to be explored.This article reviews the research progress on the func-tions and partial mechanisms of the small integral membrane protein(SMIM)family encoded by lncRNAs in tumor ini-tiation and progression.

In recent years,artificial intelligence(AI)technologies,particularly those represented by deep learn-ing,have demonstrated tremendous potential in the advancement of medical applications.This article reviews recent re-search progress in AI applications for the diagnosis and treatment of triple-negative breast cancer,aiming to inform the development of clinically relevant AI algorithms that align with real-world practice scenarios.The ultimate objectives in-clude enhancing diagnostic accuracy through efficient computational approaches,reducing manual labor burdens,im-proving patient prognosis,and facilitating the identification of therapeutic targets in oncology through AI-driven predic-tive modeling.

Objective:To establish a multi-factor prediction model for vascular aging based on psychological behavior and physical exercise using nomogram and structural equation method.Methods:A total of 701 inpatients or physical examination patients who underwent carotid ultrasound examination in the Affiliated Hospital of Qingdao University from October 2021 to March 2023 were selected by cross-sectional method. The subjects were randomly divided into training queue( n=492) and verification queue( n=209) according to the ratio of 7∶3.The psychological and behavioral factors, lifestyle, demography and accompanying diseases data were collected. Multi-factor binary Logistic regression method in SPSS 25.0 software was used to screen independent influencing factors of vascular aging, R 4.2.2 software was used to build a nomogram prediction model of vascular aging, and the ROC curve, calibration chart and decision curve analysis were used to evaluate the nomogram, and AMOS software was used to build a structural equation model of vascular aging. Results:Multivariate Logistic regression analysis showed that type A behavior( B=1.757, OR(95% CI)=5.790(2.750-12.210), P<0.001), physical exercise( B=-3.019, OR(95% CI)=0.050(0.020-0.100), P<0.001), high-fat diet( B=0.679, OR(95% CI)=1.970(1.350-2.880), P<0.001), sleep quality( B=-1.451, OR(95% CI)=0.230(0.120-0.460), P<0.001), tea drinking habits( B=-2.349, OR(95% CI)=0.100(0.050-0.200), P<0.001), age( B=0.061, OR(95% CI)=1.060(1.020-1.110), P=0.005), sex( B=-1.263, OR(95% CI)=0.280(0.140-0.570), P<0.001), hyperlipidemia( B=0.679, OR(95% CI)=1.970(1.350-2.880), P<0.001) and diabetes( B=0.838, OR(95% CI)=2.310(1.140-4.700), P=0.021)were independent influencing factors of vascular aging. The nomogram model showed that type A behavior, physical exercise, high-fat diet, sleep quality, tea drinking habits, age, sex, hyperlipidemia and diabetes were independent influencing factors of vascular aging.Advanced age, type A behavior, hyperlipidemia, diabetes and the score of high-fat diet were risk factors for vascular aging, while better sleep quality, tea drinking habit and the score of physical exercise were protective factors for vascular aging.Men were more prone to vascular aging than women. Structural equation model showed that type A behavior had the strongest direct positive effect on vascular aging (the effect coefficient=0.197, P<0.01), and physical exercise had the strongest direct negative effect on vascular aging (the effect coefficient=-0.452, P<0.01), which could indirectly affect vascular aging through various factors. Conclusions:The nomogram model shows the independent influencing factors of vascular aging and has certain predictive value.Structural equation model shows that many factors such as psychological behavior and lifestyle can directly or indirectly affect the occurrence of vascular aging, among which type A behavior and physical exercise have more extensive effects.

Objective To evaluate the potential of serum exosomal miR-148a-5p as a biomarker and to investigate its role in the pathogenesis of rheumatoid arthritis(RA).Methods A total of 80 participants(30 healthy controls,HCs;50 RA patients)were recruited.Serum exosomes were extracted and identified.The expressions of exsomal miR-148a-5p will be screened by next-generation sequencing,validated by qRT-PCR and assessed its clinical significance.Target genes and their functions were determined by the luciferase reporter assays,cell transfection,and ELISA.Results Fifty-five differentially expressed serum exomiRNAs were identified(44 upregulated,11 downregulated).The high expression of the exo-miR-148a-5p in the serum of patients with RA was validated by qRT-PCR,comparing to HCs(P<0.000 1),which showed a strong correlation with the disease activity score(DAS)28,rheumatoid factor(RF),and erythrocyte sedimentation rate(ESR)and exhibited higher sensitivity and specificity of diagnostic(AUC 0.8633,95%CI 0.77～0.95).CREB5 was the potential target gene of miR-148a-5p.CCK-8 assays showed that miR-148a-5p mimic significantly promoted proliferation of MH7A and M0 macrophages at 48 h and 72 h(P<0.005).The miR-148a-5p inhibitor inhibited proliferation of MH7A and M0 macrophage at 48 h slightly(P<0.05),and better effects shown at 72 h(P<0.001).Additionally,miR-148a-5p mimic significantly reduced CREB5 protein expression in MH7A cells and increased the levels of MMP3 and CXCL10 in culture supernatant(P<0.001),which could be reversed by miR-148a-5p inhibitor.However,miR-148a-5p had no impact on protein expression of RBMXL1 or CREB5 in M0 macrophages.Conclusion Serum exosomal miR-148a-5p is a diagnostic marker and involves in the pathogenesis of RA,which promotes MH7A cell proliferation by affecting protein levels of CREB5 and excessive secretion of MMP-3,CXCL10.

Objective To evaluate the potential of serum exosomal miR-148a-5p as a biomarker and to investigate its role in the pathogenesis of rheumatoid arthritis(RA).Methods A total of 80 participants(30 healthy controls,HCs;50 RA patients)were recruited.Serum exosomes were extracted and identified.The expressions of exsomal miR-148a-5p will be screened by next-generation sequencing,validated by qRT-PCR and assessed its clinical significance.Target genes and their functions were determined by the luciferase reporter assays,cell transfection,and ELISA.Results Fifty-five differentially expressed serum exomiRNAs were identified(44 upregulated,11 downregulated).The high expression of the exo-miR-148a-5p in the serum of patients with RA was validated by qRT-PCR,comparing to HCs(P<0.000 1),which showed a strong correlation with the disease activity score(DAS)28,rheumatoid factor(RF),and erythrocyte sedimentation rate(ESR)and exhibited higher sensitivity and specificity of diagnostic(AUC 0.8633,95%CI 0.77～0.95).CREB5 was the potential target gene of miR-148a-5p.CCK-8 assays showed that miR-148a-5p mimic significantly promoted proliferation of MH7A and M0 macrophages at 48 h and 72 h(P<0.005).The miR-148a-5p inhibitor inhibited proliferation of MH7A and M0 macrophage at 48 h slightly(P<0.05),and better effects shown at 72 h(P<0.001).Additionally,miR-148a-5p mimic significantly reduced CREB5 protein expression in MH7A cells and increased the levels of MMP3 and CXCL10 in culture supernatant(P<0.001),which could be reversed by miR-148a-5p inhibitor.However,miR-148a-5p had no impact on protein expression of RBMXL1 or CREB5 in M0 macrophages.Conclusion Serum exosomal miR-148a-5p is a diagnostic marker and involves in the pathogenesis of RA,which promotes MH7A cell proliferation by affecting protein levels of CREB5 and excessive secretion of MMP-3,CXCL10.

Enterotoxigenic Escherichia coli（ETEC）infection can induce watery diarrhea，leading to dehydration，electrolyte disturbance，and even death in severe cases. Recombinant B subunit/inactivated whole-cell cholera（rBS/WC）vaccine is effective in preventing ETEC infectious diarrhea. On the basis of the latest evidence on etiology and epidemiology of ETEC，as well as the effectiveness，safety，and health economics of rBS/WC vaccine，National Clinical Research Center for Child Health（The Children’s Hospital，Zhejiang University School of Medicine）and Zhejiang Provincial Center for Disease Control and Prevention invited experts to develop expert consensus on rBS/WC vaccine in prevention of ETEC infectious diarrhea. It aims to provide the clinicians and vaccination professionals with guidelines on using rBS/WC vaccine to reduce the incidence of ETEC infectious diarrhea.

Objective To investigate the effect of long non-coding RNA (lncRNA) LNC01309 on the proliferation and migration abilities of human hepatocellular carcinoma (HCC) cells and its mechanism of action. Methods HCC samples and corresponding adjacent tissue samples were collected from 12 patients with HCC who underwent surgical treatment in The Sixth Medical Center of PLA General Hospital from February 2018 to June 2019, and quantitative real-time PCR was used to measure the relative expression level of LNC01309. Quantitative real-time PCR was also used to measure the expression level of LNC01309 in human hepatoma cell lines (HepG2, SNU-398, and Hep3B) and the human immortalized normal liver cell line THLE-2. After LNC01309 was overexpressed in HepG2 cells, the cells were divided into plasmid control group (pEXP-control) and overexpression group (pEXP-LNC01309). CCK-8 assay was used to observe the change in cell proliferation, and wound healing assay and Transwell assay were used to observe migration ability. RNA co-immunoprecipitation was used to detect the interaction between LNC01309 with RBM38, with cells divided into IgG group and RBM38 antibody group, and cycloheximide chase assay was used to analyze the effect of LNC01309 on the stability of RBM38 protein. RBM38 was overexpressed in HepG2 cells to conduct the recovery experiment, and CCK-8 assay, wound healing assay, and Transwell assay were used to observe the changes in cell proliferation and migration abilities. The t -test was used for comparison of continuous data between two groups. Results The mean expression level of LNC01309 in HCC tissue was significantly higher than that in adjacent tissue (4.225±2.285 vs 1.541±0.530, t =3.618, P =0.004), and the relative expression level of LNC01309 in hepatoma cells (HepG2, SNU-398, and Hep3B) was also significantly higher than that in normal hepatocytes (THLE-2) ( t =4.231、6.489、14.480, all P < 0.05). Compared with the control group, HepG2 cells with the overexpression of LNC01309 had significant increases in growth rate (OD 450 value at 96 hours: 1.885±0.107 vs 2.527±0.234, t =4.330, P =0.012) and migration ability (11.65%±2.40% vs 35.66%±4.90%, t =9.837, P < 0.001; 100.00%±3.11% vs 161.00%±35.93%, t =4.399, P =0.005); however, the upregulated proliferation and migration abilities of hepatoma cells induced by LNC01309 overexpression were partially inhibited by RBM38 (OD 450 value at 96 hours: 2.500±0.227 vs 1.913±0.282, t =2.812, P =0.048; 168.00%±9.43% vs 117.20%±18.03%, t =6.622, P < 0.001). Compared with the IgG control group, RBM38 antibody significantly enriched the precipitation of LNC01309 ( t =3.846, P =0.031). The results of cycloheximide chase assay showed that the LNC01309 overexpression group had a significant reduction in the stability of RBM38 protein ( t =8.038, P =0.001). Conclusion The newly identified LNC01309 reduces the stability of RBM38 protein through interaction with RBM38 and promotes the proliferation and migration of HCC cells.