Objective To analyze the epidemiological characteristics of epidemic mumps in Chongqing Wanzhou district,and provide scientific basis for taking effective prevention and control measures.Methods Epidemic data of mumps in Wanzhou district from January 2011 to December 2014 were investigated retrospectively.Results A total of 2 785 cases of epidemic mumps were reported,there was no death case,the incidence of mumps was 44.02/100 000.Incidence of mumps in population under 15 years old was the highest,accounting for 84.45% (2 352/2 785 ).Mumps mainly occurred among students (1 674 cases,60.11 %).The peaks were from April to July and Oc-tober to December,the number of mumps increased significantly from October to December in 2013.Difference in incidence among each year of 2011 -2014 was statistically different(χ2 =40.52,P <0.01).Incidence of mumps was statistically different between the city streets and villages/towns(63.99/100 000 vs 32.13/100 000,χ2 =20.168,P<0.01).Incidence was statistically different between the city streets and villages/ towns each year of 2011 -2014 (all P < 0.01 ),except 2012,the incidence of mumps of city streets was significantly higher than villages/ towns. Conclusion It is important to conduct “Five early”for the prevention and treatment of infectious diseases,strength-en the vaccination of measles-mumps-rubella (MMR)vaccine or vaccine against epidemic mumps,especially the vaccination for students and children in nurseries,popularize the knowledge about prevention and control of mumps, improve diagnosis and treatment level,and strengthen the epidemic monitoring.

Objective To investigate the expressions of Krüppel like factor 5 (KLF5) and tumor necrosis factor receptor superfamily member 11a (TNFRSF11a) in cervical cancer tissues and their effect on proliferation,migration,and invasion of HeLa cells. Methods Microarray technology was used to detect the mRNA expression of gene in cytocine stimulusin cervical tissues,and the result was verified by real-time fluorescence quantitative polymerase chain reaction. The expressions of KLF5 and TNFRSF11a in cervical tissues were detected by double immunofluorescence staining. HeLa cells were transfected with specific small interfering RNA to knock down the endogenous TNFRSF11a and KLF5 and were infected with adenovirus containing KLF5 to over-express KLF5,respectively. Protein level was detected by Western blot. The regulatory effect of KLF5 on candidate target gene (TNFRSF11a) was determined by dual-luciferase reporter assay. The activity of the cell proliferation,migration,and invasion was detected by using cell counting kit-8 assay and Transwell assay. Results The results of microarray technology showed that the expressions of KLF5 and TNFRSF11a were significantly higher in cervical squamous cell carcinoma tissues compared with normal cervical tissues (P=0.002,P=0.045),and real-time fluorescence quantitative polymerase chain reaction showed that the mRNA expressions of KLF5 and TNFRSF11a were significantly higher in cervical intraepithelial neoplasia (CIN) Ⅰ,CINⅡ-Ⅲ and cervical squamous cell carcinoma tissues compared with normal cervical tissues (KLF5:F=32.79,P=0.018,P=0.014,and P=0.011;TNFRSF11a:F=36.72,P=0.013,P=0.010,and P=0.009) and double immunofluorescence staining showed that the protein expressions of KLF5 and TNFRSF11a were significantly higher in CIN Ⅰ,CIN Ⅱ-Ⅲ and cervical squamous cell carcinoma tissues compared with normal cervical tissues (KLF5:F=42.38,P=0.014,P=0.008,and P=0.002;TNFRSF11a:F=35.42,P=0.021,P=0.012,and P=0.004) and increased with the carcinogenesis. The experiment in vitro confirmed that KLF5 promotes proliferation,migration,and invasion of HeLa by up-regulating TNFRSF11a expression. Clinical analysis showed that the expression of TNFRSF11a mRNA was positively correlated with tumor pathological grading,clinical stage,depth of invasion,and lymph node metastasis (all P<0.05). Conclusion KLF5 and TNFRSF11a are related to cervical cancer. KLF5 promote the proliferation,migration,and invasion of cervical cancer cells partly by upregulating the transcription of TNFRSF11a.