简介:摘要:分类推进人才评价机制改革,建立科学的人才分类评价机制,调动人才创新创业积极性,对于国有企业转型升级、全面深化改革成功具有十分重要的战略意义,所以我们必须加快分层分类人才评价机制的建立健全。以“德”、“能”、“勤”、“绩”、“廉”五个要素,研究建立以企业中基层员工为对象的岗位人才评测模型,并对各要素数据量化、权重分配进行深入研究。。
简介:AbstractAfrican swine fever (ASF) is a highly infectious, transboundary viral disease of domestic and wild pigs, and is currently the most serious threat to world swine production, resulting in significant economic loss. In the absence of vaccines and treatments, the control of the disease entirely depends on accurate and early diagnosis accompanied by the culling of infected pigs. Thus, a highly specific and sensitive diagnostic assay is required during an outbreak and surveillance of the disease. In this study, a highly sensitive, specific, rapid and repeatable P22-monoclonal antibody-based blocking enzyme-linked immunosorbent assay (bELISA) assay was developed for the detection of antibodies against genotype I and II African swine fever viruses(ASFVs). A total of 806 pig serum samples were tested to evaluate the performance of the diagnostic assay. To determine the PI (percent Inhibition) cut-off value, receiver-operating characteristic (ROC) analysis was applied. According to the ROC analysis of the data, 98.10% specificity and 100% sensitivity were recorded when the threshold cut-off value of PI was established at 47%. In addition, the assay was able to detect ASFV antibodies as early as 9 days post-infection when serum samples from experimentally infected pigs were used. Taking all together, the results of the present study indicated that the P22-mAb based bELISA assay can be used for rapid and accurate detection of antibodies against ASFV, which could play a valuable role in the containment and prevention of ASFV as an alternative to other serological diagnostic methods. Also, this study will assist researchers to further investigate the immunogenic importance of P22 protein in ASFV infection.
简介:摘要目的探讨微小RNA(miRNA)-4795-3p通过靶基因表皮生长因子受体(epidermal growth factor receptor,EGFR)抑制胃癌细胞增殖和侵袭。方法本研究于2020年6月至12月分别转染阴性对照模拟物(阴性对照组)和miR-4795-3p模拟物(miR-4795-3p组)至胃癌BGC823细胞。实时定量聚合酶链反应(qRT-PCR)检验转染效率。淋巴细胞增殖检测(MTS)法和Transwell实验检测BGC823细胞的增殖情况及侵袭能力。生物信息学软件miRcode预测miR-4795-3p的靶基因,采用双荧光素酶报告基因实验验证miR-4795-3p与靶基因的结合。qRT-PCR和蛋白质免疫印迹试验(Western blot)检测靶基因的表达。采用SPSS 21.0软件分析数据,组间比较应用独立样本t检验,P<0.05为差异有统计学意义。结果miR-4795-3p组和阴性对照组BGC823细胞中miR-4795-3p表达分别为(1.02±0.11)和(11.04±1.23),阴性对照组miR-4795-3p表达明显低于miR-4795-3p组(t=8.14,P<0.01)。与阴性对照组比较,miR-4795-3p组BGC823细胞吸光度值明显下降(P<0.05),细胞侵袭数明显减少(P<0.01)。miR-4795-3p与EGFR存在互补结合位点,miR-4795-3p可互补结合EGFR(P<0.01)。与阴性对照组比较,miR-4795-3p组BGC823细胞中EGFR表达明显降低(P<0.01)。结论miR-4795-3p通过靶向负调控EGFR抑制胃癌BGC823细胞的增殖和侵袭能力。
简介:AbstractBackground:Gene promoter methylation is a major epigenetic change in cancers, which plays critical roles in carcinogenesis. As a crucial regulator in the early stages of B-cell differentiation and embryonic neurodevelopment, the paired box 5 (PAX5) gene is downregulated by methylation in several kinds of tumors and the role of this downregulation in esophageal squamous cell carcinoma (ESCC) pathogenesis remains unclear.Methods:To elucidate the role of PAX5 in ESCC, eight ESCC cell lines, 51 primary ESCC tissue samples, and eight normal esophageal mucosa samples were studied and The Cancer Genome Atlas (TCGA) was queried. PAX5 expression was examined by reverse transcription-polymerase chain reaction and western blotting. Cell apoptosis, proliferation, and chemosensitivity were detected by flow cytometry, colony formation assays, and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assays in ESCC cell lines with PAX5 overexpression or silencing. Tumor xenograft models were established for in vivo verification.Results:PAX5 methylation was found in 37.3% (19/51) of primary ESCC samples, which was significantly associated with age (P = 0.007) and tumor-node-metastasis stage (P = 0.014). TCGA data analysis indicated that PAX5 expression was inversely correlated with promoter region methylation (r = -0.189, P = 0.011 for cg00464519 and r = -0.228, P = 0.002 for cg02538199). Restoration of PAX5 expression suppressed cell proliferation, promoted apoptosis, and inhibited tumor growth of ESCC cell lines, which was verified in xenografted mice. Ectopic PAX5 expression significantly increased p53 reporter luciferase activity and increased p53 messenger RNA and protein levels. A direct interaction of PAX5 with the p53 promoter region was confirmed by chromatin immunoprecipitation assays. Re-expression of PAX5 sensitized ESCC cell lines KYSE150 and KYSE30 to fluorouracil and docetaxel. Silencing of PAX5 induced resistance of KYSE450 cells to these drugs.Conclusions:As a tumor suppressor gene regulated by promoter region methylation in human ESCC, PAX5 inhibits proliferation, promotes apoptosis, and induces activation of p53 signaling. PAX5 may serve as a chemosensitive marker of ESCC.