现代信息技术（IT）尤其是互联网技术的兴起，已经将世界的各个行业结构扁平化。移动智能设备广泛普及、信息及时分享，成为促进社会进步的新动力，催化各个行业改革。现代IT与医学教育的结合必将给医学临床教育带来变革，运用IT，加强教师与学生的紧密联系，增强临床实习的效果与效率，推进实践教学方法和手段的创新。

Objective To determine the effect of HCV core protein on HepG2 cells proliferation after construction of a retroviral vector containing the protein,and detect the expression of Wnt1 and microRNA152 in the HepG2 cells after transfection.Methods A recombinant adenovirus expressing HCV core protein along with EGFP with high titer was used to transfect the HepG2 cells.The expression of HCV core protein in the transfected cells was evaluated by real-time PCR and Western blot analysis.Cell viability of HepG2 cells was measured by MTT assay,flow cytometry and colony formation assay after the transfection of Ad-EGFP and Ad-HCV core.Real-time PCR and Western blot analysis was employed to detect the expression of Wnt1 and miR-152 in HepG2 cells transfected with HCV core protein and miR-152 inhibitor.Results The titer of the recombinant adenovirus expressing HCV core was 1.6×1010 pfu/mL,and that of Ad-EGFP was 1.5×109 pfu/mL The recombinant viruses could effectively transfected into HepG2 cells,and HCV core protein was highly expressed after the transfection of Ad-HCV core.The transfection of the virus Ad-HCV core resulted in an increase in cell proliferation,and promotion in G1/S cell cycle progression and formation of cell colonies in 48 h after transfection(P<0.05).Transfection of the adenovirus of HCV core caused up-regulation of Wnt1 and down-regulation of miR-152(P<0.05).miR-152 inhibitor also upregulated the expression of Wnt1 at mRNA and protein levels(P<0.05).Subsequent bioinformative analysis revealed that the 3′-UTR of Wnt1 mRNA contained a complementary site for miR-152.Conclusion HCV core protein might attenuate the degradation and transcription of Wnt1 mRNA through inhibiting miR-152,and then activate the Wnt signaling pathway in order to promote the proliferation of hepatoma carcinoma cells.

目的 观察3,6-二羟黄酮对HER-2/neu高表达人乳腺癌细胞株MDA-MB-453移植瘤生长和miRNA表达谱的影响.方法 以18只雌性BALB/c裸鼠建立乳腺癌MDA-MB-453细胞移植瘤模型,按照完全随机设计原则平均分入对照组和高、低剂量作用组,移植后72 h开始给予各处理因素,低、高剂量组分别以10、20 mg/( kg·d)的3,6-二羟黄酮灌胃,对照组以等量的生理盐水灌胃.每4天测量1次肿瘤体积和裸鼠体质量,处理28 d后取材,提取肿瘤组织总RNA并分离miRNA,样品采用PolyA Polymerase加尾后利用T4RNA连接酶将带有生物素标记的信号分子与之连接,进而与微阵列杂交,通过芯片扫描和数据分析获得miRNAs表达谱.结果 高、低剂量组移植瘤生长速度低于对照组,肿瘤体积分别在处理12 d和16 d后显著低于对照组(P＜0.05)；处理24d后高、低剂量组移植瘤质量均显著低于对照组(P＜0.01).miRNAs表达谱分析显示,高剂量组瘤组织miRNAs表达与对照组相比显著上调的有12个,显著下降的有15个.结论 3,6-二羟黄酮可显著抑制人乳腺癌细胞株MDA-MB-453移植瘤的生长并影响其miRNAs表达谱.

Objective To investigate the effects of 3,6-dihydroxyflavone on the miRNA expression profile in 1-methyl-1-nitrosourea(MNU)-induced breast carcinogenesis of rats.Methods Female SD rats were equally randomized into 3 groups including normal control,model control and treatment groups.Rats in treatment groups were fed orally with 20 mg·kg-1·d-1 of 3,6-dihydroxyflavone;rats in the normal and model control groups were fed orally with vehicle alone(normal saline).Except the normal control group,all the rats were given a single intraperitoneal injection of MNU(50 mg/kg).18 weeks later,we calculated the tumor incidence in each group.In the same way as mentioned above,the total RNA in breast tissue of rats was extracted at 0,4,8,18 weeks after MNU injection,and miRNA were isolated and hybridized with miRNA microarrays.Results Oral administration of 3,6-dihydroxyflavone significantly decreased the cancer incidence of MNU-induced breast carcinogenesis.MiRNA array analysis revealed that after MNU injection for 4,8,18 weeks,11,12 and 17 miRNA were up-regulated respectively,whereas 18,17 and 18 miRNA were down-regulated.In comparison to the control,10,15,11 miRNA were up-regulated in treatment group at 4,8,18 weeks respectively,while 9,10,12 were down-regulated.Conclusion Oral administration of 3,6-dihydroxyflavone effectively suppressed MNU-induced carcinogenesis in rats,and affected the miRNA microarrays.

Objectives:This work aims to investigate the effect of insulin-like growth factor binding protein 5(IGFBP5 ) on the proliferation and invasion of human osteosarcoma cells(143B ).Methods:The effects of IGFBP5 on the growth,migration,and invasion of osteosarcoma 143B cells were studied.The 143B cell lines were infected with IGFBP5-overexpressing recombinant adenovirus(Ad -IGFBP5 ) and small interfering RNA-mediated knockdown of IGFBP5 recombinant adenovirus(Ad - silGFBP5 ).Cell proliferation,cell wound healing assay,and Transwell invasion assay were performed to determine the effect of IGFBP5 on the osteosarcoma cells.Results: Cell proliferation assay and functional analysis revealed that the osteosarcoma cells infected with Ad-IGFBP5 had significantly lower cell growth rates,wound closure rates,and invasiveness compared with the cells in the control group(P<0.05 ).Meanwhile,after infection with Ad-siIGFBP5,the cells exhibited the opposite biological effects.Conclusion:IGFBP5 may inhibit the tumorigenesis and metastasis of osteosarcoma.