Objective To investigate the effects of artesunate(Art)on the proliferation,apoptosis,and autophagy of nephroblastoma cell line(SK-NEP-1).Methods SK-NEP-1 cells were intervened with different concentrations of Art(0,10,20,40 and 80 μmol/L),and MTT method was applied to calculate the cell proliferation inhibition rate to screen the optimal intervention concentration;SK-NEP-1 cells were separated into control group,Art group,3-MA group(Art+autophagy inhibitor,3-methyladenine),and Rapa group(Art+autophagy activator rapamycin).EdU and flow cytometry were applied to detect cell proliferation and apoptosis,respectively;MDC staining was applied to detect autophagy in cells;the level of reactive oxygen species(ROS)in cells was detected by DCFH-DA fluorescent probe;the expression of proliferating cell nuclear antigen(PCNA),anti apoptotic factor B cell lym-phomatoma-2(Bcl-2),Bcl-2 associated X protein(Bax),microtubule junction protein 1 light chain 3 Ⅱ/3 Ⅰ(LC3 Ⅱ/LC3 Ⅰ),selective autophagy junction protein 1(p62),and benzyl chloride 1(Beclin-1)proteins in cells were detected by Western blot.Results Compared with 0 μmol/L Art,the proliferation inhibition rate of SK-NEP-1 cells was gradually increased after 10,20,40 and 80 μmol/L Art treatment(P＜0.05),and the IC50 value was 46.881 μmol/L,so 40 μmol/L Art was selected for follow-up experiments.Compared with the control group,the apoptosis rate,relative autophagy fluorescence intensity,ROS level,Bax,LC3 Ⅱ/LC3 Ⅰ,Beclin-1,PINK1,and Parkin protein expression levels of SK-NEP-1 cells in the Art group were obviously increased,the EdU positive cell rate,PCNA,Bcl-2,and P62 protein expression levels were obviously reduced(P＜0.05);The auto-phagy inhibitor 3-MA inhibited the promoting effect of Art on apoptosis and autophagy of nephroblastoma cells and inhibit proliferation(P＜0.05).Conclusions Art inhibits the proliferation of nephroblastoma cell line SK-NEP-1,and promotes autophagy and apoptosis.

Neovascularization plays an important role in many physiological and pathological processes, but its mechanism is still unclear. Since vascular cells are subjected to a variety of biochemical and biomechanical stimulations in vivo and live in a complex microenvironment, it is necessary to construct the vascular model in vitro and simulate the in vivo microenvironment to explore the mechanism of neovascularization. Recently, owing to the advance of micromachining and microfluidic technology, various in vitro microvascular models have emerged. Variables such as shear stress, interstitial flow and biochemical gradient of angiogenic factors have been controlled in these models, which greatly promotes the research of neovascularization. The construction, development and biomechanical design of various microvascular models are reviewed in this paper.

Objective To investigate the impairment and the effect factors of encoding of episodic memory in patients with cerebral infarction. Methods 112 cases cerebral infarction patients and 115 healthy elders as controls were tested for episodic memory encoding with episodic pictures accomplished in computer, and compare the differences of encoding of episodic memory between the two groups. Results The remember indexes ( REM )of encoding memory test in patient group was significantly lower than that in control group( (70.81 ± 6.08 )vs (84.67 ± 4.49), P ＜ 0.01 ). The REM in patients with different impaired areas was significantly different ( (65.88 ± 5.73 ), (68.92 ± 4.65 ), (73.39 ± 6.20), ( 73.53 ± 3.44), P ＜ 0. 01 ). The REM in frontal lobe infarction group was significantly lower than that in temporal lobe infarction group (P ＜ 0.05 ), and in temporal lobe infarction group was significantly lower than that in basal ganglia infarction group and corona radiate infarction group (P＜0.05, P＜0. 01). The REM in cortex infarction group was significantly lower than that in under cortex group ( ( 67.37 ± 5.40 ), ( 73.46 ± 4.99 ), P ＜ 0.01 ). The REM in small cerebral infarction group was significantly higher than that in large cerebral infarction group( (72.67 ±4.47 ), (67.56 ± 6.18 ), P＜0.01 ). The size of cerebral infarction diameter was related with the REM( r= -0.39, P＜0. 01 ). The REM among control group,infarction with atrophy group, and infarction without atrophy group were significantly different( (67.03 ± 6. 17 ),( 72.84 ± 5. 00 ), ( 84.67 ± 4.49 ), P ＜ 0. 01 ). The REM in infarction with atrophy group was significantly lower than that in infarction without atrophy group and control group( both P＜0.01 ) ,The REM in infarction without atrophy group was significantly lower than that in control group (P ＜ 0.01). Conclusion The encoding of episodic memory was impaired in cerebral infarction patients. The infarction parts,size of infarction area and atrophy was related with the impairment of encoding of episodic memory.

[Objective]To explore the combined curative effect of the ginkgo leaf and benazepril on the early diabetic nephropathy(DN).[Method]Ninety patients with the early diabetic nephropathy(DN)were randomly divided into single group(n=45,the ginkgo leaf injection 20ml,once a day for 3 months)and combined group(n=45,added benazepril 10mg,once a day for 3 months).The changes in glycosylated hemoglobin(Hba1c) and 24-hour urinary microalbum inuria were observed before and after treatment.[Result]Hba1c remained unchanged throughout the course of the treatment,urinary microalbum inuria decreased in both groups,a more profound reduction was achieved after the combined treatment(P