Objective To detect the expression characteristics of lncRNA SNHG16 in hepatocellular carcinoma, and observe the proliferation regulatory effect by miR-141-3p/FOXJ3 on the hepatocarcinoma cells. Methods Potential binding sites were predicted between SNHG16 and miR-141-3p, miR-141-3p and FOXJ3 by bioinformatics analyses. Forty-nine cases of hepatocellular carcinoma were collected, the tumor tissue and the adjacent liver tissue were retained. The normal human hepatocyte HL-7702, hepatocarcinoma cells of Hep-3B and Huh7 were selected. The pc-DNA3.1-SNHG16 group, si-SNHG16 group, miR-141-3p inhibitor group, miR-141-3p mimic group, and si-FOXJ3 group were constructed The cell proliferation activity was detected through CCK-8 method. The expression of SNHG16 and miR-141-3p was detected by real-time fluorescence quantitative PCR(qRT-PCR), FOXJ3 and Ki67 were detected through immunohistochemistry method, FOXJ3 were detected by Western blot. Target relationship was verified between SNHG16 and miR-141-3p, miR-141-3p and FOXJ3 by double luciferase reporter gene experiment. Results Possible combination of base sequences were found between SNHG16 and miR-141-3p, miR-141-3p and FOXJ3 by bioinformatics analysis. The expression of SNHG16 and FOXJ3 were higher in human hepatoma cell line than in normal hepatocyte line. The expression of miR-141-3p was lower in human hepatoma cell line than that in normal hepatocyte line. Compared with the control group and the empty vector transfection group, the proliferation activity was increased at 48h in pc-DNA3.1-SNHG16 group, while it was decreased in si-SNHG16 group, which lasted to 96h. Target relationship was found between SNHG16 and miR-141-3p, miR-141-3p and FOXJ3 in double luciferase reporter gene test. The rescue experiment showed that the inhibition of miR-141-3p could partially reverse the inhibition effect of si-SNHG16 and si-FOXJ3 on cell proliferation. The expression of SNGHN16 and the positive rate of FOXJ3 in hepatocellular carcinoma were significantly higher than that in adjacent liver tissues, and the expression of miR-141-3p was significantly lower than that in adjacent liver tissues. SNHG16 was negatively correlated with miR-141-3p, miR-141-3p and FOXJ3, and positively correlated with FOXJ3 and Ki67 in hepatocellular carcinoma. Conclusion Expression of SNHG16 is increased in hepatocellular carcinoma, which promotes the proliferation through miR-141-3p/FOXJ3 pathway.

Objective: To characterize the clinical distribution and drug resistance of hospital-acquired infections due to Enterococcus spp and provide basis for clinical treatment. Methods: The clinical data of hospital-acquired enterococcus infection patients from 2013.1 to 2015.12 in Chinese PLA General Hospital were retrospectively analyzed. Results: A total of 883 strains of Enterococci were isolated in this study. Most of them were isolated from ICU (292 strains, 33.07%) and hepatobiliary surgery department (125 strains, 14.16%); Urine was the most common sources of these strains (347, 39.30%), followed by body fluids (315, 35.67%) and blood samples (202, 22.88%); The top organism was Enterococcus faecium (596, 67.50%), followed by Enterococcus faecalis (244, 27.63%). The resistance rates of Enterococcus faecium to ampicillin, penicillin, streptomycin, tetracycline, erythromycin, vancomycin and ciprofloxacin were obviously higher than Enterococcus faecalis (P<0.05). Conclusions: Enterococcus faecium and Enterococcus faecalis are the main pathogens in hospital-acquired enterococcus infection, and Enterococcus faecalis has higher resistance rate. It's necessary to choose the appropriate antibiotics according to drug susceptibility test in clinical treatment.

Objective: To explore the effects of aminophylline on proliferation of adipose tissue-derived stem cells (ASCs) of SD rats. Methods: ASCs of SD rats were isolated and cultured to the third generation. Trypan blue staining was used to detect the survival rate of ASCs, MTT methods to draw growth curve after the ASCs were cultured with aminophylline of different concentration (0μg/ml, 5μg/ml, 10μg/ml, 20μg/ml) for 48h. Results: There was no significant difference about survival rate of ASCs in different concentration aminophylline group (P>0.05). There was no significant difference about proliferation of ASCs at same culture time and of different concentration of aminophylline (P>0.05). Conclusions: Treatment concentration of aminophylline has no obvious effects on survival rate and proliferation of ASCs in vitro.