miRNA-10a-5p inhibits cell metastasis in hepatocellular carcinoma via targeting SKA1.

A variety of microRNAs (miRNAs) are involved in the occurrence and development of hepatocellular carcinoma (HCC). However, the role of miR-10a-5p in the progression of HCC remains unclear. Therefore, the purpose of this study was to determine the role of miR-10a-5p in the development of HCC and the possible molecular mechanism. miR-10a-5p expression in HCC tissues and plasma from patients was detected by quantitative real-time polymerase chain reaction. Migratory changes in HCC cells were detected after the overexpression of miR-10a-5p. Epithelial-mesenchymal transition (EMT)-related proteins were detected by Western blot. Finally, through luciferase assay and rescue experiments, the mechanism by which miR-10a-5p regulates its downstream gene, human spindle and kinetochore-associated complex subunit 1, SKA1 and the interaction between these molecules in the development of HCC were determined. The expression of miR-10a-5p was markedly downregulated in HCC tissues, cell lines, and plasma. The overexpression of miR-10a-5p significantly inhibited the migration, invasion, and EMT of HCC cells. Furthermore, SKA1 was shown to be a downstream gene of miR-10a-5p. SKA1 silencing had the same effect as miR-10a-5p overexpression in HCC. In particular, the overexpression of SKA1 reversed the inhibitory effects of miR-10a-5p in HCC. Taken together, low miR-10a-5p expression is associated with HCC progression. miR-10a-5p inhibits the malignant development of HCC by negatively regulating SKA1.

[Effect of compound glycyrrhizin on peripheral T-lymphocyte subset in AIDS patients].

OBJECTIVE: To probe the effect and mechanism of Compound Glycyrrhizin in treating AIDS. METHODS: Forty AIDS patients were randomly divided into a treatment group and a control group, both treated with HAART. In addition, the former was given Compound Glycyrrhizin for 6 months, and the CD4+ T count and the expressions of CD8+ and HLA-DR on the surface of peripheral blood lymphocytes (PBL) were studied before and after the treatment. RESULTS: After 6 months of treatment, the expressions of CD8+ and CD38+ of PBL in the treatment group [(6.6 +/- 2.1)%] were found lower than in the control [(11.4 +/- 3.8)%] (t = 5.043, P < 0.01) and CD4+ T count [(243.6 +/- 91.2) x 10(6)/L vs (170.8 +/- 55.7) x 10(6)/L] rose more significantly (t = 3.045, P < 0.01). CONCLUSION: Compound Glycyrrhizin can lower the expression of active T-lymphocyte subset, inhibit HIV and help immune reconstitution.

Antiviral therapeutic efficacy of foscarnet in hepatitis B virus infection.

Foscarnet (PFA), a viral DNA polymerase inhibitor, is a clinical agent for herpes viruses. The goal of the study was to evaluate the therapeutic efficacy of PFA in hepatitis B virus (HBV) infection. Intravenous infusion of PFA (1 g/day) for 4 weeks significantly reduced serum HBeAg (p<0.01) and HBV DNA copies (p<0.05) in 31 patients who were diagnosed with active chronic HBV infection (CHB) and had not received antiviral treatment previously. Alanine aminotransaminase (ALT), aspartate aminotransaminase (AST) and gamma glutamyl transpeptidase (gamma-GT) of the patients declined (p<0.001, 0.001 and 0.01, respectively). Kidney function (blood creatinine and urea nitrogen) remained unchanged. Another 21 lamivudine-resistant CHB patients with mutations at the tyrosine-methionine-aspartate-aspartate motif (YMDD) displayed a response to PFA similar to that mentioned above, with reductions in HBeAg (p<0.05), HBV DNA (p<0.01) and liver enzymes (ALT and AST, p<0.001; gamma-GT, p<0.05). Moreover, PFA reduced serum HBeAg (p<0.01), HBV DNA (P<0.05), AST (p<0.05) and ALT (p<0.02) in a cohort of 13 severe CHB patients with advanced liver damage. PFA was also evaluated in vitro and in vivo. PFA inhibited HBV DNA replication in HBV-transfected human HepG2 cells (2.2.15 cells) with reduced amount of HBV RC-DNA and DS-DNA. In the duck HBV-infected ducklings, PFA reduced viral DNA and duck HBsAg in the serum (p<0.01 for both).

[Coreceptors CCR5 and CXCR4 expressions on peripheral blood T lymphocytes in HIV/AIDS patients].

OBJECTIVE: To investigate the coreceptors CCR5 and CXCR4 expressions on the peripheral blood T lymphocytes in HIV/AIDS patients, with an analysis of their clinical value. METHODS: Thirty HIV/AIDS patients and 16 normal controls were selected and flow-cytometry was used to detect the coreceptors CCR5 and CXCR4 expressions in whole blood samples taken from the patients and controls. An analysis was made of the correlation of the coreceptor expression with CD4 T cell counts and the activation of CD4+/ CD8+ T cells (HLA-DR+/CD38+). RESULTS: The CCR5 expression on CD8+ lymphocytes and the CXCR4 expression on the CD4+/ CD8+ T lymphocytes of the HIV/AIDS group were higher than those of the normal controls (P < 0.01). The CCR5 and CXCR4 expressions on the CD4+/CD8+ T lymphocytes of the HIV/AIDS patients was significantly correlated with the activation of CD4+/CD8+ T cells (HLA-DR+/CD38+) (P < 0.05). CONCLUSION: The expressions of CCR5 and CXCR4 are significantly correlated with the immune system reaction to HIV and the disease progression in HIV infected patients.

Self-assembled biomimetic monolayers using phospholipid-containing disulfides.

Several phospholipid-based disulfide molecules were synthesized and attached onto the gold-coated silicon wafer using the self-assembling method. The syntheses of these surface-modifying agents were conducted by introducing bromoethylphosphorate (PBr), phosphorylcholine (PC) or phosphorylethanolamine (PE) groups on the terminals of a dialkyl disulfide. After disulfides adsorption onto gold substrate surfaces, the composition, the film thickness, and the conformational order of self-assembled monolayer surfaces were explored and discussed in detail based on reflection-absorption infrared spectroscopy, contact angle measurement, Auger electron spectroscopy, X-ray photoelectron spectroscopy, and so on. The monolayer having the PBr end group could also be converted to a PC surface by treating with trimethylamine. The model functional surfaces of Au-SC11-PC, -PE, -PBr, -OH or corresponding mixed layers were used to mimic biomembrane surfaces. The monolayer having PC groups was found to reduce fibrinogen adsorption as evaluated from protein adsorption experiments using quartz crystal microbalance. It also showed relatively low platelet adherence compare to the glass, PBr and PE surfaces. The cell viability test also revealed that the PC surface displayed lower cytotoxicity than other surfaces.