In order to identify problems in the use of antibiotics and propose corresponding countermeasures, a statistical analysis was made into 6 000 prescriptions and medical records detailing the use of antibiotics by outpatients and inpatients randomly selected from the years 2002～2003. It was found that the irrational use of antibiotics was prevalent. It is pointed out that high attention ought to be paid to the issue and countermeasures be adopted, including strengthening physician training in the "three basics", implementing various rules and regulations, adhering to the standards and guides for the use of antibiotics, dynamically tracing the use of antibiotics by means of the computer, and providing timely analysis and feedback of information on the use of antibiotics.

Objective To investigate the anti-proliferation mechanisms of Phenethyl isothiocyanate (PEITC)in human lung cancer cells line NCI-H446. Methods Human lung cancer cell line NCI-H446 was cultured in vitro,and treated with 10,30,50μmol/L PEITC for 24 h respectively. Cell viability and apoptosis were analyzed by methylthiazolyldiphenyl-tetrazolium bromide (MTT)assay and flow cytometry,respectively. Phosphorylation of Akt,activation of caspase-3 and caspase-9 in NCI-H446 cells,and production of cytochrome C in cytoplasm were detected by Western blot. Expression of phosphatase and tensin homologue (PTEN)was detected by real-time PCR. Results PEITC significantly reduced NCI-H446 cells proliferation in dose-dependent manner (P<0.05 ),and apoptosis was also inducted after PEITC administration. PEITC also markedly induced expression of caspase-3 and caspase-9,as compared with control group. And the level of cytochrome C in the cytoplasm was also increased after treatment with PEITC.Furthermore,PEITC treatment significantly increased the mRNA level of PTEN in NCI-H446 cells. Conclusion PEITC may be used as a potential anti-lung cancer agent by regulationg PI3K/AKT pathway and increasing PETN expression.

[Abstract] Objective: To investigate the effect of RG108 on the proliferation and apoptosis of human non-small cell lung cancer (NSCLC) cell lines (A549, H1299) and explore its molecular mechanism. Methods: A549 and H1299 cells were cultured in vitro and treated with different concentrations of RG108. The cell proliferation, cell cycle and apoptosis were detected by MTT assay and Flow cytometry, respectively. qPCR and Western blotting (WB) were used to detect the TFPI-2 mRNA and protein expressions as well as the expression of TMPRSS4 in cells. Meanwhile, the methylation status and degree of TFPI-2 promoter in cells were detected with Methylation-specific PCR (MSP) and colorimetry. Finally, siRNA-TFPI-2 and pcDNA3.0-TMPRSS4 plasmids were used to silence TFPI-2 or overexpress TMPRSS4, and then the changes in cell proliferation and apoptosis were detected. Results: After treatment with RG108, the proliferation rate of A549 and H1299 cells were significantly decreased (all P<0.05), while the apoptosis rate were significantly increased(P<0.05), the cell cycle were arrested in G1/S phase (P<0.05), and the intracellular mRNA and protein expressions of TFPI-2 were significantly increased (P<0.01 or P<0.05). Meanwhile, the methylase degree in TFPI-2 promoter region and the expression of TMPRSS4 in cells were all significanly decreased ( all P<0.05). After TFPI-2 silence, the proliferation levels of A549 and H1299 cells were significantly increased(all P<0.05); however, the apoptosis rate of A549 and H1299 cells were significantly reduced after transfection with pcDNA3.0-TMPRSS4(all P<0.05). Conclusion: RG108 can inhibit proliferation of A549 and H1299 cells and promote apoptosis by inhibiting the methylation of TFPI-2 and negatively regulates the expression of TMPRSS4.