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Evaluating the impacts of genetically modified crops on biodiversity is a necessary step before their release to the field and obtaining environmental safety certificates. To assess the ecological safety of herbicide-resistant soybean ZUTS-33, we compared arthropod diversity, diseases occurrence, nodule number, and weed diversity through spraying herbicide or water on ZUTS-33, and its parental control receptor HC-3 and main cultivar soybean ZH-13 in a field experiment. The results showed that there was no significant difference of arthropod diversity (number of insects per 100 plants, Shannon index, Simpson index and Pielou index), diseases incidence rates and disease index, nodules and weed diversity between ZUTS-33 and non-genetically modified control soybean HC-3 and ZH-13. Spraying herbicide on ZUTS-33 had no significant effect on arthropod diversity, diseases and rhizobium compared with those treatments of spraying clear water on ZUTS-33, non-genetically modified control HC-3 and ZH-13, and the abundance of weeds were significantly decreased.

Objective: To investigate the effect of demethylating agent 5-Aza-CdR (5-aza-2'- deoxycytidine) on demethylation and transcription-regulating of RASSF1A gene in gastric cancer cell SGC7901 in vitro, as well as on the growth inhibition of cells., Methods: After SGC7901 cells were treated with 5-Aza-CdR, MTT assay, flow cytometry, and Annexin V-FITC staining were performed to analyze the cell proliferation, cell cycle and apoptotic rate respectively. Methylation- specific PCP (MSP), RT-PCR and Western blotting were used to detect methylation state, expression of mRNA and protein of RASSF1A gene., Results: After SGC7901 cells were treated with different concentrations of 5-Aza-CdR, the cell growth was inhibited(P<0.05), the cell cycle was blocked at G(1) phase, and the apoptotic rate increased significantly(P<0.05). Hypermethylation was detected in the promoter region of RASSF1A gene in SGC7901 cells, and no expression of RASSF1A mRNA and protein was found. After treated with 5-Aza-CdR, demethylation occurred in RASSF1A gene,which subsequently induced re-expression of this gene at both mRNA and protein level., Conclusion: Demethylating agent 5-Aza-CdR can regulate demethylation and re-expression of RASSF1A gene in gastric cancer cell SGC7901,and inhibit its growth.

Objective: To investigate the effects of sodium butyrate (NaB), a histone deacetylase inhibitor (HDACI), on the proliferation of human gastric cancer cells and the expression of p16, an important negative-regulatory factor of the cell cycle G1., Methods: Human gastric cancer cells of the lines SGC7901 and BGC823 were cultured in RPMI1640 medium and treated with NaB of different concentrations: 5 x10(-4), 1 x 10(-3), 3 x 10(-3), and 5 x 10(-3) mol/L for 24 h or 72 h. MTT assay, flow cytometry, and annexin V-fluorescein isothiocyanate staining were performed to analyze the cell proliferation activity, cell cycle, and apoptotic rate. RT- PCR, Western blotting, and methylation-specific PCR (MSP) were used to detect the e mRNA and protein expression and methylation state of p16 gene respectively., Results: Exposure to different concentrations of NaB inhibited the growth of the SGC7901 and BGC823 cells. Treated with NaB of the concentrations of 1 x 10(-3), 3 x 10(-3), and 5 x 10(-3) mol/L respectively for 72 h, the numbers of the SGC7901 and BGC823 cells at G0/G1 stage increased significantly and those at S stage decreased significantly (all P <0.01), which showed that the cell cycle was blocked at G1 phase. The apoptosis rates of the SGC7901 and BGC823 cells treated with NaB of different concentrations for 72 h all increased significantly (all P <0.01). P16 was expressed in the SGC7901 and BGC823 cells at low levels, and hypermethylation was detected in its promoter region in both cells before the treatment of NaB. After treated with NaB the mRNA and protein expressions of p16 gene were increased in both cells., Conclusion: NaB inhibits the growth of human gastric cancer cells by blocking cell cycles, inducing apoptosis and upregulating the expression of p16 gene by increasing acetylation and reducing methylation.