Genetic analysis of group A streptococcus isolates recovered during acute glomerulonephritis outbreaks in Guizhou Province of China.

In this study, 68 group A streptococcus (GAS) isolates associated with two outbreaks of acute glomerulonephritis (AGN) in China were analyzed by emm typing. A total of 11 different emm types were identified. Analysis of emm type distribution suggested that AGN outbreaks in two counties were caused by emm60.1- and emm63.0-type GAS. These two types were further characterized by pulsed-field gel electrophoresis, multilocus sequence typing, sof sequence typing, and PCR-based identification of streptococcal pyrogenic exotoxin A, B, and C (speA, speB, and speC) genes. In antimicrobial susceptibility tests, all outbreak strains were resistant to erythromycin and tetracycline, and the rates of resistance of nonoutbreak strains to the two antibiotics were 63.6% and 90.9%. This study is also the first to report a nephritogenic M63 GAS strain.

[The effects of acrylonitrile on cell apoptosis, proliferation and related genes expression of rat normal and tumor glial cells].

OBJECTIVE: To study the effect of acrylonitrile (ACN) to cell growth, apoptosis, proliferation and related gene expression of rat normal glial cells (DI TNC1) and tumor glial cells (C6). METHODS: The concentration of ACN on DI TNC1 and C6 were 25, 50 and 75 microg/ml. For cell growth, proliferation and apoptosis assay, the treated time was 24 hours, for microarray assay, the treated time was 4 and 24 hours. RESULTS: After treatment of DI TNC1 cell with 25,50 and 75 microg/ml ACN, the DNA synthesis index were decreased 93.1%, 81.3% and 74.9% as compared to control respectively, the apoptosis index was increased 118%, 122% and 143% as compared to controls respectively. The DNA synthesis and apoptosis indexes of C6 cell showed no change after treatment with ACN. The cell cycle and apoptosis pathway related genes, such as cyclin and p53, also showed changes after treatment with ACN. CONCLUSION: ACN inhibited the cell proliferation of DI TNC1, induced the apoptosis of DI TNC1 and had no effect on cell proliferation and apoptosis of C6 cells, and the related regulation gene expression changes further confirmed the results.

[Effects of cell growth and apoptosis of preneoplastic Syrian hamster embryo cells by green tea constituent epigallocatechin-3-gallate].

OBJECTIVE: The co-culture model of Syrian hamster embryo (SHE) normal (primary cell) and preneoplastic cells mimicking in vivo status was established and used to study the chemopreventive effects of epigallocatechin-3-Gallate (EGCG) on cell growth, proliferation, apoptosis and regulated genes expression of SHE preneoplastic cells and discussed on the mechanism of EGCG's chemopreventive effect of carcinogenesis. METHODS: The SHE cell preneoplastic and normal cells were cultured on the plates with 1:10,000, 1:1000, 1:100, 1:10 rates for 7 days, and the co-culture model was established. The different concentration of EGCG (0, 0.5, 1, 5, 10, 50 micromol/L) were used to treat the cells and the SHE cells growth assay, in situ cell apoptosis assay, in situ cell proliferation assay and microarray assay were used to determined the growth, apoptosis and proliferation of SHE preneoplastic cells. RESULTS: The co-culture model of SHE cells with the 1:100 rate between SHE preneoplastic cells and normal cells was established. 0.5, 1, 5, 10 micromol/L EGCG increased the colony growth and proliferation of SHE normal cells. In the coculture model of SHE cells with 1:200 rate, compared the the control group, 5, 10 micromol/L EGCG suppressed the growth of different size of SHE preneoplastic cells clone. The DNA proliferation index and apoptosis index in the control group were 39.3% and 6.5%, respectively. After treatment of 5, 10 micromol/L EGCG, the proliferation index were decreased to 25.6% and 24.8%, and the apoptosis index were increased to 12.65% and 14.5%. EGCG suppressed the growth and proliferation of SHE preneoplastic cells in co-culture model and increased its apoptosis. The pathway of cell apoptosis was regulated through the P53, NF-kappaB, bcl-2 signal pathway, and the pathway of cell proliferation was regulated through the growth arrest at G1/S phase of cell cycle. CONCLUSION: The selective regulation of EGCG to normal and preneoplastic cells, the interaction of EGCG, SHE normal cells and SHE preneoplastic cells in co-culture model indicate that the suppression of proliferation and induction of apoptosis of preneoplastic cells by EGCG might be the mechanism of green tea' s chemopreventive effects to tumorigenicity.

[Determination and analysis of cellular fatty acids composition of Burkholderia gladioli].

OBJECTIVE: To determine and analyse the composition of cellular fatty acids of Burkholderia gladioli. METHODS: The cellular fatty acids composition of different pathovar strains of Burkholderia gladioli were determined by GC method and analyzed by MIDI-FAME. RESULTS: The results showed that the composition of cellular fatty acids of these strains, including original food poison strains of, were similar and were identified as, and this confirmed the conclusion that Pseudomonas cocovenenans subsp farinofermentans and Burkholderia cocovenenan were the junior synonym of Burkholdria gladioli. It was interesting to find that fatty acids of C16: 0.20H, C18: 1.20H and C16: 1.20H were related to the Bongkrekic acid (BA) producing of Pseudomonas cocovenenans subsp farinofermentans. CONCLUSION: It provide more data for the study of the mechanism of BA production and pathogenesis.