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 acrylonitrile on the activation of nuclear factor-kappaB signaling pathways and related gene expression in rat brain and rat glial cells].

OBJECTIVE: To study the effects of acrylonitrile on the activation of nuclear factor kappaB (NF-kappaB) signaling pathways and related gene expressions in rat brain and rat glial cells. METHODS: The microarray and EMSA (electrophoretic mobility shift assay) techniques were used to investigated NF-kappaB pathway and related gene expressions changes in rat brain after treated with 0 mg/kg and 200mg/kg ACN for 14,28 and 90 days and rat normal glial cells after treated with 0, 25, 50 and 75 microg/ml ACN for 4 and 24 hours. RESULTS: ACN induced the NF-kappaB pathway related gene expression (NIK, IKK, NF-kappaB1, NF-kappaB 2, IkappaBa, c-myc) in rat brain (in vivo) and in rat glial cells (in vitro). It was confirmed by EMSA results that ACN caused activation of the NF-kappaB pathway in rat brain and rat glial cells. CONCLUSION: There is some relationship between gene expression of NF-kappaB pathway and ACN-induced oxidative stress.

[Mechanism study of tea pigment on the selective against the colony growth of preneoplastic and normal Syrian hamster embryo cells].

OBJECTIVE: To use co-cultures of SHE normal and preneoplastic cells in order to study the chemopreventive effects of doses of tea pigment (TP) from black tea on growth, proliferation, apoptosis and related regulation gene expression of normal and preneoplastic SHE cells. METHODS: The different dose of TP (0, 0.5, 1, 5, 10 and 50 microg/ml) were used to treat the cells and the SHE cells growth growth assay and in situ apoptosis assay, in situ proliferation assay and microarray assay were used to determine the growth, proliferation, apoptosis, regulation gene expression of SHE preneoplastic cells. RESULTS: TP induced the colony growth and proliferation of SHE normal cells and had no effect on its apoptosis. TP suppressed the growth and proliferation of SHE preneoplastic cells and induced its apoptosis. TP suppressed the growth and proliferation of SHE preneoplastic cells and induced its apoptosis in co-cultures. The pathways of cell apoptosis were up-regulated through the Caspase3, Casp ase8, P53, bad, bax, GADD45 and down-regulated mdm2 signal pathways, and the pathways of cell proliferation were regulated through blockage of G2 phase of cell cycle. CONCLUSION: The suppression of transferring from preneoplastic cells to tumor cells was both directly through inducing preneoplastic cell apoptosis and indirectly through induced surrounding normal cells proliferation. This selective effect should be helpful to clarifying mechanism of TP's chempreventive effect on tumorigenecity in rodent assays.

[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.

Need to differentiate lethal toxin-producing strains of Burkholderia gladioli, which cause severe food poisoning: description of B. gladioli pathovar cocovenenans and an emended description of B. gladioli.

Burkholderia cocovenenans produces a lethal toxin (Bongkrekic acid) that leads to high fatality in food poisoning cases. However, B. cocovenenans was combined in Burkholderia gladioli in 1999. B. gladioli was originally described as a phytopathogenic bacteria that sometimes causes pneumonia in humans and that acts as an opportunistic pathogen. We thought that it was clinically dangerous to describe these two species without considering their pathogenicities. From our data of 16S rRNA sequence analysis, DNA-DNA hybridization, and fatty acid analysis, we could confirm that B. cocovenenans and B. gladioli should be categorized as a single species. However the species really weaved lethal toxin-producing strains with non-lethal strains. To emphasize that B. gladioli contains two different pathogens, we describe a new pathovar, B. gladioli pathovar cocovenenans, for the lethal toxin-producing strains. We provide characteristics that differentiate this lethal toxin-producing pathovar from other phytopathogenic pathovars within B. gladioli, together with an emended description of B. gladioli.