Multisite survey of bacterial contamination in ready-to-eat meat products throughout the cooking and selling processes in urban supermarket, Nanjing, China.

OBJECTIVE: Ready-to-eat (RTE) meat is a kind of popular instant food easily contaminated by microbes, which is one of the causes of foodborne diseases. This study analyzes the possible sources of RTE food bacterial contamination during processing and subsequent selling. METHOD: Samples of eight kinds of RTE meat were collected from four supermarkets in Nanjing, China. The knives, chopping boards, trays(containers of food), clamps, air, water, and hands of the sales staff were sampled, and the enumeration of aerobic plate count and total coliforms and pathogenic bacteria was performed. RESULTS: The survey revealed that poor hygienic levels was the causes that RTE meat products were contaminated by bacteria at different levels. With regard to pathogen, the incidences of Salmonella spp. and Staphylococcus aureus were 4.2% and 2.1%, respectively. These results also revealed that the bacterial contamination of RTE food was caused by the air, as well as clamps, chopping boards, knives, trays, and hands of the operators. The total number of aerobic colonies were positively correlated with the amount of RTE food in one pot (r = .87728, p = .0217), and negatively correlated with the maximum temperature in the center of the meat (r = -.81633, p = .0475). CONCLUSION: The high number of bacteria in RTE foods indicates potential food safety risks and the need to improve the health of supermarket sales staff. The most important thing is to determine how to raise hygiene awareness of employees through food safety education. Meanwhile, a comprehensive set of regulations on hand cleaning and disinfection should be developed to facilitate public health and reduce foodborne illness caused by the consumption of RTE food.

Attenuation of Pseudomonas aeruginosa biofilm by hordenine: a combinatorial study with aminoglycoside antibiotics.

Pseudomonas aeruginosa is a ubiquitous pathogen that is the leading cause of chronic infections. Bacterial biofilm formation facilitates CF development and restricts the anti-bacterial potential of many current antibiotics. The capacity of P. aeruginosa to form biofilms and resist antibiotics is closely correlated with quorum sensing (QS). Disrupting QS by QS inhibitors is a promising strategy for treating chronic infections. Here, we evaluated the effect of hordenine, a recently characterized QS inhibitor, on the susceptibility of aminoglycoside antibiotics against P. aeruginosa biofilms. Hordenine significantly enhanced the susceptibility of aminoglycoside antibiotics tobramycin, gentamycin, and amikacin against P. aeruginosa PAO1 biofilm formation. Combinations of hordenine and aminoglycoside antibiotics showed potent efficiency in disrupting the preformed biofilms of P. aeruginosa. Microscopic observations showed flat, scattered, and unstructured biofilm architecture after treatment with hordenine. Mechanistic study further revealed that hordenine treatment led to the downregulation of genes involved in QS and biofilm formation. Thus, our results suggest that hordenine has the potential to function as an antibiotic accelerant in treating P. aeruginosa infections.

Stimulation of the proliferation of human normal esophageal epithelial cells by fumonisin B1 and its mechanism.

Previous epidemiological studies have demonstrated a correlation between fumonisin B1 (FB1) and human esophageal cancer in China, Iran and South Africa. The purpose of this study was to investigate the effects of FB1 on the proliferation, cell-cycle and apoptosis of normal human esophageal epithelial cells (HEECs) and to explore the molecular mechanisms of these effects. The proliferation of HEECs treated with FB1 was assessed using a colorimetric assay, while analyses of the cell cycle and apoptosis were performed using flow cytometry and the measurement of the protein expressions of genes associated with the cell cycle was conducted using western blotting. The results showed that FB1 stimulated the proliferation of HEECs, decreased the percentage of cells in the G0/G1 phase and reduced apoptosis. The western blotting results showed that FB1 significantly increased the protein expression of cyclin D1 and significantly decreased the protein expression of cyclin E, p21 and p27. The results indicated that FB1 stimulated the proliferation of HEECs by affecting the cell cycle and apoptosis. This mechanism was associated with changes in cyclin D1, cyclin E, p21 and p27 expression.

Effect of fumonisin B1 on the cell cycle of normal human liver cells.

Fumonisin B1 (FB1) is a well-known liver and kidney carcinogen in rodents and humans. The aim of the present study was to investigate the effect of FB1 on the proliferation and cell cycle of the normal human liver cell line HL-7702 and to explore the underlying molecular mechanisms of action. The cells were treated with FB1 (0.0, 0.1, 1.0, 10.0 and 100.0 µmol/l) for 24, 48, 72 and 96 h. Cell proliferation was assessed by colorimetric assay. Cell cycle analysis was performed by flow cytometry. The mRNA and protein expression of cyclin E and P21 were determined by RT­PCR and western blot analysis, respectively. FB1 was initially demonstrated to significantly inhibit the proliferation of HL-7702 cells; however, cell proliferation increased with increasing treatment time. The percentage of cells in the G0/G1 phase was significantly increased by FB1; however, significantly decreased with an increasing concentration of FB1. The mRNA expression of cyclin E was upregulated and then gradually downregulated with increasing treatment time. The mRNA expression of P21 was significantly increased following treatment with 0.1 µmol/l FB1, and decreased following treatment with 10.0 and 100.0 µmol/l FB1 for different treatment durations. Western blot analysis showed that FB1 significantly increased the protein expression of cyclin E and significantly decreased the protein expression of P21 at various concentrations and treatment durations. Our results demonstrated that FB1 affects the cell cycle of normal human liver cells and that the underlying mechanism of action is associated with alterations in the expression levels of cyclin E and P21 induced by FB1.