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Objective@#To analyze the etiological characteristics of an outbreak of Campylobacter foodborne disease in a middle school in Suzhou City, so as to provide insights into the identification of pathogenic factors of Campylobacter foodborne disease outbreaks.@*Methods@#Eighteen anal swabs from patients, 10 anal swabs from canteen workers, 43 food samples, 2 drinking water samples, 2 food original material samples and 31 environmental samples were collected, and the pathogens were rapidly screened using the gastrointestinal infection detection strip. The pathogens were isolated and cultured using the double-pore filtration membrane method, and cluster analysis of bacterial isolates was performed using pulsed field gel electrophoresis ( PFGE ). In addition, the susceptibility of Campylobacter isolates to antibiotics was tested using the Campylobacter agar dilution method.@*Results@#A total of 63 cases with Campylobacter infections were reported, and the major clinical symptoms included diarrhea ( 51 cases, 80.95% ) and fever ( 39 cases, 61.90% ), while no inpatients or deaths were found. Twelve Campylobacter-positive samples were detected, including 11 anal swabs sampled from patients and one food original material sample. Among the 11 positive anal swabs, there were 10 samples positive for Campylobacter jejuni and one sample positive for C. coli, and of the one positive food original material, C. coli was identified. PFGE analysis showed that 10 C. jejuni isolates of had 100.0% homology, and these 10 isolates were 100.0% resistant to naphthyridic acid, ciprofloxacin and tetracycline, appearing multidrug resistance.@*Conclusions@#This is an outbreak of foodborne disease caused by C. jejuni infections. Gastrointestinal infection detection strips, double-pore filtration membrane and PFGE typing are rapid and accurate to identify pathogenic factors.
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Objective To investigate the effect and mechanism of oxymatrine on invasion and metastasis of human pancreatic cancer line SW1990 in vitro. Methods Human pancreatic cancer cell line SW1990 was cultured in vitro. Oxymatrine was added into the culture media of SW1990 cells. Then MTT assay was used to determine the effect on proliferation. The adhesive capability, the mobile ability and invasive ability of SW1990 cells were detected by the adhesion assay, the crossing-river test, the transwell migration assay and the matrigel invasion method, respectively. RT-PCR was used to detect the mRNA expression of MMP-2 and VEGF. ELISA method was used to detect the protein levels of the VEGF. Results The growth of SW1990 cells was inhibited by oxymatrine in a dose and time-dependent manner. After 2 mg/ml of oxymatrine treatment for SW1990 cells for 1 h, the adhesive capability inhibitory rate was (35.23 ±8.56) % ; 24 h later, crossing-river time was (65.46 ±4.25) h, which was significantly longer than that in control group [ (34.50 ± 4.12) h, P <0.05)], the number of penetrating cells was 91.9 ±9.6, which was significantly lower than that in control group (144.2±17.2, P <0.05). The mRNA expression of MMP-2 and VEGF, expression of protein of VEGF in SW1990 cells was significantly down-regulated [0.515 ±0.063 vs. 0.817 ±0.054, 0.343 ± 0.072 vs. 0.650 ±0.068; (265.50 ±5.45) pg/ml vs. (441.06 ±16.70) pg/ml, P <0.05]. Conclusions Oxymoron can inhibit the invasion and metastasis ability of pancreatic cancer line SW1990 in vitro, and the mechanism is possibly related to the down-regulation of MMP-2 and VEGF expression.
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AIM: To investigate the effects of PAR-2 agonist peptide on the proliferation and cytosolic calcium concentration ([Ca~(2+)]_c) in human hepatoma cells HepG2. METHODS: Human hepatoma cell line HepG2 was cultured. The cells were treated with PAR-2 agonist peptide SLIGKV-NH_2 and the reverse PAR-2 agonist peptide VKGILS-NH_2, respectively. The [Ca~(2+)]_c of hepatoma cells were measured by microfluorimetric techniques based on calcium indicator fura-2/AM. The influences on proliferation of hepatoma cells were determined by MTT method. The changes of cell cycle were evaluated by flow cytometry, and the changes of cyclin D1 mRNA expression were detected by RT-PCR. RESULTS: After treated with 50 μmol/L SLIGKV-NH_2, a rapid rise of [Ca~(2+)]_c in HepG2 cells was induced (P<0.01), percent S phase, G_2/M phase and proliferation index (PI) of HepG2 cells were elevated (P<0.01), and cyclin D1 mRNA expression was significantly upregulated (P<0.01). The proliferation rates of HepG2 cells treated with 1-50 μmol/L SLIGKV-NH_2 were significantly increased, and the effect was in a dose-dependent manner (P<0.01 or P<0.05). No statistical significance of the difference between VKGILS-NH_2 and control group was observed (P>0.05). CONCLUSION: PAR-2 agonist peptide induces the rise of [Ca~(2+)]_c in HepG2 cells, upregulates the expression of cyclin D1 mRNA, accelerates the progress of cell cycle, promotes the synthesis of DNA and the proliferation of hepatoma cells via activating PAR-2 in vitro.