ABSTRACT
According to CLSI,agar dilution method was used to analyze the minimum inhibitory concentrations (MIC) of the nalidixic acid and ciprofloxacin for the isolates from different sources.Mutations in the quinolone resistant determining region (QRDR) of gyrA and gyrB were examined by DNA sequencing of 102 resistant C.jejuni isolates and 27 sensitive isolates.The results showed that 218 isolates(93.16％) were resistant to nalidixic acid among the entire tested 234 isolates.Among these,the resistant rates of the isolates from chicken feaces,duck feaces,human feaces,food animal and cow feaces were 100.00％,100.00％,97.96％,97.83％ and 77.97％,respectively.The 211 isolates(90.17％) were resistant to ciprofloxa-cin.Among these,the resistant rates of the isolates from chicken feaces,duck feaces,human feaces,food animal and cow feaces were 100.00％,100.00％,91.84％,95.65％ and 77.97％,respectively.The differences were both statistically significant.All of the resistant isolates on the QRDR of gyrA had Thr-86-Ile mutation.However,the point substitutions in gyrB gene were synonymous mutations.The results indicated that the C.jejuni isolates in this study showed highly resistant to nalidixic acid and ciprofloxacin.The Thr-86-Ile mutation on the QRDR of gyrA can cause highly resistant to quinolone and fluoroquinolone for C.jejuni.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate genetic and antibiotic resistance characteristics of Campylobacter jejuni (C. jejuni) isolated from Shenzhen.</p><p><b>METHODS</b>Multilocs sequence typing and agar dilution methods were used to define the genotype and antibiotic resistance of C. jejuni, respectively.</p><p><b>RESULTS</b>In total, 126 C. jejuni strains were isolated. The prevalence of C. jejuni was 5.3% in diarrheal patients. The prevalence in poultry meat (36.5%) was higher than that in cattle meat (1.1%). However, the prevalence in poultry cloacal swabs (27.0%) was lower than that in cattle stool (57.3%). Sixty-two sequence types were obtained, among which 27 of the STs and 10 alleles were previously unreported. The most frequently observed clonal complexes were ST 21 (11.9%), ST-22 (10.3%), and ST-403 (7.1%). ST-21, ST-45, ST-354, ST-403, and ST-443 complexes overlapped between isolates from patients and cattle, whereas ST-45 and ST-574 complexes overlapped between isolates from patients and poultry. All C. jejuni were resistant to at least one antibiotic. The highest resistance rate was toward ciprofloxacin (89.7%), followed by tetracycline (74.6%), and nalidixic acid (69.0%).</p><p><b>CONCLUSION</b>This is the first report of the genotypes and antibiotic resistance of C. jejuni in Shenzhen. Overlapping clonal complexes were found between isolates from patients and cattle, and between patients and poultry.</p>
ABSTRACT
PURPOSE: To provide the insight into the role of LXR alpha on the progression of diabetic nephropathy, we measured the production of extracellular matrix in the cultured mesangial cells treated with the LXR agonist. METHODS: With the mesangial cells extracted from C57BL6 mice, we cultured them in the presence of 25 mM glucose with or without TO901317, an agonist of LXRalpha We transfected siRNAs of SREBP1 and LXR alpha into the mesangial cell to suppress the activity of the two genes. RESULTS: TO901317 increased expressions of LXR alpha, SREBP-1, TGF beta-1, and collagen IV and triglyceride amount in mesangial cells cultured in 25mM glucose. These effects of TO901317 were attenuated by inhibiting transcription of LXR alpha or SREBP-1 with transfection of siRNAs. In mesangial cells transfected with siRNA of SREBP-1, changes by TO901317 were attenuated regardless of increased expression of LXR alpha. That suggested the activation of SREBP-1, an downstream gene of LXR alpha, would be more important to induce changes in mesangial cells by TO901317. CONCLUSION: The TO901317, an agonist of LXR alpha, increases extracellular matrix, collagen IV, and TGF beta-1 production in cultured mesangial cells. The SREBP-1 as well as dyslipidemia in mesangial cells enhanced by LXR agonist would be the important mechanism to induce those changes.