METHODS： We determined the serum level of apolipoprotein A-I （APO A-I）, haptoglobin （HPT） and a-2 macroglobulin （A2I） with an automatic nephelometer in 63 children （age range 4-17 years, mean 10 years） with b...METHODS： We determined the serum level of apolipoprotein A-I （APO A-I）, haptoglobin （HPT） and a-2 macroglobulin （A2I） with an automatic nephelometer in 63 children （age range 4-17 years, mean 10 years） with biopsy-verified chronic HBeAg-positive hepatitis B. Fibrosis stage and inflammation grade were assessed in a blinded fashion according to Batts and Ludwig. We defined mild liver fibrosis as a score ≤2 and advanced fibrosis as a score equal to 3. ROC analysis was used to calculate the power of the assays to detect advanced liver fibrosis （AccuROC, Canada）. RESULTS： Serum concentrations of APO A-I, HPT and A2M were not significantly different in patients with chronic hepatitis B compared to controls. However, APO A-I level of 1.19 ng/L had a sensitivity of 85.7% and a specificity of 60.7% （AUC = 0.7117, P = 0.035） to predict advanced fibrosis. All other serum biochemical markers and their combination did not allow a useful prediction. None of these markers was a good predictor of histologic inflammation. CONCLUSION： Apolipoprotein A-I may be a suitable serum marker to predict advanced liver fibrosis in children with chronic hepatitis B.展开更多
118 clinical strains of Shigella were serotyped, in which 116 strains were tested to be S. flexneri. The susceptibilities of the S .flexneri strains to quinolones were measured by the disk-diffusion method. It was fou...118 clinical strains of Shigella were serotyped, in which 116 strains were tested to be S. flexneri. The susceptibilities of the S .flexneri strains to quinolones were measured by the disk-diffusion method. It was found that most S .flexneri strains were susceptible to norfloxacin and ciprofloxacin, but resistant to nalidixic acid. To study the correlation between gyrA mutations and quinolones resistance, a fragment within the gyrA gene was amplified by PCR. The SSCP （Single-Strand Conformation Polymorphism） analysis was applied to detect mutations in PCR products of different strains. The mutations were then confirmed by DNA sequencing. Altogether, two types of mutation were revealed, in which one type was single mutation （ C42-T）, and the other was double mutations （ C42-T and A54- G）. By statistical analysis, C42-T （encoding Ser83-keu substitution） was shown to have correlation with nalidixic-acid resistance in the clinical strains of Shigella, while A54-G （encoding Asp87-Gly substitution） was shown to have correlations with both norfloxacin resistance and ciprofloxacin resistance.展开更多
文摘METHODS： We determined the serum level of apolipoprotein A-I （APO A-I）, haptoglobin （HPT） and a-2 macroglobulin （A2I） with an automatic nephelometer in 63 children （age range 4-17 years, mean 10 years） with biopsy-verified chronic HBeAg-positive hepatitis B. Fibrosis stage and inflammation grade were assessed in a blinded fashion according to Batts and Ludwig. We defined mild liver fibrosis as a score ≤2 and advanced fibrosis as a score equal to 3. ROC analysis was used to calculate the power of the assays to detect advanced liver fibrosis （AccuROC, Canada）. RESULTS： Serum concentrations of APO A-I, HPT and A2M were not significantly different in patients with chronic hepatitis B compared to controls. However, APO A-I level of 1.19 ng/L had a sensitivity of 85.7% and a specificity of 60.7% （AUC = 0.7117, P = 0.035） to predict advanced fibrosis. All other serum biochemical markers and their combination did not allow a useful prediction. None of these markers was a good predictor of histologic inflammation. CONCLUSION： Apolipoprotein A-I may be a suitable serum marker to predict advanced liver fibrosis in children with chronic hepatitis B.
文摘118 clinical strains of Shigella were serotyped, in which 116 strains were tested to be S. flexneri. The susceptibilities of the S .flexneri strains to quinolones were measured by the disk-diffusion method. It was found that most S .flexneri strains were susceptible to norfloxacin and ciprofloxacin, but resistant to nalidixic acid. To study the correlation between gyrA mutations and quinolones resistance, a fragment within the gyrA gene was amplified by PCR. The SSCP （Single-Strand Conformation Polymorphism） analysis was applied to detect mutations in PCR products of different strains. The mutations were then confirmed by DNA sequencing. Altogether, two types of mutation were revealed, in which one type was single mutation （ C42-T）, and the other was double mutations （ C42-T and A54- G）. By statistical analysis, C42-T （encoding Ser83-keu substitution） was shown to have correlation with nalidixic-acid resistance in the clinical strains of Shigella, while A54-G （encoding Asp87-Gly substitution） was shown to have correlations with both norfloxacin resistance and ciprofloxacin resistance.
