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英文摘要
Helicobacter pylori, a primate-specific gastric pathogen, infects most of human population in the world and plays an important role in the pathogenesis of various gastroduodenal diseases. The cag pathogenicity island (PAI) of H. pylori contains approximate 40 genes. The genes, cagA and cagE are in the cagI region of PAI, but cagT is in the cagII region. The previous studies have shown that at least part of the PAI encodes a type IV secretion system and it may involve in the export of virulence factors and interaction between bacteria and host. CagA is one of the major virulence factors in H. pylori. However, its true function and genomic variations related to clinical outcome remain unclear. In order to understand whether the genes in PAI correlate with clinical disease, cagA, cagE, and cagT were selected. A total of 100 clinical isolates of H. pylori were collected from NCKUH. Using three different pairs of the cagA primers (cagA1, cagA2, and cagA3), the presence of the cagA1 gene, was found in 26 strains. All isolates were positive for cagA2, cagA3, cagE and cagT primers. The sequence identity of the cagA1, cagA2, and cagA3 region compared with published sequence is about 88%. These results show that the geographic difference between Taiwanese''s and western strains really exists and the presence of cagA1 is associated with malignancy (p < 0.05). In addition to epidemiological studies, we also conducted the in vivo piglet study to test gastric juice levels of two promising antibiotics (clarithromycin and amoxicillin) for H. pylori eradication, and to compare the difference of bactericidal effects of these two antibiotics between with and without co-usage of intravenous omeprazole (Ome). In part I study, ten piglets (15-20 kg) were used for a 2-week session, one with amoxicillin (Amo) only and the other co-usage with Ome. In part II study, during a consequent 3-week period, clarithromycin (Cla), co-usage with Cla plus Ome, co-usage with Cla, Amo, plus Ome were used in this session. In each session of part I and II studies, serial serum and gastric juice were collected before bolus and 0.5, 1, 2, 3 hour after bolus. In bioassay, the peak serum level of Amo after bolus was found at 30 min, and the peak gastric juice level was at 2 hour. While co-using Ome, the peak level was not altered in both timing and concentration. The co-usage of Ome seems not enhance the level of antimicrobial agent in gastric juice by applying the bioassay. Levels of Amo in serum and gastric juice were estimated by high-performance liquid chromatographic (HPLC) . The results showed that the mean of serum level has two-fold difference between with and without co-usage Ome, but it does not have significance because the larger standard deviation . However, the concentrations of Amo in gastric juice between with and without co-usage Ome are significant difference at 3 hour. Based on these data, the role of omeprazole in co-usage study may decrease the secretion of gastric juice and slow down the empty of stomach.
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