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AIM:To establish stock of clinical Helicobacter pylori (H.pylon) isolates,to perform cagA and vacA typing of theseisolates,to evaluate the relationship between genotypes ofcagA and vacA and upper gastrointestinal diseases and toassess the association of vacA genotypes with presence ofthe pathogenicity marker-cagA.METHODS:Clinical H.pylori strains were isolated from theantrum of 259 patients in Clumbia agar.The isolated H.pylori strains were identified by histology,and16SrRNA PCR.CagA genotypes were detected by colony hybridization,theprobe was derived from the cloned plasmid PcagA,anddigested by EcoRI-Hind Ⅲ and the isolated PcagA DNAfragment was radioactively labelled by the random primingmethod,vacA genes types (s,m)and subtypes (s1a,s1b,s2) were typed by PCR.Vacuolating toxin was detected withneutral red absorb test.The results were treated statisticallyby χ~2 test,ttest,and rank sum test.RESULTS:A total of 192 clinical H.pylori strains were isolatedand the stock of Helicobacter pylori was established.Thetotal positive rate of cagA was 87 % in all gastric diseases,and 95 % in gastric cancer group.There was a differencebetween gastric cancer group and the other groups (P<0.05)except duodenal ulcer group.The expression of type s1 ofvacA was more than type s2 (P<0.05),and,the expressionof type m1 was equal to type m2.In gastric cancer group,there was a difference between s1a and s1b (P<0.05),ands1a was more than s1b.Vacuolating toxins were more inXi’an area isolates.CONCLUSION: The cagA~+ vacA type si clinical isolates are more in Xi’an area, but this can not serve as an index to predict gastric cancer.
AIM: To establish stock of clinical Helicobacter pylori (H. pylon) isolates, to perform cagA and vacA typing of these isolates, to evaluate the relationship between genotypes of cagA and vacA and upper gastrointestinal diseases and toassess the association of vacA genotypes with presence of the pathogenicity marker -cagA.METHODS: Clinical H. pylori strains were isolated from the antrum of 259 patients in Clumbia agar. The isolated H. pylori strains were identified by histology, and 16S rRNA PCR. CagA genotypes were detected by colony hybridization, the probe was derived from the cloned plasmid PcagA, anddigested by EcoRI-Hind III and the isolated PcagA DNA fragment was radioactively labeled by the random primingmethod, vacA gene types (s, m) and subtypes (s1a, s1b, s2) were typed by PCR.Vacuolating toxin was detected with neutral red absorb test.The results were treated by necrosis test χ ~ 2 test, ttest, and rank sum test .RESULTS: A total of 192 clinical H.pylori strains were isolated and the stock of Helicobacter pylori was established. The total positive rate of cagA was 87% in all gastric diseases, and 95% in gastric cancer group. There was a difference between gastric cancer group and the other groups (P <0.05) except duodenal ulcer group. The expression of type s1 ofvacA was more than type s2 (P <0.05), and, the expression of type m1 was equal to type m2.In gastric cancer group, there was a difference between s1a and s1b (P <0.05), ands1a was more than s1b. Vacuolating toxins were more inXi’an area isolates.CONCLUSION: The cagA ~ + vacA type si clinical isolates are more in Xi’an area, but this can not serve as an index to predict gastric cancer.