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1. It is now generally acknowledged that Helicobacter pylori infection is the major cause of antral gastritis.

2. The Pyloriset detects IgG antibodies by agglutination, using Latex particles coated with acid extracted antigen of H pylori.

3. It has also been proposed that H pylori ammonia production will lead to mucosal damage by denaturing the protective mucus layer.

4. After eradication of H pylori, duodenal ulcers do not usually recur and the associated chronic gastritis gradually disappears.

5. One month after completion of this treatment their C-urea breath test was repeated to assess the H pylori state.

6. Therefore, additional evidence clearly pointing to a causal relation between H pylori infection and gastric ulcer disease has to be provided.

7. This was done by using the pylorus and the anatomical antrum-corpus boundary as reference points.

8. The high rate of H pylori ammonia production in uraemic patients should accentuate any ammonia induced effects.

9. Twelve of these children received previous antibiotic therapy for various reasons, with possible inadvertent effects on the diagnosis of H pylori.

10. However, acid secretion in old subjects without atrophy was not different to that in young subjects, irrespective of H pylori status.

11. In the present study we also analysed the relation between active H pylori infection and serum pepsinogen-I and pepsinogen-II concentrations.

12. Decreased concentrations of activated pepsinogen were found in H pylori positive patients only. Duodenal biopsies were tested in 76 patients.

13. H pylori has variable effects on serum gastrin concentrations and gastric acid secretion.

14. The strong association between antral tumours and chronic active gastritis suggests the possibility that H pylori infection may have a pathogenic role.

15. In healthy volunteers, H pylori state was determined by the C urea breath test.

16. Helicobacter pylori is recognised as a significant cause of chronic antral gastritis and important in the aetiology of peptic ulceration.

17. The primary aim of the second trial was to see if eradication of H pylori led to resolution of intestinal metaplasia.

18. H pylori infection has been shown in prospective epidemiological studies to be a risk factor for gastric cancer.

19. This study aimed to analyse H pylori infection within family groups.

20. One explanation for this finding would be that H pylori infection is acquired by people throughout their lives.

21. Conclusions Neuromuscular tissue of pylorus originates from mesenchyme.

22. Serial panendoscopy in the following years discovered double pylorus formation in 1992 and 1993.

23. The double pylorus is a rare condition consisting of fistulous communication between the gastric antrum and the duodenum .

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24. The hindgut consists of pylorus, ileum and rectal. The structure of the ileum is different from rectal.

25. Objective: To provide anatomic data for pylorus - preserving pancreaticoduodenectomy ( PPPD ).

26. Most of amylases located at pylorus and foregut, few of them can be found in the stomach.

27. Excuse me the following bacterium of screw of which formulary and eradicative pylorus is best?

28. Conclusions Stomach adynamia after PD procedure is mainly caused by interruption of vagus branches to pylorus and gastric antrum. The VTPPD procedure can effectively prevent this complication.

29. Because the distribution of lipase is the same as that of amylose, the lipases between pylorus and foregut had much more important effection than those of stomach.

30. Follow up panendoscopy 4 months later showed gastric ulcer with double pylorus.