The study has a limitation of just providing 181 isolates for the analysis of the dupA status of H. pylori, which disclose a rather low 20% dupA-positive prevalence rate. Accordingly, the study S3I-201 in vitro became limited to only 103 patients to provide both analyses
on the infected isolate’s dupA status and the host’s SNPs (Figure 2). It thus cannot provide an adequate statistical power to determine the exact impact of MMP-3 www.selleckchem.com/products/sis3.html SNPs under dupA-negative specific conditions. Conclusions In conclusion, this study provides evidence that host promoter polymorphisms of MMP-3 contribute to increased individual susceptibility to duodenal ulcers in females after H. pylori infection in Taiwan. The MMP-3 promoter genotypes may serve to screen out patients at risk and target for H. pylori eradication in order to stop the ulceration process among H. pylori-infected patients without ulcers yet. Acknowledgements This study was supported by grants from the National Science Council, Taiwan (95-2314-B-006-029-MY3 and 98-2628-B-006-013-MY3), NHRI-EX99-9908BI from the National Health Research Institute, and DOH99-TD-C-111-003 from Department of Health, Taiwan. The authors also thank Miss Hunt-Wen Wu for her assistance. References 1. Labigne A, de Reuse H: Determinants of Helicobacter pylori pathogenicity. Infect Agents Dis 1996,5(4):191–202.PubMed 2. Maeda S, Mentis AF: Pathogenesis MG-132 ic50 of Helicobacter pylori infection. Helicobacter
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