003). Moreover, the odds ratios of age, gender and LY2874455 concentration p-CagA intensity on the gastric IM were showed in Table 2. As compared

to those infected with strains with sparse p-CagA intensity, the crude odds ratio to have IM was 4.38 for those with weak p-CagA intensity, and increased to 8.34 for those with strong p-CagA intensity. Based on the logistic regression analysis to adjust the age, gender, and clinical diagnoses, the odds ratios to have IM were 3.93 for the patients infected with weak RAD001 datasheet p-CagA intensity isolates and 10.45 for those with strong p-CagA intensity. Table 2 The impacts of the p-CagA intensity of H. pylori on the gastric intestinal metaplasia in the 122 selected non-cancer patients by stratified analysis and logistical regression   Odd ratio (95% CI) Crude: Age < 50 years 1 < 50 years 8.14 (3.49~18.98)    Gender - Male 1 - Female 2.36 Cytoskeletal Signaling inhibitor (1.12~5.11)    p-CagA – Sparse 1 – Weak 4.38 (1.15~16.72) – Strong 8.34 (2.21~31.55) Age and gender adjusted      Sparse p-CagA 1    Weak p-CagA 3.67 (0.93~14.37)    Strong p-CagA 8.44 (2.08~34.12) Age, gender and disease adjusted      Sparse p-CagA 1    Weak p-CagA 3.93 (0.92~16.94)    Strong p-CagA 10.45 (2.25~48.48)

Correlation between H. pylori p-CagA intensity and gastric histological features In Figure 4, this study also analyzed whether there were an association between the p-CagA intensity and the severity of gastric inflammation in histology. Farnesyltransferase The patients infected with H. pylori isolates with stronger p-CagA

intensity may have more severe acute inflammation (p = 0.04) and also chronic inflammation (p = 0.002). Nevertheless, the p-CagA intensity of H. pylori isolates was not associated with the HPD or gastric atrophy (p > 0.05). Figure 4 The H. pylori density, inflammation and atrophy by gastric histology among the 146 patients infected with H. pylori isolates with different p-CagA intensity. The isolates with stronger p-CagA intensity were significantly associated with more severe acute inflammation (p = 0.01) and chronic inflammation (p = 0.005) but not with H. pylori density or gastric atrophy (p = NS) (Pearson chi-square test). In Figure 5, a higher proportion of patients infected with a strain with strong p-CagA intensity had corpus-predominant gastritis (59.6%), as compared to those infected with strains with weak (40%) or sparse (25.9%) p-CagA intensity (p = 0.001). The adjusted odds ratio for age, gender, and clinical diagnoses by logistic regression was 3.15 (1.07~9.31) for patients infected with H. pylori with strong p-CagA intensity and 1.49 (0.51~4.35) for those infected with strains with weak p-CagA intensity, as compared with those with sparse p-CagA intensity. Figure 5 The patients infected with strains with strong or weak p-CagA intensity had more corpus-predominant gastritis than those infected with strains with sparse p-CagA intensity ( p = 0.001, Pearson chi-square test). Discussion This study shows the clinical impacts of H.