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The presence of active inflammation at baseline (in 46 of 96 patients) was found to be a highly significant predictor of early detection of LGD, HGD, or EAC (Figure 1b; Table 2). The univariate HR associated with active inflammation was estimated to be 3.4 from the Cox model (P=0.0005, 95% CI=(1.7, 7.5); Table 2). Figure 1 (a) Overall detection of LGD, HGD, or EAC in BE patients with IND; (b) detection of LGD, HGD, or EAC in IND patients with active inflammation at baseline; (c) detection of LGD, HGD, or EAC in IND patients with abnormal DNA flow cytometric results at baseline ... Table 2 Univariate and multivariate Cox proportional Buparlisib ic50 hazards models with LGD/HGD/EAC or HGD/EAC as the outcome Both aneuploidy and elevated 4N fraction were also associated with an increased risk of subsequent detection of dysplasia or EAC. Patients with aneuploidy had an estimated HR of 4.0 (P=0.007, 95% CI=(1.4, 12.1)), whereas patients with elevated 4N fraction had an HR of 4.4 (P=0.005, 95% CI=(1.4, 13.6); Figure 1c,Table 2). For patients who had either DNA flow cytometric abnormality or active inflammation, the difference in the detection rate of neoplasia was highly significant (P=0.003) among the 39 patients who had DNA flow cytometric data available, but the HR was not estimable (infinite), because no patients without any of the abnormalities were found to have dysplasia or EAC during follow-up (Figure 1d,Table 2). Patients Oxacillin with neither active inflammation nor a DNA flow cytometric abnormality had a stable 1-, 2-, and 3-year detection rates of 0%, whereas patients with any of these risk factors had 1-, 2-, and 3-year detection rates of 18%, 45%, and 50%, respectively (Figure 1d). To obtain an estimate of the HR for the combination markers of active inflammation and DNA flow cytometric abnormality, a multiple imputation (unbiased) method was used with a large number of imputations (1,000) to account for imputation error, resulting in an estimated HR of Angiogenesis inhibitor 18.8 (P