INTRODUCTION: Although the 9-minute mean withdrawal time (m-WT) is often reported to be associated with the optimal adenoma detection rate (ADR), no randomized trials of screening colonoscopy have confirmed the impact of a 9-minute m-WT on adenoma miss rate (AMR) and ADR. METHODS: A multicenter tandem trial was conducted in 11 centers. Seven hundred thirty-three asymptomatic participants were randomized to receive segmental tandem screening colonoscopy with a 9-minute withdrawal, followed by a 6-minute withdrawal (9-minute-first group, 9MF, n = 366) or vice versa (6-minute-first group, 6MF, n = 367). The primary outcome was the lesion-level AMR. RESULTS: The intention-to-treat analysis revealed that 9MF significantly reduced the lesion-level (14.5% vs 36.6%, P < 0.001) and participant-level AMR (10.9% vs 25.9%, P < 0.001), advanced adenoma miss rate (AAMR, 5.3% vs 46.9%, P = 0.002), multiple adenomas miss rate (20.7% vs 56.5%, P = 0.01), and high-risk adenomas miss rate (14.6% vs 39.5%, P = 0.01) of 6MF without compromising detection efficiency ( P = 0.79). In addition, a lower false-negative rate for adenomas ( P = 0.002) and high-risk adenomas ( P < 0.05), and a lower rate of shortening surveillance schedule ( P < 0.001) were also found in 9MF, accompanying with an improved ADR in the 9-minute vs 6-minute m-WT (42.3% vs 33.5%, P = 0.02). The independent inverse association between m-WT and AMR remained significant even after adjusting ADR, and meanwhile, 9-minute m-WT was identified as an independent protector for AMR and AAMR. DISCUSSION: In addition to increasing ADR, 9-minute m-WT also significantly reduces the AMR and AAMR of screening colonoscopy without compromising detection efficiency.

Introduction: CC chemokine receptor 5 (CCR5) and the NF-κB signaling pathway play important roles in the pathophysiology of inflammatory bowel disease (IBD). Previously, we synthesized two peptides (GH and HY peptides) that specifically bind to the first and the second extracellular loops (ECL1 and ECL2, respectively) of CCR5 and preliminarily found an inhibitory effect of these peptides on colitis. However, the specific mechanism by which these two peptides regulate trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats remains unclear.Material and methods: Experimental colitis was induced by 5% TNBS. CCR5 antagonist peptides were administered intravenously once a day for a week. Histological evaluation, real-time PCR, western blotting and correlation analysis were performed to examine the effects of the CCR5 binding peptides on the infiltration of inflammatory cells and the NF-κB signaling pathway.Results: GH and HY peptides ameliorated mucosal damage and reduced the infiltration of neutrophils, lymphocytes and macrophages in experimental colitis (P < 0.05). The expression of NF-κB-related genes, including p105, p100, IKK and TNF-α, was reduced after GH and HY peptide administration (P < 0.01), and the protein level of TNF-α and the phosphorylation of IKK, IκBα and p65 were also suppressed. Furthermore, CCR5 antagonist peptides inhibited nuclear translocation of p65. Spearman correlation analysis showed that the infiltration of inflammatory cells was significantly correlated with the NF-κB pathway.Conclusions: Antagonistic peptides that specifically bind to ECL1 and ECL2 of CCR5 inhibit the infiltration of neutrophils, lymphocytes and macrophages in the colonic mucosa of SD rats with TNBS-induced colitis via regulation of the NF-κB signaling pathway.