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 5 366) or vice versa (6-minute-first group, 6MF, n 5 367). 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 5 0.002), multiple adenomas miss rate (20.7% vs 56.5%, P 5 0.01), and high-risk adenomas miss rate (14.6% vs 39.5%, P 5 0.01) of 6MF without compromising detection efficiency (P 5 0.79). In addition, a lower false-negative rate for adenomas (P 5 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 5 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.

This study assesses the effect and mechanism of BMSC in IBD rat. Fifty SDF-grade rats were assigned into divided into NC group, model group, BMSC group, blocking agent group and positive NC group randomly with 10 rates in each group. The histopathological changes of colon tissue, expression of Musashi-1, DAPI, SDF-1 and CXCR4 was measured. There was notable inflammatory cell infiltration in model group and agonist group. The structure of gland was destructed notably with notable-visible phenomenon of hyperemia and edema in colon tissue. They could be improved significantly in positive control group and BMSC group. The necrotic colonic mucosal tissue began to be recovered slowly. The phenomenon of hyperemia and edema was alleviated notably without abnormality in colon tissue in control group. The positive level of Musashi-1 in control group, model group and agonist group was the highest. In conclusion, BMSC could be migrated into colonic damage position and differentiated into intestine stem cells to exert recovery effect on IBD rats. The molecular mechanism might be related with SDF-1/CXCR4 axis.