Background/Aims: The adenoma detection rate (ADR) of screening colonoscopies performed by trainees is often lower than that of colonoscopies performed by experts. The effcacy of cap-assisted colonoscopy (CAC) in adenoma detection is well documented, especially that of CACs performed by trainees. Endocuff, a new endoscopic cap, is reportedly useful for adenoma detection; however, no trials have compared the effcacy of Endocuff-assisted colonoscopy (EAC) and CAC conducted by trainees. Therefore, the present study retrospectively compared the effcacy between EAC and CAC in trainees. Methods: This was a single-center, retrospective study involving 305 patients who underwent either EAC or CAC performed by three trainees between January and December 2018. We evaluated the ADR, mean number of adenomas detected per patient (MAP), cecal intubation rate, cecal intubation time, and occurrence of complications between the EAC and CAC groups. Results: The ADR was significantly higher in the EAC group than in the CAC group (54.3% vs. 37.3%, p=0.019), as was the MAP (1.36 vs. 0.74, p=0.003). No significant differences were found between the groups with respect to the cecal intubation rate or cecal intubation time. No major complications occurred in either group. Conclusions Our results suggest that EAC exhibits increased ADR and MAP compared to CAC when performed by trainees.

Background/Aims: Intestinal fibrosis is a major complication of Crohn’s disease (CD). The profibrotic protein transforming growth factor-β (TGF-β) has been considered to be critical for the induction of the fibrotic program. TGF-β has the ability to induce not only the expression of extracellular matrix (ECM) including collagen, but also the production of plasminogen activator inhibitor-1 (PAI-1) that prevents enzymatic degradation of the ECM during the onset of fibrotic diseases. However, the significance of PAI-1 in the developing intestinal fibrosis has not been fully understood. In the present study, we examined the actual expression of PAI-1 in fibrotic legion of intestinal inflammation and its correlation with the abnormal ECM deposition. Methods: Chronic intestinal inflammation was induced in BALB/c mice using 8 repeated intrarectal injections of 2,4,6-trinitrobenzene sulfonic acid (TNBS). TM5275, a PAI-1 inhibitor, was orally administered as a carboxymethyl cellulose suspension each day for 2 weeks after the sixth TNBS injection. Results: Using a publicly available dataset (accession number, GSE75214) and TNBS-treated mice, we observed increases in PAI-1 transcripts at active fibrotic lesions in both patients with CD and mice with chronic intestinal inflammation. Oral administration of TM5275 immediately after the onset of intestinal fibrosis upregulated MMP-9 (matrix metalloproteinase 9) and decreased collagen accumulation, resulting in attenuation of the fibrogenesis in TNBS-treated mice. Conclusions PAI-1-mediated fibrinolytic system facilitates collagen degradation suppression. Hence, PAI-1 inhibitor could be applied as an anti-fibrotic drug in CD treatment.