Background and aims Improving the rate of polyp detection is an important measure to prevent colorectal cancer (CRC). Real-time automatic polyp detection systems, through deep learning methods, can learn and perform specific endoscopic tasks previously performed by endoscopists. The purpose of this study was to explore whether a high-performance, real-time automatic polyp detection system could improve the polyp detection rate (PDR) in the actual clinical environment. Methods The selected patients underwent same-day, back-to-back colonoscopies in a random order, with either traditional colonoscopy or artificial intelligence (AI)-assisted colonoscopy performed first by different experienced endoscopists (> 3000 colonoscopies). The primary outcome was the PDR. It was registered with clinicaltrials.gov. (NCT047126265). Results In this study, we randomized 150 patients. The AI system significantly increased the PDR (34.0% vs 38.7%, p < 0.001). In addition, AI-assisted colonoscopy increased the detection of polyps smaller than 6 mm (69 vs 91, p < 0.001), but no difference was found with regard to larger lesions. Conclusions A real-time automatic polyp detection system can increase the PDR, primarily for diminutive polyps. However, a larger sample size is still needed in the follow-up study to further verify this conclusion. Trial Registration clinicaltrials.gov Identifier: NCT047126265
Cell adhesion molecule 1 (CADM1/TSLC1), a putative tumor suppressor involving in cell adhesion, proliferation and apoptosis, is frequently inactivated in several carcinomas due to promoter hypermethylation. But alterations of CADM1/TSLC1 in colorectal carcinogenesis and clinical significance have not been elucidated yet. The aim of this study was to determine the role of functional inactivation of CADM1/TSLC1 gene in colorectal tumorigenesis and its potential as a novel epigenetic marker for clinical assessment of patients with colorectal cancer. We measured CADM1/TSLC1 expression levels in 8 colorectal cancer cell lines, 54 primary colorectal carcinomas and their corresponding non-cancerous tissues by reverse transcription polymerase chain reaction, western blot analysis and immunohistochemistry. We analyzed CADM1/TSLC1 promoter methylation status by bisulfite genomic sequencing and the methylation special polymerase chain reaction, and evaluated its correlation with clinicopathological characteristics. All statistical tests were 2-sides. Downregulation of CADM1/ TSLC1 expression was observed in 7 of 8 (88%) colorectal cancer cell lines and in 39 of 54 (72%) primary colorectal carcinomas. Hypermethylation of CADM1/TSLC1 promoter region occurred in 6 of 8 (75%) colorectal cancer cell lines and 32 of 54 (59%) primary colorectal carcinomas, and was correlated with advanced colorectal carcinoma. Epigenetic inactivation of CADM1/TSLC1 gene is a frequent alteration in development of colorectal cancer and can be a potential biomarker for molecular staging of patients with colorectal cancer.Colorectal carcinoma is one of the most common malignancies, which is attributable much to the inactivation of tumor suppressor genes (TSGs). Besides gene mutations and deletions, DNA methylation of CpG islands in the promoter of TSGs is a major mechanism underlying TSGs inactivation. Lots of studies have shown that the promoter hypermethylation of many TSGs, such as MLH1, P16, TIMP3 and P14, is associated with colorectal carcinoma. 1 A recent study further showed that promoter hypermethylation of methylguanine DNA methyltransferase, human Mut L homolog-1 and vimentin in stool samples could be used as a feasible epigenetic biomarker for colorectal carcinoma screening. 2 Thus, promoter methylation of TSGs could serve as potential diagnostic, therapeutic and prognostic targets for colorectal carcinoma.
Low molecular weight heparin (LMWH) exhibits anti-inflammatory properties, but its effect on inflammation in colitis remains unclear. This study aimed to evaluate the therapeutic effects of LMWH on dextran sulfate sodium (DSS)-induced colitis in mice, in which acute colitis progresses to chronic colitis, and to explore the potential mechanism involved in this process. C57BL/6 mice were randomly divided into control, DSS, and DSS plus LMWH groups (n = 18). Disease activity was scored by a disease activity index (DAI). Histological changes were evaluated by hematoxylin and eosin (HE) staining. The mRNA levels of syndecan-1, interleukin (IL)-1β, and IL-10 were determined by quantitative reverse transcription polymerase chain reaction. Protein expression of syndecan-1 was detected by immunohistochemistry. The serum syndecan-1 level was examined by a dot immunobinding assay. LMWH ameliorated the disease activity of colitis induced by DSS administration in mice. Colon destruction with the appearance of crypt damage, goblet cell loss, and a larger ulcer was found on day 12 after DSS administration, which was greatly relieved by the treatment of LMWH. LMWH upregulated syndecan-1 expression in the intestinal mucosa and reduced the serum syndecan-1 level on days 12 and 20 after DSS administration (P<0.05 vs. DSS group). In addition, LMWH significantly decreased the expression of both IL-1β and IL-10 mRNA on days 12 and 20 (P<0.05 vs. DSS group). LMWH has therapeutic effects on colitis by downregulating inflammatory cytokines and inhibiting syndecan-1 shedding in the intestinal mucosa.
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