Background and Aims In recent years, high-resolution microendoscopy (HRME) has shown potential to improve screening for esophageal squamous cell neoplasia (ESCN). Furthering its utility in a clinical setting, especially in lower-resource settings, could be accomplished by reducing the size and cost of the system as well as incorporating the ability of real-time, objective feedback. This article describes a tablet-interfaced HRME with fully automated, real-time image analysis. Methods The performance of the tablet-interfaced HRME was assessed by acquiring images from the oral mucosa in a normal volunteer. An automated, real-time analysis algorithm was developed and evaluated using training, test, and validation images from a previous in vivo study of 177 patients referred for screening or surveillance endoscopy in China. The algorithm was then implemented in a tablet HRME that was used to obtain and analyze images from esophageal tissue in 3 patients. Images were displayed alongside the probability that the imaged region was neoplastic. Results The tablet-interfaced HRME demonstrated comparable imaging performance at lower cost compared with first-generation laptop-interfaced HRME systems. In a post-hoc quantitative analysis, the algorithm identified neoplasia with a sensitivity and specificity of 95% and 91% in the validation set, compared with 84% and 95% achieved in the original study. Conclusion The tablet-based HRME is a low-cost tool that provides quantitative diagnostic information to the endoscopist in real-time. This could especially be beneficial in lower-resource settings for operators with less experience interpreting HRME images.

Single ICD-9 codes are inadequate to accurately define IBD patients; however, ICD-9 code algorithms can be used to identify patients with UC or CD with high positive predictive value. The 2 code, at least 1 outpatient code algorithm was observed to have a high PPV and low miss rate.

BackgroundmicroRNAs (miRNAs) have been implicated in the control of many biological processes and their deregulation has been associated with many cancers. In recent years, the cancer stem cell (CSC) concept has been applied to many cancers including pediatric. We hypothesized that a common signature of deregulated miRNAs in the CSCs fraction may explain the disrupted signaling pathways in CSCs.Methodology/ResultsUsing a high throughput qPCR approach we identified 26 CSC associated differentially expressed miRNAs (DEmiRs). Using BCmicrO algorithm 865 potential CSC associated DEmiR targets were obtained. These potential targets were subjected to KEGG, Biocarta and Gene Ontology pathway and biological processes analysis. Four annotated pathways were enriched: cell cycle, cell proliferation, p53 and TGF-beta/BMP. Knocking down hsa-miR-21-5p, hsa-miR-181c-5p and hsa-miR-135b-5p using antisense oligonucleotides and small interfering RNA in cell lines led to the depletion of the CSC fraction and impairment of sphere formation (CSC surrogate assays).ConclusionOur findings indicated that CSC associated DEmiRs and the putative pathways they regulate may have potential therapeutic applications in pediatric cancers.

Summary Background The proportions of patients with oesophageal adenocarcinoma (OAC) diagnosed by Barrett's oesophagus surveillance or with pre‐existing Barrett's oesophagus are unclear. Aim To estimate the prevalence of prior and concurrent Barrett's oesophagus diagnosis among patients with OAC or oesophagogastric junction adenocarcinomas (OGJAC). Methods We searched PubMed and Embase to identify studies published 1966‐1/8/2020 that examined the prevalence of prior (≥6 months) or concurrent Barrett's diagnosis (at cancer diagnosis) among OAC and OGJAC patients. Random effects models estimated overall and stratified pooled prevalence rates. Results A total of 69 studies, including 33 002 OAC patients (53 studies) and 2712 patients with OGJAC (28 studies) were included. The pooled prevalence of prior Barrett's oesophagus diagnosis in OAC was 11.8% (95% confidence interval [CI] 8.4%‐15.6%). The prevalence of prior Barrett's oesophagus diagnosis was higher in single‐centre resection studies (16.0%, 95% CI 8.7%‐24.9%) than population‐based cancer registry studies (8.4%, 95% CI 5.5%‐11.9%). The prevalence of concurrent Barrett's oesophagus in OAC was 56.6% (95% CI 48.5%‐64.6%). Studies with 100% early stage OAC had higher prevalence of concurrent Barrett's oesophagus (91.3%, 95% CI 82.4%‐97.6%) than studies with <50% early OAC (39.7%, 95% CI 33.7%‐45.9%). In OGJAC, the prevalence of prior and concurrent Barrett's oesophagus was 23.2% (95% CI 7.5%‐44.0%) and 26.3% (95% CI 17.8%‐35.7%), respectively. Conclusions Most patients with OAC have Barrett's oesophagus. Our meta‐analysis found ~12% of OAC patients had prior Barrett's diagnosis, but concurrent Barrett's oesophagus was found in ~57% at the time of OAC diagnosis. This represents a considerable missed opportunity for Barrett's oesophagus screening.

OBJECTIVES: The risk of noncardia gastric cancer is increased in the presence of gastric intestinal metaplasia. We aimed to identify demographic and lifestyle factors independently associated with the risk of gastric intestinal metaplasia. METHODS: We used data from a cross-sectional study of patients attending primary care and endoscopy clinics at the Michael E. DeBakey VA Medical Center in Houston, Texas, between February 2008 and August 2013. All patients completed standardized questionnaires and underwent endoscopy with gastric mapping biopsies. Gastric intestinal metaplasia cases included patients with intestinal metaplasia on any noncardia gastric biopsy; we defined extensive gastric intestinal metaplasia as antrum and corpus involvement. We estimated odds ratios (ORs) and 95% confidence intervals (CIs) using multivariate logistic regression models. RESULTS: We identified 423 cases with gastric intestinal metaplasia and 1,796 controls without gastric intestinal metaplasia. Older age (vs <60 years: 60–69 years AdjOR, 1.50; 95% CI, 1.17–1.93; ≥70 years AdjOR, 2.12; 95% CI, 1.48–3.04), male sex (AdjOR, 2.76; 95% CI, 1.50–5.10), nonwhite race/ethnicity (vs non-Hispanic white: Hispanic, AdjOR, 2.66; 95% CI, 1.89–3.76; black, AdjOR, 2.36; 95% CI, 1.85–3.02), and current smoking status (AdjOR, 1.78; 95% CI, 1.29–2.48) were independently associated with gastric intestinal metaplasia. These risk factors remained statistically significantly associated with gastric intestinal metaplasia after adjusting for Helicobacter pylori infection, and their effect sizes were larger for associations with extensive gastric intestinal metaplasia compared with focal gastric intestinal metaplasia. DISCUSSION: Older age, male sex, nonwhite race/ethnicity, and current smoking status were the nonendoscopic factors independently associated with gastric intestinal metaplasia in a predominantly nonimmigrant US population.