Enhanced Risk of Gastroesophageal Reflux Disease and Esophageal Complications in the Ulcerative Colitis Population.

Background: Although heartburn and reflux are frequently reported in ulcerative colitis [UC], the correlation between UC and gastroesophageal reflux disease [GERD], and its complications, esophageal stricture and Barrett's esophagus [BE], is not well understood. This study aims to examine the prevalence and associated risk of GERD and its complications within the UC population. Methods: We analyzed the National Inpatient Sample (NIS) dataset, consisting of 7,159,694 patients, comparing GERD patients with and without UC to those without GERD. We assessed the degree of colonic involvement in UC and the occurrence of esophageal complications. Bivariate analyses were conducted using the chi-squared test or Fisher exact test (two-tailed). Results: A higher prevalence of GERD (23.0% vs. 16.5%) and GERD phenotypes, such as non-erosive reflux disease (NERD) (22.3% vs. 16%) and erosive esophagitis (EE) (1.2% vs. 0.6%), was found in UC patients (p < 0.01), including pancolitis, proctitis, proctosigmoiditis, left-sided colitis, and indetermined UC (with undefined colonic involvement). UC patients were more likely to develop GERD (1.421), NERD (1.407), and EE (1.681) (p < 0.01). A higher prevalence of esophageal stricture (16.9 vs. 11.4 per 10,000 patients) and BE without dysplasia (94.5 vs. 39.3 per 10,000 patients) was found in UC (p < 0.05). The odds of developing BE without dysplasia were higher (1.892) in patients with UC (p < 0.01), including ulcerative pancolitis, proctitis, and indeterminate UC (OR of 1.657, 3.328, and 1.996, respectively) (p < 0.05). Conclusions: Our study demonstrates an increased risk of developing GERD and its complications in UC. This highlights the importance of vigilant monitoring and early intervention to minimize associated GERD-related risks in patients with UC.

Elucidating the Link: Chronic Obstructive Pulmonary Disease and the Complex Interplay of Gastroesophageal Reflux Disease and Reflux-Related Complications.

Background and Objective: Presenting chronic obstructive pulmonary disease (COPD) patients frequently report concurrent symptoms of gastroesophageal reflux disease (GERD). Few studies have shown a correlation between GERD and COPD. We aimed to examine the correlation between GERD and COPD as well as secondary related reflux complications, such as esophageal stricture, esophageal cancer, and Barrett's esophagus. Methods: This population-based analysis included 7,159,694 patients. Patients diagnosed with GERD with and without COPD were compared to those without GERD. The enrollment of COPD included centrilobular and panlobular emphysema and chronic bronchitis. Risk factors of COPD or GERD were used for adjustment. Bivariate analyses were performed using the chi-squared test or Fisher exact test (2-tailed) for categorical variables as appropriate to assess the differences in the groups. Results: Our results showed that COPD patients had a significantly higher incidence of GERD compared to those without COPD (27.8% vs. 14.1%, p < 0.01). After adjustment of demographics and risk factors, COPD patients had a 1.407 times higher risk of developing non-erosive esophagitis (p < 0.01), 1.165 higher risk of erosive esophagitis (p < 0.01), 1.399 times higher risk of esophageal stricture (p < 0.01), 1.354 times higher risk of Barrett's esophagus without dysplasia (p < 0.01), 1.327 times higher risk of Barrett's esophagus with dysplasia, as well as 1.235 times higher risk of esophageal cancer than those without COPD. Conclusions: Based on the evidence from this study, there are sufficient data to provide convincing evidence of an association between COPD and GERD and its secondary reflux-related complications.

A "Failed" Assay Development for the Discovery of Rescuing Small Molecules from the Radiation Damage.

With improving survival rates for cancer patients, the side effects of radiation therapy, especially for pediatric or more sensitive adult patients, have raised interest in preventive or rescue treatment to overcome the detrimental effects of efficient radiation therapies. For the discovery of rescuing small molecules for radiation damage to the endothelium, we have been developing a 96-well microplate-based in vitro assay for high-throughput compatible measurement of radiation-induced cell damage and its rescue by phenotypic high-content imaging. In contrast to traditional radiation assays with detached cells for clonogenic formation, we observed cells with live-cell imaging in two different kinds of endothelial cells, up to three different cell densities, two gamma-infrared radiation dose rates, more than four different radiation doses, and acute (within 24 h with one to two h intervals) and chronic (up to 7 days) responses by phenotypic changes (digital phase contrast) and functional assays (nuclear, live-cell, and dead-cell staining) at the end of the assay. Multiple potential small molecules, which have been reported for rescuing radiation damage, have been tested as assay controls with dose responses. At the end, we did not move ahead with the pilot screening. The lessons learned from this "failed" assay development are shared.