Supplementary Material for: The Characteristics and Treatment Outcomes of 71 Duodenal Brunner’s gland Adenomas with Endoscopic Submucosal Dissection

Abstract Background: The aim of this study was to investigate outcomes of patients with duodenal Brunner’s gland adenomas (BGAs) that were treated endoscopically. Methods: We identified consecutive 71 patients treated at our center with endoscopic submucosal dissection (ESD) for their duodenal tumors diagnosed pathologically as BGAs over the period between January 1, 2011 and December 31, 2021. We retrospectively analyzed our experience and short- and long-term outcomes of ESD therapy on patients with BGAs. Results: Among 71 BGA patients with an average age of 57 ± 11.7 years (range: 30-82), 48 (67.6%) were male and 23 (32.4%) were female. The accuracy of preoperative diagnosis with endoscopic ultrasonography was 44.0% (22/50). The H. pylori infection was found in 29 patients (29/71, 40.8%). The median size of BGAs was 1.5 cm [interquartile range (IQR) 0.8-2.7cm]. The most common location was the duodenum bulb (50/71, 64.8%). For the ESD procedure, the median operation time was 15.0 minutes (IQR 9.5-25.5 minutes). The en-bloc and the complete resection rates were 97.2% and 92.3%, respectively. ESD-related mild acute obstructive pancreatitis was present in two patients (2/4, 50%) with BGAs located in the ampulla region. During the follow-up period, one patient with a positive peripheral margin experienced tumor recurrence 2 years after the initial ESD. There was no disease-related death for the cohort. Conclusion: ESD was an effective and safe therapeutic option for BGA patients with excellent outcomes. Long-term follow-up is needed

Supplementary Material for: Late Embryonic and Postnatal Development of Interstitial Cells of Cajal in Mouse Esophagus: Distribution, Proliferation and Kit Dependence

This paper investigates alterations in interstitial cells of Cajal (ICC) in the esophagus of mice from embryonic day 13.5 (E13.5) to 36 days postpartum (P0–P36) using immunohistochemistry. At E13.5, Kit+ cells presented in clusters and differentiated into spindle-like cells with biopolar processes within the outer (longitudinal) and inner (circular) muscle layers at E17.5. These Kit+ ICC with long processes were also Ano1+ and prominent at birth. The density of ICC gradually decreased, and at P36 it became about one twentieth of that at birth. Kit ligand (stem cell factor) expression is lower in striated muscle cells than that in smooth muscle cells. The ICC number was higher in the distal (close to the cardia) than in the proximal esophagus (close to the pharynx). Some Kit+/Ki67+ and Kit+/bromodeoxyuridine+ cells were observed within the muscle layers, and proliferation persisted from birth through adulthood (P28) with a gradually decreasing cell number. At 24 h, Kit+ ICC were dramatically decreased and almost missing 48 h after administration of imatinib (a Kit inhibitor). Our results indicate that ICC proliferation is age dependent and persists throughout the postnatal period. There is a dramatic decrease in the ICC number from P0 to adult life. The Kit signal is essential for the postnatal development of ICC in the esophagus

Erratum: Abnormal Epigenetic Modifications in Peripheral T Cells from Patients with Abdominal Aortic Aneurysm Are Correlated with Disease Development

<b><i>Background:</i></b> Increasing evidence suggests that abdominal aortic aneurysm (AAA) is a T-cell-mediated autoimmune condition. This study investigates the epigenetic modifications that occur in the T cells of AAA patients and evaluates the correlation of these modifications with disease development. <b><i>Methods and Results:</i></b> Peripheral T cells were collected from 101 AAA patients and 102 healthy controls (HCs). DNA methylation and histone acetylation levels were measured by ELISA. Methyl-CpG-binding domain, DNA methyltransferase (DNMT) and histone deacetylase (HDAC) mRNA levels were determined by real-time PCR. DNA from the T cells of the AAA patients exhibited significant hypomethylation compared with the HCs (1.6-fold, p < 0.0001). Expression of DNMT1 at the mRNA level in the T cells of the AAA patients was 1.52-fold lower than that of the HCs (p < 0.0001). The extent of DNA methylation in the AAA patients was negatively correlated with the corresponding aortic diameter (r = -0.498, p < 0.0001). H3 (1.59-fold, p < 0.0001) and H3K14 (2.15-fold, p < 0.0001) acetylation levels in the T cells of the AAA patients were higher than those of the HCs, but the HDAC1 mRNA level was 2.33-fold lower than that of the HCs (p < 0.0001). <b><i>Conclusions:</i></b> DNA methylation and the histone modification status are significantly altered in the T cells of AAA patients. These changes could play a pivotal role in the activation of pathological immune responses and may influence AAA development