Effect of an avatar-based discharge education application on knowledge and behaviour in people after acute coronary syndrome: protocol for a pragmatic prospective randomised controlled trial.

INTRODUCTION: Many hospital presentations for acute coronary syndrome (ACS) occur in people previously hospitalised with coronary heart disease (CHD), leading to increased costs and health burden. Secondary prevention education including a prehospital discharge plan is recommended for all individuals to reduce the risk of recurrence. However, many clinicians lack the time or support to provide education, and patients' uptake of secondary prevention programmes is limited. An avatar-based education app is a novel and engaging way to provide self-delivered, evidence-based secondary prevention information during the hospital admission and remains accessible after discharge. This protocol aims to evaluate the effect of an avatar-based education app on individuals with ACS. METHODS AND ANALYSIS: This protocol describes a prospective, randomised controlled trial with 3-month follow-up and blinded assessment of 72 participants. Intervention group participants will download the app onto their own device during the hospital admission and independently complete six interactive education modules based on the National Heart Foundation's six steps to cardiac recovery. All participants will receive a text message reminder of the study after 3 weeks. Both groups will receive usual care consisting of bedside education and a pamphlet about cardiac rehabilitation. The primary outcome is knowledge of CHD, assessed using the Coronary Artery Disease Education Questionnaire II. Secondary outcomes include quality of life, response to heart attack symptoms, cardiac-related readmissions and mortality and modifiable cardiac risk factors. Engagement with the app will be evaluated objectively. Intention-to-treat analysis will be conducted, with between-group comparisons and 95% CIs of the primary outcome analysed using analysis of covariance, adjusting for baseline values. ETHICS AND DISSEMINATION: This study protocol has been approved by the Western Sydney Local Health District Human Research Ethics Committee. The results of this study will be disseminated via a peer-reviewed journal and research thesis. TRIAL REGISTRATION NUMBER: Australian New Zealand Clinical Trials Registry (ACTRN12622001436763).

Deletion of Mtgr1 sensitizes the colonic epithelium to dextran sodium sulfate-induced colitis.

BACKGROUND & AIMS: The disruption of homeostasis between proliferation and apoptosis in the colonic epithelium contributes to the pathogenesis of human ulcerative colitis. Mice lacking the transcriptional corepressor myeloid translocation gene related-1 (Mtgr1) display impaired secretory cell lineage development in the small intestine and an increase in proliferation in the crypts of both the small and large intestines. Despite the increase in proliferating cells, the colons of Mtgr1-null mice have a normal cell lineage distribution and normal architecture. To uncover colonic phenotypes in Mtgr1(-/-) mice, we stressed the colonic epithelium with low-molecular-weight dextran sodium sulfate (DSS), which is a well-studied model of murine ulcerative colitis. METHODS: Mtgr1-null mice were given 3% DSS in their drinking water for 4 days and the colons examined at various times thereafter for ulceration and for changes in proliferation and apoptosis. RESULTS: Treatment with DSS resulted in severe colitis in Mtgr1(-/-) mice, at least partially due to increased epithelial apoptosis rates. Transplantation of wild-type and Mtgr1-null bone marrow into irradiated wild-type mice demonstrated that the severe DSS-induced ulceration seen in Mtgr1-null mice was due to a colonic, rather than a hematologic, defect. Importantly, the epithelium of DSS-treated Mtgr1-null mice failed to completely regenerate, showing changes consistent with chronic colitis, even 10 weeks after a single DSS treatment. CONCLUSIONS: These findings suggest that Mtgr1 has an important role in crypt survival and regeneration after colonic epithelial ulceration.

Mtgr1 is a transcriptional corepressor that is required for maintenance of the secretory cell lineage in the small intestine.

Two members of the MTG/ETO family of transcriptional corepressors, MTG8 and MTG16, are disrupted by chromosomal translocations in up to 15% of acute myeloid leukemia cases. The third family member, MTGR1, was identified as a factor that associates with the t(8;21) fusion protein RUNX1-MTG8. We demonstrate that Mtgr1 associates with mSin3A, N-CoR, and histone deacetylase 3 and that when tethered to DNA, Mtgr1 represses transcription, suggesting that Mtgr1 also acts as a transcriptional corepressor. To define the biological function of Mtgr1, we created Mtgr1-null mice. These mice are proportionally smaller than their littermates during embryogenesis and throughout their life span but otherwise develop normally. However, these mice display a progressive reduction in the secretory epithelial cell lineage in the small intestine. This is not due to the loss of small intestinal progenitor cells expressing Gfi1, which is required for the formation of goblet and Paneth cells, implying that loss of Mtgr1 impairs the maturation of secretory cells in the small intestine.