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Basic and Translational Advances in Intestinal and Pancreatic Disease
Do not miss the bridge
A myocardial bridge is a congenital coronary artery anomaly that involves the left anterior descending artery in most cases. It is characterized by the presence of a segment of the coronary artery, the tunneled segment, that takes an intramural course through the myocardium underneath muscular fibers, the muscular bridge.1,2 The muscular bridge is not a new entity, having first been described in autopsies by Reyman in 1737, and has been reported to have a prevalence as great as 86% in autopsy series.Surgical intervention for myocardial bridges: To do or not do to? That is the question
Myocardial bridge, a congenital abnormality in which a portion of the epicardial coronary artery takes an intramuscular course, can be a controversial topic. Most coronary blood flow occurs in diastole, and so the impact of a myocardial bridge, at least theoretically, should be minimal. Nevertheless, systolic compression of the coronary artery has been associated with angina,1 ventricular dysfunction,2 and even sudden cardiac death,3 and systolic compression of the coronary artery has been demonstrated to impact diastolic flow in the coronary artery.Zooming in on Inflammatory Bowel Disease: Microbial and Proteomic Features Associated With IBD in Colonic Microenvironments
Inflammatory bowel disease (IBD) is a multifactorial chronic intestinal inflammatory disorder characterized both by genetic and environmental factors.1 Among the latter, the microbiome recently emerged as one of the most promising avenues of research to understand the pathogenesis of IBD. Several studies have shown differences in microbiome composition and diversity in IBD patients compared with healthy controls.2,3 Larger cohorts have allowed for further characterization of the gut microbiota in IBD patients, including assays that determine function and activity of the microbiome and thus provide better mechanistic insights.Dissecting the Requirement for Secondary Lymphoid Organs in Peripheral Regulatory T-Cell Development
Intestinal mucosal immunity requires the ability to induce a proinflammatory response to clear invasive pathogens while also maintaining self-tolerance in the face of continuous immune activation by luminal contents. Regulatory T cells (Tregs) expressing the transcription factor Foxp3 promote immunologic homeostasis by suppressing dendritic cells1 and effector T-cell responses through the production of transforming growth factor β, interleukin (IL)10, and IL35.2 In this manner, Foxp3+ Tregs play a central role in the development of oral tolerance to food antigens and commensal bacteria.Opening CFTR in the Intestine: Flushing on Demand
A new paper by Cil et al1 has described the discovery and characterization of a small molecule capable of opening the Cl- channel cystic fibrosis transmembrane regulator (CFTR). CFTR accounts for the majority of salt and water secretion across mucosal surfaces and into the ducts of secretory glands, and it is important for mucosal hydration in the intestine, lung, and cornea. The new channel opener was identified from a library of 120,000 drug-like synthetic compounds by using a high-throughput, single-cell screen for agonists of Cl- transport.Macrophages: The Missing Link in Diabetic Gastroparesis?
Gastroparesis is a clinical condition associated with delayed gastric emptying in the absence of mechanical obstruction. Patients present with nausea, vomiting, bloating, and early satiety. The underlying cause may be related to diabetes but also can be caused by upper gastrointestinal surgery, neurologic disease, collagen vascular disease, viral infections, and drugs.1 In approximately 35% of patients there is no underlying cause. The pathogenesis and underlying cellular changes in diabetic gastroparesis are largely unknown.
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