ABSTRACT
In the intestine, finger-like villi provide abundant surface area for nutrient absorption. During murine villus development, epithelial Hedgehog (Hh) signals promote aggregation of subepithelial mesenchymal clusters that drive villus emergence. Clusters arise first dorsally and proximally and spread over the entire intestine within 24 h, but the mechanism driving this pattern in the murine intestine is unknown. In chick, the driver of cluster pattern is tensile force from developing smooth muscle, which generates deep longitudinal epithelial folds that locally concentrate the Hh signal, promoting localized expression of cluster genes. By contrast, we show that in mouse, muscle-induced epithelial folding does not occur and artificial deformation of the epithelium does not determine the pattern of clusters or villi. In intestinal explants, modulation of Bmp signaling alters the spatial distribution of clusters and changes the pattern of emerging villi. Increasing Bmp signaling abolishes cluster formation, whereas inhibiting Bmp signaling leads to merged clusters. These dynamic changes in cluster pattern are faithfully simulated by a mathematical model of a Turing field in which an inhibitor of Bmp signaling acts as the Turing activator. In vivo, genetic interruption of Bmp signal reception in either epithelium or mesenchyme reveals that Bmp signaling in Hh-responsive mesenchymal cells controls cluster pattern. Thus, unlike in chick, the murine villus patterning system is independent of muscle-induced epithelial deformation. Rather, a complex cocktail of Bmps and Bmp signal modulators secreted from mesenchymal clusters determines the pattern of villi in a manner that mimics the spread of a self-organizing Turing field.
Subject(s)
Body Patterning , Bone Morphogenetic Proteins/metabolism , Intestines/embryology , Microvilli/metabolism , Signal Transduction , Animals , Bone Morphogenetic Protein Receptors, Type I/metabolism , Epithelium/embryology , Hedgehog Proteins/metabolism , In Situ Hybridization , Ligands , Mesoderm/embryology , Mice, Inbred C57BL , Models, Biological , Muscle, Smooth/embryology , Organ Size , Tensile StrengthABSTRACT
Herniation of the cecum, terminal ileum, and ascending colon through the epiploic foramen is an uncommon presentation of an internal hernia. An 82-year-old female presented with a small bowel obstruction; Computed Tomography (CT) imaging showed a herniation of the terminal ileum, cecum, and ascending colon through the foramen of Winslow into the lesser sac, with cecal volvulus. Prompt surgical treatment included laparotomy and reduction of the hernia, followed by an extended right hemicolectomy with primary anastomosis and functional closure of the epiploic foramen. This report reviews the natural history and management of this rare pathology.
ABSTRACT
INTRODUCTION: Fecal incontinence (FI) is a common complaint and is often associated with diarrhea and urgency. Foods high in fermentable oligo-, di-, and mono-saccharides and polyols (FODMAP) cause symptoms of diarrhea and urgency. Therefore, this study assesses the impact of a low FODMAP diet on the occurrence of FI due to loose stool. METHODS: This study is a retrospective chart review of patients with FI seen in the Michigan Bowel Control Program clinic between August 2012 and December 2017. Patients who had FI with loose stool without red flag signs and who were recommended a low FODMAP diet and underwent formal dietary instruction with a Michigan Medicine dietician were included. RESULTS: Sixty-five patients with FI who underwent formal dietary teaching were included in this study. Eighty-eight percent of the patients were white, and 87% were women with a mean age of 62 years (±14 years). Additionally, the chart review showed that 35% of the patients had FI daily, 21.5% had FI weekly, and 5% had FI monthly. About 64.6% of the patients (42) had reported a reduction in their FI symptoms with the low FODMAP diet. There was no demographic or clinical characteristic that predicted the response to a low FODMAP diet. DISCUSSION: In this case series, dietary manipulation with a low FODMAP diet was a useful tool to treat patients who suffer from FI due to loose stool. Further confirmatory, prospective randomized controlled trials are required to see the true efficacy of a low FODMAP diet in patients who suffer with FI.