Multiple studies have implicated the POZ-ZF and methyl-DNA-binding transcription factor, Kaiso, in the regulation of genes and pathways that are important for development and tumorigenesis. In Xenopus embryos and mammalian cultured cells, Kaiso has been implicated as a negative regulator of the canonical Wnt signaling pathway. Paradoxically however, Kaiso depletion extends lifespan and delays polyp onset in the ApcMin/+ mouse model of intestinal tumorigenesis, where aberrant activation of Wnt signaling results in the development of neoplasias. These findings call into question Kaiso’s role as a negative regulator of canonical Wnt signaling and led us to hypothesize that Kaiso promotes intestinal tumorigenesis by a mechanism independent of its role in canonical Wnt signaling. To further delineate Kaiso’s role in intestinal tumorigenesis and to determine Kaiso’s role in regulating canonical Wnt signaling in the murine intestine, we generated a Kaiso transgenic mouse model expressing an intestine-specific murine Kaiso transgene. We then crossed our Kaiso transgenic mice with ApcMin/+ mice and analyzed the resultant progeny. Unexpectedly, Kaiso transgenic mice exhibited intestinal inflammation, increased expression of Wnt target genes and deregulated progenitor cell differentiation, although ectopic expression of Kaiso was not sufficient to drive tumorigenesis in the intestine. In agreement with previous studies, ectopic Kaiso expression in ApcMin/+ mice resulted in a significantly shortened lifespan and increased tumour burden. While we were unable to determine the precise mechanism by which Kaiso promotes intestinal tumour development, we found that Kaiso-induced inflammation is enhanced in the ApcMin/+ background and ectopic Kaiso expression further intensifies Wnt target gene expression in this model. Collectively, these studies have identified novel roles for Kaiso in regulating inflammation and cell-fate determination in the intestine. Furthermore, our findings suggest that Kaiso may contribute to intestinal tumorigenesis by promoting inflammation, which has been shown to be a predisposing factor for colorectal cancer development. Lastly, we have demonstrated distinct tissue and organism-specific roles for Kaiso in regulating canonical Wnt signaling. While, the aforementioned studies were the primary focus of this thesis, we also examined Kaiso’s role in DNA methylation-dependent repression of two tumour-associated genes, cyclinD1 and HIF1A. Our studies revealed that Kaiso binds and regulates the cyclinD1 locus via both sequence-specific and methylation-dependent DNA binding, suggesting that these alternate modes by which Kaiso binds to DNA may not be mutually exclusive. Furthermore, we identified a previously unexplored role for Kaiso in regulating the expression of the master regulator of hypoxia, HIF1A, which implicates Kaiso in modulating hypoxia-driven tumorigenic processes. / Thesis / Doctor of Philosophy (PhD)

No description available.

The chicken yolk sac and small intestine are connected through the yolk stalk and share many biological similarities. During the embryonic stage, the extra-embryonic yolk sac helps the embryo to absorb nutrients primarily in the last two weeks of incubation. The chicken yolk sac physically moves yolk contents from the yolk sac to the small intestine at the end of embryogenesis. This is the time when the small intestine replaces the yolk sac in assimilating nutrients for the embryo and later for the posthatch chicken. Additionally, both chicken small intestinal epithelia and the yolk sac secrete beta defensins for promoting intestinal health. Since there are heterogeneous cell types along the mammalian intestinal villus, which are derived from the intestinal stem cells in the crypts, we investigated if cells of the chicken yolk sac and small intestine have the same ontogeny as mammalian intestinal epithelial cells. In this dissertation, we mainly focused on the spatial expression of nutrient transporters (PepT1 and SGLT1), intestinal stem cell markers (Lgr5 and Olfm4), and avian beta defensins in the chicken yolk sac and small intestine during the embryonic and early posthatch stages. RNAscope in situ hybridization was used to identify the distribution of cells expressing PepT1 mRNA in both the chicken yolk sac and small intestine. PepT1 mRNA was found to be expressed by epithelial cells in both the yolk sac and small intestine. In the yolk sac, PepT1 mRNA was uniformly distributed in each endodermal epithelial cell along the villus-like structure. The pattern of PepT1 mRNA expression observed in the chicken yolk sac during the last 10 days of incubation revealed that PepT1 mRNA was increased from e11 to e13, and decreased from e15 to day of hatch. The peak of PepT1 mRNA expression was between e13 and e15, when the yolk sac reaches maximum absorptive area and the growth of the chicken embryo is at its fastest rate. However, the expression of PepT1 mRNA in the intestine was only detected in columnar enterocytes along the villus and not in goblet cells or cells in the crypts. The immunofluorescence assay confirmed that PepT1 protein was located at the brush border membrane of the enterocytes and that protein expression of PepT1 was restricted to the intestinal epithelial cells from approximately the middle to the tip of the villus. In order to identify intestinal stem cells, we used the known mammalian stem cell markers, Lgr5 and Olfm4. Both Lgr5 and Olfm4 are specifically expressed by cells in the chicken intestinal crypts, suggesting that they can be used as biomarkers for chicken intestinal stem cells. Dual labelling of PepT1 and Olfm4 mRNA on the same chicken intestinal sample revealed that there was a gap between PepT1-expressing enterocytes and Olfm4-expressing intestinal stem cells. The cells in this gap were presumably transit amplifying (TA) cells. Additionally, we also found that the TA cell zone along the intestinal villus was reduced during chicken growth. This TA cell population could be clearly detected at day of hatch and d1 posthatch but not later. The expression of SGLT1 mRNA was localized to yolk sac endodermal epithelial cells and showed a sharp increase at the end of incubation. This increase of SGLT1 mRNA coincided with the increase in glucose in the yolk, indicating that the chicken embryo needs glucose as energy for hatching. The mRNA expression profiles of various avian beta defensins have been examined by qPCR and in situ hybridization to investigate the immune function of the yolk sac and small intestine. We found that AvBD10 mRNA showed the highest expression level in the yolk sac and was expressed predominantly in the yolk sac endodermal epithelial cells. Additionally, the expression of AvBD10 mRNA showed a development-specific pattern, which increased from e9 to e11, and decreased from e13 towards day of hatch. The expression patterns of AvBD1, 2, and 7 mRNA were similar to each other. These three genes were found to be expressed by chicken heterophils distributed in the yolk sac blood islands and small intestinal blood vessels. Only a subset of heterophils, which might be activated, were able to express AvBD1, 2, and 7 mRNA. In the intestine, the expression of AvBD10 mRNA was localized to cells along the villus at e19 and day of hatch, but later to only a few cells located above the intestinal crypts. In summary, the endodermal epithelial cells are responsible for the absorptive and immune functions of the chicken yolk sac. The yolk sac mesoderm is critical for embryonic hematopoiesis and innate immunity. The chicken small intestinal epithelial cells are derived from the intestinal stem cells in the crypts. These epithelial cells have different cell types, which are functioning to absorb nutrients and secrete antimicrobial peptides. / Ph. D. / The chicken yolk sac and small intestine are connected to each other and share many biological similarities. Both chicken small intestinal and yolk sac epithelia play critical roles for nutrient absorption and immune defense. In this dissertation, the mRNA for nutrient transporters such as the peptide transporter, PepT1 and the sodium-glucose co-transporter, SGLT1 were found to be expressed by absorptive epithelial cells in both the yolk sac and small intestine. Additionally, both intestinal and yolk sac epithelial cells expressed avian beta defensins (AvBDs), which are important chicken host defense peptides. In the small intestine, there are a number of differentiated cell types that originate from stem cells in the crypt that express the known mammalian stem cell markers, Olfm4 and Lgr5 mRNA. However, in the chicken yolk sac, only the stem cell marker Lgr5 mRNA was expressed by endothelial cells. In summary, the yolk sac epithelial cells are responsible for the absorptive and immune functions for the embryonic stage. The chicken small intestinal epithelial cells are derived from the intestinal stem cells in the crypts. These epithelial cells have different cell types, which function to absorb nutrients and secrete antimicrobial peptides.

The gross intestinal configuration of the Nile tilapia intestine changed dramatically from a short, straight intestinal tube at hatch (day 0) to a very complex, coiling pattern first attained at 9 weeks post-hatch. During the developmental period, gut length increased from 90% to 410% of body length. The rate of increase in both intestinal and body lengths took place at an accelerating rate as the fish aged. The great intestinal length provides an advantage to the fish in digestion and absorption of nutrients present in the less energy-efficient herbivorous diet. Formulation of commercial diets to match the development of the fish's intestine may offer commercial advantage. Appearance, localization and distribution of intestinal enzymes were observed in the fish at hatch and at mature stages using enzyme histochemistry. At hatch (day 0), most gut enzymes were already present in the intestinal brush border. As the fish matured, activities of the enzymes were widely distributed along the intestinal tract. The early appearance and broad distribution of activities of all studied intestinal enzymes may be one factor contributing to the rapid growth rate characteristic of tilapia, which differs markedly from other fish species. To investigate the possibility of using alfalfa as a potential protein food replacement in tilapia, the effects of different levels of alfalfa in feeds on growth and intestinal enzyme activities were observed in the fish aged 3-15 weeks. Results demonstrated that replacing 20% and 40% of a commercial diet with alfalfa had an overall negative effect on body and intestinal growth, as well as the intestinal enzyme activities from age 3-9 weeks. Thus, using alfalfa as a food replacement is not optimal for fish of these young ages, but may yet be suitable for older fish. / Ph. D.

The objective of this study was to evaluate developmental regulation of the expression of nutrient transporter and brushborder hydrolase genes in the small intestine of piglets. Seventy piglets from seven sows were killed at birth (d 0), during suckling (d 1, 3, 7, 14, 21) and postweaning (d 22, 24, 28, 35), and intestinal segments (duodenum, jejunum and ileum) were collected. The mRNA abundance was determined by Northern blot using specific cDNA probes for three disaccharidases (lactase-phlorizin hydrolase, LPH, sucrase-isomaltase, SI, and maltase-glucoamylase, MGA), three peptide hydrolases (aminopeptidase A, APA, aminopeptidase N, APN, and dipeptidyl peptidase IV, DPP IV), two sugar transporters (Na+-dependent glucose transporter 1, SGLT1, and facilitated glucose transporter 5, GLUT5), a peptide transporter (H+-dependent peptide transporter 1, PepT1), four amino acid transporters (excitatory amino acid carrier 1, EAAC1, Na+-dependent neutral amino acid transporter, ATB0, the light chain of a heterodimeric transport system b0,+ involved in the heteroexchange of cationic and neutral amino acids, b0,+AT, and Na+-independent large branched and aromatic neutral amino acid transporter 2, LAT2), and two iron transporters (divalent metal ion transporter 1, DMT1, and iron-regulated transporter 1, IREG1). Protein expression was quantified by Western blot using specific antibodies for LPH, SI, SGLT1, and PepT1. During suckling, the abundance of LPH, APA, APN, DPP IV, b0,+AT mRNA increased quadratically (P < 0.001) with age from birth to d 7 or 14 then remained unchanged or slightly declined with age to d 21. The mRNA abundance of SI increased and LAT2 decreased linearly (P < 0.001) with age, and the abundance of MGA and GLUT5 mRNA remained unchanged with age. There was an age x intestinal segment interaction (P < 0.001) for the abundance of EAAC1 and ATB0 mRNA. The abundance of EAAC1 mRNA increased from d 0 through 14 and remained stable to d 21 in the ileum, and it was low and slightly increased with age through d 21 in the duodenum and jejunum. The abundance of ATB0 mRNA generally increased from d 0 to 21 in the duodenum and ileum, and increased from d 0 to 7 and then decreased to d 21 in the jejunum. The abundance of SGLT1 and PepT1 mRNA was substantial at birth and transiently declined to d 1. The abundance of SGLT1 mRNA generally increased from d 1 to 21, and PepT1 mRNA abundance increased to d 3 and then plateaued through d 21. Postweaning, the mRNA abundance of all of these carbohydrate and protein assimilation related genes increased during the first day (3 d for ATB0) after weaning then declined to the levels at weaning in the jejunum and ileum, followed by a subsequent change pattern that varied among genes. During suckling, the mRNA abundance of LPH, SGLT1, and APA was greater in the duodenum and jejunum than the ileum (P < 0.001). The PepT1 and APN mRNA was evenly distributed among intestinal segments, and the expression of MGA, DPP IV, EAAC1, b0,+AT, ATB0, and LAT2 mRNA was generally greater in the jejunum and ileum than the duodenum or greatest in the ileum. Postweaning, the mRNA abundance of all of these carbohydrate and protein assimilation related genes examined was generally greater in the jejunum and ileum than the duodenum or highest in the ileum. From d 0 through 35, DMT1 and IREG1 mRNA was predominantly (P < 0.05) distributed in the duodenum, where the abundance of DMT1 and IREG1 mRNA increased with age during suckling, and then rapidly decreased after weaning. The protein expression of LPH and SI exhibited a similar developmental pattern as that for the mRNA abundance. Unlike the developmental regulation of their respective mRNA abundance, the protein expression of SGLT1 exhibited a general decline from suckling to postweaning. The protein expression of PepT1 gradually decreased with age from birth to d 35 in the duodenum, and initially declined from birth to the lowest value then slightly increased with age through d 21, followed by an increase to d 35 in the jejunum and ileum. In conclusion, the gene expression of these brushborder hydrolases and nutrient transporters was not only differentially regulated by age but also differentially distributed along the small intestine of piglets at early stages of life. These differences in ontogenetic regulation and the distribution may be related to the luminal substrate concentration as well as the nutrient categories, and the developmental regulation of these genes may occur not only at the transcriptional level but also at the posttranscriptional level. / Ph. D.

The role of nutrition in providing optimal broiler growth and intestinal health is essential, especially during stress or disease challenge. Feed enzymes are useful for improving performance of poultry, particularly when nutrition, management, or health status is not favorable. The objective of the following experiments was to evaluate the effect of dietary phytic acid (PA) and phytase on the performance and intestinal health of birds that were vaccinated with a live coccidial oocyst vaccine. For each experiment, half of the chicks were spray-vaccinated at day-of-hatch with Coccivac®-B and grown out in floor pens with ad libitum access to diets formulated to meet Cobb nutrient recommendations. In the first experiment, birds were given one of three diets that included different levels of a PA solution to obtain dietary PA levels of 0.74, 0.87, and 1.12% for low, medium, and high PA diets, respectively. In the second experiment, two levels of PA were included to obtain dietary PA levels of 0.75 and 1.05% for low and high PA diets, respectively. In addition, phytase was added over the top to half of the diets at 1000 FTU/kg, resulting in four diets: low PA without phytase, low PA with phytase, high PA without phytase, and high PA with phytase. Live performance parameters including body weight, body weight gain, feed intake, feed conversion, and mortality were measured as well as tibia ash (experiment 2) and indicators of small intestinal health including morphology, apparent ileal amino acid digestibility (IAAD), and pH (experiment 2). The results presented here indicated that giving broilers vaccinated against coccidiosis a medium level of PA was detrimental to feed intake, body weight gain, and it induced necrotic enteritis (P ≤ 0.05). Adding phytase on top of nutritionally adequate diets did not improve performance (P ≥ 0.05), but did improve (P ≤ 0.05) apparent IAAD and morphology of the small intestine, especially in younger birds. In addition, it has been determined that important considerations in diet formulation also can include the phytate: protein as well as calcium: total phosphorus ratios, as these may critically affect how phytate impacts bird health and performance. / Ph. D.

Carolina Rinse (CRS) has been shown to be effective in decreasing vascular permeability and neutrophil infiltration in reperfused equine small intestine. The objective of this study was to show that CRS applied topically and intraluminally could prevent immediate reperfusion injury after low flow ischemia or distention in the equine jejunum. Materials & Methods: Two groups of 5 horses were used to evaluate CRS treatment after low-flow ischemia (Group 1) and intraluminal distention (Group 2) of distal jejunum. Mesenteric blood flow, osmotic reflection coefficient (ORC), wet weight to dry weight ratios (WW/DW), and neutrophil accumulation in the serosa were measured. ORC is defined as the lymph protein concentration to plasma protein concentration ratio subtracted from one (1- Cl / Cp) at maximal lymph flow. The ORC from baseline values and at 60 minutes after initiating reperfusion was compared between Groups 1 and 2. Pair wise comparisons were made for mesenteric blood flow, tissue volume, neutrophil number, and WW/DW proximal control and CRS treated jejunal segments were made using a Mann Whitney U test (P< 0.05). Results: The mean ORC of bowel treated topically and intraluminally with CRS was similar to that recorded in normal bowel or ischemic intestine treated with CRS by arterial perfusion. The ORC after distention and decompression increased and was similar to that reported in untreated intestine. The WW/DW after both ischemia and distention increased compared to the proximal control segments. There was no difference in neutrophil number in either ischemic or distended intestine compared to the proximal control segments. Discussion: Carolina CRS was effective in preventing alterations in microvascular permeability during reperfusion afterischemia but not distention. Neutrophil migration curtailed in both groups suggesting that combined topical and intraluminal application of CRS to ischemic intestine may reduce the acute inflammatory responses during reperfusion thereby decreasing complications after ischemia or distention. / Master of Science

No description available.

Une multitude de voies endocytiques existent à la surface de la membrane plasmique, ce qui conduit à l'endocytose de la majeure partie des membranes ainsi que de leurs protéines associées, des molécules de signalisation, des facteurs de croissance et autres cargos (Smith et al. 2017). Pendant des décennies, la voie majeure dite clathrine dépendante a été la plus étudiée, Cette voie d’endocytose se caractérise par la polymérisation de molécules de clathrine et de protéines adaptatrices au niveau de récepteurs liés à leurs ligands, entrainant la courbure de la membrane, avant sa scission et son endocytose (Smith et al. 2017). Récemment, plusieurs mécanismes alternatifs ont été découverts facilitant l'absorption endocytique des protéines cargo et des récepteurs membranaires, même en l'absence de la voie clathrine dépendante (Mayor et al.2014). Un modèle d'endocytose qui ne requiert pas de clathrine mais à la place des galectines et des glycolipides a été proposé par le groupe de Ludger Johannes (Lakshminarayan et al. 2014). Les galectines sont des lectines qui se lient aux bêta-galactosides et qui, à ce jour, regroupent 15 membres (galectine-1 à galectine-15) chez les mammifères et sont retrouvées dans de nombreux types de cellules et tissus (Leffler et al., 2004). Les galectines sont probablement sécrétées extra-cellulairement par une voie inconnue et non-classique (Hughes, 1999). Les glycosphingolipides (GSL) sont des constituants membranaires ubiquitaires, divisés en fractions neutres ou acides. Le terme GSL s'applique aux composés contenant au moins un monosaccharide et une céramide. Il est à noter que l’enzyme UDP-glucose céramide glucosyltransférase (Ugcg) catalyse l’étape initiale de la biosynthèse de GSLs à base de glycosylcéramides.Notre modèle de travail actuel, impliquant les glycolipides et les lectines, a été qualifié d'hypothèse GL-Lect (Johannes et al. 2016), et préliminairement soutenu par des données expérimentales comme décrit par Lakshminarayan et al. en 2014. Il peut être décrit comme suit:i) le monomère Gal3 se lie aux glycoprotéinesii) Gal3 commence alors à oligomériseriii) Gal3 oligomérisé a la capacité de se lier aux glycosphingolipides, ce qui peut induire la formation de clusters de GSLsiv). Ces clusters Gal3-GSL induisent une invagination de la membrane plasmique, une endocytose des protéines cargo liées à Gal3 et la formation subséquente de CLIC (clathrin-independent carriers ), endosomes pré-précoces.Selon ce modèle, l’oligomère Gal3 est capable de se lier aux GSLs et d’induire une déformation de la membrane de la même manière qu’une autre lectine, la sous-unité pathogène shiga toxine-B (STxB). Par conséquent, les deux processus pourraient être résumés sous la même hypothèse GL-Lect, où GL représente les glycosphingolipides (Gb3 pour STxB et des GSLs non identifiés pour Gal3) et Lect corresponds aux lectines (STxB, Gal3 et éventuellement d'autres). Comprendre si les voies d'internalisation indépendantes de la clathrine, mais dépendantes de la galectine 3, sont conservées, non seulement pour les modèles in vitro mais également in vivo, est un défi majeur dans le domaine du trafic cellulaire.Nous avons caractérisé, pour la première fois, un nouveau mécanisme dans l’intestin facilitant le transport endocytique d’un cargo. Ce mécanisme est conduit par la Galectine 3 et agit dans les entérocytes intestinaux dans le processus analogue de transcytose et dépend des glycosphingolipides. En effet, nous avons découvert que la lactotransferrine (LTF), un cargo de Gal3 que nous avons identifié par Mass spec, dépendait fortement de la Galectine3 pour son endocytose efficace, et des GSLs pour son mode de distribution analogue à la transcytose. Sur la base de ces découvertes dans l'épithélium intestinal de souris, nous avons établi un système modèle in vivo fonctionnel dans lequel le mécanisme endocytique récemment proposé, appelé dans notre laboratoire GL-Lect, a été étudié physiologiquement. / A host of endocytic pathways exist at the surface of eukaryotic cells, which lead to the internalization of the bulk of membranes along with membrane proteins, signaling receptors, growth factors, and other cargoes (Smith et al. 2017). For decades, the clathrin-mediated pathway has been the major well characterized endocytic process where clathrin polymerizes along with the associated adaptor proteins to include ligand-bound receptors, leading to membrane bending, membrane scission, and endocytosis (Smith et al. 2017). Recently, multiple alternative mechanisms have been uncovered which facilitate the endocytic uptake of cargo molecules and membrane receptors even in the absence of clathrin machinery (Mayor et al.2014). A model of endocytosis that doesn’t require clathrin but rather sugar-binding galectins and glycolipids has been proposed by my host laboratory (Lakshminarayan et al. 2014). Galectins constitute a family of beta-galactoside–binding lectins, which to date consists of 15 members in mammals. Galectins are broadly distributed in a variety of cells and tissues (Leffler et al. 2004). They are translocated from the cytosol to the extracellular space by a process of non-classical secretion (Hughes 1999). Glycosphingolipids (GSLs) are ubiquitous membrane constituents that are subdivided in neutral or acidic fractions. The term GSLs applies to compounds that contain at least one monosaccharide and a ceramide. Of note, the enzyme UDP-glucose ceramide glucosyltransferase (Ugcg) catalyzes the initial step for the biosynthesis of glycosylceramide-based GSLs.Our current working model, which involves glycolipids and lectins, was termed the GL-Lect hypothesis (Johannes et al. 2016). It is backed up by experimental data as described in Ref. (Lakshminarayan et al. 2014) and can be described as follows:i) Monomeric Gal3 binds to glycoproteinsii) Gal3 then starts to oligomerizeiii) Oligomerized Gal3 has the capacity to bind to glycosphingolipids and this may induce clustering of GSLsiv) Gal3-GSL cluster are inducing the invagination of the plasma membrane to generate tubular endocytic pits from which clathrin-independent carriers (CLICs, which are pre-early endosomes) are generated.Oligomeric Gal3 is indeed able to bind to GSLs and to induce membrane deformation (Lakshminarayan et al. 2014) in a similar way the pathogenic lectin Shiga toxin-B subunit (STxB) does. Therefore, both processes could be summarized under the same hypothesis, the GL-Lect hypothesis, where GL stands for the glycosphingolipids (Gb3 for STxB and gangliosides for Gal3) and Lect summarizes the lectins (STxB, Gal3 and possibly others as well).Understanding if this clathrin-independent but Gal3-dependent internalization mechanism is conserved not only in vitro model systems but in vivo is a main challenge in the field of trafficking.We characterized for the first time that in the gut a new mechanism facilitates endocytic uptake of cargo. This mechanism is driven by Galectin3 and operates in intestinal enterocytes for transcytosis like process and is glycosphingolipid dependent. Indeed, we have found that the lactotransferrin (LTF), a Gal3 cargo that we have identified by Mass spec, strongly required Gal3 and GSLs for its efficient endocytosis and its transcytosis like distribution pattern, respectively. Based on these findings in mouse intestinal epithelium, we established a functional in vivo model system where the newly proposed endocytic mechanism termed in our lab as GL-Lect, was physiologically investigated.

The effects of intraluminal distention (25 cm H₂O, 120 minutes) and subsequent decompression (60 minutes) on the intramural vascular patterns of the equine small intestine was evaluated in 7 anesthetized horses. The vascular system of experimental and control segments were injected with a blue-colored radiopaque medium for microangiography and histology or a diluted methyl methacrylate (MERCOX CL-2B) for scanning electron microscopy. The distended segments had shortened villi that were separated by expanded crypts and mesothelial cell loss, neutrophil infiltration and edema in the seromuscular layer. The number of filled vessels was decreased in the seromuscular layer and to a lesser extent in the mucosal layer in the distended segments compared to controls. Following reperfusion, the morphologic lesions progressed and the number of observed vessels increased in all layers; however the vascular density did not return to the pre distention state. This study identifies altered intramural vascular patterns in the equine jejunum during luminal distention and reperfusion. / Master of Science