Thesis (D. Miss.)--Trinity Evangelical Divinity School, 1994. / Abstract. Includes bibliographical references (leaves 190-198).

L’objectif de ce travail est de développer une approche de type science des surfaces pour étudier l’effet de support sur la genèse et la structure de la phase active des catalyseurs d’hydrotraitement à base de sulfure de molybdène supporté sur alumine, utilisés pour la purification des coupes pétrolières. L’originalité réside dans une approche science des surfaces en solution avec un dépôt du précurseur métallique (molybdates) en phase aqueuse selon deux voies de synthèse (adsorption à l’équilibre et imprégnation) sur des monocristaux d’alumine α (modèle de l’alumine γ) de 4 orientations différentes (C (0001), R "(1" ¯("1" ) "02)" , A "(11" ¯("2" ) "0)" et M "(10" ¯("1" ) "0)" ). La combinaison de techniques (XPS, AFM, MET, EXAFS) a permis de montrer que chaque orientation cristalline gouverne la force des interactions métal-support à l’état oxyde et donc le taux de sulfuration et la taille des particules de la phase sulfure. Cette phase sulfure a ainsi pu être reliée à une phase de type I (interactions métal-support fortes, plus faible sulfurabilité) pour la face R "(1" ¯("1" ) "02)" et de type II (interactions métal-support plus faibles et meilleure sulfurabilité) pour les faces C (0001), A "(11" ¯("2" ) "0)" et M "(10" ¯("1" ) "0)" . Les résultats obtenus sur la face C (0001) par EXAFS suggèrent une orientation majoritairement basale des feuillets de phase sulfure tandis qu’une orientation aléatoire est mise en évidence sur les autres faces. Les analogies structurales établies entre alumine α et γ ont permis de transposer ces résultats au support industriel (γ-Al2O3) pour conclure que le contrôle de la morphologie du support constitue un levier pour maîtriser la genèse de la phase sulfure et améliorer les performances des catalyseurs d’HDT. / The objective of this work was to develop a surface science approach to study the support effect on the genesis and structure of the active phase (molybdenum sulfide) on alumina supported Mo based hydrotreating catalysts supported on alumina which are used for petroleum refining. The originality of the work lies in the aqueous phase metal precursor deposition (molybdates) according to two synthetic routes (equilibrium adsorption and impregnation) on α alumina single crystals (γ alumina surrogate) with 4 different orientations (C (0001), R "(1" ¯("1" ) "02)" , A "(11" ¯("2" ) "0)" and M "(10" ¯("1" ) "0)" ). The combination of several physico-chemical characterization techniques (XPS, AFM, TEM, EXAFS) has shown that the surface structure of each crystal orientation governs the strength of metal/support interaction in the oxide state and thus the sulfidation degree and size of the sulfide active phase nanoparticles. This sulfide phase has been associated to a type I (strong metal/support interactions, lower sulfurability) for the R "(1" ¯("1" ) "02)" plane and to a type II (weaker metal/support interactions and better sulfurability) for C (0001), A "(11" ¯("2" ) "0)" and M "(10" ¯("1" ) "0)" planes. In addition, EXAFS results suggest a predominantly basal orientation of the sulfide phase on the C (0001) plane while a random orientation is highlighted on the other faces. The surface structural analogies between α and γAl2O3 polymorphs allows us to transpose these results to the industrial support (γ-Al2O3) and hence, to conclude that a proper control of the industrial support morphology constitutes a way to tune the genesis of the sulfide phase and improve the performances of hydrotreating catalysts.

The human GI tract has evolved to simultaneously absorb nutrients and be the frontline in host defence. These seemingly mutually exclusive goals are achieved by a single cell thick epithelial barrier, and a complex resident immune system which lives in symbiosis with the intestinal microflora and is also able to rapidly respond to invading pathogens. An immunological balance is therefore required to permit tolerance to the normal intestinal microflora, but also prevent the dissemination of pathogenic micro-organisms to the rest of the host. Inappropriate immune responses in genetically susceptible individuals are the hallmark of human inflammatory bowel disease (IBD) and are thus targeting effector immune cells and their cytokines remains the mainstay of treatment. However despite vigorous efforts to delineate the genetic contribution to IBD disease susceptibility using large multinational cohorts, the majority of disease heritability remains unknown. Epigenetics describes heritable changes in chromatin that are not conferred by DNA sequence. These incorporate changes to histones, chromatin structure and DNA methylation, which confer changes to gene transcription and thus gene expression and cellular function. Methylbinding proteins (MBD) have the ability to bind to methylated DNA and recruit large chromatin remodeling complexes that underpin a variety of epigenetic modifications. Methyl- CpG-binding domain protein 2 (MBD2) is one such MBD that is required for appropriate innate (dendritic cell) and adaptive (T cell) immune function, though its role has not been investigated in the GI tract. We hypothesized that alterations in chromatin are central to the reprogramming of normal gene expression that occurs in disease states. By defining the phenotype of immune cells in the absence of MBDs we hope to understand the mechanisms of chromatin-dysregulation that lead to immune-mediated diseases such as IBD. We therefore aimed to assess the role of MBD2 in colon immune cells in the steady state and in murine models of GI tract inflammation, thereafter identifying the culprit cell types and genes responsible for any observed changes. We envisaged that investigating heritable, epigenetic changes in gene expression that are inherently more amenable to environmental manipulation than our DNA code, may provide novel insight to a poorly understood mechanism of disease predisposition. In addition identifying the cellular and gene targets of Mbd2 mediated changes to immune homeostasis that may provide exciting and novel approaches to therapeutic modulation of pathological inflammatory responses. In chapter 3 we assessed the expression of Mbd2/MBD2 in the murine/human GI tract. Consistent with existing mouse data, levels of Mbd2 mRNA increased between anatomical divisions of small (duodenum, ileum, terminal ileum) and large intestine (caecum, colon, rectum). In addition MBD2 mRNA was greater in the rectum versus ileum, with active IBD associated with lower rectal MBD2 mRNA compared to quiescent IBD controls. Thus we sought to understand the role of Mbd2 in the colon, where mRNA levels were the highest in the GI tract and where appropriate immune function is central to prevent damaging inflammation. To address these aims required the development of existing methods of cell surface marker expression analysis using flow cytometry techniques to simultaneously identify multiple innate and adaptive immune populations. Using naïve Mbd2 deficient mice (Mbd2-/-) we observed CD11b+ CD103+ DCs were significantly reduced in number in Mbd2 deficiency. To understand the role of Mbd2 in colonic inflammation we employed a mouse model of chemical (DSS) and infectious (T. gondii) colitis comparing Mbd2-/- and littermate controls (WT). Mbd2-/- were extremely sensitive to DSS and T. gondii mediated colonic inflammation, characterized by increased symptom score, weight loss and histological score of tissue inflammation (DSS) and increased antibody specific cytokine responses (T. gondii) in Mbd2 deficient animals. Flow cytometry analysis of colon LP cells in both infectious and chemical colitis revealed significant accumulation of monocytes and neutrophils in Mbd2-/-. Indeed monocytes and neutrophils were the principal myeloid sources of IL-1b and TNF in DSS colitis and the number of IL-1b/TNF+ monocytes/neutrophils was significantly greater in Mbd2-/-. Lastly we employed our colon LP isolation techniques to analyse immune populations in active and quiescent IBD and healthy controls, using endoscopically acquired biopsy samples. Analysis revealed that as in murine colitis, active human IBD is characterized by the accumulation of CD14High monocyte-like cells, with an associated increased ratio of macrophage:monocyte-like cells. In Chapter 4 we sought to understand the cellular sources of Mbd2 that may explain the predisposition of Mbd2-/- to colitis. Firstly we restricted Mbd2 deficiency to haematopoietic cells using grafting Mbd2-/- bone marrow (BM) into lethally irradiated WT mice. These animals treated with DSS displayed increased weight loss, symptom score, neutrophil accumulation and histopathology score compared to mice irradiated and grafted with WT BM. Given the accumulation of monocytes in Mbd2-/- DSS treated mice, and existing literature supporting a pathogenic role in this model, we then investigated the role of Mbd2 in monocyte function. Colon monocytes sorted from Mbd2-/- and WT DSS treated mice displayed similar expression for many pro-inflammatory genes (Il6, Il1a, Il1b, Tnf), but demonstrated significantly dysregulated expression for some others (Regb, Lyz1, Ido1, C4a). To investigate this in a more refined model, we lethally irradiated WT mice and repopulated them with a WT:Mbd2-/- BM mix. This enabled the analysis of WT and Mbd2-/- haematopoietic cells in the same animal. Colon WT and Mbd2-/- monocyte recruitment and cytokine production in DSS treated mixed BM chimeras was equivalent between genotypes suggesting that Mbd2 deficiency in monocytes alone did not explain the increased susceptibility of Mbd2-/- to DSS colitis. We then restricted Mbd2 deficiency to CD11c expressing cells, given the known role for Mbd2 in their function, and for CD11c+ cells in DSS, using a CD11cCreMbd2Fl/Fl system. DSS treated mice with Mbd2 deficient CD11c+ cells demonstrated increased weight loss, symptoms score, histolopathology score, monocyte and neutrophil colon accumulation compared to controls. To further explore the role of Mbd2 in colon CD11c+ cells, macrophage and DCs from DSS treated WT and Mbd2-/- mice were purified and their gene expression analysed. Mbd2-/- versus WT macrophages demonstrated significantly altered expression of both pro- (Il1a, C6, Ido1, Trem2) and antiinflammatory (Tgfbi, Retnla) pathways that we hypothesized was a method for attempted host control of excessive colon damage in Mbd2-/- mice. DC gene expression analysis was hampered by small sample size, but demonstrated a large number of small expression changes, including IL-12/IL-23 (Jak2) and autophagy (Lrrk2) pathways. Lastly levels of costimualtory molecules (CD40/CD80) were increased in Mbd2-/- but not CD11cΔMbd2 colon LP DCs/macrophages suggesting that non-CD11c+ cellular sources of Mbd2 were required to produce increased activation phenotype in these cells. Finally in Chapter 5 we explored the role for Mbd2 in non-haematopoietic cells, namely the colonic epithelium. Here we first developed a novel method for identifying and purifying these cells using flow cytometry. Mbd2 deficient colonic epithelium demonstrated increased expression of activation markers MHC II and LY6A/E in the steady state and in DSS / T. muris mediated colonic inflammation. Indeed FACS purified colon epithelial cells from naive and DSS treated, Mbd2-/- and WT mice revealed conserved dysregulated gene expression independent of inflammation: Both naïve and inflamed Mbd2 deficient epithelium displayed significantly increased expression of genes responsible for antigen processing/presentation (MHC I, MHC II, immunoproteasome) and decreased expression of genes involved in cell-cell adhesion (Cldn1, Cldn4). Lastly we investigated whether the observed differences in Mbd2-/- cell types conferred alterations in the makeup of the intestinal microflora. Interestingly independent of co-housing of Mbd2-/- and WT animals, Mbd2 deficiency consistently predicted the microbial composition, with increased levels of Clostridales and decreased levels of Parabacteroides bacteria. Collectively we have identified CD11c+ cells, monocytes and colon epithelial cells as key cell types for Mbd2 mediated changes in gene expression that affect mucosal immune responses. These data thus identify Mbd2 gene targets within these cell types as exciting new areas for investigation and therapeutic modulation to limit damaging GI tract inflammation.

Contrairement aux autres chimiokine, CX3CL1 a la particularité d'exister sous deux formes protéiques fonctionnelles : une forme soluble chimio-attractante impliquée dans le recrutement leucocytaire comme toutes les chimiokines et une forme membranaire qui confère au couple CX3CL1/CX3CR1, une propriété surprenante de molécule d'adhésion participant à l'arrêt et à la transmigration des leucocytes circulants. Le CX3CR1 appartient à la famille des Récepteurs Couplés aux Protéines Gi, c'est-à-dire qu'il inhibe l'enzyme de synthèse de l'AMP cyclique (AMPc), l'adénylate cyclase. L'étude de la cinétique et du rôle du signal AMPc déclenché en aval du CX3CR1, activé par la forme soluble ou membranaire du CX3CL1 font l'objet de ce travail de thèse. La réponse à la forme membranaire est de même amplitude que celle induite par la forme soluble, mais présente une cinétique considérablement ralentie. Ce ralentissement corrèle avec une moindre internalisation du CX3CR1, qui semble être retenu en surface par le ligand membranaire. Un recrutement plus lent des ? arrestines sur le CX3CR1 activé par le CX3CL1 membranaire renforce cette hypothèse d'une internalisation plus tardive du CX3CR1 comparé à une activation par la forme soluble. Le rôle physiologique de l'AMPc a été également exploré sur les deux fonctions principales du couple CX3CL1/CX3CR1 : le chimiotactisme et l'adhésion. Le rôle inhibiteur de l'AMPc sur ces deux fonctions, confirme une action immunosuppressive de ce messager secondaire. Ces résultats indiqueraient que, grâce à leurs réponses AMPc inhibitrices, les cellules activées par les chimiokines seraient sélectionnées pour une réponse efficace en milieu inflammatoire. / CX3CL1 is a particular chemokine which, in contrast to other chemokines exists in two physiological forms: a soluble form is implicated in chemotaxis and cellular migration like all chemokines; whereas a membranous form confers to the CX3CL1/CX3CR1 couple an adhesive role, contributing in particular to the arrest of circulating leukocytes and their migration to the site of inflammation. The CX3CR1 belongs to the family of Receptor Coupled with Proteins Gi (RCPG), which inhibits the enzyme that syntheses cyclic AMP (cAMP), the adenylyl cyclase. The study of the kinetics and the role of the cAMP signal triggered downstream of CX3CR1, activated by soluble or membranous form of the CX3CL1 are the aims of this work of thesis. The response induced by the membranous form has the same amplitude as the one induced by the soluble form, but has a significantly slowed kinetic. This slowdown correlates with less internalization of CX3CR1, which seems to be retained on the surface by the membranous ligand. A slower recruitment of β-arrestin on the CX3CR1-activated by membranous CX3CL1 strengthens the hypothesis of a later internalization of CX3CR1 compared to activation by the soluble form. The physiological role of cAMP was also explored in the two principal functions of the couple CX3CL1 / CX3CR1: chemotaxis and adhesion. The inhibiting effect of cAMP in these two functions confirms an immunosuppressive action of this second messenger. These results indicate that through their inhibitory cAMP responses, cells activated by chemokines are selected for an effective response in the inflammatory conditions.

African American, male, veteran (AAMV) students are not completing their degrees at a local community college. The purpose of this qualitative research study was to examine veteran student perspectives regarding factors that influence community college completion to better understand their unique needs as veteran students. The conceptual framework was Bean and Metzner's model of nontraditional student attrition. The Schlossberg situation, self, support, and strategies transition model served as a foundation to examine each veteran student's personal experience of navigating available community college services to reach their educational goals. Data were collected from interviews with 10 AAMV students. Interview transcripts were coded, and an inductive data analysis was used to develop the study findings and identify emerging themes. The findings highlight veteran student service progress, identify challenges, and make recommendations for an overview of the key results of the data analysis. The project was an executive summary that addresses the experience of AAMV community college students who are not completing their degrees based on the data analysis of the research. The findings of this study may influence social change by helping veterans have a better understanding of resources and support that are needed to assist them in completing their community college degree. The results also provide information that may assist academic leaders in identifying ways to support AAMV students successfully complete their community college degrees.

No description available.

Benefits for soldiers follow the formation of ancient and present day armies raised for the purpose of extending the national or state will. Veterans' benefits for defenders of the U.S. emerged during the American colonial period. College benefits began after WWII with the GI Bill of Rights. This study examines the variations in purpose for nationally established educational benefits for veterans and the singular value to the veterans of these 5educational benefits. The study begins with an overview of the history of veterans' benefits. Primary emphasis is then placed on the educational portion of the World War II Servicemen's Readjustment Act and the current educational benefit, the Montgomery GI Bill. As the purpose of awarding educational benefits changed from World War II to the latest U.S. war, the Gulf War of 1990-1991, the economic value to the individual veteran also changed. The WWII GI Bill featured an educational provision intended to keep returning veterans out of the changing economy whereas current GI Bills is intended as a recruiting incentive for an all-volunteer force. Correspondingly, the economic value to the individual veteran has changed. Data supporting this study were extracted from historical documents in primary and secondary scholarly studies and writings, government documents, national newspapers and periodicals, Veterans Administration publications, service newspapers, and anecdotal writings. The study offers conclusions regarding the shifting purposes and economic value and recommends changes to current and future GI Bills. The conclusions of this study are: (a) the purpose of the Montgomery GI Bill is to serve as a recruitment tool for the armed force, whereas the WWII GI Bill emphasized concern over the return of millions of veterans to a changing wartime economy unable to offer full employment and, (b) the present GI Bill funds less than 50% of the costs for a 4-year degree while the first GI Bill fully funded a college degree, including tuition and living expenses.

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No description available.

In patients with a functional gastrointestinal (GI) tract, enteral feeding is preferred over parenteral feeding as it has fewer complications and a relatively lower cost. Nasogastric and nasoenteric feeding tubes are available options but when long-term enteral feeding is desired, a percutaneous endoscopic gastrostomy (PEG) tube is more convenient. PEG tube can be associated with multiple complications; however, its displacement which causes gastric outlet obstruction (GOO) is a rare one. Here we present a case of an 81-year-old woman with dementia who presented with upper GI bleeding and was found to have GOO causing reflux esophagitis due to PEG tube displacement.