Thesis (M. Sc.)--York University, 2000. Graduate Programme in Biology. / Typescript. Includes bibliographical references (leaves 111-119). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://wwwlib.umi.com/cr/yorku/fullcit?pMQ59179.

Thesis (Ph. D.)--University of Washington, 1997. / Vita. Includes bibliographical references (leaves 171-191).

Thesis (doctoral)--Amsterdam, 1981.

No description available.

INTRODUCTION: Small intestinal bacterial overgrowth refers to the proliferation of abnormal numbers and types of microorganisms in the lumen of the proximal bowel. Bacterial overgrowth has been implicated as a possible factor in prolonging some episodes of infantile gastroenteritis. This thesis examines 2 different aspects of the duodenal flora of infants with gastroenteritis, and has therefore been divided into 2 separate studies. CARBOHYDRATE STUDY: Objective: To test the hypothesis that during a diarrhoeal episode the presence of malabsorbed carbohydrate in the duodenal lumen acts as a factor promoting bacterial proliferation. Patients and methods: Infants admitted to the rehydration ward with acute gastroenteritis were selected for study if they fulfilled various criteria in terms of age, nutritional status, previous diarrhoeal episodes and antibiotic administration. They were admitted to the research ward. Weights were measured and if they had severe diarrhoea (≥ 30g/kg) were included in the study. Twenty patients were entered into the study. On admission into the trial the first duodenal intubation was done to measure the duodenal flora quantitatively and qualitatively. Thereafter the patients were assigned on an alternate basis to one of 2 groups. One group (carbohydrate-containing group) received a soy-based infant formula containing carbohydrates (Isomil, Ross). The other group (carbohydrate-free group) received an identical milk but from which all carbohydrate had been omitted (Ross CHO-free). To these infants carbohydrate was given intravenously. Stool output was measured daily. After 3 days of the respective diets the duodenal flora was re-examined. Results: Longitudinal analysis of the duodenal flora of the carbohydrate-containing group showed a small decrease in the number of bacterial isolates and in their magnitude. The duodenal flora of the carbohydrate-free group was virtually unchanged. Comparing the duodenal bacteriology of the groups the only significant difference was that the number of isolates and the magnitude of Haemophilus was greater in the carbohydrate-free group- (p < 0.05). The diarrhoea resolved in 5 patients: 2 in the carbohydrate-containing and 3 in the carbohydrate-free group. Conclusions: The lack of difference in the response of the duodenal flora between the two groups studied suggests that the presence of carbohydrates in the lumen is not important in encouraging the growth of bacteria in that site. The possible causes for an increase in Haemophilus numbers in the carbohydrate-free group are discussed. BOWEL COCKTAIL STUDY: Objective: Small intestinal bacterial overgrowth has been proposed as a cause of progression of acute diarrhoeal episodes to persistence. The "bowel cocktail", a combination of oral gentamicin and cholestyramine, has been shown to be effective in terminating episodes of persistent diarrhoea. It has been postulated to work by eradicating small intestinal bacterial overgrowth, but its mode of action is not known. The objective of this study was to examine the changes in the duodenal flora associated with administration of the bowel cocktail in order to elucidate its possible mechanism or mechanisms of action. Patients and methods: The study group comprised 15 patients. Fourteen were infants from the carbohydrate study who had ongoing diarrhoea. The remaining infant (the "late entry") was selected from the rehydration ward. Severe diarrhoea, as defined by a stool output equal to or greater than 30g/kg/day, was a pre-requisite for entry into the study. The investigation involved 2 duodenal intubations for microbiological analysis of the duodenal fluid. After the first intubation (which was the second intubation for the 14 infants who had been in the carbohydrate study) the bowel cocktail was administered. This comprised a 3-day course of oral gentamicin and 5 days of oral cholestyramine. Forty-eight hours after the start of therapy the duodenal bacteriology was repeated. The patient management was the same as during the carbohydrate study and the feeding regimen of the infants was not altered. The study ended immediately after completion of the bowel cocktail course. Results: Administration of the bowel cocktail was associated with a decreased stool output in all patients. Bacteriological analysis of the duodenal flora after this treatment showed a statistically significant decrease in the total microbial count, the aerobic microbial fraction and the Enterobacteriaceal fraction. On analysis of the bacterial genera a significant decrease was noted in Neisseria, Haemophilus, and aerobic lactobacilli. Analysis of individual patients' duodenal fluid bacteriology in conjunction with the stool bacteriology results before administration of the bowel cocktail often provided an explanation as to the possible aetiology of the diarrhoea and its resolution by therapy. Conclusions: Small intestinal bacterial overgrowth, in the accepted sense of a luxuriant flora teeming with faecal organisms, did not appear to be a feature of the patients in this study. The total bacterial count was only slightly above the accepted upper limit of normal. Although the decrease in the number of Enterobacteriaceae could possibly be interpreted in the context of bacterial overgrowth, a study of the individual patients' duodenal flora shows that these microorganisms were more likely to be acting as specific enteric pathogens. It is concluded that small intestinal bacterial overgrowth, as currently defined, is not an important cause of persistent diarrhoea. The efficacy of the bowel cocktail is more likely to reside in its ability to eradicate specific enteric pathogens. The author ends by questioning the validity of the whole concept of small intestinal bacterial overgrowth.

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The characteristic loops of the small intestine arise during embryonic development from differential growth as the intestinal tube elongates against the constraint of its attached dorsal mesentery, which compresses the tube until it buckles into loops. The number and shape of loops are conserved for a given species and are predictable from tube and mesentery geometries and stiffnesses. Importantly, the mesentery readily accommodates a certain amount of stretch from the elongating tube before stiffening by several orders of magnitude and resisting further extension—thereby dictating how differential growth translates into buckling forces. While such constitutive nonlinearity is well appreciated in adult soft tissues, its determinants and consequences remain largely unexplored in buckling morphogenesis and embryogenesis as a whole. In this work, we undertake to establish a mechanistic link between molecular control of cell behaviors and organ-scale buckling morphogenesis of the small intestine. Using pharmacological treatments, mechanical testing, image analysis of tissue microstructure, and computational modeling, we test the hypothesis that actomyosin contractility regulates mesentery constitutive nonlinearity and thereby organ-scale buckling of the small intestine through its effects on extracellular matrix recruitment. Our findings suggest that highly contractile cells could act as a mechanical ‘clutch’, modulating the stiffening transition of the mesentery by compacting stiff matrix fibers that must be decompressed by applied forces before contributing to stretch resistance. However, we also find that low levels of contractility control the initial soft response of the mesentery through a mechanism largely independent of matrix fiber straightness and alignment. Despite the apparent simplicity of buckling from a mechanical standpoint, its underlying biological determinants are evidently quite complex. The present study begins to unpack those intricate links between the molecular and biophysical aspects of buckling morphogenesis by revealing how cell forces and matrix organization interactively dictate tissue-scale mechanics during development in sometimes counterintuitive ways.

published_or_final_version / abstract / Surgery / Doctoral / Doctor of Philosophy

Thesis (Ph. D.)--University of Hong Kong, 2006. / Title proper from title frame. Also available in printed format.

Thesis (Ph. D.)--University of Missouri--Columbia, 2001. / "May 2001." Typescript. Vita. Includes bibliographical references (leaves 168-199). Also available on the Internet.