Although there is abundant scientific information regarding vitamin E and selenium deficiency disease in domestic poultry, there is only scant information on exotic species, such as ratites. Several necropsy cases involving ostriches, emus and rheas were presented to the Oregon State University Veterinary Diagnostic Laboratory with gross and/or histologic lesions of degenerative myopathy. Investigation of these cases led to determination of tissue levels of vitamin E and selenium and to determination of the dietary levels of these same substances. A small group of emus with a post-mortem diagnosis of degenerative myopathy was supplemented with dietary vitamin E with excellent clinical results. This success prompted a survey of vitamin E and selenium levels in blood and feed from clinically normal ratites. This information was then used to make recommendations for dietary levels of vitamin E and selenium in ratite formulated diets. Since overzealous supplementation can result in selenium toxicosis in birds, a safe, but effective level of dietary selenium and vitamin E is necessary for optimal propagation of the various ratites species. / Graduation date: 1998

The present study was performed to determine whether ongoing oxidative stress in some BPD infants contributes to their increased energy expenditure leading to growth failure. The study consisted of two parts. The first is a descriptive census of BPD infants (n = 38) followed at the outpatient clinics at The Montreal Children's Hospital (MCH). The second is a cross-sectional study of fifteen patients wherein anthropometric parameters, energy intake, and oxidative stress measures (red cell glutathione (GSH) and plasma malondialdehyde (MDA)) were assessed. Nine infants with growth failure were compared to six thriving infants with respect to their nutritional and oxidative stress status. Growth failure was defined as weight for age and weight for height for age less than the tenth percentile (z score $ leq - 1).$ Results revealed that the prevalence of growth failure in the BPD infants followed at MCH ranged between 45% and 55%. The mean ($ pm$ SD) energy intakes for thriving and failing to thrive infants expressed as a percent of the recommended nutrient intake were 104 $ pm$ 46% and 133 $ pm$ 35% respectively. Six infants had reduced mean ($ pm$ SD) blood glutathione per hemoglobin (3.63 $ pm$ 0.37 umol/g) compared to adult controls (6.57 $ pm$ 1.04 umol/g). Four of the six infants had growth failure while two were thriving. Fourteen Infants including all failing to thrive infants had elevated mean ($ pm$ SD) plasma MDA levels compared to adult controls (129 $ pm$ 48 vs 55 $ pm$ 3 nmol/l). Differences in oxidative stress markers were not observed between the two groups. These results suggest that growth failure is associated with an increase in caloric consumption and not with a decrease in caloric intake. The preliminary findings on oxidative stress markers suggest a depletion of the GSH antioxidant in some infants and marked lipid peroxidation in the BPD population.

Motivation and study design: Iron deficiency is a common condition in infancy, particularly in lower socio-economic groups. In Cape Town it remains a problem in spite of public health measures taken against it: a recent survey found a prevalence of iron deficiency anaemia of 34% in healthy 1-year old term infants who had ready access to a municipal health clinic where iron fortified milk formula is sold at subsidized prices. The consequences of iron deficiency extend beyond anaemia- to involve all organ systems including the immune system. Since Helen Mackay's report in 1928 of a striking decrease in incidents of infection in infants treated with iron, clinicians have assumed that iron deficiency predisposes to infection. Despite a sound theoretical basis for this belief, the clinical evidence for the assumption is poor as studies to date have displayed methodological deficiencies. On the other hand, iron is also essential for the growth of micro-organisms. As such, supplemental iron may predispose to infection. Indeed, there is much laboratory and clinical evidence to show that excess iron can result in the recrudescence of quiescent infections and increase the virulence of newly acquired infections. Thus, the competition between host and parasite may sometimes hinge on the relative availability of iron and it has been speculated that excess iron in infant milk formula may increase susceptibility to infectious diarrhoeal disease. The problem addressed by this thesis was to determine the utility of increasing the level of iron fortification of infant milk formula. Three questions were posed: Does increasing the level of iron fortification of conventional infant milk formula improve the iron nutrition of normal infants fed on the formula? Does increased iron fortification of infant milk formula alter immunity as reflected by incidence of infection and laboratory tests of immune function? Are there any handful effects of increasing the quantity of iron in conventional infant milk formula? A double blind randomized trial was carried out in 1983 and 1984 to answer these questions. A group of 149 healthy, well-nourished infants from a lower socio-economic community of so called Cape Coloureds were followed from the age of 3 months to 1 year. Half of the infants, the Control group, were given a commercially available infant milk formula (Lactogen Full Protein) which has 8.3 mg Fe/ 100 g formula and 37 mg ascorbic acid/ 100 g. The other half of subjects, the Test group, were given the same milk formula but fortified with iron to a concentration of 40 mg Fe/ 100 g. The children were examined every 3 or 4 weeks and any infection or history of infection was noted. Laboratory tests were done at the start of the trial and again on completion. During the trial, laboratory tests were performed only if clinically indicated. The tests included full blood count and differential analysis, red cell zinc protoporphyrin, plasma ferritin, plasma and hair zinc and lymphocyte subtyping with monoclonal antibodies. Within each group, half of the infants were randomly selected for assay of neutrophil bactericidal activity. The other half were assayed for lymphocyte blastogenic response to stimulation with phytohaemagglutinin. Tests of delayed cutaneous hypersensitivity to Candida antigen and PPD were done and all children and their mothers had antibodies to tetanus and polio determined. Results: 74 infants in the Control group started the trial and 62 completed it. In the Test group, 75 infants began and 70 completed the study. Intake of milk and solid foods was not quantified, but the ages of weaning and of introduction of new foods were determined. The Control and Test groups did not differ significantly on any test item. The mean age of completion of weaning was 3.60 months for the Control group and 4.04 months for the Test group. The Control group was first given meat or fish at a mean age of 5.19 months; the Test. group had meat or fish introduced to their diets at a mean age of 4.36 months. These differences were not statistically significant. The children in the Control group were lighter and shorter than the Test group at the end of the year. Mean standard deviation scores for weight were 0.23 and 0.48 respectively (P = 20%), while for length the SD scores were -0.13 and 0.06 (P = 20%).

No description available.

Call number: LD2668 .T4 1954 B5 / Master of Science

The statistical correlations between habitual diet and plasma risk factors for coronary heart disease CHD were analyzed using multiple regression. Thirty-one male subjects between 30-56 years kept complete dietary records for 7 days. Daily means of nutrient consumption were calculated using a computerized data base. Fourteen independent variables (total kilocalories, protein %, carbohydrate %, fat %, ethanol %, caffeine, P/S ratio, cholesterol, age, weight, height , weight**.75, Body Mass Index, kilocalories/weight**.75) were created. Plasma samples were analyzed and the following simple (total plasma cholesterol (TC), VLDL-C, LDL-C, HDL2-C, HDL3-C, apo A-I, apo A-II, apo B) and derived (VLDL-C+LDL-C, LDL-C/TC, LDL-C/HDL-C, HDL-C, HDL2-C/HDL3-C, HDL-C/TC, apo B/apo A-I, apo B/apo A-II, apo A-Il/apo A-I) dependent variables were created. Dependent variables were individually regressed against the entire set of independent variables. An F-value of 4.00 to enter an independent variable in the model and of 3.99 to remove one were used to achieve significance of p<05. Age appeared in 5 regression models (TC, apo B, apo B/apo A-I, apo B/apo A-II, apo A-Il/apo A-I) and was positively correlated with increased risk for CHD. Total kilocalories appeared in 4 models (LDL-C, apo B, VLDL-C+LDL-C, LDL/TC) and was negatively correlated with risk. Fat % appeared in 4 models (VLDL-C+LDL-C, LDL/TC, LDL-C/HDL-C, HDL-C/TC) and was associated with increased risk. Body Mass Index was entered in 2 models (HDL2-C, HDL-C) and was positively correlated with risk. P/S ratio was negatively correlated with risk in the three models (HDL2, apo A-I, HDL-C) in which it appeared. The independent variable carbohydrate % was negatively associated with risk in 2 models, LDL-C and apo B. Kcal/wt**.75 was also negatively correlated with risk in the VLDL-C, LDL-C/TC and HDL-C/TC models. One independent variable, EtOH %, was positively associated with risk in the apo A-II and apo A-II/apo A-I models. Two dependent variables did not have any independent predictors (HDL3-C, HDL2-C/HDL3-C) entered in their regression models. Six independent variables did not appear in any regression model (protein %, caffeine, cholesterol, weight, height, weight**.75). Independent variables positively correlated with increased risk for CHD were therefore fat %, ethanol %, age, and Body Mass Index. Independent variables correlated with decreased risk for CHD were total kilocalories, carbohydrate %, P/S ratio, and kilocalories/weight**.75. / Graduation date: 1985

No description available.

Typescript (photocopy). / Digitized by Kansas Correctional Industries

Typescript (photocopy). / Digitized by Kansas Correctional Industries

Bibliography: leaves 204-215. / xviii, 215, [14] leaves : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / This study investigates the food consumption of overweight women over three menstrual cycles within a randomised double blind placebo controlled design. The aims of the study were: 1) to determine whether women identified as exhibiting PMS symptoms including increased appetite, have a preference for carbohydrate; 2) to determine if low brain levels of serotonin are involved in contributing to increased carbohydrate intake, and whether increasing the availablility of serotonin by using dexfenfluramine reduces total food intake or solely selectively reduces carbohydrate intake in women with PMS; 3) to determine whether there is a link between changes in food consumption, and the severuty of PMS symptoms. / Thesis (Ph.D.)--University of Adelaide, Dept. of General Practice, 2003