Thesis (doctoral)--Umeå University, Sweden, 1995. / Added t.p. with thesis statement inserted. Includes bibliographical references.

Thesis (Ph.D.) - University of Glasgow, 1999. / Ph.D. submitted to the Faculty of Medicine, Department of Human Nutrition, University of Glasgow, 1999. Print version also available.

Thesis (Ph. D.)--Göteborg University, 2000. / Includes bibliographical references.

Thesis (M.S.)--University of Wisconsin--Madison. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 37-42).

Thesis (doctoral)--Umeå University, Sweden, 1995. / Added t.p. with thesis statement inserted. Includes bibliographical references.

Thesis (M.S.) in Food Science and Human Nutrition--University of Maine, 2005. / Includes vita. Includes bibliographical references (leaves 108-118).

From November 2001 through to March 2002, 100 boys and 108 girls, aged 12.0 ± 0.8 years were assessed for coronary heart disease (CHD) risk factors. Rural (school 1) and valley (school 2) comprehensive schools (age range 11 to 18 years) were selected to represent differing socio-economic status (SES). Informed written consent was sought from head teachers, parents, and schoolchildren. All measurements were made in the subjects' respective schools, with the author making a total of 60 visits to these schools. Tests were carried out at the same relative time intervals and by an identical team of researchers. Physical and physiological measurements included stature (m), body mass (kg), body mass index (BMI) (kg m'2), skinfold measurements (£ SKF) (mm), waist to hip ratio (WHR), aerobic fitness (20 MST) (shuttles), systolic (SBP) (mm Hg) and diastolic blood pressure (DBF) (mm Hg). Total cholesterol (TC) (mmol-L' 1 ), high density lipoprotein-cholesterol (HDL-C) (mmol-L" 1 ), low density lipoprotein-cholesterol (LDL-C) (mmol-L" 1 ), TC: HDL-C, triglyceride (TG) (mmol-L' 1 ), lipoprotein(a) (Lp(a)) (mg-dL'1), glucose (Glu) (mmol-L' 1), fibrinogen (Fg) (mg-dL" 1), folate (ng-mL"1 ), vitamin Bn (pmol-L' 1), and homocyst(e)ine (Hey) (umol-L" 1 ) were measured for haematological concentrations. Lifestyle assessments included dietary and physical activity analysis. Familial risk of coronary heart disease was also determined. Blood analyses were conducted at the Biochemistry Laboratories of the Royal Glamorgan Hospital, Llamtisant, and Llandough Hospital, Penarth.

The possibility that loss of intestinal motility occurs as a result of potassium or sodium depletion has been investigated. A new technique, based on the passage of a solution containing the dye, gentian violet, was developed for estimating upper bowel motility. Lower bowel motility was not objectively studied. The sodium and potassium content of various portions of the gut from rats on a low sodium, low potassium diet and on a high sodium, low potassium diet have been determined and compared with that of similar portions of the gut of animals on a control diet. The possibility that excess adrenal cortical or medullary hormones may cause or permit electrolyte and motility changes has been studied. The response to dietary potassium restriction in the presence of a high sodium intake were also determined after adrenalectomy, both with and without medullory or cortical hormonal supplementation. The electrolyte pattern of plasma liver and of skeletal muscle from different portions of the body were analysed and compared in order to aid in understanding the overall electrolyte shifts. Analyses of the selected tissues of the body indicated that initial electrolyte concentrations and responses to diets and hormones vary within similar tissues as well as between different organs. It was not possible to correlate alterations in the gastro-intestinal tract content of sodium and/or potassium with changes in motility. Dietary potassium deprivation led to depletion of potassium only in plasma, skeletal muscle and certain portions of the gastro-intestinal tract in intact animals. This effect was prevented by adrenalectomy. Evidence is presented that cortisone can influence the electrolytes of the body by acting in the cells of peripheral tissues as well as on the kidney and that the high dose administered (4 mgm/day) had direct dietary potassium deficiency actions in addition to permitting depletion to occur in the presence of certain tissues. The hypothesis that excess adrenal cortical hormones cause intestinal immotility through loss of potassium or a gain of sodium in this tissue was not confirmed by the data. Evidence is presented indicating that adrenalin can partially restore the ability to excrete potassium and the ability of tissues to undergo potassium depletion in adrenalectomized animals on a potassium deficient diet. It does not correct the electrolyte levels in adrenalectomized animals on a control diets The possibility that adrenalin may play some role in maintaining electrolyte homeostatis is discussed. / Medicine, Faculty of / Anesthesiology, Pharmacology and Therapeutics, Department of / Graduate

Catherine Foy Walters / Typescript / M.S. Florida State College for Women 1934 / Includes bibliographical references

Typescript / M.S. Florida State College for Women / Includes bibliographical references