No description available.

Thesis (Ph.D.). / Written for the School of Dietetics and Human Nutrition, Macdonald College of McGill University. Title from title page of PDF (viewed 2008/08/04). Includes bibliographical references.

Thesis (Doctoral)--Department of Internal Medicine, Lund Institute of Technology. / Added t.p. with thesis statement inserted. Includes bibliographical references.

No description available.

Typescript (photocopy). / Digitized by Kansas Correctional Industries

Thesis (MNutr)--University of Stellenbosch, 2008. / Bibliography. Also available via the Internet.

Thesis (M.S.)--Ball State University, 2009. / Title from PDF t.p. (viewed on Dec. 14, 2009). Includes bibliographical references (p. 52-54).

No description available.

The objectives of this research were to determine the impact of 4 different bedtime snack compositions on prevention of nocturnal hypoglycemia and to determine whether optimized titration and delivery of bedtime insulin using multiple daily injections of insulin (MDI) or continuous subcutaneous insulin infusion (CSII) could prevent nocturnal hypoglycemia in the absence of bedtime snacks. We also sought to determine whether 3 months of CSII therapy would improve catecholamine response and symptom awareness to experimentally-induced hypoglycemia. The need for and the most appropriate composition of bedtime snacks were dependent on the glycemic level at bedtime. No bedtime snacks were necessary at bedtime glycemic levels > 10 mmol/L. At bedtime glycemic levels between 7-10 mmol/L , a standard snack and cornstarch-containing snack worked best and at bedtime glycemic levels < 7mmol/L, a standard and protein-rich snack were most effective. Despite optimized titration and delivery of bedtime insulin, including the use of CSII, "the gold standard" of nocturnal insulin replacement, the incidence of nocturnal hypoglycemia over 181 nights was 54 episodes per 100 patientnights. However, there was a substantial reduction, by 36% (p=0.17), in the incidence of nocturnal hypoglycemia with the use of bedtime snacks. Therefore bedtime snacks, tailored to the bedtime glycemic level, are recommended for ail adults undergoing intensive management with MDI or CSII. Although, 3 months of CSII therapy did not improve catecholamine response and symptom awareness to experimentally-induced hypoglycemia, it did not deteriorate the responses either. Therefore, CSII therapy is a viable option in intensive management of adults with type 1 diabetes.

Controversy remains about the contribution of hypoglycemia to brain damage in the newborn. Therefore, the objective of this study was to determine the effects of isolated hypoglycemia on damage to the immature rat brain. Seven-day-old rats, equivalent to a late preterm human newborn, were placed in either Sham or hypoglycemic groups. Hypoglycemia was induced by insulin infusion for variable periods of time. Outcomes were assessed by behavioral, neurochemical and neuropathologic determination. Rats were categorized as having mild, moderate, or severe hypoglycemia. Behavioral tests revealed no abnormality in hypoglycemic animals. Floro-JadeB showed significant damage in the thalamic reticular nucleus (TRN) of the severe hypoglycemic animals at PD9. However, neuronal (Neu-N), astrocytic (GFAP), and myelin (MBP) staining at PD21 showed no brain injury. There was a significant rise in aspartate and arginine, and drop in glutamine and alanine of hypoglycemic brains. Oxidative stress markers were also increased in hypoglycemic brains. We conclude that isolated prolonged severe hypoglycemia caused a transient, region specific increase in neuronal cell death within the TRN. Though transient in nature, the associated neurochemical alterations warrant further research to determine if more subtle long-term effects may result.