An Evaluation of the Inhibitory Action of 4-Tertiary-Butyl-Pyrocatechol on Aerobacter Aerogenes, Bacillus Megaterium and Pseudomonas Fluorenscens and a Soil Isolate

vii, 67 p.The topic for this thesis developed from exploratory work undertaken during a six month experimental work period at the Biochemical Research Laboratory, The Dow Chemical Company, Midland, Michigan. As an assistant to Dr. William H. Riley, a microbiologist and biochemist in the laboratory, the author studied the effects of 4-tertiary-butyl-pyrocatechol on soil microflora. This experience gave him an appreciation of the time required to formulate and complete a research project. Fortunately, he was able to return to the laboratory to write his senior thesis on a comparison of the inhibitory effects of TBC on bacteria

The Effects Of Hypophysectomy On The Digestive Glands Of The Mouse.

PhDAnatomy & physiologyUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/184456/2/6701761.pd

Gluconeogenesis And Fatty Acid Oxidation In Chick Embryo Liver.

PhDAnatomy & physiologyAnimalsUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/188579/2/7021701.pd

Studies on the control of fatty acid oxidation in liver preparations from chick embryos

The characteristics and developmental pattern of the metabolic pathway for fatty acid oxidation were investigated in liver slices and mitochondria prepared from chick embryos of varying ages. In 8-day-old chick embryos, hepatic fatty acid oxidation was readily measurable. The incorporation of labelled palmitate into CO2 was increased twofold by carnitine in liver slices of 8-day-old chick embryos but by nearly sixfold to tenfold in tissues prepared from 10- or 12-day-old embryos. A similar increase was seen in the degree of augmentation of ketogenesis induced by carnitine in liver slices prepared from the 10-day-old embryo, suggesting an increased carnitine palmitoyltransferase activity in liver cells during the stage of development from 8 to 10 days. Palmitoyl-CoA was not metabolized in the absence of carnitine, whereas the palmitoyl portion of palmitoylcarnitine readily supported respiration by embryonic chick liver mitochondria. In the presence of adequate amounts of albumin, good respiratory control was evident.The administration of glucose to chick eggs which had previously been incubated for approximately 4.5 days resulted in changes in the metabolism of embryos killed 5 days later, which indicated that tissues of the chick embryo were capable of integrative metabolic adaptations in response to changes in substrate supply. </jats:p

Glucoregulation during insulin and glucagon deficiency: role of catecholamines

Glucose production decreases markedly following acute reduction in insulin and glucagon secretion (induced by somatostatin). After about an hour, however, glucose production is restored nearly to basal rates. To study the mechanism by which this occurs, islet hormone deficiency was superimposed on beta-adrenergic blockade. It was found that the hypoglycemia that accompanies insulin and glucagon deficiency is an adequate stimulus for catecholamine secretion. During combined hormone deficiency and beta-blockade, glucose production fell and remained very low for 2-3 h. This resulted in a profound hypoglycemia (glucose less than 30 mg/dl). We conclude from these studies that restoration of glucose production during sustained insulin and glucagon deficiency is not attributable to a) onset of insulin deficiency because insulin is equally depressed in both experimental settings, b) glucose autoregulation even though adequate substrate is available, or c) an alpha-adrenergic mechanism because plasma catecholamines were very high and alpha-receptors were not blocked. Rather, the glucose counterregulation during insulin and glucagon deficiency must be heavily dependent on a beta-adrenergic mechanism. </jats:p