The fatty acid composition of whole tissue and plasma membrane fractions of mammary adenocarcinomas and normal mammary glands excised from Strong A female mice fed a 15% safflower oil and 15% tallow diets were studied. Previous work has indicated that high fat diets in general and high unsaturated fat diets in particular, influenced tumorigenesis. The mechanism is not clear. Alternig the normal composition and structure of the plasma membrane can result in altered physiological responses.The fatty acid composition of the dietary fat used in this study affected the fatty acid distribution of mammary gland tissue to a greater degree than tumor tissue. Tumor tissue had almost twice the percentage of linoleic acid as normal tissues (17.0% vs. 9.2%). Oleic acid was also elevated in tumor tissue (24.5% vs. 10.9). The normal tissues contained significantly higher proportions of eicosatrienoic acids (13.5%, 12.2%) than did tumorous tissues, regardless of diet (5.8%, 1.1%). It may be that some of these prostaglandin-active fatty acids in tumorous tissues have been diverted into prostaglandin synthesis.Results of this study indicate that the effect of dietary fat on plasma membranes of tumor cells and normal mammary gland cells was minimal. The saturated or unsaturated state of the fatty acids in the diet appear to play a role in the genesis of tumors by changing the availability of linoleic acid and other prostaglandinactive fatty acids.

The purpose of this study was to determine the substrate (malonate or acetate) used to elongate palmitic acid to stearic acid by Aspergillus niger.

This study was developed from the original protocol which was to examine the role of long chain polyunsaturated fatty acids (LCPUFA) in the maturation of the auditory system in the preterm infant. The particular dietary components under investigation were arachidonic (AA) and docosahexaneoic( DHA) acids. This study investigates the wider aspects and implications of the preterm birth on the maturation of the preterm auditory system. Testing was performed using Auditory brainstem response (ABR) on preterm infants in Hillingdon Hospital's neonatal intensive care unit (NICU). The recruitment criteria was <32 weeks gestational age (GA) or <1500g. A normative data set was produced using term infants (3742 weeks GA). Tympanometric testing was also introduced to assess middle ear (ME) function in both preterm and term infants. The susceptance and conductance components were recorded at frequencies between 226 and 2000Hz. This testing enabled normative data to be established for multi-component, multi-frequency tympanometric analysis. The effect of the preterm birth on tympanometric data was also examined. A total of 22 preterm infants were recruited onto the study. The maturational characteristics of ABR parameters relating to neural transmission and synaptic efficacy were investigated. The peripheral auditory system (PAS) and the lower brainstem region were found to have maturation in their neural transmission properties. The auditory nerve, however, displays constant neural transmission properties throughout the preterm period. Maturation of the synaptic efficacy (using the rate effect) of the PAS was not identified. However, both auditory nerve and lower brainstem regions display reductions in the rate effect. This was greatest in the auditory nerve. The effect of the preterm birth was assessed. The PAS showed lesser conductive properties for the preterm infant during the term period. This behaviour was confirmed by poor tympanometric data for the preterm infants. The auditory nerve showed the same transmission properties for both term and preterm infants. This indicates that the lack of maturation in this region is replicating the characteristics of the term infant developing in utero. The lower brainstem region would seem to be the most susceptible to delayed development in the preterm infant. The rate effect for the PAS and auditory nerve indicate that the extra-uterine environment has not been detrimental to the maturation of synaptic efficacy as measured by the rate effect. The lower brainstem region rate effect is slightly higher for the preterm infants. This may indicate that this region is the most susceptible to possible synaptic deficiency. There is indication of a gender effect for transmission properties in the preterm infant. This suggests superior properties for females in the central auditory system. It is possible that this also occurs on a synaptic level. Dietary analysis suggested that the preterm infants (on this study) fed formula milk enriched with a LCPUFA composition have comparable auditory function (as measured by ABR) with breastfed infants. It is concluded that breastmilk would be the diet of choice due to the additional medical benefits. Tympanometry was found to be well tolerated in both term and preterm neonate populations. Testing in enclosed style incubators in the NICU was successful. Normative characteristics for multi-component tympanornetry at various frequencies was established. The ear canal acoustic and mechanical properties were identified as a source of variability for tympanogram morphology in the neonate populations. The interaction of the neonate external auditory meatus (EAM) violates assumptions relating to numerical data. A lack of maturation was found for preteen data, there was no evolution to the normative term data over the period studied. The more complex nature of the preterm tympanometric data was still observed during the term period. This indicates that there is a difference between the maturational characteristics of the term infant and those for the preterm infant in the clinical environment. The PAS ABR characteristics were compared with tympanometric data collected from the preterm infants. The lack of maturation in the tympanometric data suggests that the major contribution to the ABR maturation during the preterm period is due to the cochlear transduction and basic synaptic delay components. In addition, that poorer ME function (as displayed in the tympanometric data) contributes to the lesser PAS ABR conductive properties in the preterm population by the term period.

No description available.

Graduation date: 1970

Bibliography: leaves 186-193 / vi, 193 leaves ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Organic Chemistry, 1991

Obesity and type 2 diabetes are the most prevalent metabolic diseases in the western world and affect over 50% of the world’s population. During obesity non-adipose tissues such as the liver and skeletal muscle take up and store excess fatty acids (FA) as lipids such as triacylglycerols (TAG) and diacylglycerols (DAG). Excessive lipid storage in non-adipose tissues can result in the dysfunction of cellular processes and lead to programmed cell death (apoptosis). Lipid-induced apoptosis was investigated in the key glucoregulatory tissues, the liver and skeletal muscle. Lipid-induced apoptosis was detected in vitro in both hepatocytes and myotubes but was not detected in the livers or skeletal muscles of genetically obese mice or high-fat fed mice. Further investigation discovered despite exacerbated TAG accumulation, endoplasmic reticulum stress (ER) was not activated in the liver and pathways of cellular remodelling (proteolysis and autophagy) were not initiated in skeletal muscle. These studies demonstrated that the liver and skeletal muscle are adaptable to increased lipid storage in physiological models but not isolated cell culture systems. In vitro experiments demonstrated unsaturated FAs could protect hepatocytes from lipoapoptosis and it has been suggested this is due to driving FA accumulation into TAG lipid droplets. Adipose triglyceride lipase (ATGL) is one of the primary TAG lipases. To explore TAG metabolism in the liver, primary hepatocytes were derived from ATGL null mice and ATGL was over-expressed in the livers of chronically obese mice. / It was found that cellular FA uptake and TAG esterification was increased and TAG lipolysis and FA oxidation were decreased in the ATGL null hepatocytes. This resulted in exacerbated TAG and diacylglycerol (DAG) storage. The gene expression of metabolic regulators such as cytochrome c oxidase subunit 2 (COX2), medium chain acyl Co-A dehydrogenase (MCAD), peroxisome proliferators-activated receptor co-activator 1! (PGC1!), nuclear respiratory factor 1 (NRF1) and FA translocase/cluster of differentiation 36 (FAT/CD36) were increased in ATGL null hepatocytes compared with wild type hepatocytes, suggesting that the reduction in FA oxidation in the ATGL null hepatocytes was probably due to limited FA substrate availability. Interestingly, despite increased TAG and DAG, the hepatocytes remained insulin sensitive. To investigate hepatic ATGL over-expression an adenovirus containing an ATGL insert was injected into chronic high fat fed mice. Hepatic ATGL over-expression in the iii chronically obese mice reduced TAG, DAG and ceramide content in the liver. This resulted in improved hepatic insulin signalling and whole body insulin sensitivity. In summary, studies from this thesis suggested the use of in vitro systems are not a substitute for in vivo models when assessing the toxic effects of lipid oversupply, TAG accumulation may be a protective mechanism against cellular remodelling and programmed cell death, and increased ATGL expression in the liver can reduce hepatic steatosis and enhance whole body insulin sensitivity. Therefore, increasing hepatic ATGL expression could be a therapeutic approach to treat obesity and type 2 diabetes.

Thesis (Ph. D.)--George Mason University, 2007. / Title from PDF t.p. (viewed Jan. 18, 2008). Thesis director: Ancha Baranova Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biosciences. Vita: p. 213 Includes bibliographical references (p. 188-212). Also available in print.

Thesis (Ph. D.)--University of Adelaide, Dept. of Physiology, 1992. / Includes bibliographical references (leaves 257-286).

Thesis (Ph.D.) -- University of Adelaide, Dept. of Medicine, 2003. / "October 2003" Bibliography: leaves 190-210.