Thesis (M.Phil.)--Hong Kong University of Science and Technology, 2008. / Includes bibliographical references (leaves 41-44).

No description available.

No description available.

Thesis (Ph.D.)--University of Wollongong, 2008. / Typescript. Includes bibliographical references: leaf 150-165.

Call number: LD2668 .T4 1950 H35 / Master of Science

No description available.

Originally presented as the author's thesis, M.S. in the M.I.T. Alfred P. Sloan School of Management, 1979.

This study was undertaken to assess rates and timing of mortality and hatchability, to identify pathological changes and compare them to those observed in chicken embryos, and to determine whether mallard duck chorioallantoic membrane (CAM) is a target organ of toxicity of Prudhoe Bay crude oil (PBCO). Mortality and hatchability were determined in embryos exposed to 10[mu]l of PBCO on days 3, 6, 9 and 12 of incubation. Pathological changes in embryos and the CAM, hematological parameters and body and plasma calcium concentration were assessed in live embryos exposed to PBCO on day 12. Oil-exposed embryos had high mortality, low hatchability and high prevalence of pathological changes. Mortality was characterized by initial death that coincided with development and maturation of the CAM and a sublethal effect that resulted in live, mature embryos, which were unable to hatch. This mortality at hatching contributed greatly to total mortality. Lesions included hepatic and renal necrosis, liver enlargement, subcutaneous edema, reduced body weight and ratio of body weight to fresh egg weight, short crown-rump, third toe and metatarsal lengths, depletion of lymphocytes in the bursa of Fabricius, renal hematopoiesis, and diffuse changes in the CAM which included necrosis and hyperplasia, of chorionic epithelium, soft swelling of mesenchymal cells, hemorrhages and reduced vascular density. There also were high proportions of reticulocytes and polychromatophilic and primary erythrocytes. Prevalence of lesions in the CAM was greatest during the stage of acute toxicity, suggesting that injury to the CAM may have a role in acute oil. toxicity. The distribution of lesions in the CAM suggests a direct effect on the CAM cells of toxic components or their metabolites. Injury to the CAM did not affect its role in mobilization of calcium from the eggshell. Body and plasma calcium in oil-exposed and control embryos were not different. Embryos exposed to PBCO did not develop anemia nor any damage to the red blood cells. The spectrum of morphological changes in oil-exposed embryos suggests retarded and altered development The rate and timing of mortality and pathological changes in oil-exposed mallard embryos were similar to those reported in oil-exposed chicken embryos.

The physics of oil and petroleum evaporation are investigated. Literature on oil spill evaporation shows that most workers use boundary-layer equations adapted from water evaporation work. These equations predict a constant evaporation mass-transfer rate, dependent on scale size and wind speed. Evaporation was studied further by measuring evaporation of commercial oil products. An experimental apparatus for the study of evaporation was developed. Evaporation was determined by weight loss measured on a balance and recorded constantly on a computer. Examination of the data shows that most oil and petroleum products evaporate at a logarithmic rate with respect to time. This is attributed to the overall logarithmic appearance of many components evaporating at different linear rates. Petroleum products with fewer chemical components such as diesel fuel, evaporate at a rate which is square root with respect to time. The particular behaviour is shown to be a result of the number of components evaporating. Oils with greater than seven to ten components can be predicted with logarithmic equations, those with three to seven components, with square root equations. Evaporation of oils and petroleum products is not strictly boundary-layer regulated. This is largely a result of the high saturation concentrations of oil components in air, which is associated with a high boundary-layer regulated rate. Typical oil evaporation rates do not exceed that of molecular-diffusion, and thus turbulent diffusion does not increase the evaporation rates. Some volatile oils and petroleum products show some effect of boundary-layer regulation at the start of the evaporation process, but after several minutes, evaporation slows because of the loss of the more volatile components, at which point evaporation ceases to be boundary-layer regulated. Overall, boundary-layer regulation can be ignored in the prediction of oil and petroleum evaporation. A simple equation relating only the logarithm of t

Thesis (M.B.A.)--University of North Carolina Wilmington, 2008. / Title from PDF title page (viewed May 28, 2009). Includes bibliographical references (p. 30-31).