Thesis (doctoral)--Swedish University of Agricultural Sciences, 2000. / Includes bibliographical references.

Thesis (MMedVet. (Veterinary Tropical Diseases, Veterinary Science))--University of Pretoria, 1999. / Also available in print format.

The distribution of five Na,K-ATPase subunit isoforms (α1, α2, α3, β1 and β2) in rat cochlear and vestibular tissues was determined by immunocytochemical techniques using subunit isoform specific polyclonal antibodies. The expression of Na,K-ATPase α and β subunit isoforms varied among different cell regions of the inner ear. The α1 subunit isoform was more extensively distributed in all inner ear tissues than the α2 or α3 subunit isoforms. The β1 subunit isoform was distributed primarily in spiral ligament and inner hair cells of the cochlea, and in crista ampullaris and macula of the saccule. The β2, subunit isoform was most abundant in the stria vascularis, dark cells of the ampullae and utricle. The α1β1 subunit combination of Na,K-ATPase was most commonly found in the spiral ligament, while the α1β2 combination was most abundant in the stria vascularis. Similarly, α1β2 was confined more to the dark cells of the ampullae and utricle. The α3β1 suhunit combination of Na,K-ATPase was identified in the inner hair cells of the cochlea and the sensory regions of the vestibular end organs. These observations may reflect functional diversity of Na,K-ATPase in the individual inner ear regions and may provide insight into the differences between fluid and ion transport in the inner ear and that of other transporting tissues. Overall, the distribution pattern further indicates that the different isoform combinations have specific roles.

Please read the abstract in the section 00front of this document / Dissertation (MMed Vet (FER))--University of Pretoria, 1999. / Veterinary Tropical Diseases / unrestricted

No description available.

This research studied the iron deficient condition of the nitrogen-fixing filamentous cyanobacteria Trichodesmium in neighboring oligotrophic northern South China Sea and upstream Kuroshio. The iron deficiency was detected by the immunocytochemical analysis of the expression of iron deficiency induced protein A (IdiA), a protein translated by Trichodesmium cells under iron deficiency. IdiA expression rate (percentage of cells stained by IdiA antiserum in total cells) was used to represent the iron deficiency status. Trichodesmium samples were collected in four cruises by net-towing or bottle-sampling in the Kuroshio and the shelf, slope and basin of the South China Sea between December 2008 and May 2010, representing three seasons: Spring (CR899 and CR1455), Summer (CR910) and Winter (CR886). The results showed that the IdiA expression rates vaied greatly among the stations in the South China Sea. Iron supplies from various sources decreased the IdiA expressions rates (i.e., less iron deficient). These sources include: (1) Mixing from deep layer, such as in the continental shelf of the South China Sea in which internal wave occured, and upwelling occurred in the continental slope; (2) Mixing at some stations in the South China Sea basin from the input of river dischange, especially in the events after typhoon. During these events, stations with lower surface water salinities usually implied lower IdiA expression rates. In contrast, the basin station that were high in salinities showed high IdiA expression rates, higher than the rates in the Kuroshio. These stations generally had strongly stratified water coulumn, and therefore might limit the ward mixing of deep water. The incubation experiment conducted showed that 24 hours after adding iron, Trichodesmium IdiA expression rates were significantly decreased. The Kuroshio, with its water column stratification weaker than South China Sea, the IdiA expression rates were lower than the basin stations in South China Sea, and positively relatied with the stratification index, indicating that deep advection may be the main source of iron. In the incubation experiments in Kuroshio, the expression rates did not significantly differ with iron or without iron addition. The IdiA expression rates in both regions were not related to flux of atmospheric dust, indicating the input from the dust was not key point to decrease iron deficiency of Tricodesmium in this two region. This study shows that iron deficient condition of diazotrophic Trichodesmium in South China Sea and upstream Kuroshio were related to vertical mixing and horizontal discharge, but not dust flux. This study is first time to apply immunocytochemical analysis on field experiments to explain iron deficiency in the ocean.

No description available.

Mitochondria perform functions which are central to the life of most eukaryotic cells. These organelles can be considered the ultimate energy power house of a living cell. The role of mitochondria in cancer phenotype remains a fertile area of research. Several carcinogens are known to enter the mitochondria, resulting in impaired functioning and altered structure. Aflatoxin BI (AFB1) a primary type I mycotoxin elaborated by Aspergillus flavus and Aspergillus parasiticus, is carcinogenic for a wide species range. The epoxide is capable of binding to nucleic acids and proteins, resulting in induced mutations, cellular toxicity, and eventually carcinogenesis. Approximately 250 000 deaths occur annually in both China and Africa due to patients presenting with Hepatocellular Carcinoma (HCC). The causative agents being AFB1-ingestion via contaminated foods and feeds, and the Hepatitis B Virus infection. The toxin has a multifaceted mode of attack, capable of being activated to a highly reactive and carcinogenic derivative, the AFB1-8,9-epoxide, via the cytochrome P450 enzyme system of the microsomes, endoplasmic reticulum and also the mitochondria. The epoxide is capable of binding to nucleic acids and proteins, resulting in the formation of covalent adducts. The repeated occurrence of gold labelled toxin within mitochondria from hepatomas of patients presenting with HCC suggested that these organelles were direct sites of toxin binding. Despite observations that mitochondria appear as direct and perhaps preferential targets for attack by AFB1, the actual in vivo immunolocalisation and characterisation of bound AFB1 within liver mitochondria has not been reported previously. In addition the role of AFB1-protein binding within mitochondria was investigated to determine the mode of action of the toxin, within the mitochondrial system. Liver sections from rats treated with a single lethal dose of AFB1, showed distinct ultrastructural abnormalities viz. large nuclei, increased heterochromatin, and swollen mitochondria. Immunocytochemistry revealed for the first time, the selective localisation of conjugated gold labelled toxin within the mitochondria. Toxin was found in the intracristal and peripheral spaces and frequently within the mitochondrial matrix. The mitochondria isolated from treated rats revealed significant alterations and damage to the mitochondrial membranes. The cristae were also markedly swollen with the associated clearing of the mitochondrial matrix. Western blot immunoassays revealed the presence of five AFB1-bound proteins (150kDa, 50kDa, 25kDa, 18kDa, 14kDa) in the inner mitochondrial fraction of isolated mitochondria. High pressure liquid chromatography also revealed that a significant proportion (84%) of an initial dose of toxin, was absorbed by mitochondrial protein. This study is the first to show the presence of specific mitochondrial proteins involved in toxin binding. In addition, the presence of toxin within the mitochondria and the specific binding to inner mitochondrial proteins suggest that the toxin specifically targets the electron transport chain and hence effects ATP production. This study conclusively indicates that mitochondria are direct targets for attack by AFB1 during experimental carcinogenesis. Mitochondria therefore play an important role in AFB1-mediated carcinogenesis. / Thesis (M.Med.Sc.)-University of Natal, Durban, 1998.

Thesis (MAppSc (Medical Laboratory Sc)) --University of South Australia, 1993

Thesis (M.S.)--Duquesne University, 2003. / Title from document title page. Abstract included in electronic submission form. Includes bibliographical references (p. 59-61) and abstract.