Bibliography: leaves 133-144 / 144 p., [15] leaves of plates : ill ; 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 Biochemistry, 1986

Studies in a number of human tissues have revealed that the activities of mitochondrial respiratory chain enzyme complexes decline during the aging process. Other studies have suggested that aging increases the frequency of mitochondrial DNA (mtDNA) mutation and leads to the accumulation of mutant mtDNA species, mainly those with large deletions and point mutations. Although the mitochondrial theory of aging may be more applicable to post mitotic tissues, abnormalities of mtDNA have also been reported in tissues which retain a mitotic capacity. Fresh tissues from elderly patients are difficult to obtain and only a limited number of studies on biochemical examination of respiratory chain enzyme complex activities have been carried out. Prostate tissue is readily available in elderly male subjects because of the high prevalence of benign prostatic hypertrophy in this sub-group of the population, and endoscopic surgery is routinely performed for excision of the diseased prostate. In this study, mitochondrial respiratory function and the mtDNA mutations in prostate tissues of elderly patients (aged from 56 to 92) were studied in 24 subjects. This included the measurement of the activities of the respiratory chain enzyme complexes and screening for mitochondrial point mutations and deletions at sites commonly affected in neurodegenerative diseases. (For complete summary open document)

Progressive Atrophic Rhinitis (PAR) is a serious complex disease of young swine characterized by sneezing, atrophy of the nasal turbinates, shortening and twisting of the snout and reduction in weight gain. Although the aetiology of the disease is complex, infection with the bacterium toxigenic Pateurella multocida, is considered essential. A dermonecrotic toxin (DNT) produced by toxigenic strains of type D P. multocida is central to the resorption of the nasal bone structures characteristic of the infection. The P. multocida DNT gene toxA has been previously cloned, sequenced and genetically manipulated in order to develop a vaccine for PAR. These earlier studies demonstrated that DNT-specific antibodies produced in pigs by vaccination with the purified genetically inactivated DNT derivative (toxoid) resulted in the protection of the animals against experimentally induced PAR. An alternative approach to using a subunit vaccine for PAR is to express the toxoided gene from P. multocida either from the chromosome or a plasmid thus providing a live vaccine that could present to the porcine immune system a full spectrum of bacterial antigens in addition to the DNT. (For complete abstract open document)

Corrigenda pasted onto back end-paper. / Bibliography: leaves 167-189. / 191, [229] leaves : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / In this study the wbh region responsible for O-antigen biosynthesis was isolated and partially characterised. The operon appears to be made up of genes that were acquired from other bacteria. The presence of IS1358 indicates that it may have played a role in the acquisition or rearrangement of the polysaccharide biosynthesis genes in V. anguillarum 01. / Thesis (Ph.D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1999

Typescript (photocopy) / xiii, 209 leaves : ill., (1 col.) ; 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 Genetics, 1983

This thesis describes the construction and evaluation of six knockout mutants in Neisseria meningitidis serogroup B strain MC58. The genes that were inactivated were NMB0711, NMB1048, NMB1525, NMB1898, NMB1948 and NMB1966. Attempts to inactivate a seventh gene, NMB0768, were not successful. These genes were chosen as they had been observed previously to be up-regulated following incubation in whole blood using Differential Fluorescence Induction. Mutant strains were constructed by allelic exchange with a plasmid construction in which a kanamycin resistance cassette had been incorporated within the coding sequence of each cloned target gene. Confirmation of successful allelic exchange was achieved by Southern blotting. The phenotype of all mutant strains were evaluated by assessment of in vitro growth and in the infant mouse model of infection. Of the six mutants, all except that involving NMB1966, showed no differences compared with wild-type. The mutant knockout of NMB1966 showed (1) impaired growth beyond the mid-logarithmic phase in shaking broth culture but normal growth on solid medium, (2) reduced virulence in a mouse model of infection, (3) impairment in its capacity to invade (although not adhere to) cultured human bronchial epithelial cells, and (4) more rapid killing in ex vivo human blood. NMB1966 is predicted to encode the ATP-binding subunit of an ABC transporter and, after experiments for this thesis had been completed, it was demonstrated, by others, that this ABC transporter is responsible for uptake of L-Glutamate at low sodium concentrations. It is likely that defective uptake of L-Glutamate explains the observed defect in shaking broth culture and intracellular survival, both of which are associated with low ambient concentrations of sodium. However, it is not certain if this mechanism explains the observed defect in survival in human blood and in the infant mouse model which test predominantly extracellular survival and represent environments with high sodium concentrations.

Thesis (Ph.D)--Biology, Georgia Institute of Technology, 2009. / Committee Chair: Dr. Soojin Yi; Committee Member: Dr. Eric Vigoda; Committee Member: Dr. James Thomas; Committee Member: Dr. John McDonald; Committee Member: Dr. Kirill Lobachev; Committee Member: Dr. Michael Goodisman. Part of the SMARTech Electronic Thesis and Dissertation Collection.

Prefatory material introducing a collection of articles spanning fifty years of research into inborn errors of metabolism. Table of Contents: 1. Introduction -- 2. Background information about inborn errors of metabolism -- 3. Lessons from phenylketonuria [PKU] -- 4. My role in developing new medical foods -- 5. My role in solving an epidemic of benzyl alcohol poisoning in premature infants -- 6. My role in galactosaemia research -- 7. My start in the metabolic world - screening tests in urine -- 8. My experiences in disaster relief -- 9. My first appearance in the medical literature -- 10. A selection of rare and unusual diseases -- 11. Tyrosinaemia type II; tyrosine aminotransferase deficiency -- 12. Iminodipeptiduria due to prolidase deficiency -- 13. Citrullinaemia -- 14. Rippling muscle disease -- 15. A fatal X-linked disorder of diarrhoea, diabetes mellitus and immune dysregulation -- 16. Infantile Refsum disease -- 17. Hereditary hypocalcuric hypercalcaemia -- 18. Carbohydrate deficient glycoprotein disease type IAPKU -- 19. Thiamine-responsive diabetes and deafness -- 20. Folinic acid-responsive seizures: a false alarm -- 21. S-adenosylmethionine hydrolase deficiency -- 22. Deficiency of complex III of the respiratory chain -- 23. Current research: quantitation of infant sucking behaviour -- 24. Discussion and summary.

M.Sc. / DNA microsatellite primers were used to determine the population structure (genetic variation, heterozygosity, inbreeding, genetic distance and phylogenetic relationships) of Camelus dromedarius in southern Africa. A camel population from Sudan as well as an Alpaca population was included for comparison. The results obtained from the geographical distribution indicate that a number of small populations occur and that it can not be regarded as breeding units. These populations are isolated and widely distributed over South Africa, Namibia and Botswana. Information obtained from questionnaires indicates that nine true camel breeders exist in the southern African region. The genetic variation at seven loci of the southern African camel population (heterozygosity value = 0.604) is less than that of Sudan (0.680), an indication that inbreeding has occurred due to isolation. This was confirmed with the reduced number (five) of rare alleles occurring in the southern African population opposed to 30 rare alleles in the Sudan population. Both the southern African and Sudan camel populations have less genetic variation than the Alpaca population (heterozygosity = 0.757). Less genetic variation is present within the camel populations of southern Africa when results from more loci (12) are included (heterozygosity values range from 0.345 to 0.483). These values are comparable to those of endangered species such as wild dog (0.560) and cheetah (0.390). Low to moderate genetic differentiation was obtained between the three southern African populations (FST values range from 0.039 to 0.058). This was expected since the animals are derived from the same source. The results from this study will provide a scientific base for the execution of future studies. It is recommended that individuals with the identified rare alleles should be used in a breeding policy to prevent further inbreeding and to improve the current gene pool by increasing the genetic variation by either relocating or lending the individuals from and to the breeders or by making use of artificial insemination. / Prof. F.H. van der Bank

Magister Scientiae (Physiotherapy) - MSc(Physio) / Clubfoot is the most common congenital structural deformity that leads to physical impairments in children in many poor developing countries. Inadequately treated or neglected clubfoot has been found to be a common cause of ohysical disability globally among children and young growing adults. Many children are referred to the clinics for treatment but some parents do not comply with the treatment regimen whcih requires attending for consecutive treatment sessions. The purpose of this study was to investigate barriers to treatment attendance parents/caregivers of children with clubfoot encounter in complying with clubfoot treatment during the plaster csting phase in Uganda. / South Africa