Thesis (Ph. D.)--University of Hong Kong, 2006.

Thesis (Ph.D.) - University of Queensland, 2005. / Includes bibliography.

Thesis (M. D.)--University of Hong Kong, 2005. / Title proper from title frame. Also available in printed format.

Thesis (MTh(Practical Theology)--University of Pretoria, 2006. / Includes bibliographical references. Available on the Internet via the World Wide Web.

Thesis (M.D.)--University of Pennsylvania, 1800. / Dedicated to Benjamin Rush, M.D., and to Arthur May, M.D., the author's brother. Signatures: [A]⁴ B-C⁴ D1. Not in Blake. Film 633 reel 64 is part of Research Publications Early American Medical Imprints collection (RP reel 64, no. 1240). DNLM

Thesis (M.A.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / Introduction: Parkinson's disease (PO) is a neurodegenerative disorder. Medication is by far the most effective and important treatment for PO and levodopa is the most effective and commonly used medicine to control motor symptoms in PD. However, its long-term usage often induces several adverse events (AEs). Both combination therapy of monoamine oxidase type B inhibitor. (MAOBI) with levodopa and catechol-0-methyltransferase inhibitor (COMTI) with levodopa were demonstrated to provide benefits to PO patients, such as regulating motor fluctuations and reducing levodopa dose, but are accompanied by increased frequency of dopaminergic AEs. Available data is too limited to directly compare the safety of these combination therapies (MAOBI vs. COMTI). Thus the aim of this study is to investigate whether MAOBI and COMTI have different AE profiles. Methods: All the data used to analyze the AEs of different PO medications were retrieved from "The Boston University Medical Center's Parkinson's Disease and Movement Disorder Database". Ten categories of AEs, i.e. compulsive behavior, dyskinesia, dementia, depression, freezing, hallucinations, motor fluctuations, orthostatic hypotension, other autonomic dysfunction and psychosis, were compared between MAOBI and COMTI groups. Fisher's exact test and multivariable logistic regression models were applied to analyze data. Results: In total 87 subjects were included in the analysis. Out of 10 AEs, presence of dementia was significantly different between the MAOBI and COMTI groups with OR of 6.9 (COMTI vs. MAOBI, 95%CI: 1.3-37.0). Motor fluctuations were also found to be differently distributed in the two medication groups with OR of 3.1 (COMTI vs. MAOBI, 95%CI: 1.0-9.8). Conclusion: COMTI combined with levodopa therapy was more likely to be associated with dementia and motor fluctuations than MAOBI. The results need to be further tested in other independent studies. / 2031-01-01

Alzheimer’s disease is the most common cause of late-life dementia and the fourth leading cause of death in the developed world. The aetiology of AD has not yet been resolved. It has been suggested that AD could result from multifactorial process involving both a genetic predisposition and an exposure to environmental factors modulated by the biological aging process. To date, epidemiological and molecular genetic data have led to the identification of three genes, amyloid precursor protein (APP), presenilin 1 (PS1) and presenilin 2 (PS2) genes, which, when mutated, can cause an early onset form of AD. Genetic linkage studies and association studies have also shown that the ε4 allele of the apolipoprotein E gene increases risk for AD in a dose dependent manner in both early onset and late onset AD. Recently, it has also been suggested that environmental factors may interact with a genetic predisposition to modify the risk of AD. Extensive research is underway to identify environmental and genetic risk factors for this complex disease. Over 40 genes have been tested as AD candidates yet none has been clearly established as an AD risk factor. Currently scientists are investigating the interrelationship between various gene loci and how environmental factors could affect an individual’s susceptibility to AD. This study evaluated the genotoxicity of environmental agents such as hydrogen peroxide, cadmium chloride and γ radiation induced oxidative DNA damage in lymphocytes and within specific DNA sequences of APP (exon 15-18) and PS1 (exon 3-12) genes of AD patients and age-matched control subjects. As indicators of oxidative DNA damage, the frequencies of DNA strand breaks, oxidized pyrimidines and altered purines was assessed using the alkaline Comet assay modified with lesion-specific endonucleases, endo-III and fpg; and fluorescence in situ hybridisation. The number of APP and PS1 hybridisation spots per comet were used as an indicator of the extent of damage. The location of the hybridisation spots in the head or tail of the comet were recorded to further determine whether the gene of interest lies within or in the vicinity of a damaged region of DNA. With the alkaline Comet assay modified with endo-III and fpg, it was demonstrated that patients with AD had significantly increased levels of DNA strand breaks, oxidized pyrimidines and altered purines induced by hydrogen peroxide, cadmium chloride and γ radiation compared with control subjects (p<0.05). This was further confirmed by the fluorescence in situ hybridisation modification of the alkaline Comet assay by demonstrating a significant increase in the mean number of APP and PS1 gene hybridisation spots per comet in AD patients compared with control subjects. Moreover, the gene sensitivity index of APP and PS1 to hydrogen peroxide, cadmium chloride and γ radiation were found to be higher in AD patients than in control subjects. Taken together, our results suggest (i) that lymphocytes from patients with AD are sensitive to these environmental genotoxic agents and (ii) there was an overall increase in the mean number and sensitivity index of APP and PS1 genes to environmental genotoxic agents which might link a genetic cause to oxidative stress in peripheral cells of AD patients than in control subjects. Although the mechanisms by which these environmental agents induced oxidative DNA damage remained to be elucidated, our data suggest that increased oxidative stress is an inherent property of cells carrying genes associated with AD. / Dr. H. Abrahamse Mrs. J. V. Hind

No description available.

[No abstract available] / Science, Faculty of / Botany, Department of / Graduate

Includes bibliography. / This dissertation comprises an application of social marketing principles and techniques to AIDS prevention in the workplace. The overall research objective of this dissertation is to investigate the provisions which have been made for AIDS in companies in South Africa, and to gain an understanding of the "preventative AIDS provisions" which the respondents consider practical to implement in their workplace, in order to generate conclusions and recommendations. The research findings, discussions and conclusions highlight areas for future research.