In recent decades, revenue diversification has become a prevalent practice in state and local government finance. The trend of revenue diversification, according to the portfolio theory, has far-reaching implication for public financial management as it may change revenue stability, which has been an important policy objective for state and local government administrators. This study explores how revenue diversification affects revenue stability from both empirical and theoretical perspectives. Drawing on portfolio theory and regional science literature, this study develops a theoretical framework to explain how the effect of revenue diversification on revenue volatility of sub-national governments varies in terms of its economic base instability. To empirically test the theoretical framework, an econometric model that explores a series of factors that could affect revenue stability is estimated using socioeconomic and fiscal data of 156 Georgia county governments and 47 state governments during the years 1986-2004. The findings indicate that revenue diversification affects revenue stability conditional on the instability of a jurisdiction’s economic base. The county level analysis suggests revenue diversification significantly increases the revenue instability of a county that has a stable economic base and the revenue stabilizing effect of diversification is enhanced as an economic base becomes more unstable. However, the state level analysis shows that revenue diversification significantly reduces revenue volatility for a state that has a stable economic base and the revenue stabilizing effect of diversification decreases when an economic base gets more unstable. An important policy implication of the dissertation is that the degree of revenue diversification should be gauged by the condition of its corresponding economic base in order to achieve the goal of revenue stability.

Ankle sprains are among the most common injuries sustained by physically active individuals. Although ankle sprains are often considered innocuous in nature, a large percentage of individuals experience repetitive sprains, residual symptoms, and recurrent ankle instability following a single acute sprain; otherwise known as chronic ankle instability (CAI). In addition to repetitive ankle trauma, those with CAI experience reductions in functional capacity over the life span. This indicates that current intervention strategies for CAI are inadequate and require further investigation. The objective of this dissertation was to explore differences in walking and running gait parameters between individuals with and without CAI; as well as, examine the effects of a 2-week Maitland Grade III anterior-to-posterior talocrural joint mobilization intervention on self-reported function, ankle mechanics, postural control, and walking and running gait parameters in a cohort of individuals with CAI. It was hypothesized that individuals with CAI would exhibit different gait kinematics and joint coupling variability patterns compared to healthy individuals and the joint mobilization intervention would improve patient-oriented, clinician-oriented, and laboratory-oriented measures of function in those with CAI. Several observations were made from the results. In the first study, alterations in single joint kinematics and joint coupling variability were found between those with CAI and healthy individuals. In the second study, it was determined that the joint mobilization intervention improved patient-oriented and clinician-oriented measures of function as indicated by improved Foot and Ankle Ability Measure scores, increased weight-bearing dorsiflexion range of motion, and increased reach distances on the Star Excursion Balance Test. However, there were no changes in measures of instrumented ankle arthrometry or laboratory measures of postural control. In the third study, there were no changes in single joint kinematics or joint coupling variability during walking and running associated with the joint mobilization intervention. It can be concluded that joint mobilizations had a significant positive impact on patient-, and clinician-oriented measures of function. Though the laboratory measures did not detect any improvements, joint mobilizations did not produce deleterious effects on function. Therefore, future investigation on the effects of joint mobilization in conjunction with other, more active, rehabilitation strategies is warranted.

Electrospinning is a method of producing nano structured material from a polymer solution or melt using high strength electric fields. It is a process that has yet to find extensive industrial application yet shows promise if obstacles such as low rate of production overcome perhaps by more complete theoretical modelling. This work examines the effects of adding an ionic salt to a solution of poly(vinyl alcohol) in water. The direct effect was an increase the charge density and electric current. It was found that an increase in charge density decreases the mass deposition rate and forms a thinner initial jet. When the sign of the charge on the polymer solution was changed from positive to negative the charge density increased and the initial jet diameter and mass deposition rate also decreased. It was proposed that a smaller radius of curvature is formed by the Taylor cone at higher charge densities resulting in a smaller “virtual orifice”. The extent of the bending instability was explored and it was found that adding ionic salt results in a decrease in the bending instability resulting in thicker fibres. Changing the sign of the charge on the polymer solution from positive to negative resulted in an increase in the bending instability and resulted in thinner fibres. The charge transfer mechanisms used in different electrospinning models are explored and some assumptions not explicitly stated are discussed. From this discussion a generalized equation describing the charge transport mechanisms is proposed.

The Rayleigh-Taylor instability is a buoyancy driven instability that takes place in a stratified fluid system with a constant acceleration directed from the heavy fluid into the light fluid. In this study, both experimental data and numerical simulations are presented. Experiments are performed primarily using a lithium-tungstate aqueous solution as the heavy liquid, but sometimes a calcium nitrate aqueous solution is used for comparison purposes. Experimental data is obtained for both miscible and immiscible fluid combinations. For the miscible experiments the light liquid is either ethanol or isopropanol, and for the immiscible experiments either silicone oil or trans-anethole is used. The resulting Atwood number is either 0.5 when the lithium-tungstate solution is used or 0.2 when the calcium nitrate solution is used. These fluid combinations are either forced or left unforced. The forced experiments have an initial perturbation imposed by vertically oscillating the liquid containing tank to produce Faraday waves at the interface. The unforced experiments rely on random interfacial fluctuations, due to background noise, to seed the instability. The liquid combination is partially enclosed in a test section that is accelerated downward along a vertical rail system causing the Rayleigh-Taylor instability. Accelerations of approximately 1g (with a weight and pulley system) or 10g (with a linear induction motor system) are experienced by the liquids. The tank is backlit and digitally recorded with high speed video cameras. These experiments are then simulated with the incompressible, Navier-Stokes code Miranda. The main focus of this study is the growth parameter (ɑ) of the mixing region produced by the instability after it has become apparently self-similar and turbulent. The measured growth parameters are compared to determine the effects of miscibility and initial perturbations (of the small wavelength, finite bandwidth type used here). It is found that while initial perturbations do not affect the instability growth, miscibility does.

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The expansion of gene-specific trinucleotide repeats is responsible for a growing list of human disorders, including myotonic dystrophy type 1 (DM1). Repeat instability for most of these disorders, including DM1, is characterized by complex patterns of inherited and ongoing tissue-specific instability and pathogenesis. While the mechanistic basis behind the unique locus-specific instability of trinucleotide repeats is currently unknown, DNA metabolic processes are likely to play a role. My thesis involves investigating the contribution of DNA replication to the trinucleotide instability of myotonic dystrophy type 1. Herein I have designed an in vivo primate model system, based on the SV40 replication system, to assess the contribution of DNA replication to DM1 repeat instability. This system allows the assessment, under controlled conditions, and manipulation of variables that may affect replication-associated repeat instability, under a primate cellular system. Using the SV40 model system, I not only confirmed previous observations that repeat length and replication direction affect repeat instability, but also for the first time determined that the location of the replication origin relative to the repeat tract plays an important role in repeat instability. This novel observation allowed for the development of a fork-shift model of repeat instability, in which cis-elements adjacent to the repeat tract affect replication, in turn altering the propensity for repeat instability. To further my study of DNA replication in DM1 repeat instability, I have mapped the origin of replication adjacent to the DM1 locus in human patient cells and the tissues of DM1 transgenic mice actively undergoing repeat instability. The position of the replication origins adjacent to the repeat tract at the DM1 locus places several known cis-elements, including CTCF binding sites, in a position to alter replication as predicted by the fork-shift model. My analysis of the CTCF sites showed them capable of altering replication and repeat instability at the DM1 locus. Taken together these results suggest that the placement of replication origins, repeat tracts and cis-elements, may mark trinucleotide repeat tracts, such as the DM1, for locus-, tissue- and development-specific replication-associated repeat instability.

The global financial crisis has proved to have had a significant impact on countries worldwide and South Africa was not spared of this global phenomenon. The ecological systems theory, family systems theory and gestalt field theory accentuate the impact a change within the environment can have on interconnected systems and it is therefore argued that the global unstable economy can have a significant impact on families and children. Literature indicates a vast amount of confirmation on the impact of the financial crisis on already poverty stricken areas. On the contrary, less focus is offered on the impact of the financial crisis on families within middle to upper class communities. Preliminary research confirms that although the basic needs of these families (such as food and shelter) have not been affected, significant change with regards to luxuries and expenditure patterns is present. Due to the fact that parents within families are also faced with financial difficulties, these changes are not facilitated and discussed with children and adolescents, causing unresolved emotions and uncertainties. This research was therefore aimed at the development of web based assistance for parents. In addition to the set aim of this research, the study arrived at findings that indicate and emphasise the important contribution of this study. Intervention research as research method was used in the conducting of the study. The developed web based assistance proved to serve as a functional tool for parents in addressing financial issues with their children and adolescents. It also raised parents’ awareness of the impact that a change in finances in the family can have which empowered the parents as well. It was also significantly noted that the website can be utilised within an educational setting which enhances the applicability of this study. The developed assistance contributes to society as it serves as a cost effective, accessible means of providing parents with practical guidelines and activities to help their children and adolescents deal with the effects of economic instability within the family. / PhD (Psychology), North-West University, Potchefstroom Campus, 2014

Hereditary tyrosinemia type 1 (HT1) is an autosomal recessive disorder of the tyrosine degradation pathway. The defective fumarylacetoacetate hydrolase enzyme causes the accumulation of upstream metabolites such as fumarylacetoacetate (FAA), maleylacetoacetate (MAA), succinylacetone (SA) and p-hydroxyphenylpyruvic acid (pHPPA). In vitro and in vivo studies showed that the accumulation of these metabolites are detrimental to cell homeostasis, by inducing cell cycle arrest, apoptosis, and endoplasmic reticulum stress, depleting GSH, inhibiting DNA ligase, causing chromosomal instability, etc. For in vivo studies different models of HT1 were developed. Most notably was the fah deficient mouse, whose neonatally lethal phenotype is rescued by the administration of 2-(2-nitro-4-trifluoromethylbenzoyl)-1,3-cyclohexanedione (NTBC). Although, this model most closely resembles the human phenotype with elevated tyrosine levels and the development of hepatocellular carcinoma (HCC), the model is not human genome based. Both the in vitro and in vivo studies suggested that DNA repair is affected in HT1. However, it is not yet clear which DNA repair mechanisms are affected and if only protein functionality is affected, or if expression of DNA repair proteins are also affected. Characteristic of HT1 is the high prevalence of HCC and the presence of liver mosaicism. The liver mosaicism observed in HT1 patients are the result of reversion of the inherited mutation to wild-type. The general consensus is that the reversion is the result of a true back mutation. However, the mechanism underlying the back mutation is still unresolved. It was suggested that cancer develops either through a chromosomal instability mutator phenotype, a microsatellite instability mutator phenotype, or a point mutation instability mutator phenotype. In HT1 only chromosomal instability was reported. The aims of this study were to contribute to the understanding of the molecular basis of the genetic mosaicism in hereditary tyrosinemia type 1. More specifically, determine whether baseand nucleotide DNA repair mechanisms are affected and to what extent, and to determine if microsatellite instability is found in HT1. To achieve these aims, a parallel approach was followed: i.e. to develop a HT1 hepatic cell model and to use HT1 related models and HT1 patient material. To assess the molecular basis of the genetic mosaicism in HT1, the comet assay, gene expression assays, microsatellite instability assays, high resolution melting and dideoxy sequencing techniques were employed. Results from the comet assay showed that the HT1 accumulating metabolites, SA and pHPPA, decreased the capacity of cells for base- and nucleotide excision repair. Gene expression assays showed that short term exposure to SA and/or pHPPA do not affect expression of hOGG1 or ERCC1. The expression of these genes were, however, low in HT1 patient samples. Microsatellite instability assays showed allelic imbalance on chromosome 7 of the mouse genome, and microsatellite instability in the lymphocytes of HT1 patients. Although high resolution melt and sequencing results did not reveal any de novo mutations in fah or hprt1, the appearance of de novo mutations on other parts of the genome can not be ruled out. To conclude, results presented in this thesis, for the first time show that in HT1 the initiating proteins of the base- and nucleotide repair mechanisms are affected, the gene expression of DNA repair proteins are low, and microsatellite instability is found in HT1. By contributing to the elucidation of the mechanism underlying the development of HT1-associated HCC, and providing evidence for the development of a mutator phenotype, the results presented in this thesis contributes to the understanding of the molecular mechanisms underlying the genetic mosaicism in HT1. In addition to these contributions, a hypothesis is posited, which suggests that a point mutation instability (PIN) mutator phenotype is the mechanism underlying the mutation reversions seen in HT1. / Thesis (Ph.D. (Biochemistry))--North-West University, Potchefstroom Campus, 2012