Across the world, job insecurity plays a critical role in organisations. This insecurity affects not only the individual, but also the organisation. In South Africa, the Employment Equity Act (No. 55 of 1998), and the Broad-Based Socio-Economic Empowerment Charter for the South African Mining Industry (Mining Charter), brought changes to the mining industry policies and decision-making process in terms of selection and recruitment, which could in turn lead to feelings of job insecurity. Other factors such as the availability of gold left to be mined, restructuring and strikes increase work-related stress. The objectives of this study were to investigate the role of job insecurity in predicting health related behaviours, and to determine whether coping moderates the effect of job insecurity on health behaviours for a group of managers in a South African gold mining company. A cross-sectional design was used. The study population (n = 206) consisted of managers in a gold mining company in South Africa The Job Insecurity Scale, Cybernetic Coping Scale and Health Complaints Questionnaire were used as measuring instruments. Descriptive statistics (e.g. means, standard deviations and kurtosis) were used to analyse the data. Hierarchical multiple regression analysis was used to test for the hypothesized moderating effect of coping on the relation between job insecurity and health-related behaviours. The results of the regression analyses showed that qualitative job insecurity was a significant predictor of health complaints. Qualitative job insecurity was also a significant predictor of health complaints in employees who smoked cigarettes and drank alcohol, and exercised at least once a week. Quantitative job insecurity did not play a role in predicting health-related behaviour. Coping did not moderate the effects of job insecurity for employees with health complaints. Rather, it is suggested that using negative coping behaviours may actually contribute to health complaints. Recommendations for future research are made. / Thesis (M.A. (Industrial Psychology))--North-West University, Potchefstroom Campus, 2006.

Current research in stuttering suggests that individuals who stutter (IWS) may have a hyperactive error-monitoring system, leading to the exacerbation and anticipation of verbal dysfluencies. Using a neurophysiological marker of error processing known as the feedback error-related negativity, the current thesis involved three studies. First, a pilot study was conducted to ensure that word feedback cues were usable in the current paradigm. Second, a classic virtual T-maze task was used to assess the generic error processing mechanism of IWS. Third, an adaptation of the T-maze was used to assess the integrity of the reinforcement learning system of IWS and their ability to associate reward and error information of personalized problem words with predictive cues. Results suggest preliminary evidence for functional generic error processing in IWS and disrupted error processing when conditioned predictive cues are needed to predict fluent versus dysfluent outcomes. / Graduate

Considering the increasing levels of unemployment and underemployment, and the limited evidence concerning the impact of underemployment on health, my study examines the relations between subjective, objective, and time-related underemployment and employees’ health-related quality of life, as manifested through self-rated health, activity limitations and work-related stress. The study compares an expanded model of work-health relations that, along with the factors addressed by control-demand, and social capital theories, includes characteristics of the physical work environment, and employees’ economic class. In addition to the commonly examined factors related to employment and health (control-demand and social capital), my study explores the impact of the work environment (hazards, discomfort and physical demands) and economic class to determine the specific effects of underemployment on an employee’s health-related quality of life. My main argument is that underemployment, in conjunction with lower economic class, higher exposure to a harmful work environment, lack of control over work, and lower social capital, contributes to increased work-related stress and diminishes health-related quality of life. The study applies a mixed methodological approach based on data from the Canadian Work and Lifelong Learning Survey and the US General Social Survey, and qualitative analysis of interviews from the Ontario Survey on Education-Job Requirements Matching. Evidence based on cross-sectional and qualitative data analysis provides consistent findings and confirms the main assumption that high levels of underemployment have a significant effect on employees’ health-related quality of life. The study shows that employees’ economic class, characteristics of work environment and control over work carry the highest associations with health-related quality of life, while underemployment has a significant additive association with health-related quality of life, most importantly with work-related stress.

Opioid drug related death is the topic of this thesis. Each of the published works submitted in this volume has investigated an aspect of opioid drug related death. The publications have been grouped into three sub-themes: i. Characteristics of opioid drug related deaths ii. Methadone-related deaths in and out of treatment iii. Improving the quality of treatment for opioid drug dependence: a focus on injectable opioid treatment The introduction and background (Chapter1) will briefly review-the-relevant literature on opioid drug death predating my own contribution to the field. The next chapter of the thesis, 'Publications' (Chapter 2), will comprise the body of published work being submitted for the degree of Doctor of Medicine. Each article is accompanied by text on the preceding page outlining my individual contribution to that research study. The thesis will conclude with a discussion of the published works (Discussion, Chapter 3) which summarises the chief findings and reflects on the international significance and impact of the work. Finally, the Conclusion (Chapter 4) will submit suggestions for areas of future research into opioid drug related death.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2005. / Härtill 5 uppsatser.

Thesis (M.H.A.)--University of Michigan, 1963.

Thesis (M.H.A.)--University of Michigan, 1974. / Also issued in print.

Thesis (M.H.A.)--University of Michigan, 1963.

Thesis (M.H.A.)--University of Michigan, 1974. / eContent provider-neutral record in process. Description based on print version record.

Age-related macular degeneration (AMD) is a prevalent cause of vision loss and irreversible blindness that affects more than 11 million Americans. AMD is a multifactorial disease with a number of genetic, demographic, and environmental risk factors. Currently the etiology of AMD is still unclear and there are no effective cure for this devastating disease, but recent studies have demonstrated that RORA is a candidate gene involved in AMD pathophysiology. RORA is a critical regulator of multiple biological processes and has been implicated in various physiological processes including circadian rhythm, lipid metabolism, photoreceptor development, autism, and inflammation. Our current study will explore in depth the role of RORA in AMD. We will look at the effects of RORA in the retina of mice. Localization studies of retinal tissues obtained from mice with a conditional knockout of RORA in epithelial cells showed little effect of RORA on structural cells of the retina. However, there was a decrease in VEGF and TGF-B proteins in RORA knockout. This is an interesting finding because VEGF and TGF-B has an important function in angiogenesis and neovascularization which are pathophysiological effects of AMD. In addition, we will try to identify gene targets of RORA that have also been linked with AMD. By identifying the targets of RORA and discovering how RORA regulates these targets, we hope to better understand the role of RORA in AMD pathophysiology. ChIP-seq and software analysis of the data was performed to identify all genomic targets of RORA linked with AMD. A number of promising genes were found in both RORA and AMD networks. The next step of this study is to perform quantitative analysis of these genes and how their expression is affected by RORA. Also, we will perform additional conditional RORA knockout models in cone cells and developing retinal cells to further understand the role of RORA in the retina and AMD pathogenesis.