Thesis (M. A. (Social Work)) -- University of Limpopo, 2004. / The aim of this study was to explore the impact of culture on the prevention and reatment of HIV/AIDS amongst people in low-resourced areas like Malamulele. he study focused on the lifestyles, beliefs, attitudes and perceptions around ultural elements and practices, which might impact negatively on the prevention nd treatment of the HIV/AIDS epidemic. There were three groups of research espondents namely: learners from three high schools in Malamulele, some arents of the learners and the traditional/cultural leaders. The researcher ollected both qualitative and quantitative data. The data was gathered through he use of an interview schedule (questionnaire), focus group discussions and ound-table discussion sessions. The data was presented, analysed and nterpreted by means of tables and charts. t was found that people in low-resourced (rural) areas have little knowledge about HIV/AIDS, causes, symptoms and how the disease is transmitted. Despite the fact that awareness and educational campaigns and programmes are being rendered, people in low-resourced (rural) areas have little knowledge and needed skills about prevention and treatment of the pandemic. Polygamy and extra-marital relations by men is still highly valued and viewed at high esteem. Religious structures seem to be detached to the issue of HIV/AIDS as they mentioned that talking about HIV/AIDS is immoral and against their principles. The study also tried to explore the extent to which people in low-resourced areas view and use condoms as a protective means.

University of Macau / Institute of Chinese Medical Sciences

University of Macau / Institute of Chinese Medical Sciences

University of Macau / Institute of Chinese Medical Sciences

The HIV/AIDS pandemic has implications at every level of social functioning. It affects individuals, families, communities and organisations. The burden of caring for those exposed, affected and infected is vast, but one of the most significant developments which have the potential to reduce disease burden is antiretroviral therapy. Antiretroviral therapy (ART) is complex and difficult to administer, and requires a learning process which is mediated through a number of means. Vygotskian theory was utilised to better understand the process of adherence through mediated learning, and as a framework for explaining compliance. In this study, mediated learning occurs both in the context of the clinic staff and the clinic attendees, and the caregivers and the child. Therefore Vygotsky‟s theory offers useful insight into this process. This qualitative study aimed to research the factors which contribute to ART adherence in a small sample of HIV positive children who are attending a local clinic. Eight child-caregiver dyads were interviewed, and drawings utilised to better understand child and caregiver factors which contribute to compliance. There were a number of psychosocial factors identified which contribute to compliance, or lack thereof, including social support, stigma, medication fatigue, disclosure, access difficulties, psychoeducation, and motivation. A number of qualitative differences were also identified between children who knew their HIV status and those who did not. These differences emerged primarily through the analysis of the child participants‟ drawings and there appeared to be a number of inter- and intrapersonal benefits to disclosure. The factors identified in this study, if better understood, can inform interventions to improve compliance on ART. / Thesis (M.Soc.Sci.)-University of KwaZulu-Natal, Pietermaritzburg, 2010.

In recent years there has been a worldwide recognition of the disparity of HIV treatment available in the West and in Sub-Saharan Africa. The West African nation of Senegal was early to implement measures that allowed for the distribution of highly effective anti-HIV therapy known as Antiretroviral (ARV) therapy to a limited number of patients. This thesis explores how patients living in Senegal who are infected with HIV have engaged in various negotiations to obtain access to treatment and other resources to meet the needs posed by their infection. These negotiations are framed by various historically embedded notions of how to engage relationships in the search for care. Strategies are also shaped by the biopolitically-laden discourse that guides the distribution of ARV therapy. This thesis traces the structure, evolution, and effects of patients' strategic negotiations in response to the introduction of this therapeutic technology.

Stroke remains a leading cause of disability in the western world, with symptoms ranging in severity from mild congnitive or motor impairments, to severe impairments in both cognitive and motor domains. Despite ongoing research aimed at helping stroke patients the disease cannot be prevented or cured, therefore a large body of research has been aimed at identifying effective rehabilitative strategies. Based on our understanding of normal brain function, and the meachanisms mediating the limited spontaneous recovery that is observed following injury, factors that promote brain plasticity are likely to be effective treatments for stroke symptoms. The current thesis investigated three novel treatments (COX-2 inhibitor drug, vitamin supplement diet, and social experience) in a rat model of focal ischemia in the motor cortex. All three treatments have been previously shown to alter plasticity in the normal brain, however the current experiments show that the treatments have differential effects following stroke. The COX-2 inhibitors provided limited improvement in functional performance, whereas the vitamin supplement treatment had no effect. Social experience on the other hand was found to block the usually observed spontaneous improvements following the stroke. These results suggest that factors that alter dendritic plasticity may in fact serve as effective stroke treatments depending on the site and the mechanisms whereby the plastic changes are induced. / ix, 149 leaves : ill. ; 29 cm.

Middle cerebral artery (MCA) stroke can produce chronic incapacitating motor impairments. Understanding the neural basis of the motor syndromes is complicated by the diversity of neural structures damaged but the problem can be addressed in laboratory rats by inducing selective infarcts. Nevertheless, the motor syndromes that ensue from stroke in rats remain poorly understood and undermine its potential as a model for clinical stroke. The objective of the present thesis was to document the skilled reaching impairments from neocortical and subcortical MCA infarcts in rats. In addition, the integrity of the motor system components spared by the infarct was assessed neurophysiologically and neuroanatomically. Characteristic reaching impairments emerged from each infarct but there were also some overlapping features that might be explained by neural dysfunction extending beyond the boundaries of the infarct. The present studies showed that the laboratory rat is an ideal animal model for studying stroke, which should be of interest to both clinical and research scientists studying stroke. / xiii, 345 leaves : ill. ; 29 cm. + 1 CD-ROM

Alzheimer’s disease (AD) is the leading cause of dementia but despite being identified over a century ago, current treatments remain limited. To date, no disease-modifying therapies are available. Soluble, intracellular forms of β-amyloid (Aβ), a protein associated with AD, have been identified and intracellular targets of Aβ are being investigated as potential targets for new drugs. Amyloid binding alcohol dehydrogenase (ABAD) was previously identified as a mitochondrial target of Aβ and is known to be up-regulated in AD. This interaction results in production of reactive oxygen species and cell death. Using a small peptide, known as the “decoy peptide”, disruption of this interaction has been shown to reverse biochemical and behavioural symptoms in an AD mouse model. The work reported in this thesis describes the approaches taken to develop methods for in vitro and ex vivo study of the interaction between ABAD and Aβ. A fluorogenic assay for measuring the intracellular activity of ABAD in living cells was developed and using this technique, the intracellular inhibition of ABAD by Aβ was observed for the first time. Surface plasmon resonance was used to measure binding between ABAD and Aβ and also showed the first quantitative analysis of direct binding of the decoy peptide to Aβ42. In order to synthesise small molecule inhibitors of ABAD activity with the aim of developing a molecular probe of the enzyme’s activity, compounds were identified by screening a fragment-based library. Subsequent optimisation of the compound structure led to a 10-fold improvement in the IC50 and has resulted in a lead compound for future development. A similar screening strategy was employed to identify potential small molecule inhibitors of the ABAD-Aβ interaction. This research has resulted in a range of tools and methods for studying ABAD activity and interactions, which will greatly benefit future work on developing compounds that inhibit the ABAD-Aβ interaction to provide a novel method for treating Alzheimer’s disease.

Parkinson's disease (PD) is one of the most common motor neurodegenerative diseases, affecting 1-2% of the world's population over the age of 65. It is characterised by a loss of dopamine neurons within the substantia nigra, which is an integral part of the basal ganglia (BG) where dopamine is the most important modulating neurotransmitter. As the BG is primarily involved with the execution of movement, the lack of dopamine input results in dysfunctional motor control. The current PD treatment, L-DOPA, improves these motor symptoms, however only provides patients 5 to 10 years of improved quality of life before debilitating side effects, often worse than the original symptoms, begin. The neuropeptide substance P (SP) is found in high concentration in the substantia nigra, and BG in general, where it is involved in dopamine release. In the late stages of PD, SP content within the substantia nigra and BG is decreased, thus implicating SP in the pathophysiology of PD. However, SP production has not been examined in the early stages of PD when dopaminergic degeneration is first initiated. This thesis therefore sought to characterise the role of SP in dopaminergic degeneration in an experimental model of early PD, the 6-hydroxydopamine model in rats. In contrast to the prevailing dogma that a decline in SP is associated with neurodegeneration in PD, this thesis demonstrates that SP is actually increased within the striatum in early PD, particular in perivascular tissue and within surviving dopaminergic neurons during the degenerative process. Increasing exposure of the dopaminergic neurons to SP, either by inhibition of substance P breakdown with Captopril or by direct injection with SP, exacerbated the disease progression as indicated by more profound neurogenic inflammation, functional deficits and increased dopaminergic cell death. However, when SP was inhibited by treatment with a SP NK₁ receptor antagonist, dopaminergic neurons were conserved, the inflammatory response was reduced and motor function was returned to near normal levels. We conclude that SP is increased in early PD, and that increased SP plays an important role in the degenerative process, specifically, in the genesis of BBB breakdown and initiation of neurogenic inflammation. Treatment with an NK1 antagonist may thus represent a novel therapeutic approach to early stage Parkinson’s disease. / Thesis (Ph.D.) -- University of Adelaide, School of Medical Sciences, 2009