Previous studies have highlighted links between rising levels of ‘Islamophobic’ attitudes, increases in direct and structural violence towards Muslim individuals and communities, and the electoral success of the Howard Government in Australia. This thesis seeks to extend existing research by exploring how and why the wedge politics which the Government utilised so effectively during the 2004 election campaign, at the expense of Australian Muslims, failed to achieve the same endorsement from the media during the 2007 election campaign. Divergences in media representations of Muslims between 2004 and 2007 point to a crucial shift, when the Howard Government suddenly found its political currency devalued as support among key players in the media fell away. This study investigates this shift through an analysis of manifest content from one influential media genre – news reporting and commentary published in two broadsheet newspapers, The Australian and The Sydney Morning Herald. The implications of my analysis are explored by drawing on a suite of conceptual frames including Critical Discourse Analysis (CDA). This study found that Islam and issues related to Muslims were more likely to be represented through essentialist, ‘Islamophobic’ stereotypes, and were more frequently presented as a significant ‘problem’, in The Australian than in The Sydney Morning Herald. Whilst the two different publications often framed their selected stories with different emphases, the agenda-setting function of the different papers nevertheless showed a substantial overlap. For both publications, however, 2007 election reporting was characterised by increased contestation of essentialist discourses and a more adversarial stance towards the incumbent government. Analysis of this shift is utilised to suggest potential strategies for disrupting or contesting negative representational patterns in future reporting on Muslims and Islam

Anderson, Leticia

English

Dissertação de Mestrado em Biologia Celular e Molecular, apresentada ao Departamento de Ciências da Vida da Faculdade de Ciências e Tecnologia da Universidade de CoimbraA obesidade e a diabetes tipo 2 representam atualmente dois dos maiores problemas de saúde pública a nível mundial. Uma das características centrais destes distúrbios metabólicos é a resistência à insulina periférica. Curiosamente, estudos recentes sugerem que a resistência à insulina ocorre também no hipotálamo. Esta estrutura cerebral tem um papel importante na manutenção da homeostase, através da deteção de alterações metabólicas, e no controlo das respostas neuroendócrinas, que regulam o apetite, temperatura, controlo circadiano e libertação de hormonas. Tem sido proposto que a melhoria da sinalização da insulina e da neuroinflamação no hipotálamo pode restaurar a sensibilidade à insulina em órgãos periféricos.
As sirtuínas (SIRT1-7), proteínas com atividade de desacetilação dependente de NAD+, têm surgido como reguladores importantes numa variedade de processos celulares, tais como metabolismo, resposta ao stress e, possivelmente, envelhecimento. A sirtuína 2 (SIRT2) tem um papel importante na regulação do ciclo celular, neurodegeneração e supressão tumoral. Os dados agora emergentes indicam que a SIRT2 pode também desempenhar um papel importante na regulação metabólica e na neuroinflamação. Resultados obtidos previamente pelo nosso grupo, ainda não publicados, indicam que a SIRT2 é regulada negativamente em hepatócitos e fígados de ratinho insulino-resistentes e em células de sangue de humanos obesos resistentes à insulina. É importante salientar que a sobreexpressão de SIRT2 em hepatócitos insulino-resistentes melhora a sensibilidade à insulina, através da atenuação do stress oxidativo e de disfunção mitocondrial.
Este estudo demonstra que a SIRT2 é expressa no hipotálamo, encontrando-se particularmente enriquecida no VMH e presente em neurónios. A SIRT2 no VMH é regulada pela disponibilidade energética, uma vez que a sua expressão se encontra aumentada em restrição calórica e drasticamente reduzida em condições de dieta rica em gordura. Demonstramos ainda que, na presença de palmitato, um ácido gordo saturado, a SIRT2 no VMH também se encontra diminuída, de forma semelhante ao que acontece na dieta rica em gordura. Mostramos ainda que a exposição ao palmitato pode induzir resistência à insulina e diminuição da expressão de SIRT2. No entanto, a
Sirtuin 2 in hypothalamus: an emerging target in insulin resistance?
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privação de soro melhora a sensibilidade à insulina em condições normais, e evita o efeito da resistência à insulina induzida pelo palmitato, bem como a diminuição da SIRT2.
Este estudo sugere que a SIRT2 pode no futuro ser um alvo importante no tratamento da obesidade e da diabetes tipo 2.Obesity and type 2 diabetes constitute major public health problems worldwide. A central feature of these metabolic disorders is peripheral insulin resistance. Interestingly, recent studies suggest that insulin resistance also occurs in hypothalamus. This structure has an important role in the maintenance of homeostasis, by detecting metabolic changes and controlling neuroendocrine responses that regulate appetite, temperature, circadian control and release of hormones. It has been proposed that improving defective hypothalamic insulin signalling and neuroinflammation may restore insulin sensitivity in peripheral organs.
The sirtuin family (SIRT1-7) of NAD+-dependent protein deacetylases have emerged as important regulators for a variety of cellular processes, including energy metabolism, stress response and possibly aging. SIRT2 has an important role in cell cycle regulation, neurodegeneration and tumor suppression. Data now emerging indicate that SIRT2 may also play a key role in metabolic regulation and neuroinflammation. Unpublished data from the host laboratory indicate that SIRT2 is downregulated in insulin-resistant hepatocytes and mouse livers as well as in blood cells from obese insulin-resistant human subjects. Importantly, SIRT2 overexpression in hepatocytes improves insulin sensitivity by reducing oxidative stress and improving mitochondrial dysfunction.
This study demonstrates that SIRT2 is expressed in the mouse hypothalamus, being particularly enriched in the VMH, and present in neurons. SIRT2 expression in the VMH is regulated by nutritional availability since its expression is increased under caloric restriction and markedly reduced in high-fat diet conditions. We also demonstrate that direct administration of palmitate, a saturated free-fatty acid, to the VMH results in reduced SIRT2 expression, similarly to what happens in high-fat diet. We found that exposure of cultured hypothalamic neurons to palmitate induces insulin resistance and downregulates SIRT2 expression. Importantly, serum starvation improves insulin sensitivity in normal conditions, and prevents the effect of palmitate on insulin resistance and SIRT2 downregulation.
Sirtuin 2 in hypothalamus: an emerging target in insulin resistance?
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This study suggest that SIRT2 may be in future an important target in obesity and insulin resistance treatment, by modulating its expression and/or activity

Santos, Liliana Isabel Fernandes

Estudo Geral

Sirtuin 2 in hypothalamus: an emerging target in insulin resistance?

Sydney eScholarship