409 resultados para Action positive


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Recent releases from the International Federation of Accountants (IFAC) highlight the importance of ethics education. Academic institutions employ varying methods of teaching ethics and place varying levels of emphasis on ethics teaching during a business/accounting degree. This paper attempts to evaluate whether teaching ethics to final year accountancy students is beneficial. At the commencement of a semester 85 final year accounting students were given five ethical scenarios on which to make an ethical decision. During the semester they were subject to two different methods of teaching ethics, a traditional lecture/tutorial process and a group assignment. ----- After a significant gap, students were re-presented with the ethical scenarios and asked what action they now considered appropriate. In all five instances students offered a more ethical response the second time. When asked to evaluate the methodologies the students considered both training methods to have a positive effect on their ethical thinking. The results suggest it is beneficial to include ethics teaching in accountancy courses, if the profession’s goal of ethical practitioners is to be achieved.

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A Positive Buck-Boost converter is a known DC-DC converter which may be controlled to act as Buck or Boost converter with same polarity of the input voltage. This converter has four switching states which include all the switching states of the above mentioned DC-DC converters. In addition there is one switching state which provides a degree of freedom for the positive Buck-Boost converter in comparison to the Buck, Boost, and inverting Buck-Boost converters. In other words the Positive Buck-Boost Converter shows a higher level of flexibility for its inductor current control compared to the other DC-DC converters. In this paper this extra degree of freedom is utilised to increase the robustness against input voltage fluctuations and load changes. To address this capacity of the positive Buck-Boost converter, two different control strategies are proposed which control the inductor current and output voltage against any fluctuations in input voltage and load changes. Mathematical analysis for dynamic and steady state conditions are presented in this paper and simulation results verify the proposed method.

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The global financial crisis, global pandemics, global warming and peak oil are indicative of a world facing major environmental, social and economic problems. At the same time, world population continues to rise and global inequalities deepen. Children are the most vulnerable to the impacts of unsustainable living with specific harms arising because of their physical and cognitive vulnerabilities. Nevertheless, children do not have to be victims in the face of these challenges. Education, including early childhood education, has an important role to in building resilience and capabilities in children that equip them as active and informed citizens now and in the future and who are capable of contributing to healthy and sustainable ways of living. Drawing on educational change literature, action research, education for sustainability, health promotion and systems theory, this paper outlines three strategies that can help reorient early childhood education towards sustainability. One strategy is the adoption of whole centre approaches to sustainability and education for sustainability. This means working across the whole of a centre’s operations – curriculum and pedagogy, physical and social environments, its partnerships and community connections. The second strategy – applied in conjunction with the first – is the use of action research to investigate the early childhood setting and to create the desired changes. The third strategy is the adoption of systems thinking as a way of leveraging support and momentum for change so that education for sustainability goes beyond the initiatives of individual teachers and centres, and becomes a systems-wide imperative.

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This study aims to stimulate thought, debate and action for change on this question of more vigorous philanthropic funding of Australian health and medical research (HMR). It sharpens the argument with some facts and ideas about HMR funding from overseas sources. It also reports informed opinions from those working, giving and innovating in this area. It pinpoints the range of attitudes to HMR giving, both positive and negative. The study includes some aspects of Government funding as part of the equation, viewing Government as major HMR givers, with particular ability to partner, leverage and create incentives. Stimulating new philanthropy takes active outreach. The opportunity to build more dialogue between the HMR industry and the wider community is timely given the ‘licence to practice’ issues and questioned trust that applies currently somewhat both to science and to the charitable sector. This interest in improving HMR philanthropy also coincides with the launch last year by the Federal Government of Nonprofit Australia Limited (NAL), a group currently assessing infrastructure improvements to the charitable sector. History suggests no one will create this change if Research Australia does not. However, interest in change exists in various quarters. For Research Australia to successfully change the culture of Australian HMR giving, the process will drive the outcomes. Obviously stakeholder buy-in and partners will be needed and the ultimate blueprint for greater philanthropic HMR funding here will not be this document. Instead it will be the one that wears the handprint and ‘mindprint’ of the many architects and implementers interested in promoting HMR philanthropy, from philanthropists to nonprofit peaks to government policy arms. As the African proverb says, ‘If you want to go fast, go alone; but if you want to go far, go with others’.

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This manual is designed to assist human service practitioners and agencies, and the communities they work with, to enhance their skills in undertaking Participatory Action Research, and, in so doing improve the situations of people who are vulnerable. It utilises insights derived from a number of Australian Government funded programs, most notably Reconnect, NAYSS and Household Organisational Management Expenses (HOME) Advice.

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The diversity of community voices in the SEQ ‘bellwether region’ has grown from a muted murmur in the mid twentieth century supporting provision of urban services, rural conservation and green belts, to the current clamour against over-development, and in favour of protecting local and regional open space, wetlands and natural habitats. This in turn has often resulted in vigorous campaigns against unpopular roads, dams, dumps and tall buildings. In the last twenty years community issues have played a major part in local government elections throughout the region and have even helped unseat (in 1995-1996) a state government which discounted their authenticity and community resolve.

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Recently it has been shown that the consumption of a diet high in saturated fat is associated with impaired insulin sensitivity and increased incidence of type 2 diabetes. In contrast, diets that are high in monounsaturated fatty acids (MUFAs) or polyunsaturated fatty acids (PUFAs), especially very long chain n-3 fatty acids (FAs), are protective against disease. However, the molecular mechanisms by which saturated FAs induce the insulin resistance and hyperglycaemia associated with metabolic syndrome and type 2 diabetes are not clearly defined. It is possible that saturated FAs may act through alternative mechanisms compared to MUFA and PUFA to regulate of hepatic gene expression and metabolism. It is proposed that, like MUFA and PUFA, saturated FAs regulate the transcription of target genes. To test this hypothesis, hepatic gene expression analysis was undertaken in a human hepatoma cell line, Huh-7, after exposure to the saturated FA, palmitate. These experiments showed that palmitate is an effective regulator of gene expression for a wide variety of genes. A total of 162 genes were differentially expressed in response to palmitate. These changes not only affected the expression of genes related to nutrient transport and metabolism, they also extend to other cellular functions including, cytoskeletal architecture, cell growth, protein synthesis and oxidative stress response. In addition, this thesis has shown that palmitate exposure altered the expression patterns of several genes that have previously been identified in the literature as markers of risk of disease development, including CVD, hypertension, obesity and type 2 diabetes. The altered gene expression patterns associated with an increased risk of disease include apolipoprotein-B100 (apo-B100), apo-CIII, plasminogen activator inhibitor 1, insulin-like growth factor-I and insulin-like growth factor binding protein 3. This thesis reports the first observation that palmitate directly signals in cultured human hepatocytes to regulate expression of genes involved in energy metabolism as well as other important genes. Prolonged exposure to long-chain saturated FAs reduces glucose phosphorylation and glycogen synthesis in the liver. Decreased glucose metabolism leads to elevated rates of lipolysis, resulting in increased release of free FAs. Free FAs have a negative effect on insulin action on the liver, which in turn results in increased gluconeogenesis and systemic dyslipidaemia. It has been postulated that disruption of glucose transport and insulin secretion by prolonged excessive FA availability might be a non-genetic factor that has contributed to the staggering rise in prevalence of type 2 diabetes. As glucokinase (GK) is a key regulatory enzyme of hepatic glucose metabolism, changes in its activity may alter flux through the glycolytic and de novo lipogenic pathways and result in hyperglycaemia and ultimately insulin resistance. This thesis investigated the effects of saturated FA on the promoter activity of the glycolytic enzyme, GK, and various transcription factors that may influence the regulation of GK gene expression. These experiments have shown that the saturated FA, palmitate, is capable of decreasing GK promoter activity. In addition, quantitative real-time PCR has shown that palmitate incubation may also regulate GK gene expression through a known FA sensitive transcription factor, sterol regulatory element binding protein-1c (SREBP-1c), which upregulates GK transcription. To parallel the investigations into the mechanisms of FA molecular signalling, further studies of the effect of FAs on metabolic pathway flux were performed. Although certain FAs reduce SREBP-1c transcription in vitro, it is unclear whether this will result in decreased GK activity in vivo where positive effectors of SREBP-1c such as insulin are also present. Under these conditions, it is uncertain if the inhibitory effects of FAs would be overcome by insulin. The effects of a combination of FAs, insulin and glucose on glucose phosphorylation and metabolism in cultured primary rat hepatocytes at concentrations that mimic those in the portal circulation after a meal was examined. It was found that total GK activity was unaffected by an increased concentration of insulin, but palmitate and eicosapentaenoic acid significantly lowered total GK activity in the presence of insulin. Despite the fact that total GK enzyme activity was reduced in response to FA incubation, GK enzyme translocation from the inactive, nuclear bound, to active, cytoplasmic state was unaffected. Interestingly, none of the FAs tested inhibited glucose phosphorylation or the rate of glycolysis when insulin is present. These results suggest that in the presence of insulin the levels of the active, unbound cytoplasmic GK are sufficient to buffer a slight decrease in GK enzyme activity and decreased promoter activity caused by FA exposure. Although a high fat diet has been associated with impaired hepatic glucose metabolism, there is no evidence from this thesis that FAs themselves directly modulate flux through the glycolytic pathway in isolated primary hepatocytes when insulin is also present. Therefore, although FA affected expression of a wide range of genes, including GK, this did not affect glycolytic flux in the presence of insulin. However, it may be possible that a saturated FA-induced decrease in GK enzyme activity when combined with the onset of insulin resistance may promote the dys-regulation of glucose homeostasis and the subsequent development of hyperglycaemia, metabolic syndrome and type 2 diabetes.