600 resultados para genetic regulation


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Small non-profit organisations play a vital role in the creation of social capital and resilience of civil society in Australia. A number of government inquiries have recently been commissioned to propose reform to non-profit enterprise and it is timely to examine the suitability of legal structures available for small non-profit organisations. This article reviews the characteristics of small Australian non-profit organisations and the legal treatment of similar associations in New Zealand, the United Kingdom, Europe, Canada and United States to inform possible reform strategies. Reforms are then proposed for small Australian unincorporated organisations which allow them access to the benefits of separate legal entity status, but with regulation proportionate to the risks posed to the broader community.

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This article examines a preliminary review and the limited evidence of over-regulation in Australian financial services. The 1997 Wallis Report and the CLERP 6 paper resulted in the amendments to Ch 7 of the Corporations Act 2001 (Cth) by the Financial Services Reform Act. Nearly a decade later the system based upon 'one-size fits all' dual track regime and a consistent licensing regime has greatly increased the costs of compliance. In the area of enforcement there has not been a dramatic change to the effective techniques applied by ASIC over other agencies such as APRA. In particular there are clear economic arguments, as well as international experiences which state that a single financial services regulator is more effective than the multi-layered approach adopted in Australia. Finally, in the superannuation area of financial services, which is worth A$800 billion there is unnecessary dual licensing and duplicated regulation with little evidence of any consumer-member benefit but at a much greater cost

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This paper describes experiments conducted in order to simultaneously tune 15 joints of a humanoid robot. Two Genetic Algorithm (GA) based tuning methods were developed and compared against a hand-tuned solution. The system was tuned in order to minimise tracking error while at the same time achieve smooth joint motion. Joint smoothness is crucial for the accurate calculation of online ZMP estimation, a prerequisite for a closedloop dynamically stable humanoid walking gait. Results in both simulation and on a real robot are presented, demonstrating the superior smoothness performance of the GA based methods.

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Transnational mergers are mergers involving firms operating in more than one jurisdiction, or which occur in one jurisdiction but have an impact on competition in another. Being of this nature, they have the potential to raise competition law concerns in more than one jurisdiction. When they do, the transaction costs of the merger to the firms involved, and the competition law authorities, are likely to increase significantly and, even where the merger is allowed to proceed, delays are likely to occur in reaping the benefits of the merger. Ultimately, these costs are borne by consumers. This thesis will identify the nature and source of regulatory costs associated with transnational merger review and identify and evaluate possible mechanisms by which these costs might be reduced. It will conclude that there is no single panacea for transnational merger regulation, but that a multi-faceted approach, including the adoption of common filing forms, agreement on filing and review deadlines and continuing efforts toward increasing international cooperation in merger enforcement, is needed to reduce regulatory costs and more successfully improve the welfare outcomes to which merger regulation is directed.

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Cloud computing is a latest new computing paradigm where applications, data and IT services are provided over the Internet. Cloud computing has become a main medium for Software as a Service (SaaS) providers to host their SaaS as it can provide the scalability a SaaS requires. The challenges in the composite SaaS placement process rely on several factors including the large size of the Cloud network, SaaS competing resource requirements, SaaS interactions between its components and SaaS interactions with its data components. However, existing applications’ placement methods in data centres are not concerned with the placement of the component’s data. In addition, a Cloud network is much larger than data center networks that have been discussed in existing studies. This paper proposes a penalty-based genetic algorithm (GA) to the composite SaaS placement problem in the Cloud. We believe this is the first attempt to the SaaS placement with its data in Cloud provider’s servers. Experimental results demonstrate the feasibility and the scalability of the GA.

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Web service composition is an important problem in web service based systems. It is about how to build a new value-added web service using existing web services. A web service may have many implementations, all of which have the same functionality, but may have different QoS values. Thus, a significant research problem in web service composition is how to select a web service implementation for each of the web services such that the composite web service gives the best overall performance. This is so-called optimal web service selection problem. There may be mutual constraints between some web service implementations. Sometimes when an implementation is selected for one web service, a particular implementation for another web service must be selected. This is so called dependency constraint. Sometimes when an implementation for one web service is selected, a set of implementations for another web service must be excluded in the web service composition. This is so called conflict constraint. Thus, the optimal web service selection is a typical constrained ombinatorial optimization problem from the computational point of view. This paper proposes a new hybrid genetic algorithm for the optimal web service selection problem. The hybrid genetic algorithm has been implemented and evaluated. The evaluation results have shown that the hybrid genetic algorithm outperforms other two existing genetic algorithms when the number of web services and the number of constraints are large.

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Current train of thought in appetite research is favouring an interest in non-homeostatic or hedonic (reward) mechanisms in relation to overconsumption and energy balance. This tendency is supported by advances in neurobiology that precede the emergence of a new conceptual approach to reward where affect and motivation (liking and wanting) can be seen as the major force in guiding human eating behaviour. In this review, current progress in applying processes of liking and wanting to the study of human appetite are examined by discussing the following issues: How can these concepts be operationalised for use in human research to reflect the neural mechanisms by which they may be influenced? Do liking and wanting operate independently to produce functionally significant changes in behaviour? Can liking and wanting be truly experimentally separated or will an expression of one inevitably contain elements of the other? The review contains a re-examination of selected human appetite research before exploring more recent methodological approaches to the study of liking and wanting in appetite control. In addition, some theoretical developments are described in four diverse models that may enhance current understanding of the role of these processes in guiding ingestive behaviour. Finally, the implications of a dual process modulation of food reward for weight gain and obesity are discussed. The review concludes that processes of liking and wanting are likely to have independent roles in characterising susceptibility to weight gain. Further research into the dissociation of liking and wanting through implicit and explicit levels of processing would help to disclose the relative importance of these components of reward for appetite control and weight regulation.

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This chapter is about the role of law in the management of the health workforce in Australia. Health professionals play an important role in the health system as the providers of treatment and care — without health professionals health systems would not function. The relationship between health professionals and patients has always been complex and is often subject to some form of regulation by the state. The first surviving written reference to such legal regulation dates from 1795-1750 BCE when the Babylonian Code of Hammurabi stated: “If a physician make a large incision with the operating knife, and kill him, or open a tumor with the operating knife, and cut out the eye, his hands shall be cut off.” Alexander the Great recommended the crucifixion of health professionals who killed their patients. Fortunately, the law in Australia prescribes lesser penalties for erring health professionals, but at the heart of modern regulation are similar concerns to those that underpinned the ancient Babylonian Code — to create conditions to ensure the safety of patients and the provision of quality services by health professionals.

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In a consumerist society obsessed with body image and thinness, obesity levels have reached an all-time high. This multi-faceted book written by a range of experts, explores the social, cultural, clinical and psychological factors that lie behind the Obesity Epidemic . It is required reading for the many healthcare professionals dealing with the effects of obesity and for anyone who wants to know more about the causes of weight gain and the best ways of dealing with it. Fat Matters covers a range of issues from sociology through medicine to technology. This is not a book for the highly specialised expert. Rather it is a book that shows the diversity of approaches to the phenomenon of obesity, tailored to the reader who wants to be up-to-date and well-informed on a subject that is possibly as frequently discussed and as misunderstood as the weather.

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Objective: The evidence was reviewed on how physical activity could influence the regulation of food intake by either adjusting the sensitivity of appetite control mechanisms or by generating an energy deficit that could adjust the drive to eat. Design: Interventionist and correlational studies that had a significant influence on the relationship between physical activity and food intake were reviewed. Interventionist studies involve a deliberate imposition of physical activity with subsequent monitoring of the eating response. Correlational studies make use of naturally occurring differences in the levels of physical activity (between and within subjects) with simultaneous assessment of energy expenditure and intake. Subjects: Studies using lean, overweight, and obese men and women were included. Results: Only 19% of interventionist studies report an increase in energy intake after exercise; 65% show no change and 16% show a decrease in appetite. Of the correlational studies, approximately half show no relationship between energy expenditure and intake. These data indicate a rather loose coupling between energy expenditure and intake. A common sense view is that exercise is futile as a form of weight control because the energy deficit drives a compensatory increase in food intake. However, evidence shows that this is not generally true. One positive aspect of this is that raising energy expenditure through physical activity (or maintaining an active life style) can cause weight loss or prevent weight gain. A negative feature is that when people become sedentary after a period of high activity, food intake is not “down-regulated” to balance a reduced energy expenditure. Conclusion: Evidence suggests that a high level of physical activity can aid weight control either by improving the matching of food intake to energy expenditure (regulation) or by raising expenditure so that it is difficult for people to eat themselves into a positive energy balance.

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Knowledge of the regulation of food intake is crucial to an understanding of body weight and obesity. Strictly speaking, we should refer to the control of food intake whose expression is modulated in the interests of the regulation of body weight. Food intake is controlled, body weight is regulated. However, this semantic distinction only serves to emphasize the importance of food intake. Traditionally food intake has been researched within the homeostatic approach to physiological systems pioneered by Claude Bernard, Walter Cannon and others; and because feeding is a form of behaviour, it forms part of what Curt Richter referred to as the behavioural regulation of body weight (or behavioural homeostasis). This approach views food intake as the vehicle for energy supply whose expression is modulated by a metabolic drive generated in response to a requirement for energy. The idea was that eating behaviour is stimulated and inhibited by internal signalling systems (for the drive and suppression of eating respectively) in order to regulate the internal environment (energy stores, tissue needs).

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Composite web services comprise several component web services. When a composite web service is executed centrally, a single web service engine is responsible for coordinating the execution of the components, which may create a bottleneck and degrade the overall throughput of the composite service when there are a large number of service requests. Potentially this problem can be handled by decentralizing execution of the composite web service, but this raises the issue of how to partition a composite service into groups of component services such that each group can be orchestrated by its own execution engine while ensuring acceptable overall throughput of the composite service. Here we present a novel penalty-based genetic algorithm to solve the composite web service partitioning problem. Empirical results show that our new algorithm outperforms existing heuristic-based solutions.

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In cloud computing resource allocation and scheduling of multiple composite web services is an important challenge. This is especially so in a hybrid cloud where there may be some free resources available from private clouds but some fee-paying resources from public clouds. Meeting this challenge involves two classical computational problems. One is assigning resources to each of the tasks in the composite web service. The other is scheduling the allocated resources when each resource may be used by more than one task and may be needed at different points of time. In addition, we must consider Quality-of-Service issues, such as execution time and running costs. Existing approaches to resource allocation and scheduling in public clouds and grid computing are not applicable to this new problem. This paper presents a random-key genetic algorithm that solves new resource allocation and scheduling problem. Experimental results demonstrate the effectiveness and scalability of the algorithm.

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Objective. Previous studies have shown the influence of subchondral bone osteoblasts (SBOs) on phenotypical changes of articular cartilage chondrocytes (ACCs) during the development of osteoarthritis (OA). The molecular mechanisms involved during this process remain elusive, in particular, the signal transduction pathways. The aim of this study was to investigate the in vitro effects of OA SBOs on the phenotypical changes in normal ACCs and to unveil the potential involvement of MAPK signaling pathways during this process. Methods. Normal and arthritic cartilage and bone samples were collected for isolation of ACCs and SBOs. Direct and indirect coculture models were applied to study chondrocyte hypertrophy under the influence of OA SBOs. MAPKs in the regulation of the cell–cell interactions were monitored by phosphorylated antibodies and relevant inhibitors. Results. OA SBOs led to increased hypertrophic gene expression and matrix calcification in ACCs by means of both direct and indirect cell–cell interactions. In this study, we demonstrated for the first time that OA SBOs suppressed p38 phosphorylation and induced ERK-1/2 signal phosphorylation in cocultured ACCs. The ERK-1/2 pathway inhibitor PD98059 significantly attenuated the hypertrophic changes induced by conditioned medium from OA SBOs, and the p38 inhibitor SB203580 resulted in the up-regulation of hypertrophic genes in ACCs. Conclusion. The findings of this study suggest that the pathologic interaction of OA SBOs and ACCs is mediated via the activation of ERK-1/2 phosphorylation and deactivation of p38 phosphorylation, resulting in hypertrophic differentiation of ACCs.

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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.