19 resultados para Hallmarks

em Queensland University of Technology - ePrints Archive


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Mark Taylor's new essay assesses the impact of the diagram on interior design from the late 19th century to the present. Taylor identifies the pop-cultural discourse of advice writing in both books and magazines as a starting point for his analysis. Drawing on diverse sources, his analysis focuses on texts relating to the dynamics of use and flexibility by Catherine Beecher, Harriet Beecher Stowe, Melusina Fay Peirce, Mary Haweis and Christine Frederick among others. The examples in these texts use the home, domestic housekeeping and kitchens as the sites and practices of intervention through which interior design innovations can be enacted. Taylor's analysis identified the innovations in both the social and the political aspects of space and the critique of static space behind these seemingly amateurish and innocuous texts. Identifying these contributions as early precursors of Modernism's open-plan and flexible, dynamic spaces, Taylor also interprets them with a critical concern for the oppositions and hierarchies that can exist in spatial design, and which are the hallmarks of recent Postmodern, phenomenological approaches to interior design and its theorisations. The progressive and subversive "paradigms for living" implicit in these diagrams can be argued to present a model of greater economic, social and political equality as well as representing a more balanced set of power relations in the home. Progressing through the 20th century to the present, Taylor's analysis shifts byond the dressed body and on to the more intimate rituals of the revealed body to further examine how diagrams of the interior, and the interior as a set of diagrams, are also mediators, sites and grounds for the design of social and sexual intimacy. Through a consideration of the link between design, indentity and intimacy (whether of the invisible, fashioned or sexualised body), the diagrms of interiors are reconfigured as radical and critical tools for an animate, material and emancipatory "redressing" of the balance between the body, identity, sexuality, gender, function, mis(use), aesthetics and the interior.

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Neo-liberalism has become one of the boom concepts of our time. From its original reference point as a descriptor of the economics of the “Chicago School” such as Milton Friedman, or authors such as Friedrich von Hayek, neo-liberalism has become an all-purpose descriptor and explanatory device for phenomena as diverse as Bollywood weddings, standardized testing in schools, violence in Australian cinema, and the digitization of content in public libraries. Moreover, it has become an entirely pejorative term: no-one refers to their own views as “neo-liberal”, but it rather refers to the erroneous views held by others, whether they acknowledge this or not. Neo-liberalism as it has come to be used, then, bears many of the hallmarks of a dominant ideology theory in the classical Marxist sense, even if it is often not explored in these terms. This presentation will take the opportunity provided by the English language publication of Michel Foucault’s 1978-79 lectures, under the title of The Birth of Biopolitics, to consider how he used the term neo-liberalism, and how this equates with its current uses in critical social and cultural theory. It will be argued that Foucault did not understand neo-liberalism as a dominant ideology in these lectures, but rather as marking a point of inflection in the historical evolution of liberal political philosophies of government. It will also be argued that his interpretation of neo-liberalism was more nuanced and more comparative than the more recent uses of Foucault in the literature on neo-liberalism. It will also look at how Foucault develops comparative historical models of liberal capitalism in The Birth of Biopolitics, arguing that this dimension of his work has been lost in more recent interpretations, which tend to retro-fit Foucault to contemporary critiques of either U.S. neo-conservatism or the “Third Way” of Tony Blair’s New Labour in the UK.

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As part of the Australian Government’s Clean Energy Plan, the Government has attempted to harness the legal innovation of the tradeable emissions unit, within a capped carbon trading system, to reduce greenhouse gas emissions. Such an approach promises to send a price signal to the market which will influence emitting behaviours and reduce our emissions in a cost-effective manner. However, if the carbon trading scheme is to successfully achieve cost-effective emissions reductions then the carbon market must be supported by an appropriate legal framework. This paper will consider the key features of the Australian Carbon Pricing Mechanism, including the Carbon Farming Initiative, and critique whether it has all the hallmarks of an effective legal framework to reduce Australia’s net greenhouse gas emissions. The likely future of the trading scheme, following the 2013 elections, will also be addressed.

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The current regulatory approach to coal seam gas projects in Queensland is based on the philosophy of adaptive environmental management. This method of “learning by doing” is implemented in Queensland primarily through the imposition of layered monitoring and reporting duties on the coal seam gas operator alongside obligations to compensate and “make good” harm caused. The purpose of this article is to provide a critical review of the Queensland regulatory approach to the approval and minimisation of adverse impacts from coal seam gas activities. Following an overview of the hallmarks of an effective adaptive management approach, this article begins by addressing the mosaic of approval processes and impact assessment regimes that may apply to coal seam gas projects. This includes recent Strategic Cropping Land reforms. This article then turns to consider the preconditions for land access in Queensland and the emerging issues for landholders relating to the negotiation of access and compensation agreements. This article then undertakes a critical review of the environmental duties imposed on coal seam gas operators relating to hydraulic fracturing, well head leaks, groundwater management and the disposal and beneficial use of produced water. Finally, conclusions are drawn regarding the overall effectiveness of the Queensland framework and the lessons that may be drawn from Queensland’s adaptive environmental management approach.

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The cultural and creative industries contribution to the economic and social sustainability of cities is a well acknowledged phenomenon which has accelerated in the era of urban renewal since the late twentieth century. The second-tier city of Brisbane, Australia was for many years considered a cultural backwater in the national context, yet its recent urban development within a short period of time has produced a city that now has all the hallmarks of a ‘creative city’. Brisbane’s transformation has been shaped by urban and cultural policies that are largely focussed around its inner-metropolitan localities, producing a growth in cultural infrastructure and the aestheticisation of inner-city precincts. However, like most Australian cities, the majority of Brisbane’s population live, and increasingly work in the suburbs. This article is based on a large research project that shows that creative industries workers are well represented across suburban localities. The article examines the policy and planning implications for creative industries located in Australian outer suburbs and the communities in which they are located.

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Within contemporary performance arenas young people are fast becoming part of the vanguard of contemporary performance. Performativity, convergence and openness of form are key animating concepts in the landscape of Theatre for Young People (TYP). To ignore what is taking place in the making of performance for and by young people is to ignore the new possibilities in meaning-making and theatrical form. This thesis investigates the contemporary practice within the field of Theatre for Young People. Pivotal to the study are three hallmarks of contemporary performance – shifting notions of performativity; convergence articulated in the use of technology and theatrical genres; and Umberto Eco’s realisation of openness in form and authorship. The thesis draws from theatre and performance studies, globalisation theory and youth studies. Using interviews of Theatre for Young People practitioners and observation of thirty-nine performances, this thesis argues that young people and Theatre for Young People companies are among the leaders of a paradigm shift in developing and delivering performance works. In this period of rapid technological change young people are embracing and manipulating technology (sound, image, music) to represent whom they are and what they want to say. Positioned as ‘cultural catalysts’ (McRobbie, 1999), ‘the new pioneers’ (Mackay, 1993) and ‘first navigators’ (Rushkoff, 1996) young people are using mediatised culture and digital technologies with ease, placing them at the forefront of a shift in cultural production. The processes of deterritorialisation allows for the synthesis of new cultural and performance genres by fragmenting and hybridising traditional cultural categories and forms including the use of new media technologies. Almost half of all TYP performances now incorporate the technologies of reproduction. The relationship between live and mediatised forms, the visceral and the virtual is allowing young people to navigate and make meaning of cultural codes and cultural forms as well as to engage in an open dialogue with their audiences. This thesis examines the way young people are using elements of deterritorialisation to become producers of new performance genres. The thesis considers the contemporary situation in relation to issues of performance making and performance delivery within a global, networked and technology-driven society.

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The sheep (Ovis aries) is commonly used as a large animal model in skeletal research. Although the sheep genome has been sequenced there are still only a limited number of annotated mRNA sequences in public databases. A complementary DNA (cDNA) library was constructed to provide a generic resource for further exploration of genes that are actively expressed in bone cells in sheep. It was anticipated that the cDNA library would provide molecular tools for further research into the process of fracture repair and bone homeostasis, and add to the existing body of knowledge. One of the hallmarks of cDNA libraries has been the identification of novel genes and in this library the full open reading frame of the gene C12orf29 was cloned and characterised. This gene codes for a protein of unknown function with a molecular weight of 37 kDa. A literature search showed that no previous studies had been conducted into the biological role of C12orf29, except for some bioinformatics studies that suggested a possible link with cancer. Phylogenetic analyses revealed that C12orf29 had an ancient pedigree with a homologous gene found in some bacterial taxa. This implied that the gene was present in the last common eukaryotic ancestor, thought to have existed more than 2 billion years ago. This notion was further supported by the fact that the gene is found in taxa belonging to the two major eukaryotic branches, bikonts and unikonts. In the bikont supergroup a C12orf29-like gene was found in the single celled protist Naegleria gruberi, whereas in the unikont supergroup, encompassing the metazoa, the gene is universal to all chordate and, therefore, vertebrate species. It appears to have been lost to the majority of cnidaria and protostomes taxa; however, C12orf29-like genes have been found in the cnidarian freshwater hydra and the protostome Pacific oyster. The experimental data indicate that C12orf29 has a structural role in skeletal development and tissue homeostasis, whereas in silico analysis of the human C12orf29 promoter region suggests that its expression is potentially under the control of the NOTCH, WNT and TGF- developmental pathways, as well SOX9 and BAPX1; pathways that are all heavily involved in skeletogenesis. Taken together, this investigation provides strong evidence that C12orf29 has a very important role in the chordate body plan, in early skeletal development, cartilage homeostasis, and also a possible link with spina bifida in humans.

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The 'human topoisomerase I (htopoI) damage response' was reported to be triggered by various kinds of DNA lesions. Also, a high and persistent level of htopoI cleavage complexes correlated with apoptosis. In the present study, we demonstrate that DNA damage-independent induction of cell death using colcemid and tumor necrosis factor is also accompanied by a strong htopoI response that correlates with the onset of apoptotic hallmarks. Consequently, these results suggest that htopoI cleavage complex formation may be caused by signaling pathways independent of the kind of cellular stress. Thus, protein interactions or signaling cascades induced by DNA damage or cellular stress might lead to the formation of stabilized cleavage complexes rather than the DNA lesion itself. Finally, we show that p53 not only plays a key role in the regulation of the htopoI response to UV-C irradiation but also to treatment with colcemid.

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One of the hallmarks of progressive renal disease is the development of tubulointerstitial fibrosis. This is frequently preceded by macrophage infiltration, raising the possibility that macrophages relay fibrogenic signals to resident tubulointerstitial cells. The aim of this study was to investigate the potentially fibrogenic role of interleukin-1beta (IL-1beta), a macrophage-derived inflammatory cytokine, on cortical fibroblasts (CFs). Primary cultures of human renal CFs were established and incubated for 24 hours in the presence or absence of IL-1beta. We found that IL-1beta significantly stimulated DNA synthesis (356.7% +/- 39% of control, P <.003), fibronectin secretion (261.8 +/- 11% of control, P <.005), collagen type 1 production, (release of procollagen type 1 C-terminal-peptide, 152.4% +/- 26% of control, P <.005), transforming growth factor-beta (TGF-beta) secretion (211% +/- 37% of control, P <.01), and nitric oxide (NO) production (342.8% +/- 69% of control, P <.002). TGF-beta (1 ng/mL) and the phorbol ester phorbol 12-myristate 13-acetate (PMA, 25 nmol/L) produced fibrogenic effects similar to those of IL-1beta. Neither a NO synthase inhibitor (N(G)-methyl-l-arginine, 1 mmol/L) nor a protein kinase C (PKC) inhibitor (bis-indolylmaleimide 1, 1 micromol/L) altered the enhanced level of fibronectin secretion or DNA synthesis seen in response to IL-1beta treatment. However, addition of a TGF-beta-neutralizing antibody significantly reduced IL-1beta-induced fibronectin secretion (IL-1beta + IgG, 262% +/- 72% vs IL-1beta + alphaTGF-beta 156% +/- 14%, P <.02), collagen type 1 production (IL-1beta + IgG, 176% +/- 28% vs IL-1beta + alphaTGF-beta, 120% +/- 14%, P <.005) and abrogated IL-1beta-induced DNA synthesis (245% +/- 49% vs 105% +/- 21%, P <.005). IL-1beta significantly stimulated CF DNA synthesis and production of fibronectin, collagen type 1, TGFbeta, and NO. The fibrogenic and proliferative action of IL-1beta on CF appears not to involve activation of PKC or production of NO but is at least partly TGFbeta-dependent.

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It was Dvorak in 1986 that postulated 'tumours are wounds that do not heal' as they share common cellular and molecular mechanisms, which are active in both wounds and in cancer tissue. Inflammation is a crucial part of the innate immune system that protects against pathogens and initiates adaptive immunity. Acute inflammation is usually a rapid and self-limiting process, however it does not always resolve. This leads to the establishment of a chronic inflammatory state and provides the perfect environment for carcinogenesis. Inflammation and cancer have long had an association, going back as far as Virchow in 1863, when leucocytes were noted in neoplastic tissue. It has been estimated that approximately 25% of all malignancies are initiated or exacerbated by inflammation caused by infectious agents. Furthermore, inflammation is linked to all of the six hallmarks of cancer (evasion of apoptosis, insensitivity to anti-growth signals, unlimited replicative potential, angiogenesis, increase in survival factors and invasion and metastasis). It is thought that inflammation may play a critical role in lung carcinogenesis given that individuals with inflammatory lung conditions have an increased risk of lung cancer development. Cigarette smoking can also induce inflammation in the lung and smokers are at a higher risk of developing lung cancer than non-smokers. However, exposure to a number of environmental agents such as radon, have also been demonstrated as a causative factor in this disease. This chapter will focus on inflammation as a contributory factor in non small cell lung cancer (NSCLC), concentrating primarily on the pathological involvement of the pro-inflammatory cytokines, TNF-α, IL-1β, and the CXC (ELR+) chemokine family. Targeting of inflammatory mediators will also be discussed as a therapeutic strategy in this disease. © 2013 by Nova Science Publishers, Inc. All rights reserved.

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The expression of neutrophil gelatinase-associated lipocalin (NGAL) has been shown to be upregulated in ovarian cancer cells. In this study, we report that the expression of immunoreactive NGAL (irNGAL) in ovarian tumors changes with disease grade and that this change is reflected in the concentration of NGAL in peripheral blood. A total of 59 ovarian tissues including normal, benign, borderline malignant and grades 1, 2 and 3 malignant were analyzed using immunohistochemistry. irNGAL was not present in normal ovaries and the NGAL expression was weak to moderate in benign tissues. Both borderline and grade 1 tumors displayed the highest amount of NGAL expression with moderate to strong staining, whereas in grade 2 and 3 tumors, the extent of staining was significantly less (p < 0.01) and staining intensity was weak to moderate. Staining in all cases was confined to the epithelium. NGAL expression was analyzed by ELISA in 62 serum specimens from normal and different grades of cancer patients. Compared to control samples, the NGAL concentration was 2 and 2.6-fold higher in the serum of patients with benign tumors and cancer patients with grade 1 tumors (p < 0.05) and that result was consistent with the expression of NGAL performed by Western blot. NGAL expression was evaluated by Western blot in an immortalized normal ovarian cell line (IOSE29) as well as ovarian cancer cell lines. Moderate to strong expression of NGAL was observed in epithelial ovarian cancer cell lines SKOV3 and OVCA433 while no expression of NGAL was evident in normal IOSE29 and mesenchyme-like OVHS1, PEO.36 and HEY cell lines. NGAL expression was downregulated in ovarian cancer cell lines undergoing epithelio-mesenchymal transition (EMT) induced by epidermal growth factor (EGF). Down-regulation of NGAL expression correlated with the upregulation of vimentin expression, enhanced cell dispersion and downregulation of E-cadherin expression, some of the hallmarks of EMT. EGF-induced EMT phenotypes were inhibited in the presence of AG1478, an inhibitor of EGF receptor tyrosine kinase activity. These data indicate that NGAL may be a good marker to monitor changes of benign to premalignant and malignant ovarian tumors and that the molecule may be involved in the progression of epithelial ovarian malignancies.

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Molecular interactions that underlie pathophysiological states are being elucidated using techniques that profile proteomicend points in cellular systems. Within the field of cancer research, protein interaction networks play pivotal roles in the establishment and maintenance of the hallmarks of malignancy, including cell division, invasion, and migration. Multiple complementary tools enable a multifaceted view of how signal protein pathway alterations contribute to pathophysiological states.One pivotal technique is signal pathway profiling of patient tissue specimens. This microanalysis technology provides a proteomic snapshot at one point in time of cells directly procured from the native context of a tumor micro environment. To study the adaptive patterns of signal pathway events over time, before and after experimental therapy, it is necessary to obtain biopsies from patients before, during, and after therapy. A complementary approach is the profiling of cultured cell lines with and without treatment. Cultured cell models provide the opportunity to study short-term signal changes occurring over minutes to hours. Through this type of system, the effects of particular pharmacological agents may be used to test the effects of signal pathway inhibition or activation on multiple endpoints within a pathway. The complexity of the data generated has necessitated the development of mathematical models for optimal interpretation of interrelated signaling pathways. In combination,clinical proteomic biopsy profiling, tissue culture proteomic profiling, and mathematical modeling synergistically enable a deeper understanding of how protein associations lead to disease states and present new insights into the design of therapeutic regimens.

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One of the hallmarks of cancer is the ability to activate invasion and metastasis (Hanahan et al., 2011). Cancer morbidity and mortality are largely related to the spread of the primary, localised tumour to adjacent and distant sites (Pantel et al., 2004). Appropriate management and treatment decisions of predicting metastatic disease at the time of diagnosis is thus crucial, which supports better understanding of the metastatic process. There are common events that occur during metastasis: dissociation from the primary tumour mass, reorganisation/remodelling of extracellular matrix, cell migration, recognition and transversal of endothelial cells and the vascular circulation and lodgement and proliferation within ectopic stroma (Wells, 2006). One of the key and initial events is the increased capability of cancer cells to move, escaping the regulation of normal physiological control. The cellular cytoskeleton plays an important role in cancer cell motility and active cytoskeletal rearrangement can result in metastatic disease. This active change in cytoskeletal dynamics results in manipulation of plasma membrane and cellular balance between cellular adhesion and motility which in turn determines cancer cell movement. Members of the tetraspanins play important roles in regulation of cancer migration and cancer-endothelial cell interactions, which are critical for cancer invasion and metastasis. Their involvements in active cytoskeletal dynamics, cancer metastasis and potential clinical application will be discussed in this review. In particular, tetraspanin member, CD151, is highlighted for its major role in cancer invasion and metastasis

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Significance Reactive oxygen species (ROS) such as superoxide, hydrogen peroxide, and peroxynitrite are generated ubiquitously by all mammalian cells and have been understood for many decades as inflicting cell damage and as causing cancer by oxidation and nitration of macromolecules, including DNA, RNA, proteins, and lipids. Recent Advances A current concept suggests that ROS can also promote cell signaling pathways triggered by growth factors and transcription factors that ultimately regulate cell proliferation, differentiation, and apoptosis, all of which are important hallmarks of tumor cell proliferation and angiogenesis. Moreover, an emerging concept indicates that ROS regulate the functions of immune cells that infiltrate the tumor environment and stimulate angiogenesis, such as macrophages and specific regulatory T cells. Critical Issues In this article, we highlight that the NADPH oxidase family of ROS-generating enzymes are the key sources of ROS and, thus, play an important role in redox signaling within tumor, endothelial, and immune cells thereby promoting tumor angiogenesis. Future Directions Knowledge of these intricate ROS signaling pathways and identification of the culprit NADPH oxidases is likely to reveal novel therapeutic opportunities to prevent angiogenesis that occurs during cancer and which is responsible for the revascularization after current antiangiogenic treatment.

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Many techniques in information retrieval produce counts from a sample, and it is common to analyse these counts as proportions of the whole - term frequencies are a familiar example. Proportions carry only relative information and are not free to vary independently of one another: for the proportion of one term to increase, one or more others must decrease. These constraints are hallmarks of compositional data. While there has long been discussion in other fields of how such data should be analysed, to our knowledge, Compositional Data Analysis (CoDA) has not been considered in IR. In this work we explore compositional data in IR through the lens of distance measures, and demonstrate that common measures, naïve to compositions, have some undesirable properties which can be avoided with composition-aware measures. As a practical example, these measures are shown to improve clustering. Copyright 2014 ACM.