975 resultados para Guadalupe, Our Lady of.
Resumo:
Reinforced concrete structures are susceptible to a variety of deterioration mechanisms due to creep and shrinkage, alkali-silica reaction (ASR), carbonation, and corrosion of the reinforcement. The deterioration problems can affect the integrity and load carrying capacity of the structure. Substantial research has been dedicated to these various mechanisms aiming to identify the causes, reactions, accelerants, retardants and consequences. This has improved our understanding of the long-term behaviour of reinforced concrete structures. However, the strengthening of reinforced concrete structures for durability has to date been mainly undertaken after expert assessment of field data followed by the development of a scheme to both terminate continuing degradation, by separating the structure from the environment, and strengthening the structure. The process does not include any significant consideration of the residual load-bearing capacity of the structure and the highly variable nature of estimates of such remaining capacity. Development of performance curves for deteriorating bridge structures has not been attempted due to the difficulty in developing a model when the input parameters have an extremely large variability. This paper presents a framework developed for an asset management system which assesses residual capacity and identifies the most appropriate rehabilitation method for a given reinforced concrete structure exposed to aggressive environments. In developing the framework, several industry consultation sessions have been conducted to identify input data required, research methodology and output knowledge base. Capturing expert opinion in a useable knowledge base requires development of a rule based formulation, which can subsequently be used to model the reliability of the performance curve of a reinforced concrete structure exposed to a given environment.
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This paper focuses on participatory research and how it can be understood and employed when researching children and youth. The aim of this paper is to provide a theoretically and empirically grounded discussion of participatory research methodologies with respect to investigating the dynamic and evolving phenomenon of young people growing up in networked societies. Initially, we review the nature of participatory research and how other researchers have endeavoured to involve young people (children and youth) in their research projects. Our review of these approaches aims to elucidate what we see as recurring and emerging issues with respect to the methodological design of involving young people as co-researchers. In the light of these issues and in keeping with our aim, we offer a case study of our own research project that seeks to understand the ways in which high school students use new media and network ICT systems (Internet, mobile phone applications, social networking sites) to construct identities, form social relations, and engage in creative practices as part of their everyday lives. The article concludes by offering an assessment of our tripartite model of participatory research that may benefit other researchers who share a similar interest in youth and new media.
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This is an important book that ought to launch a debate about how we research our understanding of the world, it is an innovative intervention in a vital public issue, and it is an elegant and scholarly hard look at what is actually happening. Jean Seaton, Prof of Media History, U of Westminster, UK & Official Historian of the BBC -- Summary: This book investigates the question of how comparative studies of international TV news (here: on violence presentation) can best be conceptualized in a way that allows for crossnational, comparative conclusions on an empirically validated basis. This book shows that such a conceptualization is necessary in order to overcome existing restrictions in the comparability of international analysis on violence presentation. Investigated examples include the most watched news bulletins in Great Britain (10o'clock news on the BBC), Germany (Tagesschau on ARD) and Russia (Vremja on Channel 1). This book highlights a substantial cross-national violence news flow as well as a cross-national visual violence flow (key visuals) as distinct transnational components. In addition, event-related textual analysis reveals how the historical rootedness of nations and its symbols of power are still manifested in televisual mediations of violence. In conclusion, this study lobbies for a conscientious use of comparative data/analysis both in journalism research and practice in order to understand what it may convey in the different arenas of today’s newsmaking.
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Height is a complex physical trait that displays strong heritability. Adult height is related to length of the long bones, which is determined by growth at the epiphyseal growth plate. Longitudinal bone growth occurs via the process of endochondral ossification, where bone forms over the differentiating cartilage template at the growth plate. Estrogen plays a major role in regulating longitudinal bone growth and is responsible for inducing the pubertal growth spurt and fusion of the epiphyseal growth plate. However, the mechanism by which estrogen promotes epiphyseal fusion is poorly understood. It has been hypothesised that estrogen functions to regulate growth plate fusion by stimulating chondrocyte apoptosis, angiogenesis and bone cell invasion in the growth plate. Another theory has suggested that estrogen exposure exhausts the proliferative capacity of growth plate chondrocytes, which accelerates the process of chondrocyte senescence, leading to growth plate fusion. The overall objective of this study was to gain a greater understanding of the molecular mechanisms behind estrogen-mediated growth and height attainment by examining gene regulation in chondrocytes and the role of some of these genes in normal height inheritance. With the heritability of height so well established, the initial hypothesis was that genetic variation in candidate genes associated with longitudinal bone growth would be involved in normal adult height variation. The height-related genes FGFR3, CBFA1, ER and CBFA1 were screened for novel polymorphisms using denaturing HPLC and RFLP analysis. In total, 24 polymorphisms were identified. Two SNPs in ER (rs3757323 C>T and rs1801132 G>C) were strongly associated with adult male height and displayed an 8 cm and 9 cm height difference between homozygous genotypes, respectively. The TC haplotype of these SNPs was associated with a 6 cm decrease in height and remarkably, no homozygous carriers of the TC haplotype were identified in tall subjects. No significant associations with height were found for polymorphisms in the FGFR3, CBFA1 or VDR genes. In the epiphyseal growth plate, chondrocyte proliferation, matrix synthesis and chondrocyte hypertrophy are all major contributors to long bone growth. As estrogen plays such a significant role in both growth and final height attainment, another hypothesis of this study was that estrogen exerted its effects in the growth plate by influencing chondrocyte proliferation and mediating the expression of chondrocyte marker genes. The examination of genes regulated by estrogen in chondrocyte-like cells aimed to identify potential regulators of growth plate fusion, which may further elucidate mechanisms involved in the cessation of linear growth. While estrogen did not dramatically alter the proliferation of the SW1353 cell line, gene expression experiments identified several estrogen regulated genes. Sixteen chondrocyte marker genes were examined in response to estrogen concentrations ranging from 10-12 M to 10-8 M over varying time points. Of the genes analysed, IHH, FGFR3, collagen II and collagen X were not readily detectable and PTHrP, GHR, ER, BMP6, SOX9 and TGF1 mRNAs showed no significant response to estrogen treatments. However, the expression of MMP13, CBFA1, BCL-2 and BAX genes were significantly decreased. Interestingly, the majority of estrogen regulated genes in SW1353 cells are expressed in the hypertrophic zone of the growth plate. Estrogen is also known to regulate systemic GH secretion and local GH action. At the molecular level, estrogen functions to inhibit GH action by negatively regulating GH signalling. GH treated SW1353 cells displayed increases in MMP9 mRNA expression (4.4-fold) and MMP13 mRNA expression (64-fold) in SW1353 cells. Increases were also detected in their respective proteins. Treatment with AG490, an established JAK2 inhibitor, blocked the GH mediated stimulation of both MMP9 and MMP13 mRNA expression. The application of estrogen and GH to SW1353 cells attenuated GH-stimulated MMP13 levels, but did not affect MMP9 levels. Investigation of GH signalling revealed that SW1353 cells have high levels of activated JAK2 and exposure to GH, estrogen, AG490 and other signalling inhibitors did not affect JAK2 phosphorylation. Interestingly, AG490 treatment dramatically decreased ERK2 signalling, although GH did stimulate ERK2 phosphorylation above control levels. AG490 also decreased CBFA1 expression, a transcription factor known to activate MMP9 and MMP13. Finally, GH and estrogen treatment increased expression of SOCS3 mRNA, suggesting that SOCS3 may regulate JAK/STAT signalling in SW1353 cells. The modulation of GH-mediated MMP expression by estrogen in SW1353 cells represents a potentially novel mechanism by which estrogen may regulate longitudinal bone growth. However, further investigation is required in order to elucidate the precise mechanisms behind estrogen and GH regulation of MMP13 expression in SW1353 cells. This study has provided additional evidence that estrogen and the ER gene are major factors in the regulation of growth and the determination of adult height. Newly identified polymorphisms in the ER gene not only contribute to our understanding of the genetic basis of human height, but may also be useful in association studies examining other complex traits. This study also identified several estrogen regulated genes and indicated that estrogen modifies the expression of genes which are primarily expressed in the hypertrophic region of the epiphyseal growth plate. Furthermore, synergistic studies incorporating GH and estrogen have revealed the ability of estrogen to attenuate the effects of GH on MMP13 expression, revealing potential pathways by which estrogen may modulate growth plate fusion, longitudinal bone growth and even arthritis.
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How and why visualisations support learning was the subject of this qualitative instrumental collective case study. Five computer programming languages (PHP, Visual Basic, Alice, GameMaker, and RoboLab) supporting differing degrees of visualisation were used as cases to explore the effectiveness of software visualisation to develop fundamental computer programming concepts (sequence, iteration, selection, and modularity). Cognitive theories of visual and auditory processing, cognitive load, and mental models provided a framework in which student cognitive development was tracked and measured by thirty-one 15-17 year old students drawn from a Queensland metropolitan secondary private girls’ school, as active participants in the research. Seventeen findings in three sections increase our understanding of the effects of visualisation on the learning process. The study extended the use of mental model theory to track the learning process, and demonstrated application of student research based metacognitive analysis on individual and peer cognitive development as a means to support research and as an approach to teaching. The findings also forward an explanation for failures in previous software visualisation studies, in particular the study has demonstrated that for the cases examined, where complex concepts are being developed, the mixing of auditory (or text) and visual elements can result in excessive cognitive load and impede learning. This finding provides a framework for selecting the most appropriate instructional programming language based on the cognitive complexity of the concepts under study.
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Neurodegenerative disorders are heterogenous in nature and include a range of ataxias with oculomotor apraxia, which are characterised by a wide variety of neurological and ophthalmological features. This family includes recessive and dominant disorders. A subfamily of autosomal recessive cerebellar ataxias are characterised by defects in the cellular response to DNA damage. These include the well characterised disorders Ataxia-Telangiectasia (A-T) and Ataxia-Telangiectasia Like Disorder (A-TLD) as well as the recently identified diseases Spinocerebellar ataxia with axonal neuropathy Type 1 (SCAN1), Ataxia with Oculomotor Apraxia Type 2 (AOA2), as well as the subject of this thesis, Ataxia with Oculomotor Apraxia Type 1 (AOA1). AOA1 is caused by mutations in the APTX gene, which is located at chromosomal locus 9p13. This gene codes for the 342 amino acid protein Aprataxin. Mutations in APTX cause destabilization of Aprataxin, thus AOA1 is a result of Aprataxin deficiency. Aprataxin has three functional domains, an N-terminal Forkhead Associated (FHA) phosphoprotein interaction domain, a central Histidine Triad (HIT) nucleotide hydrolase domain and a C-terminal C2H2 zinc finger. Aprataxins FHA domain has homology to FHA domain of the DNA repair protein 5’ polynucleotide kinase 3’ phosphatase (PNKP). PNKP interacts with a range of DNA repair proteins via its FHA domain and plays a critical role in processing damaged DNA termini. The presence of this domain with a nucleotide hydrolase domain and a DNA binding motif implicated that Aprataxin may be involved in DNA repair and that AOA1 may be caused by a DNA repair deficit. This was substantiated by the interaction of Aprataxin with proteins involved in the repair of both single and double strand DNA breaks (XRay Cross-Complementing 1, XRCC4 and Poly-ADP Ribose Polymerase-1) and the hypersensitivity of AOA1 patient cell lines to single and double strand break inducing agents. At the commencement of this study little was known about the in vitro and in vivo properties of Aprataxin. Initially this study focused on generation of recombinant Aprataxin proteins to facilitate examination of the in vitro properties of Aprataxin. Using recombinant Aprataxin proteins I found that Aprataxin binds to double stranded DNA. Consistent with a role for Aprataxin as a DNA repair enzyme, this binding is not sequence specific. I also report that the HIT domain of Aprataxin hydrolyses adenosine derivatives and interestingly found that this activity is competitively inhibited by DNA. This provided initial evidence that DNA binds to the HIT domain of Aprataxin. The interaction of DNA with the nucleotide hydrolase domain of Aprataxin provided initial evidence that Aprataxin may be a DNA-processing factor. Following these studies, Aprataxin was found to hydrolyse 5’adenylated DNA, which can be generated by unscheduled ligation at DNA breaks with non-standard termini. I found that cell extracts from AOA1 patients do not have DNA-adenylate hydrolase activity indicating that Aprataxin is the only DNA-adenylate hydrolase in mammalian cells. I further characterised this activity by examining the contribution of the zinc finger and FHA domains to DNA-adenylate hydrolysis by the HIT domain. I found that deletion of the zinc finger ablated the activity of the HIT domain against adenylated DNA, indicating that the zinc finger may be required for the formation of a stable enzyme-substrate complex. Deletion of the FHA domain stimulated DNA-adenylate hydrolysis, which indicated that the activity of the HIT domain may be regulated by the FHA domain. Given that the FHA domain is involved in protein-protein interactions I propose that the activity of Aprataxins HIT domain may be regulated by proteins which interact with its FHA domain. We examined this possibility by measuring the DNA-adenylate hydrolase activity of extracts from cells deficient for the Aprataxin-interacting DNA repair proteins XRCC1 and PARP-1. XRCC1 deficiency did not affect Aprataxin activity but I found that Aprataxin is destabilized in the absence of PARP-1, resulting in a deficiency of DNA-adenylate hydrolase activity in PARP-1 knockout cells. This implies a critical role for PARP-1 in the stabilization of Aprataxin. Conversely I found that PARP-1 is destabilized in the absence of Aprataxin. PARP-1 is a central player in a number of DNA repair mechanisms and this implies that not only do AOA1 cells lack Aprataxin, they may also have defects in PARP-1 dependant cellular functions. Based on this I identified a defect in a PARP-1 dependant DNA repair mechanism in AOA1 cells. Additionally, I identified elevated levels of oxidized DNA in AOA1 cells, which is indicative of a defect in Base Excision Repair (BER). I attribute this to the reduced level of the BER protein Apurinic Endonuclease 1 (APE1) I identified in Aprataxin deficient cells. This study has identified and characterised multiple DNA repair defects in AOA1 cells, indicating that Aprataxin deficiency has far-reaching cellular consequences. Consistent with the literature, I show that Aprataxin is a nuclear protein with nucleoplasmic and nucleolar distribution. Previous studies have shown that Aprataxin interacts with the nucleolar rRNA processing factor nucleolin and that AOA1 cells appear to have a mild defect in rRNA synthesis. Given the nucleolar localization of Aprataxin I examined the protein-protein interactions of Aprataxin and found that Aprataxin interacts with a number of rRNA transcription and processing factors. Based on this and the nucleolar localization of Aprataxin I proposed that Aprataxin may have an alternative role in the nucleolus. I therefore examined the transcriptional activity of Aprataxin deficient cells using nucleotide analogue incorporation. I found that AOA1 cells do not display a defect in basal levels of RNA synthesis, however they display defective transcriptional responses to DNA damage. In summary, this thesis demonstrates that Aprataxin is a DNA repair enzyme responsible for the repair of adenylated DNA termini and that it is required for stabilization of at least two other DNA repair proteins. Thus not only do AOA1 cells have no Aprataxin protein or activity, they have additional deficiencies in PolyADP Ribose Polymerase-1 and Apurinic Endonuclease 1 dependant DNA repair mechanisms. I additionally demonstrate DNA-damage inducible transcriptional defects in AOA1 cells, indicating that Aprataxin deficiency confers a broad range of cellular defects and highlighting the complexity of the cellular response to DNA damage and the multiple defects which result from Aprataxin deficiency. My detailed characterization of the cellular consequences of Aprataxin deficiency provides an important contribution to our understanding of interlinking DNA repair processes.
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Transmissible diseases are re-emerging as a global problem, with Sexually Transmitted Diseases (STDs) becoming endemic. Chlamydia trachomatis is the leading cause of bacterially-acquired STD worldwide, with the Australian cost of infection estimated at $90 - $160 million annually. Studies using animal models of genital tract Chlamydia infection suggested that the hormonal status of the genital tract epithelium at the time of exposure may influence the outcome of infection. Oral contraceptive use also increased the risk of contracting chlamydial infections compared to women not using contraception. Generally it was suggested that the outcome of chlamydial infection is determined in part by the hormonal status of the epithelium at the time of exposure. Using the human endolmetrial cell line ECC-1 this study investigated the effects of C. trachomatis serovar D infection, in conjunction with the female sex hormones, 17β-estradiol and progesterone, on chlamydial gene expression. While previous studies have examined the host response, this is the first study to examine C.trachomatis gene expression under different hormonal conditions. We have highlighted a basic model of C. trachomatis gene regulation in the presence of steroid hormones by identifying 60 genes that were regulated by addition of estradiol and/or progesterone. In addition, the third chapter of this thesis discussed and compared the significance of the current findings in the context of data from other research groups to improve our understanding of the molecular basis of chlamydial persistence under hormonal different conditions. In addition, this study analysed the effects of these female sex hormones and C. trachomatis Serovar D infection, on host susceptibility and bacterial growth. Our results clearly demonstrated that addition of steroid hormones not only had a great impact on the level of infectivity of epithelial cells with C.trachomatis serovar D, but also the morphology of chlamydial inclusions was affected by hormone supplementation.
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Since the 1980s, industries and researchers have sought to better understand the quality of services due to the rise in their importance (Brogowicz, Delene and Lyth 1990). More recent developments with online services, coupled with growing recognition of service quality (SQ) as a key contributor to national economies and as an increasingly important competitive differentiator, amplify the need to revisit our understanding of SQ and its measurement. Although ‘SQ’ can be broadly defined as “a global overarching judgment or attitude relating to the overall excellence or superiority of a service” (Parasuraman, Berry and Zeithaml 1988), the term has many interpretations. There has been considerable progress on how to measure SQ perceptions, but little consensus has been achieved on what should be measured. There is agreement that SQ is multi-dimensional, but little agreement as to the nature or content of these dimensions (Brady and Cronin 2001). For example, within the banking sector, there exist multiple SQ models, each consisting of varying dimensions. The existence of multiple conceptions and the lack of a unifying theory bring the credibility of existing conceptions into question, and beg the question of whether it is possible at some higher level to define SQ broadly such that it spans all service types and industries. This research aims to explore the viability of a universal conception of SQ, primarily through a careful re-visitation of the services and SQ literature. The study analyses the strengths and weaknesses of the highly regarded and widely used global SQ model (SERVQUAL) which reflects a single-level approach to SQ measurement. The SERVQUAL model states that customers evaluate SQ (of each service encounter) based on five dimensions namely reliability, assurance, tangibles, empathy and responsibility. SERVQUAL, however, failed to address what needs to be reliable, assured, tangible, empathetic and responsible. This research also addresses a more recent global SQ model from Brady and Cronin (2001); the B&C (2001) model, that has potential to be the successor of SERVQUAL in that it encompasses other global SQ models and addresses the ‘what’ questions that SERVQUAL didn’t. The B&C (2001) model conceives SQ as being multidimensional and multi-level; this hierarchical approach to SQ measurement better reflecting human perceptions. In-line with the initial intention of SERVQUAL, which was developed to be generalizable across industries and service types, this research aims to develop a conceptual understanding of SQ, via literature and reflection, that encompasses the content/nature of factors related to SQ; and addresses the benefits and weaknesses of various SQ measurement approaches (i.e. disconfirmation versus perceptions-only). Such understanding of SQ seeks to transcend industries and service types with the intention of extending our knowledge of SQ and assisting practitioners in understanding and evaluating SQ. The candidate’s research has been conducted within, and seeks to contribute to, the ‘IS-Impact’ research track of the IT Professional Services (ITPS) Research Program at QUT. The vision of the track is “to develop the most widely employed model for benchmarking Information Systems in organizations for the joint benefit of research and practice.” The ‘IS-Impact’ research track has developed an Information Systems (IS) success measurement model, the IS-Impact Model (Gable, Sedera and Chan 2008), which seeks to fulfill the track’s vision. Results of this study will help future researchers in the ‘IS-Impact’ research track address questions such as: • Is SQ an antecedent or consequence of the IS-Impact model or both? • Has SQ already been addressed by existing measures of the IS-Impact model? • Is SQ a separate, new dimension of the IS-Impact model? • Is SQ an alternative conception of the IS? Results from the candidate’s research suggest that SQ dimensions can be classified at a higher level which is encompassed by the B&C (2001) model’s 3 primary dimensions (interaction, physical environment and outcome). The candidate also notes that it might be viable to re-word the ‘physical environment quality’ primary dimension to ‘environment quality’ so as to better encompass both physical and virtual scenarios (E.g: web sites). The candidate does not rule out the global feasibility of the B&C (2001) model’s nine sub-dimensions, however, acknowledges that more work has to be done to better define the sub-dimensions. The candidate observes that the ‘expertise’, ‘design’ and ‘valence’ sub-dimensions are supportive representations of the ‘interaction’, physical environment’ and ‘outcome’ primary dimensions respectively. The latter statement suggests that customers evaluate each primary dimension (or each higher level of SQ classification) namely ‘interaction’, physical environment’ and ‘outcome’ based on the ‘expertise’, ‘design’ and ‘valence’ sub-dimensions respectively. The ability to classify SQ dimensions at a higher level coupled with support for the measures that make up this higher level, leads the candidate to propose the B&C (2001) model as a unifying theory that acts as a starting point to measuring SQ and the SQ of IS. The candidate also notes, in parallel with the continuing validation and generalization of the IS-Impact model, that there is value in alternatively conceptualizing the IS as a ‘service’ and ultimately triangulating measures of IS SQ with the IS-Impact model. These further efforts are beyond the scope of the candidate’s study. Results from the candidate’s research also suggest that both the disconfirmation and perceptions-only approaches have their merits and the choice of approach would depend on the objective(s) of the study. Should the objective(s) be an overall evaluation of SQ, the perceptions-only approached is more appropriate as this approach is more straightforward and reduces administrative overheads in the process. However, should the objective(s) be to identify SQ gaps (shortfalls), the (measured) disconfirmation approach is more appropriate as this approach has the ability to identify areas that need improvement.
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The purpose of this paper is to conduct a qualitative review of randomised controlled trials in relation to the treatment of adults with co-occurring mental health and substance use disorder (MH/SUD). In particular, integrated approaches are compared with non-integrated approaches to treatment. Ten articles were identified for inclusion in the review. The findings are equivocal with regard to the superior efficacy of integrated approaches to treatment, although the many limitations of the studies need to be considered in our understanding of this finding. Clearly, this is an extremely challenging client group to engage and maintain in intervention research, and the complexity and variability of the problems render control particularly difficult. The lack of available evidence to support the superiority of integration is discussed in relation to these challenges. Much remains to be investigated with regard to integrated management and care for people with co-occurring and MH/SUD, particularly for specific combinations of dual diagnosis and giving consideration to the level of inter-relatedness between the disorders.
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Despite increasingly sophisticated speed management strategies, speeding remains a significant contributing factor in 25% of Australia’s fatal crashes. Excessive speed is also a recognised contributor to road trauma in rapidly motorising countries such as China, where increases in vehicle ownership and new drivers, and a high proportion of vulnerable road users all contribute to a high road trauma rate. Speed choice is a voluntary behaviour. Therefore, driver perceptions are important to our understanding of the nature of speeding. This paper reports preliminary qualitative (focus groups) and quantitative (survey) investigations of the perceptions of drivers in Queensland and Beijing. Drivers’ definitions of speeding as well as their perceptions of the influence of legal factors on their reported speeds were explored. Survey participants were recruited from petrol stations (Queensland, n=833) and car washes (Beijing, n=299). Similarities were evident in justifications for exceeding speed limits across samples. Excessive speeds were not deemed as ‘speeding’ when drivers considered that they were safe and under their control, or when speed limits were seen as unreasonably low. This appears linked to perceptions of enforcement tolerances in some instances with higher perceived enforcement thresholds noted in China. Encouragingly, drivers in both countries reported a high perceived risk of apprehension if speeding. However, a substantial proportion of both samples also indicated perceptions of low certainty of receiving penalties when apprehended. Chinese drivers considered sanctions less severe than did Australian drivers. In addition, strategies to avoid detection and penalties were evident in both samples, with Chinese drivers reporting a broader range of avoidant techniques. Implications of the findings for future directions in speed management in both countries are discussed.
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The purpose of this study was to identify the pedagogical knowledge relevant to the successful completion of a pie chart item. This purpose was achieved through the identification of the essential fluencies that 12–13-year-olds required for the successful solution of a pie chart item. Fluency relates to ease of solution and is particularly important in mathematics because it impacts on performance. Although the majority of students were successful on this multiple choice item, there was considerable divergence in the strategies they employed. Approximately two-thirds of the students employed efficient multiplicative strategies, which recognised and capitalised on the pie chart as a proportional representation. In contrast, the remaining one-third of students used a less efficient additive strategy that failed to capitalise on the representation of the pie chart. The results of our investigation of students’ performance on the pie chart item during individual interviews revealed that five distinct fluencies were involved in the solution process: conceptual (understanding the question), linguistic (keywords), retrieval (strategy selection), perceptual (orientation of a segment of the pie chart) and graphical (recognising the pie chart as a proportional representation). In addition, some students exhibited mild disfluencies corresponding to the five fluencies identified above. Three major outcomes emerged from the study. First, a model of knowledge of content and students for pie charts was developed. This model can be used to inform instruction about the pie chart and guide strategic support for students. Second, perceptual and graphical fluency were identified as two aspects of the curriculum, which should receive a greater emphasis in the primary years, due to their importance in interpreting pie charts. Finally, a working definition of fluency in mathematics was derived from students’ responses to the pie chart item.
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The last few years have seen dramatic advances in genomics, including the discovery of a large number of non-coding and antisense transcripts. This has revolutionised our understanding of multifaceted transcript structures found within gene loci and their roles in the regulation of development, neurogenesis and other complex processes. The recent and continuing surge of knowledge has prompted researchers to reassess and further dissect gene loci. The ghrelin gene (GHRL) gives rise to preproghrelin, which in turn produces ghrelin, a 28 amino acid peptide hormone that acts via the ghrelin receptor (growth hormone secretagogue receptor/GHSR 1a). Ghrelin has many important physiological and pathophysiological roles, including the stimulation of growth hormone (GH) release, appetite regulation, and cancer development. A truncated receptor splice variant, GHSR 1b, does not bind ghrelin, but dimerises with GHSR 1a, and may act as a dominant negative receptor. The gene products of ghrelin and its receptor are frequently overexpressed in human cancer While it is well known that the ghrelin axis (ghrelin and its receptor) plays a range of important functional roles, little is known about the molecular structure and regulation of the ghrelin gene (GHRL) and ghrelin receptor gene (GHSR). This thesis reports the re-annotation of the ghrelin gene, discovery of alternative 5’ exons and transcription start sites, as well as the description of a number of novel splice variants, including isoforms with a putative signal peptide. We also describe the discovery and characterisation of a ghrelin antisense gene (GHRLOS), and the discovery and expression of a ghrelin receptor (growth hormone secretagogue receptor/GHSR) antisense gene (GHSR-OS). We have identified numerous ghrelin-derived transcripts, including variants with extended 5' untranslated regions and putative secreted obestatin and C-ghrelin transcripts. These transcripts initiate from novel first exons, exon -1, exon 0 and a 5' extended 1, with multiple transcription start sites. We used comparative genomics to identify, and RT-PCR to experimentally verify, that the proximal exon 0 and 5' extended exon 1 are transcribed in the mouse ghrelin gene, which suggests the mouse and human proximal first exon architecture is conserved. We have identified numerous novel antisense transcripts in the ghrelin locus. A candidate non-coding endogenous natural antisense gene (GHRLOS) was cloned and demonstrates very low expression levels in the stomach and high levels in the thymus, testis and brain - all major tissues of non-coding RNA expression. Next, we examined if transcription occurs in the antisense orientation to the ghrelin receptor gene, GHSR. A novel gene (GHSR-OS) on the opposite strand of intron 1 of the GHSR gene was identified and characterised using strand-specific RT-PCR and rapid amplification of cDNA ends (RACE). GHSR-OS is differentially expressed and a candidate non-coding RNA gene. In summary, this study has characterised the ghrelin and ghrelin receptor loci and demonstrated natural antisense transcripts to ghrelin and its receptor. Our preliminary work shows that the ghrelin axis generates a broad and complex transcriptional repertoire. This study provides the basis for detailed functional studies of the the ghrelin and GHSR loci and future studies will be needed to further unravel the function, diagnostic and therapeutic potential of the ghrelin axis.
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This study explored the role of donor prototype evaluations (perceptions of the typical organ donor) in organ donation communication decisions using an extended theory of planned behaviour (TPB) model. The model incorporated attitude, subjective norm, perceived behavioural control, moral norm, self-identity, and donor prototype evaluations to predict intentions to record consent on an organ donor register and discuss the organ donation decision with significant others. Participants completed surveys assessing the extended TPB constructs related to registering (n = 359) and discussing (n = 282). Results supported a role for donor prototype evaluations in predicting discussing intentions only. Both extended TPB structural equation models were a good fit to the data, accounting for 74 and 76% of the variance in registering and discussing intentions, respectively. Participants’ self-reported discussing behaviour (but not registering behaviour given low numbers of behavioural performers) was assessed 4 weeks later, with discussing intention as the only significant predictor of behaviour (Nagelkerke R2 = 0.11). These findings highlight the impact of people's perceptions of a typical donor on their decisions to discuss their organ donation preference, assisting our understanding of the factors influencing individuals' communication processes in efforts to bridge the gap between organ supply and demand.
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Much of what we know about lymphoedema is derived from studies involving cancer cohorts, in particular breast cancer. Yet even within this setting, and despite the known profound physical, social and psychological effects, our understanding of associated risk factors and effectiveness of prevention and treatment strategies is poorly studied with inconsistent results. The limitations of our current methods to detect and monitor lymphoedema contribute to our lack of understanding of this condition. Current measurement approaches applied in the clinical and research setting will be described during this presentation. The strengths, limitations and practical considerations relevant to measurement methods will also be addressed. Improving the way we detect and monitor lymphoedema is necessary and critical for advancing the lymphoedema field and is relevant for the detection and monitoring of lymphoedema in the clinic as well as in research.
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Background: All Canadian jurisdictions require certain professionals to report suspected or observed child maltreatment. This study examined the types of maltreatment, level of harm and child functioning issues, controlling for family socioeconomic status, age and gender of the child reported by healthcare and non-healthcare professionals. Methods: We conducted chi-square analyses and logistic regression on a national child welfare sample from the 2003 Canadian Incidence Study of Reported Child Abuse and Neglect (CIS-2003) and compared the differences in professional reporting with its previous cycle (CIS-1998) using Bonferroni-corrected confidence intervals. Results: Our analysis of CIS-2003 data revealed that the majority of substantiated child maltreatment is reported to service agencies by non-healthcare professionals (57%), followed by non-professionals (33%) and healthcare professionals (10%). The number of professional reports increased 2.5 times between CIS-1998 and CIS-2003, while non-professionals’ increased 1.7 times. Of the total investigations, professional reports represented 59% in CIS-1998 and 67% in CIS-2003 (p<0.001). Compared to non-healthcare professionals, healthcare professionals more often reported younger children, children who experienced neglect and emotional maltreatment and those assessed as suffering harm and child functioning issues, but less often exposure to domestic violence. Conclusion: The results indicate that healthcare professionals played an important role in identifying children in need of protection considering harm and other child functioning issues. The authors discuss the reasons why underreporting is likely to remain an issue.