143 resultados para Acidic transactivating domains


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Building Information Modelling (BIM) is an IT enabled technology that allows storage, management, sharing, access, update and use of all the data relevant to a project through out the project life-cycle in the form of a data repository. BIM enables improved inter-disciplinary collaboration across distributed teams, intelligent documentation and information retrieval, greater consistency in building data, better conflict detection and enhanced facilities management. While the technology itself may not be new, and similar approaches have been in use in some other sectors like Aircraft and Automobile industry for well over a decade now, the AEC/FM (Architecture, Engineering and Construction/ Facilities Management) industry is still to catch up with them in its ability to exploit the benefits of the IT revolution. Though the potential benefits of the technology in terms of knowledge sharing, project management, project co-ordination and collaboration are near to obvious, the adoption rate has been rather lethargic, inspite of some well directed efforts and availability of supporting commercial tools. Since the technology itself has been well tested over the years in some other domains the plausible causes must be rooted well beyond the explanation of the ‘Bell Curve of innovation adoption’. This paper discusses the preliminary findings of an ongoing research project funded by the Cooperative Research Centre for Construction Innovation (CRC-CI) which aims to identify these gaps and come up with specifications and guidelines to enable greater adoption of the BIM approach in practice. A detailed literature review is conducted that looks at some of the similar research reported in the recent years. A desktop audit of some of the existing commercial tools that support BIM application has been conducted to identify the technological issues and concerns, and a workshop was organized with industry partners and various players in the AEC industry for needs analysis, expectations and feedback on the possible deterrents and inhibitions surrounding the BIM adoption.

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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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Sex hormone-binding globulin (SHBG) is a homodimeric plasma glycoprotein that is the major sex steroid carrier-protein in the bloodstream and functions also as a key regulator of steroid bioavailability within target tissues, such as the prostate. Additionally, SHBG binds to prostatic cell membranes via the putative and unidentified SHBG receptor (RSHBG), activating a signal transduction pathway implicated in stimulating both proliferation and expression of prostate specific antigen (PSA) in prostate cell lines in vitro. A yeast-two hybrid assay suggested an interaction between SHBG and kallikrein-related protease (KLK) 4, which is a serine protease implicated in the progression of prostate cancer. The potential interaction between these two proteins was investigated in this PhD thesis to determine whether SHBG is a proteolytic substrate of KLK4 and other members of the KLK family including KLK3/PSA, KLK7 and KLK14. Furthermore, the effects from SHBG proteolytic degradation on SHBG-regulated steroid bioavailability and the activation of the putative RSHBG signal transduction pathway were examined in the LNCaP prostate cancer cell line. SHBG was found to be a proteolytic substrate of the trypsin-like KLK4 and KLK14 in vitro, yielding several proteolysis fragments. Both chymotrypsin-like PSA and KLK7 displayed insignificant proteolytic activity against SHBG. The kinetic parameters of SHBG proteolysis by KLK4 and KLK14 demonstrate a strong enzyme-substrate binding capacity, possessing a Km of 1.2 ± 0.7 µM and 2.1 ± 0.6 µM respectively. The catalytic efficiencies (kcat/Km) of KLK4 and KLK14 proteolysis of SHBG were 1.6 x 104 M-1s-1 and 3.8 x 104 M-1s-1 respectively, which were comparable to parameters previously reported for peptide substrates. N-terminal sequencing of the fragments revealed cleavage near the junction of the N- and C-terminal laminin globulin-like (G-like) domains of SHBG, resulting in the division of the two globulins and ultimately the full degradation of these fragments by KLK4 and KLK14 over time. Proteolytic fragments that may retain steroid binding were rapidly degraded by both proteases, while fragments containing residues beyond the steroid binding pocket were less degraded over the same period of time. Degradation of SHBG was inhibited by the divalent metal cations calcium and zinc for KLK4, and calcium, zinc and magnesium for KLK14. The human secreted serine protease inhibitors (serpins), α1-antitrypsin and α2-antiplasmin, inhibited KLK4 and KLK14 proteolysis of SHBG; α1-antichymotrypsin inhibited KLK4 but not KLK14 activity. The inhibition by these serpins was comparable and in some cases more effective than general trypsin protease inhibitors such as aprotinin and phenylmethanesulfonyl fluoride (PMSF). The binding of 5α-dihydrotestosterone (DHT) to SHBG modulated interactions with KLK4 and KLK14. Steroid-free SHBG was more readily digested by both enzymes than DHT-bound SHBG. Moreover, a binding interaction exists between SHBG and pro-KLK4 and pro-KLK14, with DHT strengthening the binding to pro-KLK4 only. The inhibition of androgen uptake by cultured prostate cancer cells, mediated by SHBG steroid-binding, was examined to assess whether SHBG proteolysis by KLK4 and KLK14 modulated this process. Proteolytic digestion eliminated the ability of SHBG to inhibit the uptake of DHT from conditioned media into LNCaP cells. Therefore, the proteolysis of SHBG by KLK4 and KLK14 increased steroid bioavailability in vitro, leading to an increased uptake of androgens by prostate cancer cells. Interestingly, different transcriptional responses of PSA and KLK2, which are androgen-regulated genes, to DHT-bounsd SHBG treatment were observed between low and high passage number LNCaP cells (lpLNCaP and hpLNCaP respectively). HpLNCaP cells treated with DHT-bound SHBG demonstrated a significant synergistic upregulation of PSA and KLK2 above DHT or SHBG treatment alone, which is similar to previously reported downstream responses from RSHBG-mediated signaling activation. As this result was not seen in lpLNCaP cells, only hpLNCaP cells were further investigated to examine the modulation of potential RSHBG activity by KLK4 and KLK14 proteolysis of SHBG. Contrary to reported results, no increase in intracellular cAMP was observed in hpLNCaP cells when treated with SHBG in the presence and absence of either DHT or estradiol. As a result, the modulation of RSHBG-mediated signaling activation could not be determined. Finally, the identification of the RSHBG from both breast (MCF-7) and prostate cancer (LNCaP) cell lines was attempted. Fluorescently labeled peptides corresponding to the putative receptor binding domain (RBD) of SHBG were shown to be internalized by MCF-7 cells. Crosslinking of the RBD peptide to the cell surfaces of both MCF-7 and LNCaP cells, demonstrated the interaction of the peptide with several targets. These targets were then captured using RBD peptides synthesized onto a hydrophilic scaffold and analysed by mass spectrometry. The samples captured by the RBD peptide returned statistically significantly matches for cytokeratin 8, 18 and 19 as well as microtubule-actin crosslinking factor 1, which may indicate a novel interaction between SHBG and these proteins, but ultimately failed to detect a membrane receptor potentially responsible for the putative RSHBG-mediated signaling. This PhD project has reported the proteolytic processing of SHBG by two members of the kallikrein family, KLK4 and KLK14. The effect of SHBG proteolysis by KLK4 and KLK14 on RSHBG-mediated signaling activation was unable to be determined as the reported signal transduction pathway was not activated after treatment with SHBG, in combination with either DHT or estradiol. However, the digestion of SHBG by these two proteases positively regulated androgen bioavailability to prostate cancer cells in vitro. The increased uptake of androgens is deleterious in prostate cancer due to the promotion of proliferation, metastasis, invasion and the inhibition of apoptosis. The increased bioavailability of androgens, from SHBG proteolysis by KLK4 and KLK14, may therefore promote both carcinogenesis and progression of prostate cancer. Finally, this information may contribute to the development of therapeutic treatment strategies for prostate cancer by inhibiting the proteolysis of SHBG, by KLK4 and KLK14, to prevent the increased uptake of androgens by hormone-dependent cancerous tissues.

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Abstract Background Recent studies show that advanced paternal age (APA) is associated with an increased risk of neurodevelopmental disorders such as autism, bipolar disorder and schizophrenia. A body of evidence also suggests that individuals who develop schizophrenia show subtle deviations in a range of behavioural domains during their childhood. The aim of the study was to examine the relationship between paternal and maternal ages and selected behavioural measures in children using a large birth cohort. Method Participants were singleton children (n = 21,753) drawn from the US Collaborative Perinatal Project. The outcome measures were assessed at 7 years. The main analyses examined the relationship between parental age and behavioural measures when adjusted for a range of potentially confounding variables, including age of the other parent, maternal race, socio-economic measures, sex, gestation length, maternal marital status, parental mental illness, and child's age-at-testing. Results Advanced paternal age was associated with a significantly increased risk of adverse ‘externalizing’ behaviours at age seven years. For every five year increase in paternal age, the odds of higher ‘externalizing’ behaviours was increased by 12% (OR = 1.12; 95% CI = 1.03, 1.21, p < 0.0001). The relationship persisted after adjusting for potential confounding factors. ‘Internalizing’ behavioural outcome was not associated with advanced paternal age. In contrast, advanced maternal age was significantly protective against adverse ‘externalizing’ behavioural outcomes, but associated with an increased risk of adverse ‘internalizing’ behavioural outcomes. Discussion The offspring of older fathers show a distinctly different pattern of behaviours compared to the offspring of older mothers. The diverse socio-cultural and biologically-mediated factors that underpin these findings remain to be clarified. In light of secular trends related to delayed parenthood, the mechanisms underlying these findings warrant closer scrutiny.

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The category of the `at-risk youth' currently underpins a good deal of youth policy, and in particular, education policy. Primarily, the category is centred around a range of programmes associated with the need for state intervention, intervention which largely occurs `at a distance' within domains such as the school and the family. While it is argued that in some ways, the `at-risk youth' simply replaces older characterisations used in the policing of the young, it will also be argued that the preventative policies associated with `risk' are constituted in terms of factors rather than individuals; that prevention is no longer primarily based upon personal expertise, but rather upon the gathering and collation of statistical knowledge which identifies `risks' within given populations; and that `risk' permits a greater number of young people to be brought into the field of regulatory strategies. Importantly, the category of the `at-risk youth' underpins crucial sections of policy documents such as the Finn Report (into credentialling/ education and vocational competency). In this case, youth is deemed to be `at-risk' of not making the transition to adulthood successfully. It will be argued that not only is the Finn Report significant in the administrative and cultural shaping of the category of `youth', but also by employing the notion of `risk', the Report puts in place yet another element of an effective network of governmental intelligibility covering the young. Finally, it will be argued that young women, as a specific example of a `risk' group (vis-a-vis obtaining certain types of employment), require particular forms of intervention, primarily through changing the vocational aspirations of their parents.

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Structural health monitoring (SHM) is the term applied to the procedure of monitoring a structure’s performance, assessing its condition and carrying out appropriate retrofitting so that it performs reliably, safely and efficiently. Bridges form an important part of a nation’s infrastructure. They deteriorate due to age and changing load patterns and hence early detection of damage helps in prolonging the lives and preventing catastrophic failures. Monitoring of bridges has been traditionally done by means of visual inspection. With recent developments in sensor technology and availability of advanced computing resources, newer techniques have emerged for SHM. Acoustic emission (AE) is one such technology that is attracting attention of engineers and researchers all around the world. This paper discusses the use of AE technology in health monitoring of bridge structures, with a special focus on analysis of recorded data. AE waves are stress waves generated by mechanical deformation of material and can be recorded by means of sensors attached to the surface of the structure. Analysis of the AE signals provides vital information regarding the nature of the source of emission. Signal processing of the AE waveform data can be carried out in several ways and is predominantly based on time and frequency domains. Short time Fourier transform and wavelet analysis have proved to be superior alternatives to traditional frequency based analysis in extracting information from recorded waveform. Some of the preliminary results of the application of these analysis tools in signal processing of recorded AE data will be presented in this paper.

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This paper addresses the following problem: given two or more business process models, create a process model that is the union of the process models given as input. In other words, the behavior of the produced process model should encompass that of the input models. The paper describes an algorithm that produces a single configurable process model from an arbitrary collection of process models. The algorithm works by extracting the common parts of the input process models, creating a single copy of them, and appending the differences as branches of configurable connectors. This way, the merged process model is kept as small as possible, while still capturing all the behavior of the input models. Moreover, analysts are able to trace back from which original model(s) does a given element in the merged model come from. The algorithm has been prototyped and tested against process models taken from several application domains.

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This report is the primary output of Project 4: Copyright and Intellectual Property, the aim of which was to produce a report considering how greater access to and use of government information could be achieved within the scope of the current copyright law. In our submission for Project 4, we undertook to address: •the policy rationales underlying copyright and how they apply in the context of materials owned, held and used by government; • the recommendations of the Copyright Law Review Committee (CLRC) in its 2005 report on Crown copyright; • the legislative and regulatory barriers to information sharing in key domains, including where legal impediments such as copyright have been relied upon (whether rightly or wrongly) to justify a refusal to provide access to government data; • copyright licensing models appropriate to government materials and examples of licensing initiatives in Australia and other relevant jurisdictions; and • issues specific to the galleries, libraries, archives and museums (“GLAM”) sector, including management of copyright in legacy materials and “orphan” works. In addressing these areas, we analysed the submissions received in response to the Government 2.0 Taskforce Issues Paper, consulted with members of the Task Force as well as several key stakeholders and considered the comments posted on the Task Force’s blog. This Project Report sets out our findings on the above issues. It puts forward recommendations for consideration by the Government 2.0 Task Force on steps that can be taken to ensure that copyright and intellectual property promote access to and use of government information.

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Process modeling grammars are used by analysts to describe information systems domains in terms of the business operations an organization is conducting. While prior research has examined the factors that lead to continued usage behavior, little knowledge has been established as to what extent characteristics of the users of process modeling grammars inform usage behavior. In this study, a theoretical model is advanced that incorporates determinants of continued usage behavior as well as key antecedent individual difference factors of the grammar users, such as modeling experience, modeling background and perceived grammar familiarity. Findings from a global survey of 529 grammar users support the hypothesized relationships of the model. The study offers three central contributions. First, it provides a validated theoretical model of post-adoptive modeling grammar usage intentions. Second, it discusses the effects of individual difference factors of grammar users in the context of modeling grammar usage. Third, it provides implications for research and practice.

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Background: Relatively little research attention has been given to the development of standardised and psychometrically sound scales for measuring influences relevant to the utilisation of health services. This study aims to describe the development, validation and internal reliability of some existing and new scales to measure factors that are likely to influence utilisation of preventive care services provided by general practitioners in Australia.----- Methods: Relevant domains of influence were first identified from a literature review and formative research. Items were then generated by using and adapting previously developed scales and published findings from these. The new items and scales were pre-tested and qualitative feedback was obtained from a convenience sample of citizens from the community and a panel of experts. Principal Components Analyses (PCA) and internal reliability testing (Cronbach's alpha) were then conducted for all of the newly adapted or developed scales utilising data collected from a self-administered mailed survey sent to a randomly selected population-based sample of 381 individuals (response rate 65.6 per cent).----- Results: The PCA identified five scales with acceptable levels of internal consistency were: (1) social support (ten items), alpha 0.86; (2) perceived interpersonal care (five items), alpha 0.87, (3) concerns about availability of health care and accessibility to health care (eight items), alpha 0.80, (4) value of good health (five items), alpha 0.79, and (5) attitudes towards health care (three items), alpha 0.75.----- Conclusion The five scales are suitable for further development and more widespread use in research aimed at understanding the determinants of preventive health services utilisation among adults in the general population.

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Multimedia-based learning has been accepted as an effective learning tool and has broadly prevailed in various types of education around the world. The Malaysian ministry of education has also adopted this information communication technology (ICT) as the means of an education reformation project called, ‘Smart School’ since 1998, aiming to improve all Malaysian Primary and Secondary students’ learning ability, attitudes, achievement, and further enhance teachers’ teaching performance. As a result, Malaysian Ministry of Education has distributed a number of interactive courseware of the key learning domains such as Mathematics, Science, Bahasa Melayu (Malay language), and English. According to recent reports by Malaysian Ministry of Education (MOE), however, the courseware has not been effectively used in schools, and many researchers point out there are vital issues concerning the interface and interaction design. Within this context, this paper presumes that one of the main reasons could derive from a structural aspect of the course development process that is devaluing or ignoring the importance of interface and interaction design. Therefore, it is imperative to conceptualise the courseware development process in terms of creating interactive and quality learning experiences through defining the stakeholders’ needs in terms of better learning and teaching. Within this context, this paper reviews the current development process and proposes a new concept called the interactive communication component which enables courseware developers to embed interactive and quality learning experiences into their courseware development process. The key objective is to provide opportunities to discuss the courseware development process from the different stakeholders’ perspectives of the educational courseware in a Malaysian context.

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A number of studies in relation to the place, impact and purpose of Wellness curricula provide insight into the perceived benefits of Wellness education in university environments. Of particular note is the recommendation by many authors that curriculum design fosters personal experiences, reflective practice and active self-managed learning approaches in order to legitimise (give permission for) the adoption of wellness as a personal lifestyle approach in the frenetic pace of student life. From a broader educational perspective, Wellness education provides opportunities for students to engage in learning self regulation skills both within and beyond the context of the Wellness construct.To realise the suggested potential of Wellness education in higher learning, it is necessary that curricula overlay the principles from the domains of both self-regulation and Wellness, to highlight authentic learning as a means to lifelong approaches. Currently, however, systematic development and empirical examination of the Wellness construct have received limited academic investigation. Despite having a multitude of intended purposes from the educative to the therapy oriented goals of the original authors, most wellness models appear to be limited to the “what” of Wellness. Investigations of the “how” and “why” aspects of Wellness may serve to enhance currently existing models by incorporating behaviour modification and learning approaches in order to create more comprehensive frameworks for health education and promotion.It is also important to note that none of the current Wellness models actually address the educative framework necessary for an individual to learn and thus become aware or understand and make choices about their own Wellness.The literature reviewed within this paper would suggest that learner success is optimised by giving learners authentic opportunities to develop and practice self regulation strategies. Such opportunities include learning experiences that: provide options for self determined outcomes; require skills development; recognise principles of successful learning as outlined by the APA; and are scaffolded according to learner needs rather than in generic ways. Thus, configuring a learner centred curriculum in Wellness Education would potentially benefit from overlaying principles from the domains of both SRL and Wellness to highlight authentic learning as a means to lifelong approaches, triggered by undergraduate experiences.Student perceptions are a rich and significant data base for the measurement of their experiences, activities, practices and behaviours. Wellness undergraduate education, such as the “Fitness, Health and Wellness” unit offered by Queensland University of Technology, offers a context in which to confirm possibilities suggested by the literature reviewed in this paper in a practical, Australian context.

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The Autistic Behavioural Indicators Instrument (ABII) is an 18-item instrument developed to identify children with Autistic Disorder (AD) based on the presence of unique autistic behavioural indicators. The ABII was administered to 20 children with AD, 20 children with speech and language impairment (SLI) and 20 typically developing (TD) children aged 2-6 years. Results indicated that the ABII discriminated children diagnosed with AD from those diagnosed with SLI and those who were TD, based on the presence of specific social attention, sensory, and behavioural symptoms. A combination of symptomology across these domains correctly classified 100% of children with and without AD. The paper concludes that the ABII shows considerable promise as an instrument for the early identification of AD.

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Purpose: The Australian Women’s Activity Survey (AWAS) was developed based on a systematic review and qualitative research on how to measure activity patterns of women with young children (WYC). AWAS assesses activity performed across five domains (planned activities, employment, childcare, domestic responsibilities and transport), and intensity levels (sitting, light-intensity, brisk walking, moderate-intensity and vigorous-intensity) in a typical week in the past month. The purpose of this study was to assess the test-retest reliability and criterion validity of the AWAS. Methods: WYC completed the AWAS on two occasions 7-d apart (test-retest reliability protocol) and/or wore an MTI ActiGraph accelerometer for 7-d in between (validity protocol). Forty WYC (mean age 35 ± 5yrs) completed the test-retest reliability protocol and 75 WYC (mean age 33 ± 5yrs) completed the validity protocol. Interclass Correlation Coefficients (ICC) between AWAS administrations and Spearman’s Correlation Coefficients (rs) between AWAS and MTI data were calculated. Results: AWAS showed good test-retest reliability (ICC=0.80 (0.65-0.89)) and acceptable criterion validity (rs= 0.28, p=0.01) for measuring weekly health-enhancing physical activity. AWAS also provided repeatable and valid estimates of sitting time (test-retest reliability ICC=0.42 (0.13-0.64), and criterion validity (rs= 0.32, p=0.006)). Conclusion: The measurement properties of the AWAS are comparable to those reported for existing self-report measures of physical activity. However, AWAS offers a more comprehensive and flexible alternative for accurately assessing different domains and intensities of activity relevant to WYC. Future research should investigate whether the AWAS is a suitable measure of intervention efficacy by examining its sensitivity to change.

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In Australia, airports have emerged as important sub-regional activity centres and now pose challenges for both airport operation and planning in the surrounding urban and regional environment. The changing nature of airports in their metropolitan context and the emergence of new pressures and problems require the introduction of a fresh conceptual framework to assist the better understanding of these complex roles and spatial interactions. The approach draws upon the meta-concept of interfaces of an ‘airport metropolis’ as an organising device consisting of four main domains: economic development, land use,infrastructure, and governance. The paper uses the framework to further discuss airport and regional interactions and highlights the use of sustainability criteria to operationalise the model. The approach aims to move research and practice beyond the traditionally compartmentalised analysis of airport issues and policy-making by highlighting interdependencies between airports and regions.