My place through my eyes : a social constructionist approach to researching the relationships between socioeconomic living contexts and physical activity

There is a growing evidence-base in the epidemiological literature that demonstrates significant associations between people’s living circumstances – including their place of residence – and their health-related practices and outcomes (Leslie, 2005; Karpati, Bassett, & McCord, 2006; Monden, Van Lenthe, & Mackenbach, 2006; Parkes & Kearns, 2006; Cummins, Curtis, Diez-Roux, & Macintyre, 2007; Turrell, Kavanagh, Draper, & Subramanian, 2007). However, these findings raise questions about the ways in which living places, such as households and neighbourhoods, figure in the pathways connecting people and health (Frolich, Potvin, Chabot, & Corin, 2002; Giles-Corti, 2006; Brown et al, 2006; Diez Roux, 2007). This thesis addressed these questions via a mixed methods investigation of the patterns and processes connecting people, place, and their propensity to be physically active. Specifically, the research in this thesis examines a group of lower-socioeconomic residents who had recently relocated from poorer suburbs to a new urban village with a range of health-related resources. Importantly, the study contrasts their historical relationship with physical activity with their reactions to, and everyday practices in, a new urban setting designed to encourage pedestrian mobility and autonomy. The study applies a phenomenological approach to understanding living contexts based on Berger and Luckman’s (1966) conceptual framework in The Social Construction of Reality. This framework enables a questioning of the concept of context itself, and a treatment of it beyond environmental factors to the processes via which experiences and interactions are made meaningful. This approach makes reference to people’s histories, habituations, and dispositions in an exploration between social contexts and human behaviour. This framework for thinking about context is used to generate an empirical focus on the ways in which this residential group interacts with various living contexts over time to create a particular construction of physical activity in their lives. A methodological approach suited to this thinking was found in Charmaz’s (1996; 2001; 2006) adoption of a social constructionist approach to grounded theory. This approach enabled a focus on people’s own constructions and versions of their experiences through a rigorous inductive method, which provided a systematic strategy for identifying patterns in the data. The findings of the study point to factors such as ‘childhood abuse and neglect’, ‘early homelessness’, ‘fear and mistrust’, ‘staying indoors and keeping to yourself’, ‘conflict and violence’, and ‘feeling fat and ugly’ as contributors to an ongoing core category of ‘identity management’, which mediates the relationship between participants’ living contexts and their physical activity levels. It identifies barriers at the individual, neighbourhood, and broader ecological levels that prevent this residential group from being more physically active, and which contribute to the ways in which they think about, or conceptualise, this health-related behaviour in relationship to their identity and sense of place – both geographic and societal. The challenges of living well and staying active in poorer neighbourhoods and in places where poverty is concentrated were highlighted in detail by participants. Participants’ reactions to the new urban neighbourhood, and the depth of their engagement with the resources present, are revealed in the context of their previous life-experiences with both living places and physical activity. Moreover, an understanding of context as participants’ psychological constructions of various social and living situations based on prior experience, attitudes, and beliefs was formulated with implications for how the relationship between socioeconomic contextual effects on health are studied in the future. More detailed findings are presented in three published papers with implications for health promotion, urban design, and health inequalities research. This thesis makes a substantive, conceptual, and methodological contribution to future research efforts interested in how physical activity is conceptualised and constructed within lower socioeconomic living contexts, and why this is. The data that was collected and analysed for this PhD generates knowledge about the psychosocial processes and mechanisms behind the patterns observed in epidemiological research regarding socioeconomic health inequalities. Further, it highlights the ways in which lower socioeconomic living contexts tend to shape dispositions, attitudes, and lifestyles, ultimately resulting in worse health and life chances for those who occupy them.

Defamation : is that a fly in my soup?

In a recent case the High Court considered whether a restaurant review was defamatory.

My "middle way" media studies

I would argue that the problems that contemporary capitalism gives rise to are not the result of the classic exercise of power and hegemony characteristic of the monopoly phase of capitalism but of the “creative destruction” of such a phase. Schumpeter’s famous phrase is reflective of Lash and Urry’s (1987) notion of “disorganised capitalism” or of Robert Reich’s (2007) claim that large corporations have significantly less power now than three decades ago. The consequence is that there is a need to explore an economic “middle way” in debates about the narrative of the relationship between culture and economy, between the Scylla of total explanatory political economy and the Charybdis of tedium-by-case-study. This involves a Schumpeterian emphasis on entrepreneurial or enterprise economics (Cunningham, Banks, and Potts 2008). Schumpeter, in 1962, in Capitalism, Socialism and Democracy, argued that Marx had “no adequate theory of enterprise” and failed to “distinguish the entrepreneur from the capitalist” (quoted in McCraw 2007: 349). Schumpeter, his most recent biographer, Thomas McCraw, “told of capitalism in the way most people experience it: as consumer desires aroused by endless advertising; as forcible jolts up and down the social pecking order; as goals reached, shattered, altered, then reached once more as people try, try again.” He knew that “creative destruction fosters economic growth but also that it undercuts cherished human values” (p. 6). Schumpeter’s most recent biographer, Thomas McCraw, says that he elucidated what capitalism “really feels like” (as quoted in McCraw 2007: 349, 6).

AITPM Email Newsletter Volume 0902, February 2009: Presidents Message

President’s Report Hello fellow AITPM members, Welcome to the first edition of the AITPM National Newsletter for 2009! I trust we all had a relaxing break and managed to lose track of all things transport for just a little while. I know I had trouble doing so when hunting for a car space at the shopping centre, and experiencing new projects such as the Tugun Bypass – the new gateway between New South Wales and Queensland. Byron Bay is now as close as Noosa for those high profile beach goers of Brisbane. There was also my experience of the reduced posted speed of 90km/h on the Bruce Highway around the troublesome Gympie stretch, when returning from a short Fraser Coast holiday. I expect that this relatively inexpensive safety improvement will pay substantial dividends in terms of crash reduction. The Newsletter took its annual leave last month and is refreshed and ready for a new year to keep us all informed of the latest in traffic and transport engineering, planning and management. I would like to take this opportunity to acknowledge the ongoing significant contributions of many volunteers in the Newsletter’s production. Mr Andrew Hulse, AITPM’s Immediate Past National President, serves as the Editorial Coordinator on behalf of the Institute. Each Branch Committee also includes a Newsletter Coordinator and committee members frequently contribute as well. And the ongoing contributions of readers enable us to offer the Newsletter as a vehicle for dialogue and debate around our sector. If you would like to contribute please email AITPM’s administration officer Josephine Mitton at aitpm@aitpm.com or through your local Branch Committee. I would also like to welcome back on deck our Editor, Mr David Brown of Driven Media, who creates a fantastic package for us each month. Lastly, members would have received the Call for Papers for the AITPM 2009 National Conference, Traffic Beyond Tomorrow, to be held at the Adelaide Convention Centre between 5 – 7 August. Abstracts will be accepted up to 20 February 2009. We look forward to seeing everyone at this, our flagship event for the year. To all a good year ahead, Jon Bunker Post Script: We all will have seen through the media the enormous scale and nature of the two natural disasters Australia is experiencing at present. AITPM’s thoughts are with all of those members, family and friends who may be experiencing hardship as a result of the Victorian bushfires and North Queensland floods. AITPM is a not for profit organisation however the National Executive has taken the decision to donate in measure to the Red Cross Victorian Bushfire Disaster Relief fund and the Queensland Premier’s Disaster Relief fund as a gesture to support our fellow Australians in their time of need. Details about these funds can be found via the Victorian and Queensland Governments’ websites.

Biochemical characterization of Aprataxin, the protein deficient in Ataxia with Oculomotor Apraxia type 1

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.

I got drunk and lost my virginity : young women's magazines and the management of sexual identity

It has often been argued that young woman’s magazine’s, like Cosmopolitan, Cleo Dolly and Seventeen, constitute a significant instrument in the patriarchal repression of young women - their hegemonic success lying in the fact that they appear to be sites wherein young women are ‘free’ from the elements of coercion so obviously in evidence within other terrains, such as the school and the family. This paper will suggest an alternative approach to these magazines. Rather than locating such texts within an overall model of repression and patriarchal domination, it will be argued here that they can be regarded as practical manuals which enrol young women to do specific kinds of work on themselves. In doing so, they form an effective link between the governmental imperatives aimed at constructing particular personas (such as, for example, ‘the sexually responsible young woman’), and the actual practices whereby these imperatives are operationalised. These manuals do not prevent young women from learning to ‘project a unique self’, they constitute a significant source of practices and techniques through which particular types of self are shaped.

Food insecurity in Brisbane : the single mother’s struggle

Using a feminist reflexive approach this paper reports on interviews with single mother’s in the Brisbane area about their experiences with food shopping and household food security. Preliminary findings suggest that most experience significant stress around the amount of money they have available for food. As the price of food and other costs of living increase, the only budget item that is flexible – groceries - is squeezed tighter. All women expressed a reluctance to ask for help from strangers at agencies instead relying on the support of family and friends to keep them food secure. Sometimes family and friends had no spare resources to help or were not aware of the extent their friend or relative might be struggling. The increased risks of poverty and food insecurity mean many go without as feeding the children takes precedence. The quality of their diets is variable with many reporting on aiming for quantity rather than being concerned with nutritional balance. Exhaustion and stress from being over-committed doing three roles, mother, father and housekeeper was self-identified as a key factor leading to mental health conditions such as depression, burnout and break down. Female single parent households are vulnerable to reducing welfare benefits as children grow or child support changes. Current policy forces single parents out to work but many can only manage part-time work for lower wages and are barely able to cope with this extra burden often resenting the reduction in benefits it brings. Public perceptions, derision and the notions of choice surrounding single parenting leave the cohort divided and silent for fear of reprisals. In my investigation issues arise about welfare policy that keep benefits low and workplace patriarchal power that can contribute to systemic poverty and the widening of the gender gap in poverty. So far analysis suggests a better support system around community food security including some hands on home help services, nutritional information, cooking classes, community gardening and other social capital building activities are needed for these women in order to avoid long-term health problems and help them better care for the next generation.

Philanthropy for Indigenous causes : more than a 'cup of tea'?

In the face of improved First Nation outcomes in many western nations, Australia is still dealing with a seemingly intractable gap between the quality of life of its Aboriginal and Torres Strait Islander peoples and the non-Aboriginal and Torres Strait Islander population. Philanthropy in Australia provides a smaller proportion of funding for community projects than is the case in other countries and Aboriginal and Torres Strait Islander causes have been significantly under - represented as recipients. This paper reports on a qualitative study aimed at understanding the issues affecting the decisions and actions of grantmaking organisations and individuals who wish to support Aboriginal and Torres Strait Islander causes in the current Australian context. The aims were to build on the limited research in this arena, add to the future research agenda and contribute to practice and policy insights for Australia and beyond. The study found that while government funding programs are perceived as output driven, inflexible and dogmatic - ‘a cup of tea mob’- participants see the Australian philanthropic sector as capable of addressing the complex Aboriginal and Torres Strait Islander ‘problem’ with more innovative and independent thinking. From the point of view of contextual impacts, success criteria, barriers, structural imposts and emotional involvement, the practical experience in grantmaking for Indigenous causes of participants in this study reflects that found elsewhere. However the focus of many grantmakers on organisational rather than community capacity and the potentially elitist emphasis on established relationships continues to hamper Aboriginal and Torres Strait Islander access to philanthropic funding in Australia. Further, if the strategic changes currently visible in the sector are unsupported by a depth of policy and a proactive transfer and distribution of skill and knowledge they may be unsustainable.

Rock pools of critical thought : finding a place to think through my higher degree and what a PhD was all about

The rock pools, salt pans, cliffs and bluffs, and the banks of the Coorooman and Pumpkin Creeks within Darumbal and Woppaburra Country are used as a backdrop in this paper, which offers an exploration of one woman’s quest to undertake her PhD and develop as an Indigenous scholar. The paper describes this Country and the use of Country to nourish, develop, stimulate and support the intellect. It draws on Australian and international literature to demonstrate the intellectual growth and development of Indigenous scholars. The paper offers a highly personal narrative of intellectual journeying which shows how we can be agents of change and power in our individual lives, even while power is being exercised over us and we are being oppressed and marginalised as Indigenous peoples.

My career chapter as a tool for reflective practice

This paper addresses reflective practice in research and practice and takes the issue of consciousness of social class in vocational psychology as a working example. It is argued that the discipline’s appreciation of social class can be advanced through application of the qualitative research method autoethnography. Excerpts from an autoethnographic study are used to explore the method’s potential. This reflexive research method is presented as a potential vehicle to improve vocational psychologists’ own class consciousness, and to concomitantly enhance their capacity to grasp social class within their own spheres of research and practice. It is recommended that autoethnography be used for research, training, and professional development for vocational psychologists.

Tips for generating a media release and media coverage : how the media ate up my research on Aussie horror movies

The focus of this paper is preparing research for dissemination by mainstream print, broadcast, and online media. While the rise of the blogosphere and social media is proving an effective way of reaching niche audiences, my own research reached such an audience through traditional media. The first major study of Australian horror cinema, my PhD thesis A Dark New World: Anatomy of Australian Horror Films, generated strong interest from horror movie fans, film scholars, and filmmakers. I worked closely with the Queensland University of Technology’s (QUT) public relations unit to write two separate media releases circulated on October 13, 2008 and October 14, 2009. This chapter reflects upon the process of working with the media and provides tips for reaching audiences, particularly in terms of strategically planning outcomes. It delves into the background of my study which would later influence my approach to the media, the process of drafting media releases, and key outcomes and benefits from popularising research. A key lesson from this experience is that redeveloping research for the media requires a sharp writing style, letting go of academic justification, catchy quotes, and an ability to distil complex details into easy-to-understand concepts. Although my study received strong media coverage, and I have since become a media commentator, my experiences also revealed a number of pitfalls that are likely to arise for other researchers keen on targeting media coverage.

Recent advances in cancer therapy targeting proteins involved in DNA double-strand break repair

Damage to genetic material represents a persistent and ubiquitous threat to genomic stability. Once DNA damage is detected, a multifaceted signaling network is activated that halts the cell cycle, initiates repair, and in some instances induces apoptotic cell death. In this article, we will review DNA damage surveillance networks, which maintain the stability of our genome, and discuss the efforts underway to identify chemotherapeutic compounds targeting the core components of DNA double-strand breaks (DSB) response pathway. The majority of tumor cells have defects in maintaining genomic stability owing to the loss of an appropriate response to DNA damage. New anticancer agents are exploiting this vulnerability of cancer cells to enhance therapeutic indexes, with limited normal tissue toxicity. Recently inhibitors of the checkpoint kinases Chk1 and Chk2 have been shown to sensitize tumor cells to DNA damaging agents. In addition, the treatment of BRCA1- or BRCA2-deficient tumor cells with poly(ADP-ribose) polymerase (PARP) inhibitors also leads to specific tumor killing. Due to the numerous roles of p53 in genomic stability and its defects in many human cancers, therapeutic agents that restore p53 activity in tumors are the subject of multiple clinical trials. In this article we highlight the proteins mentioned above and catalog several additional players in the DNA damage response pathway, including ATM, DNA-PK, and the MRN complex, which might be amenable to pharmacological interventions and lead to new approaches to sensitize cancer cells to radio- and chemotherapy. The challenge is how to identify those patients most receptive to these treatments.