Increasing socio-economic inequalities in drug-induced deaths in Australia : 1981-2002

Introduction and Aims: Since the 1990s illicit drug use death rates in Australia have increased markedly. There is a notable gap in knowledge about changing socio-economic inequalities in drug use death rates. Some limited Australian and overseas data point to higher rates of drug death in the lowest socio-economic groups, but the paucity of available studies and their sometimes conflicting findings need to be addressed. Design and Methods: This paper uses data obtained from the Australian Bureau of Statistics (ABS) to examine changes in age-standardised drug-induced mortality rates for Australian males over the period 1981 – 2002. Socio-economic status was categorised as manual or non-manual work status. Results: With the rapid increase in drug-induced mortality rates in the 1990s, there was a parallel increase in socio-economic inequalities in drug-induced deaths. The decline in drug death rates from 2000 onwards was associated with a decline in socio-economic inequalities. By 2002, manual workers had drug death rates well over twice the rate of non-manual workers. Discussion: Three factors are identified which contribute to these socio-economic inequalities in mortality. First, there has been an age shift in deaths evident only for manual workers. Secondly, there has been an increase in availability until 1999 and a relative decline in the cost of the drug, which most often leads to drug death (heroin). Thirdly, there has been a shift to amphetamine use which may lead to significant levels of morbidity, but few deaths. [Najman JM, Toloo G, Williams GM. Increasing socio-economic inequalities in drug-induced deaths in Australia: 1981–2002.

An Analysis of UK Farmland : 1981-2004

The importance of agriculture in many countries has tended to reduce as their economies move from a resource base to a manufacturing industry base. Although the level of agricultural production in first world countries has increased over the past two decades, this increase has generally been at a less significant rate compared to other sectors of the economies. Despite this increase in secondary and high technology industries, developed countries have continued to encourage and support their agricultural industries. This support has been through both tariffs and price support. Although the average farm production property may require this support to maintain long-term production, the better farms can actually achieve production levels and commodity prices that result in these units being competitive on a free market basis. This paper will analyse the total return performance of UK farmland over the period 1981-2004. This analysis will compare the total return from rural properties in the UK and compare this performance to commercial property returns (total, office, retail, industrial), equities and gilts over this 24-year period. The analysis will be based on the IPD UK let land index and the IPD property index. The portfolio diversification and risk-reduction benefits of UK farmland will be highlighted. The analysis shows that rural property has negative correlations with equities and gilts, as well as insignificant positive correlations with retail, industrial and office property. Rural property also provides portfolio diversification benefits.

Hypercapitalism:Political economy, electric identity, and authorial alienation

Hypercapitalism, with its "knowledge economy", is the form of capitalism under which thought itself is produced, commodified, and exchanged within the globally integrated system of communication technologies. As such, hypercapitalism may be seen as not so much a revolution, but rather an evolution: the progressively thorough, inexorable totalisation of social relations by Capital. The study on which this paper is based synthesises the sociological perspectives of Marx (1970, 1844/1975, 1846/1972, 1976, 1978, 1981) and Adorno (1951/1974, 1991; Horkheimer & Adorno, 1944/1998), and the Critical Discourse perspectives of Fairclough (1989, 1992) and Lemke (1995) to argue that alienated thought and language are the fundamental, irreducible commodity-forms of Cybersociety’s knowledge economy.

Psychopathology during childhood and adolescence predicts delusional-like experiences in adults : a 21-year birth cohort study

Objective: Community surveys have shown that many otherwise well individuals report delusional-like experiences. The authors examined psychopathology during childhood and adolescence as a predictor of delusional-like experiences in young adulthood. ---------- Method: The authors analyzed prospective data from the Mater-University of Queensland Study of Pregnancy, a birth cohort of 3,617 young adults born between 1981 and 1983. Psychopathology was measured at ages 5 and 14 using the Child Behavior Checklist (CBCL) and at age 14 using the Youth Self-Report (YSR). Delusional-like experiences were measured at age 21 using the Peters Delusional Inventory. The association between childhood and adolescent symptoms and later delusional-like experiences was examined using logistic regression. ---------- Results: High CBCL scores at ages 5 and 14 predicted high levels of delusional-like experiences at age 21 (odds ratios for the highest versus the other quartiles combined were 1.25 and 1.85, respectively). Those with YSR scores in the highest quartile at age 14 were nearly four times as likely to have high levels of delusional-like experiences at age 21 (odds ratio=3.71). Adolescent-onset psychopathology and continuous psychopathology through both childhood and adolescence strongly predicted delusional-like experiences at age 21. Hallucinations at age 14 were significantly associated with delusional-like experiences at age 21. The general pattern of associations persisted when adjusted for previous drug use or the presence of nonaffective psychoses at age 21. ---------- Conclusion: Psychopathology during childhood and adolescence predicts adult delusional-like experiences. Understanding the biological and psychosocial factors that influence this developmental trajectory may provide clues to the pathogenesis of psychotic-like experiences.

Monopoly, monopsony, and the value of culture in a digital age: An axiology of two multimedia resource repositories

Broadly speaking, axiology is the study of values. Axiologies are expressed materially in patterns of choices that are both culture-bound and definitive of different cultures. They are expressed in the language we use; in the friends we keep; in the clothes we wear; in what we read, write, and watch; in the technologies we use; in the gods we believe in and pray to; in the music we make and listen to—indeed, in every kind of activity that can be counted as a definitive element of culture. In what follows, I describe the axiological underpinnings of two closely related multimedia repository projects— Australian Creative Resources Online (ACRO) and The Canadian Centre for Cultural Innovation (CCCI)—and how these are oriented towards a potentially liberating role for digital repositories.

Crosstalk between developmental and tumour-specific signalling pathways : kallikrein-related serine peptidases and nodal in prostrate cancer

Prostate cancer is an important male health issue. The strategies used to diagnose and treat prostate cancer underscore the cell and molecular interactions that promote disease progression. Prostate cancer is histologically defined by increasingly undifferentiated tumour cells and therapeutically targeted by androgen ablation. Even as the normal glandular architecture of the adult prostate is lost, prostate cancer cells remain dependent on the androgen receptor (AR) for growth and survival. This project focused on androgen-regulated gene expression, altered cellular differentiation, and the nexus between these two concepts. The AR controls prostate development, homeostasis and cancer progression by regulating the expression of downstream genes. Kallikrein-related serine peptidases are prominent transcriptional targets of AR in the adult prostate. Kallikrein 3 (KLK3), which is commonly referred to as prostate-specific antigen, is the current serum biomarker for prostate cancer. Other kallikreins are potential adjunct biomarkers. As secreted proteases, kallikreins act through enzyme cascades that may modulate the prostate cancer microenvironment. Both as a panel of biomarkers and cascade of proteases, the roles of kallikreins are interconnected. Yet the expression and regulation of different kallikreins in prostate cancer has not been compared. In this study, a spectrum of prostate cell lines was used to evaluate the expression profile of all 15 members of the kallikrein family. A cluster of genes was co-ordinately expressed in androgenresponsive cell lines. This group of kallikreins included KLK2, 3, 4 and 15, which are located adjacent to one another at the centromeric end of the kallikrein locus. KLK14 was also of interest, because it was ubiquitously expressed among the prostate cell lines. Immunohistochemistry showed that these 5 kallikreins are co-expressed in benign and malignant prostate tissue. The androgen-regulated expression of KLK2 and KLK3 is well-characterised, but has not been compared with other kallikreins. Therefore, KLK2, 3, 4, 14 and 15 expression were all measured in time course and dose response experiments with androgens, AR-antagonist treatments, hormone deprivation experiments and cells transfected with AR siRNA. Collectively, these experiments demonstrated that prostatic kallikreins are specifically and directly regulated by the AR. The data also revealed that kallikrein genes are differentially regulated by androgens; KLK2 and KLK3 were strongly up-regulated, KLK4 and KLK15 were modestly up-regulated, and KLK14 was repressed. Notably, KLK14 is located at the telomeric end of the kallikrein locus, far away from the centromeric cluster of kallikreins that are stimulated by androgens. These results show that the expression of KLK2, 3, 4, 14 and 15 is maintained in prostate cancer, but that these genes exhibit different responses to androgens. This makes the kallikrein locus an ideal model to investigate AR signalling. The increasingly dedifferentiated phenotype of aggressive prostate cancer cells is accompanied by the re-expression of signalling molecules that are usually expressed during embryogenesis and foetal tissue development. The Wnt pathway is one developmental cascade that is reactivated in prostate cancer. The canonical Wnt cascade regulates the intracellular levels of β-catenin, a potent transcriptional co-activator of T-cell factor (TCF) transcription factors. Notably, β-catenin can also bind to the AR and synergistically stimulate androgen-mediated gene expression. This is at the expense of typical Wnt/TCF target genes, because the AR:β-catenin and TCF:β-catenin interactions are mutually exclusive. The effect of β-catenin on kallikrein expression was examined to further investigate the role of β-catenin in prostate cancer. Stable knockdown of β-catenin in LNCaP prostate cancer cells attenuated the androgen-regulated expression of KLK2, 3, 4 and 15, but not KLK14. To test whether KLK14 is instead a TCF:β-catenin target gene, the endogenous levels of β-catenin were increased by inhibiting its degradation. Although KLK14 expression was up-regulated by these treatments, siRNA knockdown of β-catenin demonstrated that this effect was independent of β-catenin. These results show that β-catenin is required for maximal expression of KLK2, 3, 4 and 15, but not KLK14. Developmental cells and tumour cells express a similar repertoire of signalling molecules, which means that these different cell types are responsive to one another. Previous reports have shown that stem cells and foetal tissues can reprogram aggressive cancer cells to less aggressive phenotypes by restoring the balance to developmental signalling pathways that are highly dysregulated in cancer. To investigate this phenomenon in prostate cancer, DU145 and PC-3 prostate cancer cells were cultured on matrices pre-conditioned with human embryonic stem cells (hESCs). Soft agar assays showed that prostate cancer cells exposed to hESC conditioned matrices had reduced clonogenicity compared with cells harvested from control matrices. A recent study demonstrated that this effect was partially due to hESC-derived Lefty, an antagonist of Nodal. A member of the transforming growth factor β (TGFβ) superfamily, Nodal regulates embryogenesis and is re-expressed in cancer. The role of Nodal in prostate cancer has not previously been reported. Therefore, the expression and function of the Nodal signalling pathway in prostate cancer was investigated. Western blots confirmed that Nodal is expressed in DU145 and PC-3 cells. Immunohistochemistry revealed greater expression of Nodal in malignant versus benign glands. Notably, the Nodal inhibitor, Lefty, was not expressed at the mRNA level in any prostate cell lines tested. The Nodal signalling pathway is functionally active in prostate cancer cells. Recombinant Nodal treatments triggered downstream phosphorylation of Smad2 in DU145 and LNCaP cells, and stably-transfected Nodal increased the clonogencity of LNCaP cells. Nodal was also found to modulate AR signalling. Nodal reduced the activity of an androgen-regulated KLK3 promoter construct in luciferase assays and attenuated the endogenous expression of AR target genes including prostatic kallikreins. These results demonstrate that Nodal is a novel example of a developmental signalling molecule that is reexpressed in prostate cancer and may have a functional role in prostate cancer progression. In summary, this project clarifies the role of androgens and changing cellular differentiation in prostate cancer by characterising the expression and function of the downstream genes encoding kallikrein-related serine proteases and Nodal. Furthermore, this study emphasises the similarities between prostate cancer and early development, and the crosstalk between developmental signalling pathways and the AR axis. The outcomes of this project also affirm the utility of the kallikrein locus as a model system to monitor tumour progression and the phenotype of prostate cancer cells.

Copyright future copyright freedom

If copyright law does not liberate us from restrictions on the dissemination of knowledge, if it does not encourage expressive freedom, what is its purpose? This volume offers the thinking and suggestions of some of the finest minds grappling with the future of copyright regulation. The Copyright Future Copyright Freedom conference held in 2009 at Old Parliament House Canberra brought together Lawrence Lessig, Julie Cohen, Leslie Zines, Adrian Sterling, Sam Ricketson, Graham Greenleaf, Anne Fitzgerald, Susy Frankel, John Gilchrist, Michael Kirby and others to share the rich fruits of their experience and analysis. Zines, Sterling and Gilchrist outline their roles in the genesis and early growth of Australian copyright legislation, enriching the knowledge of anyone asking urgent questions about the future of information regulation.

Hypercapitalism : a political economy of informational idealism

In this this paper I identify specific historical trajectories that are directly contingent upon the deployment and use of new media, but which are actually hidden by a focus on the purely technological. They are: the increasingly abstract and alienated nature of economic value; the subsumption of all labour - material and intellectual - under systemic capital; and the convergence of formerly distinct spheres of analysis –the spheres of production, circulation, and consumption. This paper examines the implications of the knowledge economy from an historical materialist perspective. I synthesise the systemic views of Marx (1846/1972, 1875/1972 1970 1973 1976 1978 1981), Adorno (1951/1974 1964/1973 1991; Horkheimer and Adorno 1944/1998; Jarvis 1998), and Bourdieu (1991 1998) to argue for a language-focused approach to new media research and suggest aspects of Marxist thought which might be useful in researching emergent socio-technical domains. I also identify specific categories in the Marxist tradition which may no longer be analytically useful for researching the effects of new media.

The digital Dark Ages : a retro-speculative history of possible futures

The Dark Ages are generally held to be a time of technological and intellectual stagnation in western development. But that is not necessarily the case. Indeed, from a certain perspective, nothing could be further from the truth. In this paper we draw historical comparisons, focusing especially on the thirteenth and fourteenth centuries, between the technological and intellectual ruptures in Europe during the Dark Ages, and those of our current period. Our analysis is framed in part by Harold Innis’s2 notion of "knowledge monopolies". We give an overview of how these were affected by new media, new power struggles, and new intellectual debates that emerged in thirteenth and fourteenth century Europe. The historical salience of our focus may seem elusive. Our world has changed so much, and history seems to be an increasingly far-from-favoured method for understanding our own period and its future potentials. Yet our seemingly distant historical focus provides some surprising insights into the social dynamics that are at work today: the fracturing of established knowledge and power bases; the democratisation of certain "sacred" forms of communication and knowledge, and, conversely, the "sacrosanct" appropriation of certain vernacular forms; challenges and innovations in social and scientific method and thought; the emergence of social world-shattering media practices; struggles over control of vast networks of media and knowledge monopolies; and the enclosure of public discursive and social spaces for singular, manipulative purposes. The period between the eleventh and fourteenth centuries in Europe prefigured what we now call the Enlightenment, perhaps moreso than any other period before or after; it shaped what the Enlightenment was to become. We claim no knowledge of the future here. But in the "post-everything" society, where history is as much up for sale as it is for argument, we argue that our historical perspective provides a useful analogy for grasping the wider trends in the political economy of media, and for recognising clear and actual threats to the future of the public sphere in supposedly democratic societies.

The coming of post-reflexive society : a critique of the political economy of digital capitalism

Language is a unique aspect of human communication because it can be used to discuss itself in its own terms. For this reason, human societies potentially have superior capacities of co-ordination, reflexive self-correction, and innovation than other animal, physical or cybernetic systems. However, this analysis also reveals that language is interconnected with the economically and technologically mediated social sphere and hence is vulnerable to abstraction, objectification, reification, and therefore ideology – all of which are antithetical to its reflexive function, whilst paradoxically being a fundamental part of it. In particular, in capitalism, language is increasingly commodified within the social domains created and affected by ubiquitous communication technologies. The advent of the so-called ‘knowledge economy’ implicates exchangeable forms of thought (language) as the fundamental commodities of this emerging system. The historical point at which a ‘knowledge economy’ emerges, then, is the critical point at which thought itself becomes a commodified ‘thing’, and language becomes its “objective” means of exchange. However, the processes by which such commodification and objectification occurs obscures the unique social relations within which these language commodities are produced. The latest economic phase of capitalism – the knowledge economy – and the obfuscating trajectory which accompanies it, we argue, is destroying the reflexive capacity of language particularly through the process of commodification. This can be seen in that the language practices that have emerged in conjunction with digital technologies are increasingly non-reflexive and therefore less capable of self-critical, conscious change.

Kallikrein 14 is down-regulated by androgen receptor signalling and harbours genetic variation that is associated with prostate tumour aggressiveness

Kallikrein 14 (KLK14) has been proposed as a useful prognostic marker in prostate cancer, with expression reported to be associated with tumour characteristics such as higher stage and Gleason score. KLK14 tumour expression has also shown the potential to predict prostate cancer patients at risk of disease recurrence after radical prostatectomy. The KLKs are a remarkably hormone-responsive family of genes, although detailed studies of androgen regulation of KLK14 in prostate cancer have not been undertaken to date. Using in vitro studies, we have demonstrated that unlike many other prostatic KLK genes that are strictly androgen responsive, KLK14 is more broadly expressed and inversely androgen regulated in prostate cancer cells. Given these results and evidence that KLK14 may play a role in prostate cancer prognosis, we also investigated whether common genetic variants in the KLK14 locus are associated with risk and/or aggressiveness of prostate cancer in approximately 1200 prostate cancer cases and 1300 male controls. Of 41 single nucleotide polymorphisms assessed, three were associated with higher Gleason score (≥7): rs17728459 and rs4802765, both located upstream of KLK14, and rs35287116, which encodes a p.Gln33Arg substitution in the KLK14 signal peptide region. Our findings provide further support for KLK14 as a marker of prognosis in prostate cancer.

Evaluation of the Suchey-Brooks Method of age estimation in an Australian subpopulation using computed tomography of the pubic symphyseal surface

Despite the prominent use of the Suchey-Brooks (S-B) method of age estimation in forensic anthropological practice, it is subject to intrinsic limitations, with reports of differential inter-population error rates between geographical locations. This study assessed the accuracy of the S-B method to a contemporary adult population in Queensland, Australia and provides robust age parameters calibrated for our population. Three-dimensional surface reconstructions were generated from computed tomography scans of the pubic symphysis of male and female Caucasian individuals aged 15–70 years (n = 195) in Amira® and Rapidform®. Error was analyzed on the basis of bias, inaccuracy and percentage correct classification for left and right symphyseal surfaces. Application of transition analysis and Chi-square statistics demonstrated 63.9% and 69.7% correct age classification associated with the left symphyseal surface of Australian males and females, respectively, using the S-B method. Using Bayesian statistics, probability density distributions for each S-B phase were calculated, providing refined age parameters for our population. Mean inaccuracies of 6.77 (±2.76) and 8.28 (±4.41) years were reported for the left surfaces of males and females, respectively; with positive biases for younger individuals (<55 years) and negative biases in older individuals. Significant sexual dimorphism in the application of the S-B method was observed; and asymmetry in phase classification of the pubic symphysis was a frequent phenomenon. These results recommend that the S-B method should be applied with caution in medico-legal death investigations of Queensland skeletal remains and warrant further investigation of reliable age estimation techniques.

Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990–2010 : a systematic analysis for the Global Burden of Disease Study 2010

Background Non-fatal health outcomes from diseases and injuries are a crucial consideration in the promotion and monitoring of individual and population health. The Global Burden of Disease (GBD) studies done in 1990 and 2000 have been the only studies to quantify non-fatal health outcomes across an exhaustive set of disorders at the global and regional level. Neither effort quantified uncertainty in prevalence or years lived with disability (YLDs). Methods Of the 291 diseases and injuries in the GBD cause list, 289 cause disability. For 1160 sequelae of the 289 diseases and injuries, we undertook a systematic analysis of prevalence, incidence, remission, duration, and excess mortality. Sources included published studies, case notification, population-based cancer registries, other disease registries, antenatal clinic serosurveillance, hospital discharge data, ambulatory care data, household surveys, other surveys, and cohort studies. For most sequelae, we used a Bayesian meta-regression method, DisMod-MR, designed to address key limitations in descriptive epidemiological data, including missing data, inconsistency, and large methodological variation between data sources. For some disorders, we used natural history models, geospatial models, back-calculation models (models calculating incidence from population mortality rates and case fatality), or registration completeness models (models adjusting for incomplete registration with health-system access and other covariates). Disability weights for 220 unique health states were used to capture the severity of health loss. YLDs by cause at age, sex, country, and year levels were adjusted for comorbidity with simulation methods. We included uncertainty estimates at all stages of the analysis. Findings Global prevalence for all ages combined in 2010 across the 1160 sequelae ranged from fewer than one case per 1 million people to 350 000 cases per 1 million people. Prevalence and severity of health loss were weakly correlated (correlation coefficient −0·37). In 2010, there were 777 million YLDs from all causes, up from 583 million in 1990. The main contributors to global YLDs were mental and behavioural disorders, musculoskeletal disorders, and diabetes or endocrine diseases. The leading specific causes of YLDs were much the same in 2010 as they were in 1990: low back pain, major depressive disorder, iron-deficiency anaemia, neck pain, chronic obstructive pulmonary disease, anxiety disorders, migraine, diabetes, and falls. Age-specific prevalence of YLDs increased with age in all regions and has decreased slightly from 1990 to 2010. Regional patterns of the leading causes of YLDs were more similar compared with years of life lost due to premature mortality. Neglected tropical diseases, HIV/AIDS, tuberculosis, malaria, and anaemia were important causes of YLDs in sub-Saharan Africa. Interpretation Rates of YLDs per 100 000 people have remained largely constant over time but rise steadily with age. Population growth and ageing have increased YLD numbers and crude rates over the past two decades. Prevalences of the most common causes of YLDs, such as mental and behavioural disorders and musculoskeletal disorders, have not decreased. Health systems will need to address the needs of the rising numbers of individuals with a range of disorders that largely cause disability but not mortality. Quantification of the burden of non-fatal health outcomes will be crucial to understand how well health systems are responding to these challenges. Effective and affordable strategies to deal with this rising burden are an urgent priority for health systems in most parts of the world. Funding Bill & Melinda Gates Foundation.