The burden of disease and injury in Australia 2003

The report measures mortality, disability, illness and injury arising from over 170 diseases and injuries. Burden of disease analysis gives a unique perspective on health

The burden of disease and injury in Australia

This report provides an overview of results from the Australian Burden of Disease and Injury Study undertaken by the AIHW during 1998 and 1999. The Study uses the methods developed for the Global Burden of Disease Study, adapted to the Australian context and drawing extensively on Australian sources of population health data. It provides a comprehensive assessment of the amount of ill health and disability, the ‘burden of disease’ in Australia in 1996.

Mortality, disability, impairment, illness and injury arising from 176 diseases, injuries and risk factors are measured using a common metric, the Disability-Adjusted Life Year or DALY. One DALY is a lost year of ‘healthy’ life and is calculated as a combination of years of life lost due to premature mortality (YLL) and equivalent ‘healthy’ years of life lost due to disability (YLD). This report provides estimates of the contribution of fatal and non-fatal health outcomes to the total burden of disease and injury measured in DALYs in Australia in 1996.

Health system costs of diseases and injury in Australia 1993-94 : an analysis of costs, service use and mortality for major disease and injury groups

Provides a systematic analysis of the health system use and costs associated with specific disease and injury groups in Australia in 1993-94. The estimates are presented in a consistent format and are derived using a methodology that ensures the results add across disease, age and sex groups to total Australian health expenditures for 1993-94.

Health system expenditure on disease and injury in Australia, 2000–01

This publication presents estimates of health expenditure on disease and injury in Australia in 2000-01, classified by disease or injury group, age and sex. The estimates are available by area of expenditure - hospitals, high-level residential aged care, medical services, other professional services, pharmaceuticals and research.The 2000-01 disease expenditure estimates were based on the 176 disease and injury conditions used in the first Australian burden of disease study (AIHW: Mathers et al. 1999), with the inclusion of some additional sub-categories. This report aggregates these conditions into the 19 broad disease groups used by the burden of disease study. Disease expenditure estimates are also presented for selected conditions in the seven National Health Priority Areas and by age and sex.

The burden of disease and injury in Australia

An overview of the results of the Australian Burden of Disease (ABD) study is presented. The ABD study was the first to use methodology developed for the Global Burden of Disease study to measure the burden of disease and injury in a developed country. In 1996, mental disorders were the main causes of disability burden, responsible for nearly 30% of total years of life lost to disability (YLD), with depression accounting for 8% of the total YLD. Ischaemic heart disease and stroke were the main contributors to the disease burden disability-adjusted life years (DALYs), together causing nearly 18% of the total disease burden. Risk factors such as smoking, alcohol consumption, physical inactivity, hypertension, high blood cholesterol, obesity and inadequate fruit and vegetable consumption were responsible for much of the overall disease burden in Australia. The lessons learnt from the ABD study are discussed, together with methodological issues that require further attention.

Towards a standardised methodology for estimating alcohol-caused death, injury and illness in Australia

Two key methodological issues underlying different methods for calculating estimates of the number of alcohol-caused deaths are identified and recommendations suggested for future work.

1. How to adjust alcohol aetiologic fractions across time and place to reflect different levels of risky drinking. A common approach is outlined for both acute and chronic alcohol-related conditions. In the absence of consistent, reliable and regionally specific measures of the prevalence of risky alcohol consumption from national surveys, the use of per capita consumption data as a means of adjusting alcohol population aetiologic fractions over time and across regions is recommended.

2. Whether abstainers or low-risk drinkers should be used as the reference group when assessing the impact of alcohol consumption and how the resulting information is best presented. It is recommended that when abstainers are used as the reference group, the costs and benefits for both 'low-risk' and 'risky/high-risk' drinking should be identified. Using this approach, it was estimated that for Australia in 1998 there was a net benefit of 5,100 lives saved due to low-risk drinking, while there was a net loss of 2,737 lives due to risky/high-risk drinking. On its own, the figure of a net saving of 2,363 lives per year is a simplistic and potentially misleading picture of alcohol as a net benefit to public health and safety. For public health communications, there is still value in providing estimates using the low-risk drinking contrast, of the number of lives saved if risky/high-risk drinkers all became low-risk drinkers (n=3,292 in 1998). The use of the abstinence contrast, however, allows the more complex picture of alcohol's impact on public health to be apparent, e.g. including the estimated 1,505 deaths associated with low-risk drinking (mostly from cancer).

Multifaceted role of nitric oxide in an in vitro mouse neuronal injury model: transcriptomic profiling defines the temporal recruitment of death signalling cascades

Nitric oxide is implicated in the pathogenesis of various neuropathologies characterized by oxidative stress. Although nitric oxide has been reported to be involved in the exacerbation of oxidative stress observed in several neuropathologies, existent data fail to provide a holistic description of how nitrergic pathobiology elicits neuronal injury. Here we provide a comprehensive description of mechanisms contributing to nitric oxide induced neuronal injury by global transcriptomic profiling. Microarray analyses were undertaken on RNA from murine primary cortical neurons treated with the nitric oxide generator DETA-NONOate (NOC-18, 0.5 mM) for 8–24 hrs. Biological pathway analysis focused upon 3672 gene probes which demonstrated at least a ±1.5-fold expression in a minimum of one out of three time-points and passed statistical analysis (one-way anova, P < 0.05). Numerous enriched processes potentially determining nitric oxide mediated neuronal injury were identified from the transcriptomic profile: cell death, developmental growth and survival, cell cycle, calcium ion homeostasis, endoplasmic reticulum stress, oxidative stress, mitochondrial homeostasis, ubiquitin-mediated proteolysis, and GSH and nitric oxide metabolism. Our detailed time-course study of nitric oxide induced neuronal injury allowed us to provide the first time a holistic description of the temporal sequence of cellular events contributing to nitrergic injury. These data form a foundation for the development of screening platforms and define targets for intervention in nitric oxide neuropathologies where nitric oxide mediated injury is causative.

Aging and its effects on inflammation in skeletal muscle at rest and following exercise-induced muscle injury

The world's elderly population is expanding rapidly, and we are now faced with the significant challenge of maintaining or improving physical activity, independence, and quality of life in the elderly. Counteracting the progressive loss of muscle mass that occurs in the elderly, known as sarcopenia, represents a major hurdle in achieving these goals. Indirect evidence for a role of inflammation in sarcopenia is that markers of systemic inflammation correlate with the loss of muscle mass and strength in the elderly. More direct evidence is that compared with skeletal muscle of young people, the number of macrophages is lower, the gene expression of several cytokines is higher, and stress signaling proteins are activated in skeletal muscle of elderly people at rest. Sarcopenia may also result from inadequate repair and chronic maladaptation following muscle injury in the elderly. Macrophage infiltration and the gene expression of certain cytokines are reduced in skeletal muscle of elderly people compared with young people following exercise-induced muscle injury. Further research is required to identify the cause(s) of inflammation in skeletal muscle of elderly people. Additional work is also needed to expand our understanding of the cells, proteins, and transcription factors that regulate inflammation in the skeletal muscle of elderly people at rest and after exercise. This knowledge is critical for devising strategies to restrict sarcopenia, and improve the health of today's elderly population.

The role of organisational climate factors in facilitating workplace innovation

A firm’s ability to be adaptable, entrepreneurial and innovative may assist them to maintain, or achieve competitive advantage. We investigated the relationship between organisational climate and innovation in a consulting firm. Analyses of the 98 returned surveys showed significant relationships between organisational climate subscales of autonomy, worker cohesion and innovation with workplace innovation. Co-worker cohesion and pressure (negatively) predicted organisational innovation. Autonomy, innovation, cohesion and recognition predicted innovation climate. Autonomy and innovation predicted individual innovation while cohesion predicted team innovation. The results of the linear regressions revealed that organisational innovation, was the most significant model emerging, accounting for 40% of the variance. The study concluded that organisational strategies encouraging autonomy and co-worker cohesion were conducive to workplace innovation.

Return to pre-injury health status and function 12 months after hospitalisation for sport and active recreation related orthopaedic injury

Background Hospitalised sport and active recreation injuries can have serious long-term consequences. Despite this, few studies have examined the long-term outcomes of these injuries. The purpose of this study was to establish whether patients hospitalised with orthopaedic sport and active recreation injuries, have returned to their pre-injury levels of health status and function, 12 months post injury and identify factors associated with poor outcomes. The present work was a cohort study with retrospective assessment of pre-injury status and prospective assessment of outcome at 12 months post injury.

Methods Adults with orthopaedic sport and active recreation injuries, captured by the Victorian Orthopaedic Trauma Outcomes Registry were recruited to the study. Pre-injury and 12-month outcomes were assessed using the 36-item Short Form Health Survey (SF-36) and the extended Glasgow Outcome Scale. Differences in pre-injury and post-injury SF-36 scores were examined and demographic, injury, hospital and physical activity variables were assessed for associations with outcome using multivariate linear regression.

Results Of the 324 participants 98% were followed-up at 12 months post injury. At 12 months, participants reported a mean 7.0-point reduction in physical health (95% CI 5.8 to 7.8) and a 2.5-point reduction in mental health (95% CI 1.2 to 3.0), with 58% (95% CI 52.6% to 63.4%) reporting reduced function. Sporting group (p=0.001), Injury Severity Score >15 (p=0.007) and high pre-injury vigorous activity levels (p=0.04), were related to poorer physical health outcomes.

Conclusions At 12 months post injury, most participants reported large reductions in physical health and reduced function. This information is important for furthering our understanding of the burden of sport and active recreation injury and setting priorities for treatment and rehabilitation.

Physical activity promotion for male factory workers : a realistic option?

Issue addressed: Worksites are a promising setting for health promotion initiatives. While there is an accumulated body of evidence indicating favourable health and cost outcomes, there have been difficulties identified in recruiting and influencing blue- collar workers. This descriptive study aimed to identify specific opportunities and barriers which may impact upon physical activity options at work for male blue-collar factory workers.

Methods: Fifteen manager interviews and worksite observations, and eight employee group discussions were conducted in manufacturing industry worksites.

Results: Several key barriers emerged which limit opportunities for blue-collar employees to participate in physical activity at work: time constraints; limited facilities; and lack of interest from management to facilitate physical activity due to limited resources and concerns about safety issues. Potential opportunities included the presence of change rooms, showers, outdoor areas suitable for physical activity, nearby parks and local fitness facilities, and occupational health and safety committees.

Conclusions: Increasing opportunities for workers to be active at work did not emerge as a priority of managers who may need to be convinced that allocating time and resources to physical activity is a wise investment and that workers need an environment that both supports and encourages participation in physical activity. The role of physical activity in relation to injury prevention and potential reductions in Workcover premiums is worthy of further investigation.

So what? While worksite physical activity promotion is a national health objective, there are numerous actual and perceived barriers to initiatives directed at factory workers. Rather than offering specific programs, it may be more productive to address work practices and environmental and regulatory barriers through established occupational health and safety channels. Information and education strategies to change the attitudes and beliefs of management and workers about these issues, as well as about the health benefits of physical activity, may also be helpful.

Auranofin increases apoptosis and ischaemia-reperfusion injury in the rat isolated heart

1. Auranofin, an antirheumatic gold compound, is an inhibitor of selenocysteine enzymes, such as thioredoxin reductase and glutathione peroxidase. These enzymes play an important role in protecting cardiac tissue from oxidative stress generated during ischaemia–reperfusion.

2. Auranofin (100 mg/kg) was administered to rats and their hearts were subjected to an in vitro model of ischaemia–reperfusion. The activity of thioredoxin reductase and glutathione peroxidase was determined in liver and heart tissues in an attempt to correlate enzymatic activity with heart recovery after ischaemia–reperfusion.

3. There was significantly less thioredoxin reductase activity in rat liver extracts, whereas the level of glutathione activity remained unchanged, demonstrating that the dose of auranofin used was able to selectively inhibit one of these enzyme systems. Rats administered auranofin displayed significantly impaired recovery from ischaemic insult. The end diastolic pressure was increased, whereas the rate pressure product was significantly decreased.

4. The level of postischaemic apoptosis was also assessed by examining caspase-3 activity in tissue homogenates. Auranofin significantly increased the degree of postischaemic apoptosis, leading to poor postischaemic recovery.